 years ago. And then I moved back to the Midwest so I'm in Cincinnati now and I came back just like for fun to get a lecture because I asked if I wanted to. So I actually first took the PowerPoint from Anna Newfield because then I thought I wouldn't have to make my own. But she did, I don't know if you guys are here for it, she did the review maybe last year, maybe just a year before that. But she went kind of into, she did more of like an in-depth thing on a few topics and I didn't really want to do it that way. So I still still summon for stuff. So everything that looks like a really in-depth review is probably the older slides that you might have seen. But we'll see. Anyways, in terms of the NeuroAuth anatomy, you know, these topics come up under multiple different sections, right, like plastics and pees and whatever. So you do have to know them. They always ask some questions about them. I'm not going to go through them because it's too boring and you wouldn't really learn it anyways. But you know, you have, like you had to know all of these and how they separate us. You do have to sit down and learn it. It's worth it. It will be worth at least a few questions from the OCAP. What's inside the annulus and what's outside of it? What structures are within the cavernous sinus? Everybody knows this, right? But three, four, V1, V2 travel in the lateral wall. Six in the ICA are kind of within the meat of the cavernous sinus. So they're more susceptible to traumatic injury. You have to know the sympathetic pathway. I think most people pretty much know it enough to answer the questions. But for the Horner's questions and the parasympathetic pathway for cranial nerves, three and eighties questions, you have to know those. I'm going to go through a few imaging slides. On every OCAP that I took, they always had at least one imaging picture where it's basically like, what is this structure? They will, I think they often give a stem with it, but pretty much the question is like, where is this structure? So these will probably be more helpful for my, what year are you guys? Can everybody take all your, you guys, first, second, third? First, second years. Second year? Okay. Second, okay. So it's, you know, like as, as you go along in your residency, it's going to be easier and easier. But sometimes at the beginning you haven't had that whole lot of experience picking out the structure for yourself on the scan. And so then when they ask, like, you know, they label it like, you know, what is this? You can be like, so you guys have more, you have more neuro radiology as part of your residency than I did, but I still think it's helpful to review. So you need to know which one is the superior orbital fissure and which one is the optic canal. So the optic canal is more real, right? Superior orbital fissure is a bit more lateral and inferior. But so you want to try to remember that that's like a, that's a favorite one that they ask, like, which one is the superior orbital fissure. And this is it on the coronal CT. So optic canal is more medial, superior orbital fissure, a more inferior lateral. Does anybody know what this one is? Superior ophthalmic vein, right? So if they give you a question that is related to this structure, it's almost, it's going to have something to do probably with the cavernous sinus. This then will have to do with that. But that is the superior ophthalmic vein. That's another favorite one that they like to ask. That's what it looks like on the coronal. So right underneath the superior rectus there. These are some MR slices to show you where the cavernous sinus is. It's easy on the MR usually to pick out the cavernous sinus. Sometimes it's a little tougher like on the coronal CTs because it's not as well donated, right? But the cavernous sinus is there and there. The ICA runs through it. So you get like the flow void there that you can see. And then the cavernous sinus is here and here. So they'll love to ask imaging questions about that. So if they show you a picture of a dilated superior ophthalmic vein like that, it will either be about a Cc fistula or a Cc thrombus probably. If the cavernous sinus is pretty opacified looking, like these are, if it looks diffusely opacified, it's going to be a fistula. If it's not enhancing, it's going to be a thrombus. And this is a CT scan showing the cavernous sinus. So these are, it's a bilateral cavernous sinus thrombosis, but this is where it is on the CT scan. So I think the question, I think they asked on one of my OCAPs, it was a CT, it was a coronal CT and they asked like, where is the cavernous sinus? Does anybody know what that structure is? It's the pineal gland, right? So they, do you guys know what syndrome happens with the tumor of the pineal gland? Yes, the dorsal midbrain. So this is another thing that they ask about. So the dorsal midbrain syndrome, paranoia, is