 on the anatomy of the trabecular mesh work. And so, vice, since you're in the hot seat, you know, this is a little piece of trabecular mesh work. How do we divide the trabecular mesh work anatomically? We divide by whether it's pigmented or not pigmented. Okay, even more specific. Say you're looking at the trabecular mesh work in a goniomere. What's the first thing that you see? Enter. Schwabbi's line? Schwabbi's line, what exactly is Schwabbi's line? It's the termination of decimation of membrane. Okay, so it's what decimation membrane is. So when you're looking in a goniomere, looking at the angle, you really want to know your structures because that's how you can decide is the angle open, is it narrow, is it recessed, are there synechia, what's going on in the angle? So the first part is, we'll show you another view, but there is the end of the termination of decimation membrane is called Schwabbi's line. I'm not going to make you do all these. We're just going to go down. What's the next one that you see after you see Schwabbi's line? It's the non-pigmented termination. All right, so you kind of see the non-pigmented trabecular mesh work as an axotina. Then the pigmented trabecular mesh work. Okay, welcome back. What do you see next? Scleral spur, exactly. So the scleral spur, you would see right here. Now, there's other ways of dividing the trabecular mesh work. Aside from anatomically, when you're looking at it, they've kind of divided it anatomically into zones. Can you tell me a little bit about those, Becca? Sorry, I'm not remembering the zones. Well, the zones, there's what we call a corneus sclera, there's a uveol, and there's a thurbulin area. Anybody? JCT. Just a canolecular, exactly. So when you're looking at it, you can not only divide them as looking in as here, you know, here, here, you can kind of put a line down here and divide it into the part internally, the part externally, and then the most important is the juxtacanolecular. Well, since we're talking about juxtacanolecular, Katherine, can you whisper to me what the juxtacanolecular tissue is next to? She said a vein. Or something in her home. Yeah, the aqueous vein, I said. I don't know, before that, right here. Oh, a Schlemzkanal. Schlemzkanal. All right, so Schlemzkanal. So let's look at a close-up right here. So it's important that you understand a little bit about the anatomy of the trabecular merciless. So it's made up of these bars of collagenous tissue, and they actually have some endothelial cells around them, so there is endothelial cells around them. Now this is not just a wide-open meshwork. It's not like a drain that water goes through. In the juxtacanolecular area here, there is actually not only some passive, pressure-dependent transport, but there's actually some active transport going on. So this is where the money is. This is where we think that the issues in open-angle glaucoma occurs right here in this juxtacanolecular area. And so that's the most important part we want to look at. Now we did have what Katherine mentioned one other thing. Here's Schlemzkanal, and here is an aqueous vein. So let's go back to Feisch. Let's track aqueous. Where is aqueous made? In the siler body of epithelium. More specific. Exactly, so the non-pigment epithelium of the siler bodies, what's producing aqueous? Where does it go from there, Chris? So it flows forward around the pupil in the anterior chamber. And then Tina, all right. And then where does it go from there? Then into aqueous veins. And so, exactly. So it's made in the non-pigmented part of the siler epithelium, circulates through the pupil, provides nourishment to the anterior chamber of the eye, and then eventually percolates through the meshwork, through the juxtacanolecular tissue into Schlemzkanal, and then eventually into the aqueous veins. So when you look at the trabecular meshwork here, we talked about the non-pigment of the pigment of the scleral spur. We talked about that. What is the scleral spur? You get a reprieve, because you can't. I don't read sign language. Well, I guess it's just an extension of connective tissue that the trabecular meshwork sits on. Yeah, and if you wanna think about this in three dimensions, it's almost like a little lip or a little shelf. And so the trabecular meshwork is triangular shaped. You know, the apex up near Schlemzkanal in the base, and then you've got this little spur of scleral sticking out, and it gives you a little shelf. So if you think of it in three dimensions, it kind of supports the trabecular meshwork. And then of course Schlemzkanal, when you look at it, it's not a round structure. It's more oval. It looks like a bicycle inner tube. And again, it goes 360 degrees all the way around. Now there's one other important structure that attaches to the scleral spur from the ciliary body. What is that? Attaches to the scleral spur. The iris root would be kind of behind the scleral spur. Okay, the longitudinal ciliary muscle attaches to the scleral spur. Why is that important? When you stimulate the ciliary muscle, it literally pulls on the scleral spur and actually pulls it to make the meshwork open. The very first glaucoma drop that we had available more than a hundred years ago was pylocarpe. And no, I wasn't here a hundred years ago using it. They seem that way, but