 Leisure, I wonder if you got one. Yeah. Thanks for helping me. My pleasure. And then this is postoperatively. This is traveled with a chronic six-graded ulnar pre-cis, and that's postoperative photos on the bottom row. The differential diagnosis of six-graded ulnar palsy in kids is brain tumor, brain tumor, brain tumor, or hydrocephal, something going on that's intracranial. But also, post-barrel, is it really a inflammatory process after a viral infection that causes the six-graded ulnar palsy? Yeah, probably. But you know, kids are always sick, right? So just by, I mean, if you study, do kids have six-graded ulnar palsy after a viral infection? They all do. There's so many viral infections in kids that I've always thought, well, yeah, that's probably what's going on. But I certainly never rely on that without an imaging study, OK? And trauma, definitely, is up there in kids. And if they do have hydrocephalus from a mass or other intracranial disease, they often have other neurologic signs. Differential is Duane syndrome, which we're going to talk about. Just infantile esotropia, and you can't get a child to AB duct their eye because of poor cooperation, and a few other things that I don't want to talk about in detail. Here's a differential. Get an MR, do a pediatric neurologic exam, brief one. You can do it. You know how to do just the basics, but you can always refer them to neurologists as well. If it's idiopathic or post-viral, it tends to resolve over time. And we watch in way, especially if a child is turning their head and still fusing, and often it will resolve. But it often recurs during childhood. It's an entity that we don't really understand. But these are kids whose immune system apparently is causing some post-viral inflammatory pathology at the peripheral sixth screen in there. And then if it's chronic, with sixth screen owner or palsy surgically, you really have two choices. If the lateral has function, but it's reduced function, but it's not a dead muscle and doesn't pull at all. If it has some function, but the eye is still esotropic, a recess-resect procedure will give a really nice result. But if the lateral rectus is dead and doesn't pull at all, then the only way to get abducting force on the eye, getting the eye to turn out away from the nose, is to transpose the vertical recti towards the lateral rectus and use the vertical recti to get an abducting force. And here's a pre-op photo. It's the left eye, and this is post-op. Oh, I apologize, it was bilateral on him. But much worse on the left compared to the right. Okay, so let's take a tangent. Remember I said, don't, you keep hearing this, sorry. No one wants to miss a tumor, right? So you're in your pediatric ophthalmology clinic, you've done a fellowship, or maybe not. Maybe you're just on call. And you go to the ER at Primary Children's and there's a child with an esotropia. And you know, it looks like a comatant esotropia. It looks like abduction is, you know, pretty good. Okay. And, but to kids with acquired non-accommodative comatant esotropias, ever have brain tumors and the answer actually is yes. And they probably have subtle abduction deficits because of hydrocephalus, but you can't detect it. So how are you gonna know? Okay, how are you gonna know? Optic atrophy, nystagmus, those are the two main things. Optic atrophy and nystagmus. An absence of a family history of strabismus. Okay. So esotropia tends to run in families, right? If you have a child whose psychopathic refraction is plus one sphere in both eyes, no family history of strabismus. And, you know, you've got a child with an esotropia, looks comatant, not super cooperative. Don't wanna miss a tumor, right? Look for optic atrophy, look for nystagmus. And I do get an MRI of kids who I feel like I can't get a really good exam to make sure that they have no abduction deficit. And if they have a hint of optic atrophy or are suspected at all, I go ahead and in absence of family history, I just scan them. Because if you don't, those kids, the treatment is surgery. So if you don't, and there have been case series of this following scenario, you operate, they're under corrected, you operate again, they're under corrected, then you scan them, oops. And then there's less happiness in this world at that point. Well, so not missing intracranial pathology with comatant esotropia, that's why we try to measure kids and sidegazes in the clinic. Because in comatant esotropia, due to an abduction deficit, you might pick up when you measure, that you can't see when you do version testing. So if you can, it depends on the child, their age, their level of cooperation. Okay. What was your syndrome? Anyone know what that is? It's a combined six cranial nerve, bilateral