when it's almost always due to a pineal gland tube, 90% of the time. So if they ask you about it, it's going to be related to that. But does anyone remember any of the findings of it? So they get paracys of upcase, they don't look up, they get mid-dilated pupils, convergence, retraction, and a stagmus on attempted upcase, so the eyeball head pulls back because you get co-contraction of the muscle. They have light near dissociation and upper lid retraction. So that's a really easy one because it's very localizing, right? So they can describe these findings and then say like, where is, like what structure would likely be abnormal or something like that. And that's, they will likely give it to you in a sagittal view. Oh, I could almost guarantee it will be sagittal. What are the most common intracomal tumors? Does anybody know whether they're the top three? What's number one? What are the other two? Yes? Okay, so this is a little table from the BCSC about differentiating between the optic nerve glioma and meningioma. So I've got a few pictures here, but you guys can check out that chart. It's kind of helpful, but so we'll start with the optic nerve sheath meningioma. So this is an unplugged meningioma where it's just, just surrounding the optic nerve. So that's kind of the classic picture. This is an enhanced MRI. That's the tram track appearance. So they will likely show you one like that. It can be expanse out, so it can just kind of look like a big blobby thing, but it won't enlarge the optic nerve. The other way that they may show it to you is showing calcifications on a CT. So that's an easy way to differentiate between glioma and nerve sheath meningiomas that there may be calcifications. Treatment, if somebody has an optic nerve sheath meningioma. Does anybody know? So it's going to be observation versus maybe radiation. So the typical picture is usually a woman. She's kind of middle age. She'll get progressive proptosis with some vision loss probably over time. May have optic nerve palloradema. You don't have to do anything about it unless they're losing vision and it seems like it's extending back along the optic nerve because, so basically we observe it unless it looks like it maybe is extending back. I'm going to hit the other eye and then you can radiate. And this is what a path slide might look like with the somoma bodies. So kind of the the whirls of spindle cells there. This is a more representative picture of an optic nerve glioma. So it's the big cuji mass of the optic nerve. It's usually they'll probably show you the fusiform enlargement and they usually will get some optic nerve kinkings. So that's why I picked that picture. The typical picture right in kids, like if they're less than 10, it's a low-grade astrocytoma. So they usually will have vision loss with proptosis. It may or may not be painful in a kid with strabismus, dyskidema, or atrophy. In kids, it's considered benign basically, but there is somewhere around a 15% mortality rate usually if the tumor extends back and is involving the hypothalamus. But it's basically considered benign. Does anyone know the systemic condition it's associated with? In kids, 10 to 50% of kids with an optic nerve glioma will have NF1. Yep, so that's an easy favorite. In kids, the treatment is usually observation. You can surgically excise it if it's rapidly growing. Or you can do surgical excision plus minus radiation and chemotherapy. But that's usually like to preserve vision in the other eye or if it's acute diff, it's extending back to the chiasm. In adults, this is glioblastoma and it's fatal usually within a year. And that's what the pathology will look like. This is for the kids. So as I said, it's considered a pilocytic astrocytoma. So you'll get round to spindle nucleotide and a fair number of rosenthal fibers, which are the cigar shaped eosinophilic ones. So that's for the optic nerve sheath of meningioma with the tram track appearance. And that's for the optic nerve glioma. So this is the cavernous hemangioma. So the typical picture of this, again, they're going to describe a middle-aged woman with painless proptosis. So they usually don't really get vision loss with the cavernous hemangiomas most of the time. So the picture will be middle-aged women who's noticed this progressive painless proptosis. Sometimes they get double vision with it. It's intraconal. It's well defined because you have this like dark pseudo capsule on there. And then you get this progressive enhancement on a contrasted MRI that's usually fairly heterogenous. But they'll show you something with a capsule. It'll look like that. So you could see how you maybe would get tripped up with the appearance of an optic nerve glioma. But they'll show you one that's kinking the optic nerve. And then this one, what they're trying to show in this picture is that it's actually displacing the optic nerve