no. So pylocarpe was the first drop that we used. And pylocarpe, and you'd give it to somebody, it would constrict the pupil, but it would also stimulate the ciliary body. And as a result, it would pull on the scleral spur the trabecular meshwork, you'd get increased drainage. So that was the first glaucoma drop that we had. Now there's problems with that drop. You use it four times a day. It makes your pupil small and it gives you a chronic headache. So you can imagine the compliance was excellent with that, I'm sure. So people weren't going to use it, but it was the first one that we had available. Here's the close-up of Schlem's Canal and the jyxtacanalicular tissue. Now what we're trying to show here is, here's Schlem's Canal, right there. And then here's an aqueous vein that then drains out onto the surface in the little episcleral area right there. So your assignment is when you're in the clinic today, when you're doing a slit lamp, I want you to take an extra 10 seconds and I want you to look just at the limbus with your slit lamp and then go about a millimeter from the limbus and focus down on those vessels. And you can see the aqueous veins because there's not only blood in there, but there's aqueous fluid in there, which is clear. So you get what's called boxcarrying and you'll actually see little RBCs, but then you'll see clear fluid in between them. And if you really look closely with your slit lamp, nobody pays attention to these at all, you can actually see them. And so that's your mission today, it's find these aqueous veins and they're really there. They really exist just nobody ever looks at them. So when you get increased pressure, not only can you get increased pressure from open-angle glaucoma, closed-angle glaucoma, other mechanisms, you can even get it from increased episcleral pressure. And so for example, you have an AV malformation or you have some kind of increased pressure the backup of that pressure can actually cause backup into the aqueous veins and increased pressure. So this just to remind me of talking a little bit about open-angle glaucoma, if you take a trabecular meshwork and you look at it with light microscopy and a 70-year-old with open-angle glaucoma and a 70-year-old who doesn't have open-angle glaucoma, they both look the same. And so that's the problem. Now, there's aging changes in trabecular meshwork, but on light microscopy, you really don't find changes glaucoma compared to non-glaucoma. Now, in electron microscopy, you can find changes in the actual bars and the cells around it, but on light microscopy, open-angle glaucoma looks just like a normal angle, so you really don't see much. All right, now we want to start talking a little bit about some of the variations of glaucoma. So again, when we talk about glaucoma, you want to look at open-angle, closed-angle angle recession, but when you're looking at open-angle, you want to look at primary open-angle glaucoma, which is what we just showed you, but you also want to look at secondary causes of open-angle glaucoma. All right, so what's the secondary cause pictured here? So here we see an external photo and we see these kind of radial translimination defects. So, you know, this would make me think about, like, victim dispersion, given what we're seeing here. Exactly. Look at those little radial-shaped, slit-like translimination defects in the iris. And so that tells you that something is disturbing the pigment epithelium on the posterior surface of the iris. And when that disturbs that, where does that pigment go? That pigment floats up and can cause secondary open-angle glaucoma. So here is a little piece of an autopsy eye. And this is looking from behind. Here's the iris. Here's the ciliary body. Why do you think there are those little radial areas of pigment dispersion? What causes that? So it's caused by, oh, the zonules. Exactly. So those zonular bundles that run from the ciliary body to the lens itself, if you have a posterior bowing of the iris, you can get scraping of that posterior iris pigment epithelium on these zonular bundles. And that's exactly what we think causes this. And so if you look at people with pigment dispersion glaucoma, they tend to be younger male myops, not huge myops, just mildly myopic. And if you do an OCT of the anterior segment, you'll actually see a subtle posterior bowing of the iris, which then allows it to scrape on those little zonular bundles. What are we showing here, Tina? Not only do you see pigment in the mesh work, but where else do you see pigment here? Look right here. There's pigment on the surface of the cornea. So if we look with the slit lamp in a patient with pigment dispersion, what do we see? So what happens is it kind of flows along with aqueous patterns. And so aqueous patterns will allow that pigment to deposit kind of in the center lower third of the cornea. It's almost like an upside down triangle. And so they call it Krukenberg spindle. Then you put a Goniomere on there and you'll see pigment in the angle, but also right here. Look, here's normal iris pigment epithelium. And right here, there's where it's been scraped off. So secondary open-angle glaucoma due to pigment dispersion syndrome. What do we see? What do we see in right here? Reach back from your vacation. So if you look, here's the cornea