 Okay, thank you, Isha. So now we have another visiting medical student from University of Missouri, Missouri, and Matt's going to present about acute onset of esotropia. All right. Good morning, everyone. Thank you for having me. My name is Matt Cleathamus. I'm a fourth year medical student from University of Missouri at Kansas City. Just a brief little bit about my presentation. It will be acute onset of esotropia in children, and a lot of this will be just kind of an overview for medical students, because I certainly learned a lot about this topic when I came here and started following Dr. Dries. So a little bit about me. I'm from this school, obviously, and I didn't include a slide of the picture of the School of Medicine at the University of Missouri in Kansas City, because it's not particularly pretty. So I decided to include this fountain instead, because Casey is known as the city of fountains, second only in the world to Rome, in case you guys didn't know that. Fun fact, although most people know it as the city of barbecue. So a little overview, I'm going to orient this presentation kind of differently from most. I'm going to go over the different diagnosis for multiple types of esotropias. I'm going to cover the workup. I'm going to go over the clinical exam imaging studies and patient history that plays an important role. And then I'm going to do this. I'm going to do a clinical case after we cover some of the basics, so that you guys can work through the thought process of how to diagnose what's going on. Physicians, obviously, already know how to do this. This is mostly for the students. So afterwards, I'm going to talk about some of the treatment options for this, for one diagnosis in particular of a case that I was fortunate enough to see at Primary Children's Hospital. Then we can have discussion and questions following that. So types of ET. So there's several broad categories. Most people try and divide isotropia into incombitant versus concomitant, where incombitant means that the size of the deviation varies depending on the gaze of the patient. And concomitant means that the size of the deviation is constant no matter where the patient is looking. Constant versus intermittent also are subcategories of concomitant, which are pretty much self-explanatory. More specific types of ET include congenital or infantile ET, which is present from birth or very shortly thereafter becomes a parent, and will most often require surgery to be repaired. Commodative ET is a little bit easier to fix because it's caused by most often hypertropia where patients have difficulty seeing up close so that when they try and focus on things that are near them, the eyes want to converge and accommodate at the same time. So the more they focus on something, the more the eyes will converge and come together. So this type of ET can often be treated by using glasses and reducing the amount of strain placed on the eye when trying to focus. Acquired ET is another subtype, which can be caused by a variety of different things, including six nerve palsies, hydrocephalus, intracranial masses, and so on and so forth. So that's one of the categories where you really need a little bit more help to determine the etiology. Pseudoestetropia is a very common finding. We've seen several cases of this so far over primary children's, and it's the appearance of these tropia where there is none, and you can determine this using the corneal light reflexes to figure out if the patient's eyes are actually straight or deviated. It's caused by epicanthal folds and broad nasal bridges. So here I've just got a couple of quick examples. On the left you can see what is a true estetropia, and on the right you can see the helpful arrows pointing out some epicanthal folds that make it appear as though there's less sclera on the patient's right eye over there, where there is actually an equal amount of sclera it's just covered by the skin. So a lot of people will refer these patients in for evaluation when in fact their vision is normal. So some red flags to look out for when you're evaluating a patient with estetropia. Age of onset is very important. I think most estetropias I believe present between six months and I believe about two years. Acute onset is also much more concerning if a patient has no visual problems and then within a short span develops a constant estetropia. That can be a red flag for some intracranial processes. Also low amounts of hyperopia, family history of neuro disorders, associated symptoms such as obstacle headaches, things like that are red flags to watch out for. Optic atrophy, greater estetropia at distance, and significant incompetence in side gaze is also a red flag. So here's a case presentation if you guys and the patient's name is not actually LM it's just a little shout out because I like soccer and I like Lionel Messi so let's go with that. The patient was a four year old Caucasian male who presented to clinic for a new onset eye crossing accompanied by weekly headaches worsening over the past seven months. He denies nausea vomiting or as worsening pain with activity, photophobia, and pain with eye movement. Father reports some clumsiness when the patient throws a ball compared to the patient's brother. So that's kind of a good control. And the denies balls. LM wears glasses most of the time. And his family history is unknown due to being adopted. All of their reuse systems is negative and he has no known allergies, past medical history or surgical history. So I'll give you his eye exam here. Visual acuity was 2030 in both eyes with correction. His prescription was plus 1.5 sphere. Oh, his pupils were unremarkable. He was not a very happy camper. So we couldn't really do to monetary on him. His pen light external exam and funnest exam were all normal. He did cooperate for those. Strabismus exam showed 30 diapers of ET in all gazes without any DVD. So one of the medical students here would you like to tell me what kind of dystrophy that is if it's constant all gazes? Everyone got that. It's a concomitant ET. So the next steps in diagnosis here. Anybody want to try and hazard guess the differential diagnosis so far? Okay, I'll move on and give you some more information. So we did a little bit further work up with him because his dad did report clumsiness when we were concerned