here. So it's like displacing the structures in the medial rectus, but it's encapsulated there. And it's going to slowly, progressively enhance. And then the pathology. So you have these dilated vascular spaces that are filled with blood. It's like kind of a septated thing. But if you see the blood, it's going to be the big one. So the treatment is what? What do you do with the cavernous hemangioma? Yeah, surgical excision. If you have to, you can just leave them. But if they have double vision from it or they're getting really proptotic and have exposure, you can take them out. Okay. So you can get an anterior communicating artery aneurysm that results in a visual field defect because of where the anterior communicating artery travels relative to the optic nerve. So it's usually superior that that's for the anterior communicating. So there's the chiasm with the prechiasmatic nerves running right there. But the thing to remember about that is that it will usually result in an isolated inferior visual field defect because it's laying over top. So that's kind of the picture of how okay. So we'll talk quickly about dominant optic atrophy. So it starts in younger kids, so usually before 10, it's autosomal dominant. The picture is going to be slow, progressive, loss of their central beauty that usually arrests around 2200. And they've got decreased color vision. They will have this wedge of temporal pallor. And on the visual field, they have the classic central or secocentral scatoma. So that's the picture third of looking right up. But yeah, they'll show you one where you get the wedge of temporal pallor here. Does anyone know what the gene is that it's associated with? Because they will probably ask that OPA1. That's the secocentral visual field defect, which can sometimes look by temporal. So you don't want to get thrown by that. They'll be showing you when that looks like that. But keep that in mind, secocentral scatoma. They make a by temporal one. Laborers. They'll definitely ask you a question about laborers. So it's the mitochondrial disease. Kind of a similar presentation to dominant optic atrophy, but they're older. It's usually males. It's bilateral, but it may be sequential. The picture of how the nerve looks in the beginning can be different, but later on it will probably look pretty similar. So this is an earlier picture, or picture, I guess I should say, at the onset of the disease. So you get this classic triad in laborers, where you get circumpavillary tilangioctasia on the surface of the disc. The disc looks swollen, but it's pseudoedema, so there's no leakage unforeseen. So that's going to be the big clue. Like it looks swollen, but no leakage. That's the classic thing for laborers. Okay, the systemic associations of laborers. So you can get laborers plus, where you have some of these other associated conditions. It's transmitted by female carriers, mitochondrial DNA mutation in the NADH complex. So there's the current, the genetic testing that's typically used will hit 90% of the mutations, and it tests for these three. The 11778 is the most common, but the 14484 has the best chance of some spontaneous improvement. So I would definitely know these things, the big points about the three different mutations, because they may ask that, which one do you definitely should you definitely send for an EKG connect? I want to make sure that you rule out cardiac rhythm. Okay, optic nerve drusen. So deposition of protein like material in the optic nerve head, it's usually autosomal dominant. So examining the parents can be really helpful, but it can be sporadic. They may show you, I remember seeing at least one path slide about this on the OCAPs of how the path is going to look with the basophilic, acellular stuff. Mucopolysaccharide positive. What are the rarest of all of optic nerve drusen? Can anybody tell me what, what sometimes happens with them? They're not always totally quiet and benign. So you can get neobascular membranes and hemorrhages, and if they compress the nerve enough, you can get an ischemic optic neuropathy, but peripapillary CNBM can be from drusen. What's the most common visual field defect from drusen? They can kind of do anything, but most common is infronasal. What imaging modalities can you use to visualize drusen? Yes, what else? What? Yes, what else? CT. Okay, and what are the two systemic conditions that have a higher incidence of optic nerve drusen? This would be a very high yield question because they love asking stupid shit like this. Yes, and retinitis pigment. Okay, so we'll talk briefly about the toxic or nutritional deficiencies. So the presentation is going to be fairly similar to the other, like the inherited optic neuropathies, where you get usually it's a bilateral, progressive loss of color vision, perhaps central acuity with a secocentral visual field defect. Vitamin B12 deficiency