Pigment Dispersion Syndrome

Hello, welcome to the I-3 years. You're off the mulls, you know, Cab's Board of You podcast where you're host Ben Young. And Andrew Powell, just a reminder that these episodes are meant for medical education only, not for diagnosing anything on your own eye. Each week, we take our hiotopic and talk about the wine and the how, and I, this might be more of a personal request, based on the patient's sub. I saw this 40-year-old, 40-something-year-old patient, he was there for retinolotation, repair or follow-up, but it's been a while since his repair and his IOP is 45. So it's been long enough, he's off all drops, I really can't blame it on the surgery anymore. And I was trying to look at his eye, do the, do like the anterior segment thing, and I saw like a lot of brown stuff on his coronal endothelium. It was kind of more like an align, like it wasn't like normal care to precipitates. So the patient wasn't really in pain and he was asking me if he could still play some pickup basketball, which he loved to do after our appointment. So I think the real question of this episode, Andrew, is can the man dunk, or do I tell him to hang up the basketball? I suppose it depends, and you've already pointed out a couple of really good things about his exam, that vertical line of pigment on his coronal endothelium, in particular, does worry me a bit, especially the fact that now he's inocular hypertension, and you mentioned his pressures like jacked up to the 40s. Yeah, not good. So what that pigment line on the coronal reminds me of is a Krukenberg spindle. And thanks for playing along with everybody Ben Young very much knows what Krukenberg spindles are. You don't know that. Physiciously playing along for the point of the case. But a Krukenberg spindle is very suggestive of what we worry about in this syndrome called pigment dispersion syndrome, which can lead to one of the big causes of secondary open angle glaucoma, pigmentary glaucoma. Now, how does a Krukenberg spindle come to be? We can talk about that. But should we also see if he had any other features of pigment dispersion syndrome on exam band? I did not look. What should I have looked for? If you transaluminated the iris, you normally in pigmentary would see a lot of transolubination defects. But those aren't super special in it themselves. Maybe he had previous surgery that went to rye a little bit, and the iris got snicked a little bit. What do you say in the run of fellow dead, huh? What do you say? But yeah, you can have transolubination defects from surgery. You could have it even from things like Harpies or Zoster virus. You could have it from even the pseudo X stuff we talked about. Last episode we talked about pseudo exfoliation, sometimes showing transolubination defects of the pupillary margin. The thing that's really distinct about TIDs in pigmentary is that they are very radial in appearance, and they're usually in the peripheral iris. Now let's just do a quick double check of other TIDs. We talked about if their TIDs are at the pupillary margin, think of pseudo X. If they are sectoral TIDs, only in one area think of Zoster. If they're more like patchy transolubination defects, think of Harpies, and if they are in radial lions all around the iris at the periphery, that's pigmentary, or it makes you think of that more. Two things that just to round out if you see transolubination defects doesn't match any of those. You can always consider trauma, including surgical trauma or ocular alpinism as causing transolubination defects. Those don't usually have a specific pattern like the ones Andrew mentioned. Yeah. Transolubination defects, this pigment on the corneal endothelium. We call that a Krukenberg spindle. If you did gonyoscopy, you might also see a lot of concavity or back bowing of the iris itself, which if you looked at it straight on, as we normally do with a slit lamp, it's hard to tell how that iris is what it's doing in the anterior posterior dimension, but you get a better sense of that on gonyoscopy. It's kind of like dunked into the eye. Right. Cave from your perspective. Now that we sort of got those three kind of basic exam findings, we'll talk about a few more soon. But let's talk about how those all are related to each other because really the trouble in pigmentary glaucoma, pigment dispersion syndrome is that all this pigment is coming from somewhere inappropriately and sort of obstructing, ending up in the eye's natural drainage system and plucking it up more than it should, which causes the high intracurricular pressure. But briefly, let's talk a bit more about that Krukenberg spindle again, Ben. This is something the BCSC cares about. How does a Krukenberg spindle come to be? Like, why does it distribute itself? Why does all that pigment end up being slattered in the distribution it is on the corneal endothelium? If any metastudent who's ever worked with me is listening to this, you will have heard this because it's like