six cranial nerve palsy and bilateral seventh cranial nerve palsy can be associated with systemic anomalies. Just throwing it up there so that you recognize his face. That's typically what they look like. I can't smile. Dwayne syndrome. Oh dear. Let's say you finished your fellowship, you finally got that big paycheck. You're like, yes, I'm gonna build a custom house, but you're cheap with the electrical contractor and they miswire your house. And the light switch in the kitchen on the ground floor is turning the lights on and off in the upstairs bathroom. And your spouse is up there saying, what are you doing? Okay, that's a miswiring of your new house. Dwayne syndrome is a miswiring of the cranial nerves. It's a cranial disinnovation. So what happens is these kids have hypoplasia of the sixth cranial nerve nucleus and absence or hypoplasia of the peripheral sixth cranial nerve. They have very poor, typically poor lateral rectus function and the bizarre thing is the miswiring. This is so bizarre. The third cranial, the peripheral third cranial nerve innervates the lateral rectus as if the lateral is starving for innervation during development and a branch goes over there. It's really bizarre. So not surprisingly, this disease causes the lateral rectus and the meteor rectus to contract at the same time. Isn't that weird? It's really strange, right? It doesn't make any sense unless you understand the abnormal anatomy of the peripheral third nerve sprouting an extra branch to the lateral rectus. And when you read about Dwayne syndrome, here's how you should think about it. That bilateral, that simultaneous contraction of the medial lateral rectus pulling the globe into the orbit, that unifies all of Dwayne syndrome. So you're gonna read about type one and type two and type three and less abduction, less abduction. They're exotropic. They're esotropic. They have upshoots and downshoots. And you're just gonna be like, okay, I just wanna read about Redna. But this is easy, actually. It's the co-contraction of the lateral medial rectus that unifies all of Dwayne syndrome. You know, if you look at these kids on attempted abduction from the side, from here, you can see the apex of the corneal goes back into the orbit. So when you do peeds and you see a kid with Dwayne syndrome, look at them from the side and have them follow your kids facing this way, have them look that way and look at the right eye. You'll see the globe actually goes back in the eye. I mean, we teach it that the palpibral fissure narrows. And of course that happens, that's easy to see looking face on. But to really understand this, look from the side. And then we're like, oh, okay. This unifies all of Dwayne syndrome. And all these classifications make a heck of a lot more sense. A few mutations are known, have been isolated in a few families, but in general, this is not inherited, can be, they're reported families. So they're the types. Type one, esotropia, type two, exotropia, type three, no stropismus. Okay, if you want to memorize it. But they all have co-contraction. They all have global attraction on attempted abduction. And so this miswiring I talked about, an extra branch of the third dirt going to the lateral rectus. Well, how much innervation goes to the lateral rectus? And how much innervation goes to the media rectus? Well, that varies from patient to patient. And remember there's a tug of war going on. Well, if the resting innervation of those two muscles favors the media rectus, a child will be esotropic and they'll turn their head to point their eyes straight ahead. That's type one. What if the innervation is more to the lateral rectus than the media rectus? Well, their eyes are gonna be out, right? It's gonna be an abduction. They're resting tonus. And so they want to use both eyes together so they'll turn their head. But they'll be exotropic in primary days. If the innervation is roughly equal, they'll have a straight head and straight eyes. But you'll still see the co-contraction. Okay, does that make sense? I try to teach this in a way that really makes sense. It's a springboard to learn the details. And here's a child with type one left Dwayne Center. I shouldn't look into this, right? Here you go. So his co-contraction of the medial lateral rectus is really happening in an abduction. And you can see his palpibrio fissure is narrower here than here. Look at that photo. It's easier to show it in up gaze and left here compared to here. But if you were standing to the side, getting a sagittal view of that eye, you would see the eye pull back in here, okay? So that's, what about this kid? He's a little exotropic, right? He's a little exotropic. And this doesn't show the head turn. This is type two. And