is the vitamin deficiency that's most likely to cause the issue. Usually it's in people who are drinking a lot of alcohol, they're replacing their calories with alcohol, or they've had bariatric surgery. So if they give you any stem about bariatric surgery, you almost guarantee it's going to be like a vitamin deficiency thing. Remember, from the days when we were real doctors, that B12 deficiency can result in that stocking and glove distribution of the peripheral neuropathy. So they could describe it that way. Ethanol and methanol can do the same thing. Ethanbutyl isonizide, rifamp, and the treatment for TB can result in a dose dependent thing. So the higher the dosage, the more likely you are to have to get it. Usually the discs, they'll just present it as a pale disc, but initially they can have some disc hyperemia. It's pretty rare to have actual disc swelling from it. And then you definitely need to remember about the amiodarone toxicity. So most people on amiodarone will get the vortex keratopathy, only 2% get an optic neuropathy. Two-thirds of the time, it's bilateral. So if they're presenting somebody that looks kind of like an Naion picture, but they don't have a disc at risk, and it's an insidious progressive onset that they may be talking about. Aion, we probably don't even really have to do this review because everybody knows this stuff. But they'll probably ask, they'll probably present like a typical Naion picture and then ask what's the appropriate management. So for a typical Naion picture, they'll say that it's a disc at risk. You need to have that, some sectoral paler. Usually they'll show an altitudinal field defect with it. You need to think about a phosphodasterase, 5 inhibitors in amiodarone. But the treatment is basically a complete physical evaluation to look for microvascular risk factors. So like checking blood pressure, lipids, glucose, A1C, a sleep study, and avoiding blood pressure medications at night. That's going to be the treatment. So some version of a microvascular risk factor assessment is how they'll probably ask for it. And for GCA-related ischemic opting neuropathy, you know, it's usually somebody that's older. So older than 55, but usually older, associated with polymyalgia rheumatica. So they will get pain in the shoulder and hip curtals. And then of course, everybody knows the other typical symptoms of GCA. And I'm going to say if they show a picture with paladedema or a bunch of disc hemorrhages, don't choose A1. So disc hemorrhages are relatively more uncommon. And a lot of disc hemorrhages are really uncommon in A1. So they'll probably show you like a swollen nerve with some hemorrhages, or cotton wool spots. And then you should be thinking GCA. And then you want to check the ESR-CRP. You need to get a TA biopsy no matter what the ESR-CRP is. If they're presenting a story that sounds really symptomatic for GCA, right? So you want to get the ESR-CRP, start them on steroids, and then get the TA biopsy, even if the ESR-CRP is. Okay, paladema, you know, is disc swelling that is specifically related to increased intracranial pressure. So it's bilateral. It might be kind of asymmetric, but usually both nerves. They have preserved visual function until the disc swelling is severe. So if you have a pretty swollen nerve, and then the visual field that they show you is just in large blind spots, they're going down a paladema route. So the typical headaches, I mean typical symptoms, obviously headache, transient visual obscurations. So DML, it's blackouts, when they change position for a few seconds, pulse-synchronous tinnitus, hearing the heartbeat in the ears. You can get a six nerve palsy if the pressure gets high enough. They usually don't have visual loss until it's advanced. So causes of increased intracranial pressure, the workup that you do, if you're suspecting that, you have to do the MRI brain because you can have increased intracranial pressure with a big tumor or meningitis or like a meningiocarsinomatosis. You have to do the MRV to allow venous tinnitus thrombosis, especially if they're telling you a picture about a woman on like oral contraceptives. Pseudotumor cerebri is the other sort of umbrella term for increased intracranial pressure, not from one of those other issues. So it can be sleep apnea induced. That's going to be, that hasn't really been tested. I don't think that much previously like the association, but it will be eventually they'll catch up with it and start asking questions about that. Of course, everybody knows the medication to do stuff. Just remember that IAH is a diagnosis of exclusion. So you need to have a normal MRI, MRV, and the CSF study. So obviously, we won't have an elevated opening pressure on LP, but otherwise should be normal. So, you know, everybody knows the picture for IAH, right? It's a young woman. She's gained weight or she's overweight. If