my favorite question to ask, my students, which I know is unfair and retrospect, the answer, and this isn't only seen in pigmentary dispersion, but is because there's a convection current inside the eye. So why would there be a convection current? You know, when I asked my students, like, oh, why do you think there's like a line here? Why do you think there, you know, why do you think there's a current side of the eye? I think a lot of people assume, it's because the aqueous humor is being produced and kind of being pushed in front of the eye and then that's moving backwards, I don't know, back into the back of the eye or back into direct domestic work. But you know, that wouldn't cause a convection current, that would cause a Krukenberg spindle. What actually caused the convection current is a temperature differential. So we all know that heat in our bodies are carried through the blood and where is their blood in the anterior chamber, where there's blood in the iris fasculature. So the aqueous humor that's closer to the iris is relatively heated up by that being close to that blood. But in the front of the anterior chamber, the cornea, there are no blood vessels, or at least there shouldn't be. So the cornea is relatively cool compared to the iris. So that means in the anterior chamber, it's warmer in the back of the anterior chamber than in the front of the anterior chamber. So when things fall into the back of the anterior chamber, closer to the iris, they'll rise because it's warmer back there. And then when they get to the top, they'll start moving forward closer to the cornea and there they'll fall. So you'll have this convection current where things rise in the back, fall in the front. And then that's what leads to that position in the inferior cornea, at least to the Krukenberg spindle. Right. Just to clarify, Ben's talking about a current of fluid, really. The aqueous humor itself goes on this roller coaster of up and then down. It just so happens that if there's pigment in that fluid, it's going to go on the same ride. Right. Right. So that explains why the pigment gets where it goes, why it plasteres along this sort of vertical line in the middle of the endothelium. But where does the pigment actually come from? Okay. Okay. Can I just pick one more tidy? Sorry. It's my favorite topic, so it's not just pigment, right, just like as you pointed out. It's a aqueous that rides this current and so it's not just pigment that can ride in the aqueous. It can also be white salt too. So I encourage you, next time you see a post-op, week one or day one cataract surgery patient, look at how the cell is moving. It'll fall to the exact pattern. And it's also why patients who get cure to precipitates end of getting them in the inferior part of the cornea because of the same convection current as things are deposited inferiorly. Okay. Where does the pigment come from, Andrew? Where does it come from? Sure. So you've wonderfully described for us how it kind of follows this fluid path, the convection current. But yeah. Ultimately, it actually comes from, you know, what's the part inside the eye that's got all the pigment to it? The iris. Oh, yeah, yeah. The iris. Right. Right. Okay. Sorry. From the RPE, you've got terrible. The fundamental thing is most of the stuff is coming from the iris. And specifically the back of the iris, the iris pigment epithelium. But that doesn't just spontaneously decide to jump ship and float off into the fluid space. There's a reason that that pigment comes off, right? And that's because it's chafing against something. What's it chafing on, Ben? The zonules, which motivates why it, in the lens, chafing against the zonules motivates why it has those radial lines in the kind of the mid peripheral iris because that's probably where the zonules are, right? Right. Radial, that's why those, so imagine that the iris is rubbing against those zonules and you know where the zonules are. There are 360 degrees around off to the periphery. And that's why those translimination defects look so radial. basically seeing where those are. you'll rubbed off along the iris. Why doesn't this happen to all of us, to everybody, Ben? Because our irises are flatter and more boring. Yeah, this is a big point. If you're with a glaucoma attending one day and they'll ask you, did you see this on Gonioscopy? And then you say, "Oh, I didn't look, no. Just to sketch you." If you Goni, oh, again, we talked about the concavity of the iris, you might see that. That's the reason. Their iris is just backbode so much that it is actually rubbing along those zonules and anterior lands. Gotcha. So what would you see? What else would you see in Goni, besides his backbowing? You'd see a ton of pigment deposition. So, you know, the grading scale of Gonioscopy, things you're looking for are how open does it look? What does the iris look like? How many angle structures can you identify? But of course, you're also trying to identify how pigmented