and here's the iris. This is kind of part of the cylinder body here. There's something right here and it's taking up that whole area, the angle of the entire ciliary body. And it's dark. Our metastatic tumors usually this heavily pigmented. So what would the most common cause of this be? Melanoma, exactly. So remember, you can get, you know, UVO melanoma is growing not only in the coroid, but also in the ciliary body. And if you get a ciliary body melanoma that grows forward, it can actually grow into the area that you're making or mesh work. It can cause separation of the iris here, pushing it backwards. And so you can get a secondary open-angle glaucoma from a ciliary body tumor, most commonly amylignant melanoma of the ciliary body. And that's what you're seeing here. And then when you look at a close-up here, here's cornea, here's iris root. Look at the increased space there. So this tumor is growing from ciliary body behind into the iris root and into the chiropractor mesh work. So secondary open-angle glaucoma due to malignant melanoma. Becca, what are we looking at here? Pseudo-exfoliation. Okay, so when you look at pseudo-exfoliation or exfoliation syndrome, I guess we call it now, you see this material deposited on the lens cap. So then there's this clear space and that's because the pupil acts like a windshield liper. So as your pupil goes, you know, constrict, dilate, constrict, dilate, you push that exfoliative material. So you'll see a little bit in the center and then you'll see more in the periphery. So this is classic for exfoliation syndrome, what we used to call pseudo-exfoliation. And here you can see the classic, we call this the scalloped border look. And that's what it looks like. And again, on retro-limitation, we showed these when we talked about lens a couple of weeks ago. So what this material does is as you stay in the lens capsule, you can see it kind of stands up on there. They call this iron filing. Again, as you ever take like a magnet some of those shavings of iron and they stand right up on it. That's what this looks like. But this material, we used to even call it pseudo-exfoliation of a lens capsule. It's not of the capsule itself that just where it's deposited. All of the cells in the eye make this material. Now this material is everywhere. It's not just on the lens capsule. It clogs up the mesh work. It gets into the endothelial cells so that you don't, you know, you don't have a normal endothelium so that they're more susceptible for, you know, corneal edema afterward. This stuff even gets into the iris, sphincter, and dilator muscle. And so this is like a quadruple whammy when you're doing cataract surgery. First of all, this material deposits not only on the lens capsule, but on the zonules in three places. It's where the zonules insert to the capsule. It's on the zonules themselves and it's where they insert to the ciliary body. So it makes them weaker, makes the capsule more brittle. It makes the pupil so it doesn't dilate as well. It makes you more susceptible to glaucoma afterwards and it affects the endothelium. So exfoliation syndrome can make your cataract surgery quite tricky and quite challenging. So here we have, this is our trabecular mesh work. And right in here, all of this exfoliative material just clogs up the mesh work. So the one advantage, well, two advantages of doing cataract surgery. First of all, when you take out the cataract, especially the anterior capsule, a lot of that exfoliative material leaves with it. And so when you're taking out the cataract, you get rid of a lot of that exfoliative material. But when you remove the crystalline lens, which is big, you put in a thinner implant in there that angle actually opens. And so you can get a pressure drop of up to five points in a patient with exfoliation just doing cataract surgery. Even in a normal open-angle glaucoma, you do cataract surgery, you can get a three-point drop. So I mean, you can literally treat glaucoma by taking out the crystalline lens, but especially in exfoliation syndrome. All right, so again, you get a reprieve because you can't talk. What do we see in here? So this external photograph of the left eye showing markedly injected conjunctiva as well as some corneal edema. That's a little hard to say, or if that's just a really hyper-mature cataract. All right, so let's say it's a hyper-mature cataract. He comes in with acute pain. What's his pressure gonna be? Super high, 40, 50. 60, yeah. Now, so what is this condition? Is this, yeah. Bacolytic glaucoma. Bacolytic glaucoma. So this is a setting of a hyper-mature lens. You actually get leakage of protein through the intact lens capsule. And then that protein itself can actually gum up the trabecular mesh work. But also, what kind of cells are these? Macrophages. Exactly, so macrophages, if you're British, macrophages, they come in and they'll actually gobble up this protein. And so you get these macrophages actually plugging up the mesh work in addition to the protein. So again, the treatment of this is removal of the lens and then flush it out, flush it out. If the corneal edema is not too bad and you can still see in the anterior chamber, these macrophages are huge because they engorge themselves with all of this protein that's leaked out. And so they're not just a little