it's a younger kid, they won't necessarily fit that picture. But the treatment is weight loss and headache treatment. If there's no dyskidema or if the dyskidema is mild, relatively mild and there's no vision loss, you add in acetazolamide. There's other medications that can be used to like furosomide and topomax, but if I ask about acetazolamide, if there's vision loss and, you know, aka dyskidema. For advanced or fulminate cases, you do surgical intervention with a nerve sheath administration or an outpatient. So optic neuritis, if they're giving you a question about optic neuritis, you really in your mind want to decide when you're reading it, like, are they presenting a typical optic neuritis or an atypical optic neuritis? So, the typical optic neuritis is a younger patient. It's usually unilateral. 92% of the time, you'll have pain with eye movements, an effluent pupillary defect, and dyskidema like relatively mild dyskidema in about a third. So, if it's atypical optic neuritis, like if it's bilateral, if there are hemorrhages, if it's severe dysk swelling, if it's severe vision loss, if there's no pain, then it's a little bit of a different approach, and it's going to be kind of a different answer to the questions, right? So, if it's typical, then the results of the optic neuritis treatment trial do apply, and really the only workup that you need really is the MRI. If it's atypical, those study results really don't apply, and you have to rule out other systemic conditions with a bigger workup. You will definitely get a question about the optic neuritis treatment trial. So, the objective of the study was to try to decide what the role of steroids should be in the treatment of acute unilateral optic neuritis. The studies show that IV steroids will result in a faster recovery. That's the protocol that they used. It doesn't result in more recovery after a year. IV steroids did not reduce the rate of additional attacks of optic neuritis, nor did it reduce the incidence of MS at three years compared to placebo. It did slightly reduce the incidence of the development of MS at two years, but by three years it was the same. So, you always consider treating optic neuritis with IV steroids, but you don't have to. You don't want to do oral predalone, because there's a higher risk of relapse compared to the IV steroids. Then, the optic neuritis treatment trial also showed or proved why you have to do an MRI on everybody, and it's to risk stratify them for the development of MS. So, by 15 years after the optic neuritis episode, if they had no periventricular white matter lesions, 25% went on to develop MS. If they had one or more lesion, about 75% went on to develop MS. So, they're definitely going to ask you one question about this. NMO is going to probably be more asked about more and more over the next few years, because so much more is being learned about it over time. But, you know, it's an autoimmune condition that results in primarily demyelination of the optic nerve and spinal cord, but you can hit the bright stem as well. And there is the particular autoantibody, the PITG, against aquaperm for water channel membrane protein in the oligogendrocytes. So, this is some updated criteria about diagnosing it, because you can make the diagnosis with or without positive antibodies. So, I would be basically familiar with what you need to diagnose it. So, there's the transfer to myelitis. You also want to think about NMO if they describe an area of post-tremous syndrome, where somebody has intractable hiccups and vomiting. So, third nerve palsy can be, you know, it can happen anywhere along the track. It's rare to have a nuclear third nerve palsy, but there's some really particular findings. So, you want to be basically familiar with it. If they get a nuclear third nerve palsy, they're going to have bilateral ptosis and contralateral superior rectus perisys, in addition to like the typical findings. The pupil involvement will either be both eyes or either eye, because the editor Westwell Nucleus is going to survive both pupils. There are the fascicle syndromes, which like I, you know, I learn every year and forget every year and I still don't know. And I don't know if, I can't remember if I ever actually had a question on it. So, I don't know how birthed it is to know those, but if there is an associated fourth, fifth, sixth nerve palsy or horners, make sure you're thinking about the cavernous sinus. 95% of the time, if it's a compressive etiology, the pupil will be involved, but 20% of the time, it's spared initially and then goes on to become involved. 