check out his abduction is pretty good, but it's not normal compared to this side. And his abduction, I apologize. His abduction is reduced a bit. His abduction is pretty good, but maybe not perfectly normal. But look at the globe retraction. When his right eye goes into abduction. So this is type two Dwayne Center of his right eye. Does that make sense? Okay. And she has bilateral type one Dwayne Center. Watch this eye. Retraction, you can see narrowing in the palpibrio fissure, and then whoa, it gets nice and big. Here, not that big a difference, but still an abduction deficit. Okay, so this can be bilateral, about 10, 15% of patients are bilateral. There are some other manifestations. An up shoot. Look at this. This is when the resident just comes over and says, I don't know what's going on. And so this happens, we think because the lateral rectus is super tight. Not only getting innervation with abduction, but it's restricted and tight. And it acts as a leash on the globe, and the globe goes whoop. A lot of our rectus kind of slides under the eye, and the eye goes up. And I'm gonna talk about the surgery for that in a moment. Couple other sort of boards things that I don't really care if you know, but you need to know it for boards. More common in females and males, bilateral in about 10, 15%. Usually it's sporadic. Autosomal dominant inheritance is reported in those mutations that I showed earlier are the research papers. It's been reported in association with Golden Hearth syndrome for sure. And usually they don't have amblyopia and they have good stereopsis. Why? Why is that? Well, they like to use both, kids like to use both eyes together. So they turn their head to point both eyes straight instead of allowing strabismus. But what if they allow strabismus? Hang on to that thought. Uh-oh, amblyopia is gonna happen, right? Hang on to that thought. It's one of the indications for surgery for this. So if a little kid starts to not wanna turn their head anymore for their Dwayne syndrome and their esotropic and they start to develop amblyopia, should you operate? Well, you gotta do some amblyopia therapy first, right? Do a psychopathic refraction, see if they need glasses for anisomotropia, significant refractive error. If you do all that and they're still esotropic, then you have to operate. So that's one indication for surgery. But what if they just turn their head? Why operate and when should you operate? Well, think it through. It kinda depends. Depends on a few things. Well, first of all, you don't wanna disrupt binocular visual development in the visual cortex. And isn't that amazing how that happens? Did you know there are ocular dominance columns in the primary visual cortex? Kinda like a pie. Take half a pie and make skinny slices all the way through the half of the pie. And each one of those slices is an ocular dominance column and they alternate right eye, left eye, right eye, left eye, right eye, left eye, right eye, left eye. And if you take a monkey in suture and eyelids, shut at birth and then look at the histology four months later with one eye sutured shut, every other slice is gone. It's brain damage. Primary cortical visual development, that gets disrupted by strip isthmus or suturing and eyelid shut, right? That's amblyopia. So you don't want that to happen, right? So if you do surgery and it's not successful and you have to go back and operate again, that takes time. And during that time, there's no binocular visual experience. And amblyopia is gonna start creeping in. And what about stereopsis? Stereopsis is so cool. Imagine that pie with wires spanning over all those slices. Okay, so there are binocular neurons that have dendrites and axons that they span all those pie slices and connect them together. And that's depth perception, okay? That develops during childhood, especially during the first two years of life. So you don't wanna mess that up because we really want stereopsis, right? And kind of like M&Ms, you only got one shot, right? You only got one shot at good stereopsis. My son listens to M&Ms. You don't wanna disrupt that. So should you operate early on a kid with a head turn who has a normal binocular visual experience? No, no, no, no, no, leave it alone, leave it alone. Don't operate right away. Just because a kid has a problem doesn't mean you should be operating, right? You wanna think about the ultimate visual outcome. So I tend to wait. I wait as long as I can, sometimes forever. But forever might be too long for a patient who's always turning their head. Why? Can you live with a head turn your whole life? What would you think of my lecture if I did this all the time? You'd probably say, I'm having trouble concentrating. I keep noticing that