sparkle juicy, you know, when you're looking at cells after cataract surgery, these are big juicy cells when you look at them. So facolytic glaucoma again can cause a secondary open-angle glaucoma. And this is just an aspirate. I don't know, this is a picture I copied from somebody. Nobody goes in and aspirates to see what this is, but this is an aspirate showing you macrophages again. All right, so we've talked about open-angle glaucoma, you know, primary, secondary. You know, we can get closed-angle glaucoma where the angle is blocked off and we can also get angle recession where the angle actually tears loose. So let's look at right here. What are we looking at right here? This is the right eye's injected, mid-dialated state. What would you be concerned about? Angle closure. Okay, so this is a patient that we saw in console. This was a few years ago. They had abdominal surgery. You know, for abdominal surgery, they get atropine and they get some other things. And so he was complaining about a red eye. So of course they gave him, you know, neosporin. Okay, they were giving me a spore for two days. And then he was vomiting. And they said, okay, well, it's from surgery. We'll give you, you know, some questions. Finally, about the third day when the guy had this relentless pain around his eye, it was red, they called a consult. And, you know, when you look with the slit lamp, what are we seeing here? It's an approach. Exactly. So you see the iris bowing forward. They call that iris bombe. So from the, not from the Greek, from the, from the French actually. So bombe, an E with an accent de gout, you know, the little thing sticking up over it. So bombe. And so what happens in, in these cases is you can get a primary open-angle glaucoma can occur when you have a relative pupillary block. And so the aqueous can't come through that pupil that relatively blocks off. And then it builds up behind the iris, bowing it forward, which then blocks off the angle. Now, what, why does that happen when you dilate a patient? It's not when you dilate them the widest. It's when the dilation is just beginning to wear off. And it's about halfway down and you get that maximum opposition of the iris to the crystalline lens. And then you'll get pupil block. Now, this doesn't happen in a deep angle. This is in people who have either a narrow angle from hyperopia or really swollen lens or whatever. So you can get, you know, narrow-angle glaucoma from this. So what's the treatment? Exactly. So you want to get the pressure down first because this can cause corneal edema. You want to see what you're doing. Then you can do a laser perfilaridectomy. Give the aqueous another avenue to flow through the erudectomy and then into the anterior chamber. And that will relieve the block. Vice, what are you seeing here? Another entity that can be associated with closed angle. So we see that the angle, yeah. Exactly. So here's the trabecular meshwork back here and here's this kind of scarred angle right here. And so synechia is, you know, sticking together of two things. And so this is called a peripheral anterior, meaning anterior to the isopriflantir synechia, PAS. So this can be caused by chronic angle closure. You can do this. You can get synechia. But chronic uveitis, chronic inflammation, anything that can stir things up can give you this synechia here, which will give you a secondary angle closure. And here you can see, again, here's the trabecular meshwork. Here's the iris. And then you see the iris is just totally stuck to the peripheral cornea. Closing off that angle, secondary angle closure. So, Chris, here we're looking at an iris here that's kind of closing off an angle secondarily. What's going on here? There's a lot of red here. So this makes me think about some blood vessels forming here. Exactly. There's a lot of blood in here, but if you look, look at all these little blood vessels on the anterior surface of the iris. Should you have a network of little blood vessels on the anterior surface of the iris? Not normally. Yeah, not normally. So this is another cause of secondary angle closure glaucoma. This is neovascular glaucoma. So these abnormal blood vessels grow on the surface of the iris, grow into the trabecular meshwork, and then close it off. So what's the most common causes of iris neovascularization? So you see it in poorly controlled diabetes. We could see it in van inclusions, like a CRVO could do it. I've seen it in like ocular ischemic syndrome. Sure. Anything that causes long-term ischemia. So the key word is ischemia. And so when you get ischemia, either from severe diabetes, central retinal vein occlusion, ocular ischemic syndrome, you can get abnormal blood vessels growing onto the iris. And here's the iris. Sure enough, there's those blood vessels on the surface of the trawler's condition. Rubiosis, literally red-like. Rubiosis here. So you can actually see the fine vessels on the surface of the iris. And that can give you a secondary angle closure glaucoma. All right, Tina. What are we looking at here? This is Jurassic Park. There's the dinosaur. So what do we, what's happening here? So what do we call it when the iris is stuck to the lens of the pupil? What kind of synechia? Hostereous. Hostereous synechia. So we call this PS, or posterior synechia. So you can