does the tribacular mesh work look in general. In pigmentary, it's going to look the super most pigmented it possibly could be. Pigmentary glaucoma usually gets the three or four plus designation for pigment in the angle. And that's as much as it can be. But in addition to that, you might also see another thing that we talked about last episode, the Sampleese line. Yeah, remind us what that is. Yeah. It's a line anterior to Schwalby's line, which really just looks like a so-called brown sugar appearance. It's actually, you know, it makes sense that that's there in pigmentary syndrome. We kind of always made a little less sense to me that it shows up this Sampleese line anyway, that it shows up in pseudo X2. To know the difference, just think that the more pigment there is, the more likely it is that it's pigmentary, not pseudo X-volute of. Nice. But to make the distinction between the two, you know, you'd be looking for other features of pseudo X, like the white flaky crap that we talked about in the last episode. And that should not appear in pigmentary, like you shouldn't see white flaky things. You shouldn't see that bullseye white appearance of the anterior lens capsule. We're not talking about that stuff today. Andrew, I've got a problem, though, but patients are already dilated, and I may have lost my goneo after leaving residency. Is there any other way to, so I can't find TADs? Maybe there's a Kirkkirk or Spendel. Is there anything else that I could look for an exam? Yeah. I actually love looking for this, because it takes advantage of a slit lamp maneuver that you rarely do. You know how the slit lamp is so called because you can move the beam of light in your slit, like from, you know, left or right or whatever, you can change the angle of the light. You can also change the angle of your entire viewing apparatus. If you ever kind of moved your slit lamp around, you can see that there's two parts of it that move left or right. The more inner kind of arm and then the outer arm, people rarely move the entire arm left or right. But if you do, then you're suddenly looking off at an angle. What I'm trying to get at here is there is another area where pigment deposits, and it's on the equator of the natural lens, the natural lens capsule. When you're looking straight through, like, okay, your slit beam is perfectly perpendicular to the cornea, you're just going to look straight past and kind of, you're not never going to see this accumulation of pigment at the edge, equatorial edge of the natural lens. But if you tilt your entire slit lamp viewing access way to the left or way to the right, and you ask the patient to help you out by looking in an extreme gaze, you're literally able then to see the edge, equatorial edge of the natural lens. And if you see a band of pigment along that, you've just seen something that goes by two different names. Some people call it a "shay stripe." Other people call it "Zentmire's line." Either way, it's the same thing. It's also coming there from pigment release that ends up kind of on the equatorial edge capsule, and it's very distinct. You don't really see it in other things, but you see it in pigmentary. I, so these were all very hard to memorize in residency. I have a pretty weak themonic that I will share. Do you hope, remember, the names of these different, you know, the epinems of all these different findings? So, that is, that is kisses, which is spelled, this early K-S-Z-S. So, that goes from entry to posterior about these findings. So, most interiors, Krueckerberg's Bendel, and then next, most interior is Sample Leeces line, and then posterior to that isentmire's line, which is also known as the "shay stripe." So, that's kind of the last S's that remind you that those were basically the same thing. If you also remember it according to, you know, what causes the next thing to happen? That can be helpful, and then you don't have to worry about mnemonics. Yeah. Of it that the iris backbowing causes the chafing, which causes the transillumination defects, which cause pigment release that come with pigment release that then slathers all over the Krueckerberg spindle, or the zentmire/shay stripe. Yeah, then mnemonic is really just to memorize like the literal name, in case you, you know, have just learning all these crazy different doctors from the 20th century. Actually, I'm not sure which century. Yeah. One thing that I should say, we talked a little bit about how some of these exam findings are actually also in pseudo-exfoliation. So, let's compare and contrast a bit. Peripupular ATIDs, those are in both, but they're more radial in pigmentary. The Krueckerberg spindle is actually possible in pseudo-ex too, but of course it's going to be heavier and more pigmented in pigmentary. Same goes for angle pigmentation. It's possible to be pigmented in pseudo-ex, but it's going to be more pigmented in pigmentary. Same for sample EC's line. Awesome. You know, in our pseudo-exfoliation we