he turns his head all the time, right? So that can be cosmetically unacceptable. But even worse, you can get chronic arthritis and highly, chronic arthritis and changes in facially symmetry. And so in the long term, after binocular visual development has happened in a child with a head turn, you can operate and start to help that head turn. I like to wait at least until three or four years of age for binocular visual development. And then after that, I like to get a good exam. And so it's up to the level of cooperation of the kid. So for me, beyond four years of age, and it depends too. There's some other reasons that I'll delay. And the surgeries for this generally recessing muscles, restricted muscles is the way to go to help with the abnormal head position. So for example, a type one, Dwayne syndrome with an esotropic eye, recessing the meteorrectus will help midline the eye. It's not gonna help the eye abduct at all. And in fact, the price of doing that surgery is poorer adduction than you had preoperatively, but the eye's midline and the head's straight. So if you've prevented the arthritis and facially symmetry. There is another approach. Those Arthur Rosenbaum passed away, but he pioneered vertical transposition of the vertical recti to the lateral rectus to try to not only midline the eye, but also improve abduction. And that's where the dragons are lying and waiting because I'll explain that and then tell a quick anecdote. Even after doing this for 20 years, my stress level goes very high when I'm doing transpositions of vertical recti because of induced torsion and induced vertical deviations and not getting the balance right, not getting the eye midline afterwards. And your re-operate goes up. It's just a part of it. And you have to re-operate quickly before Scar sets in typically. You gotta take them right back to the operating room. And here's the anecdote. So I found that as you get older, the bad things in the harder cases get referred to you. It's just a natural progression of things. And so child had this relatively new procedure in the hands of someone who probably didn't have the skill level to make it happen, had a very large vertical deviation, did not re-operate right away, referred to me three months later. And I said, crap, bigger than I am, that one. So I referred them down to Arthur Rosenbaum, the person who pioneered this procedure. He actually had stopped operating by then, but a doctor named Dr. Velaz, one of the partners took that on. I think it was five surgeries later. She had straight eyes looking straight ahead, but couldn't move that eye in or out up or down very far. So it was just like, woof. So don't think of, think of the, what's the name of this song my son listens to from Eminem? Just got one shot. Dun, dun, dun, dun, dun, dun, dun, dun, dun. What's the name of this song? The Eight Miles Song. Is that what it's called? The Eight Miles Song? Well, I don't know the name of it, but it's the same song. It's called The Eight Miles Song. Yes. Okay, thanks. You know what I'm talking about. It's just got one shot. And then it's like this big emotional thing. He loves that. But that's kind of true for transposition procedures. They can be reversed, but it's a really big deal. So anyway, I still like a recession of a horizontal recti for DeWayne syndrome to achieve the limited results of a straight head and binocular vision looking straight ahead. Okay, so the next entity is monocular elevation deficiency. Ooh, doesn't tell you a thing about the pathophysiology, that name. Right? What? Oh dear. How do I teach this? So, vertical deviation in little kids. Pretty much you've got fourth cranial nerve peresis, Brown syndrome, monocular elevation deficiency, very rare inferior oblique peresis. And by the way, that fourth cranial nerve peresis that I want to talk to you about, a different lecture, I can even present with a child fixing with the palsy eye and the other eye down, which confuses the heck out of the diagnosis. Then you get this little toddler who won't hold still and you can't sort it all out. It's really frustrating. And what's fascinating is all the entities have a known pathophysiology, except this one. We don't understand the underlying cause of an inability to elevate the eye. Midline, in abduction and in abduction. Okay, so what we like to say is across the board that I can't go up, all the way across, can't go up. With Brown syndrome, they can't go up looking towards the nose, but they can, in abduction, to distinguish it from Brown syndrome. It can be accompanied by true ptosis, but that's kind of hard to tell when the eye's down because the lid follows the eye because of the fascial connections between the levator and the superior