get synechia where the iris sticks to the lens posteriorly. Again, this can be chronic inflammation, it can be uveitis, whatever causes this. So you actually get iris stuck to the lens capsule. And you can get what we call an occluded pupil where you can get, it blocks it off and it can seal it up 360 degrees or you can get an actual membrane of inflammatory tissue going across the pupillary space, closing it off, we call it a succluded pupil. And so either way, you stick that iris down to the capsule and you don't allow aqueous to flow through so you can get, again, an angle closure glaucoma with that pressure building up behind it due to posterior synechia and due to iris pupillary occlusion or pupillary succlusion. All right, what do we see in right here, Rach? See a nice aqueous vein. Yeah, there's the mesh work there and the iris is clear back here. What do you think could cause that? So this is angle recession. This is the opposite. So the angle's recessed and people will talk about tearing of the iris and angle recession. What's interesting is the blunt trauma that causes this, you don't usually get the iris to tear loose from its root, but you actually get a tear here almost into the face of the ciliary body. And so you can go ahead and you'll get this angle recession and the most common cause is trauma. And so as we say when they come into the ER most common cause is two dudes, you know? Man, I was just sitting there minding my own business and these two dudes just jumped me for no reason. It's never one dude, it's always two dudes and they were always minding their business. I was just sitting there and they just jumped me, you know? Yeah, okay, sure, you know? So most common cause here is two dudes, you know? Or you can have any blunt trauma, getting hit by a ball, getting hit by, you know, in the car by an airbag. Now, what often do you see associated with this when you're looking at someone who's had trauma to the eye? Immediate, when you see them first in the ER you may not even know they have an angle recession because you can't see the angle. Why's that? Because they have a hyphaema, exactly. So, you know, if you get a bad enough trauma to tear the angle, it's a hyphaema. So you really gotta watch these people carefully because sometimes you can't see the angle recession because they'll have a hyphaema. So you'll watch them carefully till the hyphaema clears. Then once the hyphaema clears, it hasn't re-blad, you let them calm down for a month or so, then you wanna look with your goneo because you don't wanna miss this. Becca, what's the most common timeframe for angle recession glaucoma to occur after the initial injury? No, in fact, the opposite of that, seven to 10 years. So the hard thing is who usually gets angle recession? Young dudes. And so you've gotta strike the fear of God in them that they have to come back every year for follow-up because their eye will start to feel fine, they don't perceive a problem, so they'll just never occur. I've seen a couple now in my career, guys who are 40 who documented trauma when they're in their 20s just never bothered to come back till their vision went blurry. And so by the time we see them, they have a pressure of 45 and they have a visual field that's a temporal island, this big and a totally cupped-out nerve. So you gotta strike the fear of God in these guys that they're at risk for developing glaucoma seven to 10 years later. Exactly, you just get changes in the trabecular mesh work that takes a while because the initial rip occurs posterior to the mesh work, it doesn't necessarily damage the mesh work immediately once the hyphema clears. So you get a secondary angle recession, and this is just kind of a picture showing you how to compare. Here's your normal angle, here's your Irish root ciliary body, here's angle recession, here's your trabecular mesh work, here's where the Irish root should be and look at this tear into the face of the ciliary body. And so that's traumatic angle recession. And this is an angle after years later and you almost get a sclerotic look to it, it almost sclerosis off. And so you wanna warn these dudes that they wanna come back for seven to 10 years and here's a patient, this was interesting, we kind of put these two together. Here is a recessed angle. Now he also ruptured his lens and so there's a little summering dream here, but here is a totally 0.99 cupped optic disc from end stage angle recession. All right, so when we're talking about glaucoma, obviously the pressure is gonna cause an effect. Where? Where do we worry about? So in the optic nerve, ultimately, so this is a color fondness photo of the right eye and it shows some pretty significant cupping, maybe a cupped disc of like 0.8 and there's also some significant cupping. So if you looked at this in three dimensions, that would be bowing away from you. And so this is kind of the opposite of papalodema where the swelling is coming towards you, this is actually cupping that's going away from you. And the glaucoma guys will talk to you about the theories of why this is happening is that ischemia is a disruption of axoplasmic flow. Bottom line is whatever the pressure does to that area, it eventually affects the axons going into the nerve, those axons die off and you get less and less and less fibers in