talked about the genetics of pseudo-ex, is there a gene known in pigmentary? Not really. I mean, this is a bit embarrassing for me because I come, I work at an institution that's well known through the work of one of my excellent famous colleagues for glaucoma genetics. And he could have probably found some random gene somewhere that causes it, but in general, the stuff you need to know for the BCSC, there's nothing classic associated with pigmentary as far as genetics goes. We still have a lot of work to do in uncovering a lot of the genes of glaucoma, but we don't know if we're really officially classically for pigmentary. So you're off the hook. Awesome. We talked about the basketball. This is the most important part of the episode. Let's come back to the basketball. Can he dunk? Can the man dunk? Can he continue to dunk? Yeah, I guess we're not going to teach him. Anyways, what? So why did we insert this at all, right? Like, why does it come up? Yeah. This is a bit controversial, but it's been, you know, enough glaucoma docs have noticed among their more athletic young patients. Like, man, they just like had a basketball game where they were just on a tennis court watch out, Ben, I know you love tennis. And they seem to like have a lot more pressure problems right after physical intense physical activity. It's thought that maybe these like jarring physical impacts of literally when your, you know, foot hits the floor that might contribute to pigment liberation. And these are, you know, such anecdotal things. I've heard some of my old glaucoma mentors say like, yeah, I made a patient in clinic, like walk up and down the stairs for like a half hour. And then when we checked his pressure again, right after all that, it was like 10 points higher or something. The reason it's controversial is like, it's hard to replicate reliably. A lot of studies have looked at whether this truly is a thing. And, you know, it's an easy study design. Literally make all your patients walk up without stairs. And not all of them have this happen. But it's anecdotal enough. And it's kind of almost worked itself into classical textbook teaching of this that you should be aware of buzzwords in test questions, saying like this person works out a lot or they engage in a lot that are a runner or a job marathon jogger or something like that. When we talk about buzzwords that make you should make you think of pigmentary, it's this sort of physical activity that does that. Sometimes, you know, this is an aside, but sometimes that makes me confused. Sometimes for a completely non glaucomaist process, we think about Uttavs phenomenon in multiple sclerosis and optic neuritis. A lot similar sort of like that disease flares up with heat and activity, heat and physical activity. It's sort of like that here, but it's totally different mechanism, totally different disease, right? Yeah, but both should be interdifferential or transient monocular vision loss. True, yeah. We did an episode on that. Yeah, that's out there, you can find it somewhere. How many patients who have this pigment dispersion actually get pigment dispersion glaucoma? This isn't a number anybody should memorize unless you're a glaucoma fellow, I guess. But what Ben is alluding to is like, yeah, just like we said for pseudo X, you could have the syndrome before you have the actual glaucoma, right? So a lot of these fall will have all these exam findings. And if they do, you call them pigment dispersion syndrome. If they end up with glaucoma, it's pigmentary glaucoma then. Only about 15% of people end up converting from just pigment dispersion syndrome to full on pigmentary glaucoma. It's a lower number than I would have thought, you know. Yeah, yeah, it is. And you know, there's also this interesting thing to it where when I meet someone with pigmentary dispersion syndrome, I'm able to tell them, you know, it sucks that you have this. I'm sorry to be diagnosing you with it. But you're lucky in one sense. You're one of the only types of glaucoma that might just go away. Like not the glaucoma itself will not go away if you have it. But you know, there's only a certain amount of pigment that any iris has. And once it's all been shaved off, there's no more iris. There's no more pigment to contribute, you know, like this provocation has got to end at some point. So this is the one glaucoma that the provocation for which can bird itself out. If you're lucky, you'll you ostensibly could never end up with glaucoma. And eventually your iris pigment is all released and you don't have to worry about it anymore. Yeah. What age does it usually present at? Unlike pseudo X, this is more a young person's problem. It's usually ages 20 to 50. Gotcha. What about a gender? In our case that you described we on purpose that it was a guy because this has a strong predilection for men, three to one male to female ratio. Gotcha. And are Scandinavians more risk for this one? Nope. We don't know of any ethnic or geographic