rectus, right? So these kids have to be helped with surgery before you figure out if they have true ptosis or not. This is the so-called pseudotosis. And really, there are two types. There's restrictive, MED and peretic. And restrictive, MED, it just means when you go to the operating room and do four-structions. Now, for those who don't know, four-structions is you got a patient under general anesthesia. There's little or no intervention to the extraocular muscles. And you hold onto the eye and move it around, okay? And if a muscle is tight, like a leash and a dog, you know, the dog's running at your low, okay? When you move the eye, you can't, you feel restriction, it feels tight, okay? And with restrictive MED, the inferior rectus feels tight in the operating room. And if you recess that in these kids, they do well. But there's a peretic type where a nap procedure, transposition of the horizontal recti is helpful. Anyway, let me get back to basics with MED. They have a hypotropia on the affected side. They tend to have a chin-up abnormal head position, not always, kind of like Dwayne syndrome, right? Kids like to use both eyes together. So they're like, oh, wait, I want to use both eyes together. And so I wait, I wait, I wait. The pie slices are forming. The connections between the slices are forming. I wait, I wait, right? And then eventually operate. But some kids are like, I can't keep doing this. And they just allow the hypotropia, okay? And so they'll develop amblyopia. You have to treat the amblyopia. And glasses, if they need it, always do a psychopathic refraction in kids, looking for anisomotropia. So I'll just touch on the nap transposition. That's just taking the horizontal recti, the meteor rectus and the lateral rectus, and moving them up towards the insertion of the superior rectus. And it gives an elevating force to the eye for peretic MED. This is what it looks like. Can you guys see what's going on? This side can go down, but it doesn't go up. It doesn't go up here. It doesn't go up in abduction. Midline, it doesn't go up, okay? All right, so there's another entity that stops the eye from going up. Now we're moving to Brown syndrome. Oh dear. Antennas and cell phones are internal. When I grew up, antennas were really cool. My mom had a Buick Electro 225. It had a couch in the front. And she drove it. And the three kids were next to her knot and seat belts and lots of sharp things on the dashboard on that. And that car, it had a telescoping antenna that was automatic. This was the AERRA great auto design, if you ask me. You'd hit a button and it would just go zzzzzzzzzz. And you know how those antennas work, right? The telescope out click, click, click, click, click. Well it turns out the superior bleak tendons like that when it goes through the truck layer. Isn't that cool? I think that's really cool. So, you know, we used to think that this tendon was sort of like a rope going through a pulley. And Brown syndrome was there's a knot in the rope, bang. It's the, Helveston studied this in cadavers and it's pretty neat. So there's, right in the center, there are tendon fibers with, you know, scant adhesions to neighboring fibers. Kind of like the innermost smallest diameter part of the antenna. And that goes back and forth through the truck layer. And all the layers surrounding it are elastic and they allow it to go back and forth but they stop it from going too far. Does that make sense? So, when this, when the superior oblique contracts, right, it's the intorting down and out muscle, right? Has mainly in torsion, depression, abduction. So when it contracts, the tendon has to go on my left eye, the tendon has to go this way through the truck layer, right? In this direction. And when the inferior oblique contracts, the superior oblique has to relax. So the tendon has to go back the other direction. Cause if my left eye is going up and the oblique's like this, it's gotta do this. Does that make sense? It's gotta do this. If the eye, right? Does everyone know their anatomy? It's pretty complicated. What happens with Brown syndrome is that the telescoping antenna doesn't work in elevation, but it works in down gaze. So maybe that knot in the rope analogy does help a bit. There's a knot in the rope behind the truck layer so it can't elevate the eye. The eye can't elevate. It's restrictive, like a leash on a dog. All the elevators pull up, the eye can't go. Does that make sense? Well, these kids, I'd rather just show you photos. So do kids like to use both eyes together? Uh-huh, uh-huh, right? They like to use both eyes together. And so look, his eyes look pretty straight here, but look, he's looking up and to the left, this eye can't go up. So he's got Brown syndrome right