there. You get posterior bowing of the lamina crebrosa and you get an increased cupping. So that's what it looks like pathologically. And here's one that's, you know, again it's a little bit more symmetric, but it's a point, this is a good 0.8 cupping. And of course this is what you wanna avoid. This is a complete cupped out. I mean this is an autopsy eye, but this is a completely cupped out optic nerve. So you want to do everything you can to avoid that. So you wanna make sure that you treat the eye pressure, you treat whatever the cause is before it gets to that point. So again, here's our traumatic eye. This patient actually had a sharp trauma. And so that's actually called a glaucoma, a little white band adhering to the cornea, summer injury and cataract. And again, we come back here and look at that cupping. Totally 100% cupping of the optic nerve. And sometimes you can even get almost like a beanpot appearance to this. And so the atrophy gets so much that when you look at them coming in here, you can actually even see a little bit of excavation there. So when you're looking at this, you know, with your 90 diopter lens, that blood vessel will go around the edge and just disappear. So you don't even see it. And so you see this little beanpot here. And so this is the temporal edge, nasal edge, and you get that beanpot underneath. So again, posterior boeing of the lamina crebrosa totally cupped out optic nerve. So we want to do everything we can to prevent that from happening. Here's another look with that excavation. So you can see it almost like, you know, you're going around the corner of the cliff there and coming around. So totally excavated optic. All right, now there are a couple of weird conditions that I have to show you because they're going to show up on boards. And so I'll give you a bonus, but just what tissue are we looking at right here? Yeah, even posterior to it. We've been looking at the optic nerve here. So there's something funny going on with the optic nerve. This is normal out here. Splotches of white. It's kind of, yeah, splotches of white right here. And this is where you've actually got almost some hyaluronic acids and vitreous stuff being pushed into the optic nerve. So again, they'll show this every once in a while. This is called Schnabel's cavernous optic atrophy. The reason that it's important is this is going to occur in a acute attack of glaucoma. So let's say you've got someone who's got an acute angle closure. It's not recognized. Pissure is really high for a couple of days. You can literally get this vitreous-like stuff driven into focal areas of the optic nerve. So they call it Schnabel's. Sounds kind of cool, Schnabel's atrophy. Sounds like something you'd do for New Year's. Oh, man, we're going to do some Schnabel shots, you know? So Schnabel's cavernous optic atrophy. And there you see, this is actually a stain for mucin, you know, a stain, I'm sorry, a stain for hyaluronic acid. And so you can actually see this focal staining in there. But you laugh, but it shows up on boards about every third year. Now, there's another weird thing that an acute attack of glaucoma would do. Boy, Weiss, this is obscure also. What, first of all, what are we looking at right here? So we're looking at the anterior lens capsule, as well as just the anterior part of the lens, and deep in the tissue, there's these focal areas of exfoliant, vaculated spaces. That's a good, these little vaculated spaces right under the anterior lens epithelial cells. And again, this is a sign of acute glaucoma. What do you call those? Glaucoma. Yeah, another cool German word, glaucomflecken, you know, that's just kind of a cool word. So an acute glaucoma, you can also get these little pale dots under the lens caps and eventually they'll fade away. And it's an acute pressure-like ischemia that can occur on the anterior lens epithelial cells. And so they're called glaucomflecken. And that's, again, I like that just because that sounds kind of cool. I think they've been on the exam like the last five years in a row. Yeah, I mean, they always put, because they're obscure. And so, you know, exams don't test your knowledge. Exams are used to separate wheat from the chaff and so you have to, you know, memorize these obscure minutiae in order to be really wheat rather than common chaff. All right, Chris, what are we looking at here? It looks like retina to me. Okay. What are we seeing here? Well, that's what we're seeing here. And since we're talking about glaucoma, the ganglion cell layer looks a little patchy and thin to me. So next week, you guys are gonna know these layers cold when we talk about retina. But as you look right here, here's retina. You see that the outer, you know, two thirds of the retina is in pretty good shape. But right here where the ganglion cells should be there gone. And so glaucoma, again, it affects those axons at the optic nerve. Eventually you get retrograde death and the ganglion cells die off. So end stage glaucoma in a retina, you see a lack of ganglion cells, but the rest of the retina is still okay. And here you can see this is just a normal macula up on top. And then on the bottom here, you've got a glaucoma where even the macula eventually gets severely damaged and you get less and less ganglion cells. All right, now, I wanted