association for pigmentary. And I will make one kind of side comment about that because one may think, oh, if this is a pigment problem, if you are more pigmented, maybe there would be more of a problem or perhaps if you're less pigmented, like if you're a blue eyed person, there's less pigment in your iris. Why is why how can they even get it? They barely have any pigment in the iris begin with. Well, the important thing to remember is this is all about pigment on the posterior, like Angus in the very beginning, and the posterior part of your iris. And that's what's rubbing its azonyotes behind it. So while there's variability in the pigmentation of the iris stroma, which is anterior to the posterior pigment of helium of the iris, it's the almost basically everyone who has an iris as posterior pigment of helium, one exception being albinism, you know, albinism, that's the one finding if they have or they don't have that pigment back there. So like, you know, if like for some reason, you know, you ever, like, hold on the iris and surgery or something, you see the back part of the iris, you always see it's like very, very dark and like everyone does matter blue light or not. And don't ask how I know that. Well, also another condition, right? Ectropeon UVA, where the pupil margin, you can see like the posterior iris pigment has been dragged forward and around that margin so that you actually end up seeing it on the surface of the iris margin. Yeah. Anyway, yeah, that shows you the truth of things of what's going on behind there. So the one other thing that I want to point out from our case, that the patient had come for retina potassium repair fallop, and I know that there may appear to be some artifice with some of the case presentations. And for patient privacy purposes, there obviously is artifice, but we made all this up. Yeah. Yeah. These are all 100% made up, but there is actually an association between pigmentary dispersion, glaucoma and retina attachment. Andrew, can you tell us why that might be? Yeah. The retinal detachment is, you know, what are some of the other risk factors for retinal detachment? Myopia is a big one. That's a risk factor that retina detachment shares in common with pigmentary glaucoma. Ardees and pigmentary both happen more frequently in people who are really myopic. So it's not necessarily that the pigmentary is associated with the RRD, but the risk factor that they both share is, they will share it. Yeah. And I'll tell you anecdotally, like an, you know, RD clinic said, if you look, you'll actually see a decent amount of pigment dispersion. Okay. Let's say that I only saw this in the patient's RDI. Is that normal anger? It's the eye that's had more stuff happen to it, especially surgical or trauma stuff that will make pigment release more. Yeah. It's going to happen more in that eye, but usually this is a bilateral condition. And to the extent that like in the last episode, we said you can have so-called form, frust, pseudo exfoliation. Imagine that pigmentary can be worse than one eye than the other, sure. Yeah. And what about how like aggressive is pigment dispersion in your view? For your for general trainees out there, you might be off the hook because the BCSC doesn't really mention this about how aggressive is it. We said earlier in the last episode that pseudo X is the most aggressive open angle glaucoma. Right. That's what you need to know. If you're a glaucoma fellow and you're wondering about this stuff, some studies have said that that pigmentary is about analogous in aggressiveness to say like normal tension glaucoma, but it's hard to study, right? Because it all kind of depends on how much pigment got liberated, how much pigment is obstructing. When do you reach the tipping point where that obstruction can no longer be cleared out by your tribicular measures, natural self-cleaning properties? It's hard to study. Yeah. But what I do want to say about natural history, because you might get this might trip you up as a trainee, as a resident, let's say you listen to us really carefully and you're like, all right, I'm all about looking for this iris concavity on Goneo, but I don't see it. Does it mean that they don't have pigmentary well? No, because the older a person gets, the fatter their natural lens is getting, right? Don't take that personally to your listener, okay? It's okay to get bad in your age, it's okay. Or at least once you get bad. Yeah, the lens gets a kind of more poochie out in the anterior posterior dimension. And you can imagine that if your iris is initially backbode, well, as the thing behind it presses it forward, that backbowing may become less evident. So sometimes I have to make the diagnosis of pigmentary, even if I don't see the concavity of the iris that I'm looking for. The other thing that can change with time is that we mentioned already, this is the type of glaucoma that if you run out of pigment to release, then you might have less problems later on. That