here. So he's gonna wanna keep that eye away from adduction, right? And that's what he does. He's got a left head turn. Does that make sense? So he gets that eye out of the direction where his eye misalignment happens. And he can't elevate the eye in adduction. This eye looks good, good elevation. And look, superior bleak works in depression. So that's Brown syndrome. And why does it happen? What the heck? What's going on? Well, you can have a congenital abnormality of the superior bleak tendon trochlea complex. And just like that kid that I just showed you, but it can be acquired. Here's, you can give someone Brown syndrome by doing orbital surgery. It's the swan incision, the zoonins. I think so. That can happen. So you can give someone Brown syndrome with that. Or just orbital trauma. Poor guy in a car or motorcycle or something. Wow. They end up with Brown syndrome because of scarring at the trochlea. Even inflammatory diseases can cause troubles right up here. Okay? And here's the cool thing. You'll see this at some point in your career, hopefully. Some patients have a knot in the rope that stops the eye from going up, but it's a little knot. It's a small knot. If they pull hard enough, it goes through. And they feel and even hear this click and their eye goes up. Is that cool? And what's interesting in cases of inflammatory acquired Brown syndrome, steroid injections in that area can help reduce inflammation and the clicking gets better and they can move their eye better. Okay? So Brown syndrome is just a description of some kind of trouble here that can be congenital or acquired. So whether you do surgery for Brown syndrome, well, you know, it has to be a permanent situation, right? You don't want to do surgery for something that's temporary for goodness sakes, right? So the acquired cases generally are not treated surgically unless they're chronic. And obviously from urban surgery or real trauma, that's probably not gonna get better, you know, but the inflammatory ones can, so you can read about it. Don't jump straight to surgery, okay? Okay, so let's talk, you're hearing the same theme again. It's gonna get boring, but you won't forget it. Leave them alone when they're kids. Leave them alone, let them turn their head. They'll develop binocular vision. I think the earliest I've operated on kids for Brown syndrome is five, six years of age. If they adopt an abnormal head position, okay? But I've operated earlier, why? Why did it operate in a two-year-old with Brown syndrome? Because they were like, ah, I don't care. I'm gonna let my eye go down. And they developed amblyopia and we had to move, okay? Does that make sense? Okay. What's the surgery? Well, doing some sort of weakening procedure on the superior bleak tendon at the side of the globe. You know, not in the orbit, you can't get back there, right? But you can't get at the tendon in subtenon space. So that's where we operate. And all of the procedures are to lengthen or, well, cut the tendon in half. And you know, there are a lot of approaches to it. A complete tenotomy of the superior bleak tendon is a good approach. It just let the tendon fly, okay? And there are fascial attachments that surround the tendon. And they tend to keep the tendon some place close together, but it's not quantitative. And in that instance, the chance of superior bleak peresis is significant. As high as 50% even in some series, but as low as 10 in others, you do the math. Maybe the patients with the overcorrection saw a different doctor. And so I've, although I didn't train this way, I started to do a quantitative weakening the superior bleak with first silicone spacers. You know, the retina folks, they use those bands, silicone bands, you just cut one. Cut one to five millimeters, put some sutra in it, sewed on the tendon. Ken Wright was the one that started that. And, but they can erode through the conjunctiva. Stop doing that, only did a few of those and went to just using sutra, just using merciline sutra. And the reason I like this is it can be quantitative in the operating room where you can check your four stuctions based on how far you've separated the tendon. And if it's too much, you can reverse it. If it's not enough, you can let it out a bit and try to equalize the four stuctions between the two eyes. And my results of that have been really nice. I've been really happy. My re-operate is pretty low. And this is the kid pre-op. Look here, here he is, plus dot. So he's like way better. And he does not have a terrible superior bleak peresis. He does have some peresis here. Okay, I'm gonna touch on adults, myasthenia, variable ptosis and variable double vision. As you know, this can be purely ocular or systemic. Disease of the neuromile