to show you something because this is something we don't usually see often. You can have glaucoma that is congenital. And I know, I don't know if you guys see a lot impedes of congenital glaucoma or not, but when we used to think about this, people would say, what happens is, is that you get this membrane growing across the mesh working, kids with congenital glaucoma, they even call it a Barcans membrane. And you put these kids to sleep and you look at them with your lens in the operating room and you literally see this little membrane across here. And so the initial treatment for pediatric congenital glaucoma was they'd go in with a knife and they'd just slice it 180 degrees open. You'd see the iris drop back and they thought that would open it up. Well, it turns out that it's not like a true membrane going across there. It's that the mesh work just doesn't form properly. And so you get an appearance like a membrane going across there. And if you put a big goniol knife in there and slice it, it does actually allow the aqueous to flow out there. So it actually didn't improve the pressure. So this is what we see in congenital glaucoma. So it's really a maldeveloped angle. Just don't get a normal development of the angle. And you get this, it almost looks like this fine velvety membrane, Barkhans membrane across the surface. All right, now we've got to talk about some different entities here that can eventually result in glaucoma. And again, these are always on boards. So you need to memorize these. Tina, what is this, what is this you're looking at right here? Mostly polychloria. So you just have multiple kind of... Well, pupils. So this would be one of our ice syndromes and this would be essential iris atropide. What does ice stand for? Yeah, so irrital, corneal, endothelial syndrome, ice syndrome. Now, ice is an interesting entity because it can often be unilateral instead of bilateral, which is weird. And it can show up and when we look at ice, you know, it depends on if you're a lump or a splitter. You know, people who are lumpers put it all under the umbrella of ice, but there's three distinct entities in ice with some overlap between them. So the first one we talk about is this is called the central iris atrophy and you will get multiple pupils, you'll get the iris pulling away and moth eatin'. You get glaucoma with this and this is called the essential iris atrophy component. Now, Rachel, what's a second subset of ice where you get lots of corneal problems? Nope, that's the third one. Okay, so go up in your brain. Go up a level. Chandlers. Chandlers, all right, so Chandlers is the second one and Chandlers you still get some moth eatin' iris here. You get some glaucoma, but you get a lot of corneal edema. So the problem is, people when they were first looking at these many, many years ago, they would each kind of put their name under their description, then eventually someone put them all together and said, hey, wait, this is just variations of the same entity. So Chandlers is ice syndrome with lots of corneal edema, huh? Okay, so she kind of stole your thunder there, Becca. So what is this? It looks like iris nevi that you see in. Iris nevis or cogan reese is what people call this. So the third entity, you can get this little velvety, almost membrane on the surface of the iris and these little knuckles of neva cells popping up. And so that's the third entity of the ice syndrome. And now, what is the unifying theme here, Mike? What do all of these have in common? So they have, like the name suggests, they have like a layer of abnormal endothelial cells that roll over the angle onto the iris. Exactly. So people call this desmetization and remember the endothelial cells are based on membrane is decimates membrane. And so for some reason, this entity will affect the endothelial cells. They will grow onto the surface of the iris and they'll even start laying down decimates membrane. And then when they do that, you'll get the iris kind of being moth eaten and pulled over and big holes forming in it. You can also get little nevi popping up through this membrane. And then of course, if the endothelial cells are affected, then you'll get the corneal edema. But the kind of unifying field theory here is always that there's this endothelial proliferation and there's decimates membrane covering the tissues. So that's what unifies all three of these. And here you have a close-up. That's all decimates membrane. Look at that. It's like quadruple thickness. And then it comes around and here's the surface of the iris. Again, there's decimates membrane on the iris. And so that's all the unifying thing that denotes ice syndrome. And here's a peripheral air deck to me. This is one many years ago. We took this cool picture and this was actually the cover of the archives. This was my only archives cover. Well, what's it called now? Excuse me, JAMA ophthalmology, sorry, the archives. And so this was a peripheral air deck to me from an iris nevus, Cogan re-syndrome. And when we did the PIS stain on here, you'll see it had this decimates membrane along the surface with PIS stain. But it also had these little iris nevi popping through. So they almost look like little volcanoes popping through. They're little mushrooms. And so you've got decimates membrane on the surface of