about some neurologic processes going on. So we went ahead and ordered an MRI of the brain, which is one of the more common neuro imaging studies for eye manifestations, as opposed to like CT head, which is better for viewing things like strokes, bleeds and fractures. So MRI is good for looking at the soft tissues. It shows you the eye muscles, the optic nerve and areas of the optic tract and pathway. So detailed neuro exam came back a little bit less than helpful because the patient was not cooperative again, but Ellen was alert and oriented. He's able to move all extremities spontaneously and purposefully had clear speech and lacked, you know, major neuro deficits. So more or less neuro exam was normal as far as it could be conducted. So now doesn't anybody have any ideas on differential? Okay, well, he's got a concomitant esotropia and some onset began about seven months ago. So he was between three and four at that time. So it's a little bit later on set. And he's got some neuro findings that are a little bit concerning. So I'm going to call this acquired concomitant esotropia. And here is the MRI of his brain. Here's an axial view, which I like because it shows some of the eye muscles up there, which you can see are not inflamed terribly from this view. So that's probably not what's going on causing his esotropia. You can also see some of the gray matter pathways there. Here's another view where you can see a little bit better shot at the patient's cerebellum. And as you can see, it appears to be crowding the frame and magnum here. So move on some more views. The nice thing about this is these are actually the images from the patient that was seen in primary children, which I think is kind of neat. So down here, you can also see an area where the cerebellum is kind of subluxed into the frame and be it very minorly. So now does anybody, sorry, that image is kind of dark, but you can still see a little bit of the cerebellum moving down into the frame. So now does anybody have any ideas about what's going on? Probably everyone knows. Very good. Excellent. So as you all deduced, this talk is about our own curia malformations. subcategories are broken up into one through four, where curia malformation type one includes usually a syringo myelia component, and curia type two contains a myeloma ninja seal component. Whereas this patient's MRI was read as a nine millimeter deviation of the cerebellum into the frame of magnum, which is on the smaller side. So he had less severe symptoms. And he also did not have any accompanying syringo myelia or myeloma ninja seals. So the radiologist read this as a very mild atypical presentation of our own curia malformation. So this is kind of a rare presentation. It's a little bit different, which is why I wanted to bring it to you all for the grand rounds. It's another basic fact about curia that I find kind of interesting is it causes a lot of downbeat misdiagnosis. So if you have a patient in the clinic and they've got primary downbeat misdiagnosis, you should think about this because it's it's got a good chance of being the etiology. So other symptoms of this, as I already mentioned, headaches, clumsiness and ataxia, ocular manifestations, there's really two main schools of thought on treating curia malformations that affect the eye. So you can do this. You can you can have successful resolution of problems with eye muscle surgery, or you can perform neurosurgical enlargement of the frame and or both depending on how the patients symptoms present. And I was I was going to ask later on for a little bit of help from some of the more senior physicians here to speak if you have any wisdom on what you've tried in the past, if you've seen a lot of patients with this, which seems to work better. But here are my sources and I'll open it up for discussion and questions right now. Also bonus points if anyone can name this mountain and the view from here courtesy of student Michael Gilbert and Kim Lavin also joined us on this wonderful hike. So thank you very much. Does anybody have any discussion on patients they've seen with previous curia malformations and how they were treated? Very good. My experience in operating kids with Kiari, they've gotten straight state straight. So I haven't had the experience of having recur and ultimately having to have neurosurgery is decompressed to Kiari. You know, the other question here is we've got a kid who's got acquired non-incommodation of his trophia, who's got a Kiari malformation. And I'm not sure that anybody's been able to really convince me that that's the cause, you know, what's the mechanism of the use of trophia? They don't have a sixth nerve palsy. So I'll be on the side of saying, I'm not absolutely convinced that he's appropriate in those kids is absolutely due to the Kiari. I mean, the kids who straighten out when you do their, would argue pretty strongly that it's the same way, you can see this in kids who've got tethered cords. Kids with spina bifida who develop worsening of his trophia don't have limited abduction of their findings of sixth nerve palsy. They have seen that more than once and congratulated Jack Walker on his ability to straighten out crossed eyes. We didn't operate on it sooner enough to claim the Kiari, but you know, unfortunately, in all seriousness, the kids did well, and I've talked about this, I was not able to come up with a mechanism there either. So it's likely that it is related to it, but you're right, the neurosurgeons are reluctant to do this because there is much more potential morbidity associated with a neurosurgery procedure. If you were to present that to the parents and say we could either do this big surgery on, you know, the back of your child's neck and base of the skull, or we can do an eye muscle operation if it were my child, I would probably opt for the eye muscle surgery first. What would you do if it was your child? No, I believe the MRI report said, I typically follow kids that aren't decompressed every six months, and every time I see them, I send the pediatrician, the parents, and the neurosurgeon a letter letting them know that I saw them, letting them know that hopefully that kind of spurs them to... Thank you very much doctors. Anyone else have questions or comments? Yes. You win. You figured it out. It's Mount Olympus. Thank you.