junction. You know the testing. I'll let the neuro ophthalmologist go into that. And, but we see them if their diplopia is persistent. This is the ice test. This is before the ice. That's after the ice. Nice. You know, I think I was a fellow when the ice test was discovered. Shazam. That's great. I like really simple things in the clinic to make a diagnosis. I just love that. Thyroid eye disease. You guys know what this is about, right? Orbital inflammation of connective tissue in the ocular muscles with replacement of muscle tissue with glycosaminoglycans. The muscles get super tight and start pulling the eyes in bad directions. The severity of muscles affected tends to go in this order. Infiorrectus is the worst. Meteorrectus is second worst. So these patients usually end up with a hypotropion and esotropia, right? But the superior rectus, the lateral rectus can be affected and the superior bleak can be affected too. But usually, they look like this. Okay. Like that. She has an incredibly tight inferior rectus on this side and it's tight on this side as well. Here's your CT. Oh dear. Look at that. Might need an orbital decompression. It's possible in that patient, that's for sure. So eye muscle surgery for their diplopia. You can never make them normal. Just can't make them normal, okay? Their muscles are replaced by fibrous tissue. But you can try to get as large an island of single binocular vision looking straight ahead and in down gaze for driving and reading. That's really what you shoot for. These patients are so happy. Even if you can't restore rotations of the eyes. And here's the teaching point for boards in your practice if you do this. Julie. Recessions, not resections. With rare exceptions to that rule. Okay. You gotta recess. What happens if you resect a restricted muscle? It's more restricted, right? So you end up inducing Duane syndrome if you resect with thyroid disease. But there are some exceptions. I'll just touch on blowout fracture. Okay, so do patients have double vision after blowout fracture? Adults and kids. And the answer is yep, absolutely they do. What's the main pathophysiology of double vision acutely right after a fracture for the first week or two? It's edema, hemorrhage, into the orbital fascial tissues and the muscles. And that can resolve over time. And so you can't jump straight to orbital surgery or eye muscle surgery for these patients with one exception. And that's kids with a green stick fracture with the inferior rectus entrapped. That ain't gettin' better, okay? That's not gonna get better. And they need surgery. And what's really interesting, does anyone know what the ocular cardiac reflex is? I cause it all the time. Does anyone, do you guys know what it is yet? I see unfamiliar faces. You guys aren't nodding, so I assume no. If you pull out an extracurricular muscle, the heart rate goes down. We see that all the time in the operating room with eye muscle surgery, okay? It's a reflex. And it kinda makes sense. If you have a kid in the ER, let's say they have a pulse ox on something to monitor their heart rate, have them look up and the unaffected eye will go up, the other eye won't go up and their heart rate will start to drop because there's tension on that muscle. Okay, and that should tip you off. It's sorta like the ice test. I mean, you can say the heart rate just went down when he looked up, he probably needs surgery. He certainly needs his CT scan. Okay, this is what it looks like. Here's an eye that can't go up. There's the green stick fracture in the kid. Okay, now it's kind of a big deal to get it done sooner rather than later because muscles can become ischemic when they're trapped in bone and kids. And then after you lift the muscle out, they develop not a hypotropia, hyperotropia because they have a peretic inferior rectus, okay? So orbital surgery, wait at first, except for the indications for immediate surgery from oculoplastic, so I'll let them talk to you about that. Usually it has to do with gigantic floor fractures with obvious enupthalmos that can only get worse as edema and hemorrhage subside. They'll repair early. There's some other indications, but I won't talk, I won't steal their thunder. And once, if there's entrapment, if the orbital surgeons do their job, then we're dealing with double, we can be dealing with double vision that's both restrictive and peretic. And with the restrictive disease, generally you're recessing muscles to reduce restriction. And with peretic disease, you're either doing a resection of a muscle if there's some muscle function, but not normal, or transposition if it's a dead muscle that doesn't pull. Just like six great alert precess. Okay, I'll stop there. It's time to stop. Any questions?