the iris and you've got these little nevi popping through. So that's the velvety membrane with the nevi popping up. So Cogan re-syr iris nevus syndrome. And there's a nice close-up. Okay, now there's another entity that you have to memorize. There's always, you know, on boards and it has multiple parts to it. So, Baish, what are we showing here? So we're looking at the posterior surface of the cornea and the decimates membrane has a kind of big fold in it. Okay, so it's kind of thickened or folded. What do we call that? It's part of the anterior cleavage syndrome. Exactly. So there's another entity you have to remember. It's called anterior chamber cleavage syndrome and there's multiple parts. So the first thing you see is this entity. What is this? Exactly. So it's called posterior embryotoxin. And the reason is people had theorized that this is some kind of toxic insult going on to the embryo when it's forming. And so this is actually Schwab's line. This is where the decimates membrane ends, but it's more toward the center, not near the angle. So it's a little bit more toward the center and it's thickened. And so when you look at these anterior chamber cleavage syndrome, the first thing you see in all of these is a thickened little anterior displaced Schwab's line or, you know, where decimates membrane ends. They call posterior embryotoxin. Now this entity was called anterior chamber cleavage syndrome because it was thought that there would be this cleaving going on during embryology and that that cleaving was disrupted. Well, now that we've learned that, you know, the anterior chamber angle and the tissues there form successive waves of what embryologic layer that forms this, Chris? Neurocrest, so not mesoderm, neocrest. And so we know it's not really a cleavage, but that's pretty much in the literature. The best description is George Waring, sadly passed away a couple of years ago, described this, called it the stepladder classification. So if you go back even to the mid-70s, George Waring's original paper with the stepladder classification is still the best way to memorize this. And so the first thing you see is posterior embryotoxin and there you can see a close up. Now, we're looking at an angle here, Tina, posterior embryotoxin, what else is going on? It kind of looks recessed because there's kind of, the angles clear the heck back here and there's some stuff coming down from that posterior embryotoxin to the iris. So what do we call this entity? The next one in the stepladder. Regers. Yeah, both. Now they've kind of lumped them together, accent-filled regers. So again, if you're on oral boards, do not let your voice tail off. They think you're guessing. And so you say it with conviction. Axebells, even if you're wrong, you'll get credit for it. So, but if you get it right and you let your voice go up, then they'll think you're guessing. You won't get credit. So, with authority. So accent-filled regers are you. You've got posterior embryotoxin, but you've also got little bands of connective tissue coming down onto the iris. You can even get some areas of iris atrophy and you can get what's called accent-filled regers anomaly. And these kids can actually even have systemic things. They can have funny teeth, funny bones. There's a lot of systemic components to this. All right, so Rachel, we're kind of going down the stepladder. What the heck are we seeing here? So it's up against the cornea then. Look at the cornea in the center. It's totally white and opaque. So going down the stepladder, accent-filled regers, what's next? Peter's anomaly. So Peter's anomaly, you still have posterior embryotoxin. You've still got the strands, but in Peter's anomaly, you get this weird problem where you get this central loss of the posterior cornea. So they call this the ulcer of von Hippel. It's a central posterior cornea loss where decimates and endothelium just don't form well and they're gone. And so you get a focal corneal edema here. This is Peter's anomaly. And if you look at, here's the iris, here's the strands sticking up. You look at the central cornea, right in here decimates and endothelium are just gone. And so you get significant corneal edema. It's called Peter's anomaly. And here's another close-up right here or look at the cornea here. And right here in the center, decimates and endothelium are just gone. And so that's what we call Peter's anomaly. It's again kind of the lowest thing down in the stepladder classification of the anterior chamber cleavages. So again, something you have to memorize because it's rare, it's obscure. So they love it on boards. And so, you wanna know the ice syndromes, you wanna know your anterior chamber cleavage syndromes. And I like to really kind of subdivide it. My brain works by putting little cuppy holds like where you get your mail, putting the letters in there and that's how I can remember them. But you guys, however you wanna memorize them, you need to know these for boards because they're always, always on there. Okay, enough. So next week, we are going to talk about retina. Now retina has what specific feature that I always pound on? Ogres and onions have in common, layers. All right, so you gotta know those layers cold. And we'll spend a lot of time talking about the various layers of the retina. Okay, thanks.