also means that the Kruppenberg spindle can eventually sort of become less apparent over time. So there have been situations where someone was referred to me with saying like pigmentary glaucoma was diagnosed in this person 20 years ago, and I'm seeing and I'm like, what's going on? This person doesn't seem to know what pigmentary is, because I barely see a Kruppenberg spindle here. Well, it's not that I'm some smarty pants or something. It very well could have been that the Ks, the spindle was very apparent earlier, but now with less pigment circulating around, it's hard to sort of wash itself out. So be careful when you're diagnosing this stuff or at least trying to see what you're looking for in an exam, you could be less impressed than you're expecting to be depending on where they are in their chronology of their process. That's super helpful to know. So, but with this, I think it's here we've been talking about like, you know, this is very fancy. I think this is maybe the fanciest of the glaucoma, is in my opinion, but kind of like Schwarzenegger. Yeah, okay. Yeah, yeah. This is like top three, you know, Hall of Fame fancy glaucomas, but you found a fancy glaucoma. But don't you just treat it the same way and just give them drops? Like, what is different? Like, what does it matter? If you know, it's why what caused your glaucoma? Yeah, there's a couple of things. Number one is laser trabeculoplasty. We said last episode, comparing contrast again, pseudox, LTP or SLT in general, ALT if you still have it, they don't work that well for pseudox. But laser trabeculoplasty works really well for pigmentary, almost too well. Part of the reason for that is the laser energy is going to be absorbed by all this pigment. And sometimes that works in your favor, because wow, these people can have a great response to SLT. But they can also have an over-response where you've delivered too much laser energy. It's absorbed too much. And all of that makes the eye really unhappy. And the pressure actually goes crazy high. And every glaucoma specialist has a story where it's like, yeah, I treated them with SLT and I made them worse. So be judicious. Deliver less laser energy to the pigmentary angle than you would any other glaucoma disangle. That's not the only unique laser approach for pigmentary. The next thing I'm going to say is pretty controversial though. Okay, everyone brace yourself. Brace yourself, sorry. Remember going back to the back bowing of the iris that supposedly causes all this stuff to cascade on? People have said, well, why don't we just like make that iris back bowing go away? And how could we do that? Well, maybe it's also back bowed because of a pressure differential between, you know, one side of the iris is higher pressure than the other side that's contributing to pushing the iris back. So if you punch a hole through the iris, do a laser iridotomy, maybe that'll relieve that pressure imbalance, and then let the iris come forward a bit. The reason it's controversial is some studies show that that works, other studies say that it doesn't, and your glaucoma attendings are probably going to have strong opinions about this one way or another, we don't all agree. Well, you were a viewer opinion? I personally don't know that it works. My approach, which we're not here to talk about, is just if the majority of studies say that this is a thing, then I'll believe that, and if my minority of studies say that this is a thing, I probably won't believe it, but if it's half and half, I'll say, yeah, maybe we could do this in a sort of situational thing. For your patient who wants to know if he can still dunk, first I'll say, okay, is he concave? Does he have a concave iris? Yes. Sure. Let's try it. Maybe he can continue to dunk afterwards. But if they're less active or something, less high risk for that sort of thing, I'll probably not do it. Hard questions in life. One other thing that if you're doing filtering surgery on, you should be careful of this. This is more a glaucoma fellow level of knowledge, but Trabeque Electomy's tube shunts, they all work great if you have to do them. But remember that this is a type of glaucoma that happens to younger people and people who are really myopic. It turns out those two things are also risk factors for hypoteny maculopathy. So if you're doing a trabe on a person in their 40s, they're more likely if their pressure gets too low to have debilitating maculopathy from hypoteny. So you have to be careful and judicious, you can't be as much of a gunslinger and say, let's just go to Trabe right away for someone who's a younger pigmentary glaucoma patient. So I will personally not put a tube in these patients, I will let. I will let an adult make that decision. Kind of before we're almost at closing, before we finish, there has been this entity that I've seen in the literature and I saw a grand round on it at some point about this entity called, they either call baits or body, which I think stands for bilateral acute, iris transillumination or bilateral acute, deep pigmentation of the iris, so bait or body. Do looking at pigmentary dispersion, it seems very similar to those entities. Do you have any thoughts on what that might be? But I personally am a little skeptical of the bait or body diagnoses because they are so relatively newly reported in just such a few small case numbers. But there's no general consensus on how it's distinct or whether it might share some pathophys in common with pigmentary, just because it's such a new thing, it's so poorly understood. I think you can consider it separate for purposes of test taking and just don't think about it too much. It's a super exotic zebra that supposedly has maybe an association with oral moxifloxicin use. That's a case that I saw. They were like, "Oh, it's because it took moxies." I don't know. Yeah. Okay. Let's do some review. The stuff that we'd like to do now is just associations if you see pigmentary glaucoma, if you know what that's what you're dealing with. What are some things that you should be careful of to think about? We talked about retinal detachment, higher incidence, of course, right? Because they're myopic and you should be worry of that. But if you didn't know you were dealing with pigmentary, what should trigger you to consider pigmentary in your differential diagnosis? And there it's again, if it's a young man or especially somebody with maybe transient monocular vision loss, especially after exercise. Not just transient monocular vision loss, but also ocular hypertension and the visual changes that can come temporarily with that. And some test buzzer words are things like so-called reverse-pipillary bot block, which refers to that posterior bone of the iris we talked about before. And then to my line, the shea stripe, which is that finding you see at the lunsy quater, that ends you talked about that you need to turn your whole slot lamp to the left or right to be able to see in a dilated patient, the sample loci's line, which is in both the cytobox and pigmentary dispersion, and the iris concavity and radial transillumination, or spoke like transillumination defects. Yeah. We didn't say spoke like exactly, but some test, some buzz words will mention it. It's just a description. Yeah. Yeah. Radial spoke like. That's what it is. It kind of looked like bicycle spokes. So dear audio, now you know we're talking about pseudo-x and pigmentary, sometimes having things in common with each other, sometimes in contrast to each other. So Ben and I are going to go through some quick question answer stuff to illustrate the differences or similarities. So between pseudo-x and pigmentary, which of them responds to laser-tribeculoplasty better? So pigmentary responds better, but pseudo-x also responds just less well than most opening with glaucomas. All right. Question number two, which one's pathophysiology is more solely due to obstruction of the tribecular mesh work, and that's pigmentary dispersion, pseudo-x foliation, as there's more of a general issue with susceptibility. Yeah, susceptibility, the optic nerve, and the subtraction mesh work. Which of the two has a sample E.C.'s line on godioscopy? Both. But it will be like heavier, usually, in pigmentary or more pigmented looking. Next question, which of them has a zent-myer line? Pigmentary dispersion. Next question, which of them has a shade stripe? Also, pigment dispersion. Because zent-myer and shade stripes are the same thing. Which of them has a crookedberg spindle? Really pigmentary dispersion, but according to BCSE, pseudo-x can as well. Which is more common in men? Pigment dispersion in pseudo-x is the same between genders. Right. Three to one for pigmentary equivalent in pseudo-x. Which of them can burn itself out, so to speak, and kind of stop the provocation, have the stimulating provocation stop on its own? Pigment dispersion. Which is classically more common among those of Scandinavian descent? pseudo-x. Which is the most aggressive of the open-angle glaucoma? pseudo-x. Which of them is associated with the genetic mutation in loxal 1? pseudo-x. If you have the loxal 1 mutation, what's the likelihood that you'll get it's associated glaucoma? And here, I know I'm kind of being Lucy Goosey with statistical things, but let's say prevalence of this glaucoma among loxal 1 carriers, or people who have that mutation. 50%. Next question, we're almost done. Which of these might benefit from a laser-iridotomy despite being open-angle? Which of them has an association almost by the transitive property with retinal detachment? Pigment dispersion. But that's that. And that's the way for this week. If you'd like to support us, you can follow us at eyes4earys of the number 4 on Twitter, or leave us a rating review on iTunes or every founder podcast. I think this is the last episode we're going to release before OCAP, so I wish everyone the best of luck, and we'll see you guys next time. Bye. [MUSIC]