80% of the time, an ischemic or microvascular third nerve palsy will spare the pupil because the pupil fibers are running on the outside, right? So, if you have a compressive external thing smooshing on it, then it's more likely to be involved, whereas the ischemic stuff, the blood supply is more interior. So, if it's microvascular, it will get better in three to six months. It's, oh, I don't know if, I don't know if they'll ask specifically like, do you have to get an MRI, an MRA in an ischemic? So, if they're presenting a picture where it's a complete third nerve palsy, but pupil sparing, then they're going down the ischemic microvascular route. It's important to note that if it's a commercial third nerve palsy and pupil sparing, that is not a microvascular picture. Like in real life, it can be that way, but on the test, it has to be a complete third nerve palsy and pupil sparing for it to be considered like a typical microvascular picture, but you don't have to get an MRI, MRA in that particular setting, but you do have to see that really, really frequently for like several weeks, like daily or every other day or something, because 20% of the compressive ideologies will start out as pupil sparing. So, it'd be hard to go wrong with choosing the answer of like, that you have to work it up with an MRI, MRA. And then the other thing is that if the MRI, MRA is negative, then you have to get a cerebral angiogram. That's another one where the, if the real world, that's not really what we do, but on the test, that's the right answer. If it's negative, you must get a cerebral angiogram. And then always, always, always want to think about a GCA because sometimes it'll present that way. Myosthenia gravis may present with a third nerve palsy mimic, but it won't involve the pupil. Averint regeneration of the third nerve, you can have three different types, muscle to muscle, muscle to pupil, where the pupil constricts on either down gaze or adduction or muscle to lid, where the lid retracts when they move the eye. So, you want to look for that because aberrant regeneration is never seen with a microvascular third nerve palsy. So, if someone has aberrant regeneration from that, it's either from a tumor aneurysm or some other compressive cause or trauma. The fourth nerve palsy is the only one that decreases and it exits the dorsal brainstem, which is why it's the most common cranial nerve palsy in head trauma. In a congenital fourth nerve palsy, they'll have increased vertical fusional amplitudes. If it's long standing, they'll have probably like three or more diopters of vertical fusional amplitude. If it's congenital, it'll be like 10 to 15. If it's a bilateral fourth nerve palsy, the right eye, they have the crossed vertical strabismus, where the right eye is higher in left gaze, left eye is higher in right gaze, and more than 10 degrees of x-cycletortion with a double mattox rod. They may also try to show you a fourth nerve palsy by showing you a fundus photo with x-cycletortion. So, think about that. If they show you a picture like that, they're talking about the fourth nerve. The three step test, I have never had a question about a three step test that wasn't a fourth nerve palsy. I mean, you know, they could ask it, but it's always a fourth nerve palsy. And I think that's primarily because the three step test actually has relatively limited use. Like, it's helpful in the fourth nerve palsy, but other than that, most of the time, there's more than one muscle that's involved in any type of restrictives, strabismus, or whatever. So, like, you'd have to prove to yourself that it's not a fourth nerve palsy if they ask you about the Park's Bill Kassie test. Sixth nerve palsy. So, remember that the sixth nerve exits the, you know, front side of the pons next to the cerebellum pontine angle where the seventh and eighth nerve is. Then it climbs up over the clivus, goes through droll's canal, in through the cavernous sinus, and through the superior orbital fissure. And that area where it goes through droll's canal is adjacent to the pietrus bone. So, if they get a pietrus apocytus, like a kid who gets mastoiditis after, like, inner ear infections, they can get a gratin egocentral with six sevenths nerve palsy and decrease hearing. Microvascular is the most common type of sixth nerve palsy, especially if it's an older person. So, you don't have to image them unless it hasn't gotten better after three months, but they do need to be evaluated by the primary care or, you know, just evaluated for microvascular risk factors. There are a lot of mimics of a sixth nerve palsy to be aware of. If the person that they're describing is younger than 50, they must have a workup with an MRI and an LP. Kids can get a post viral sixth nerve palsy, but they will need a workup if it's less than 50. Inter-nuclear ophthalmoplegia, so they cannot adduct the ipsilateral eye, and they get abduction nystagmus in the fellow eye. It's a lesion of the medial longitudinal fasciculus. If they're still able to converge, then it's anterior, like in the midbrain. If they don't have convergence, it's posterior in the pons. If it's a young patient, it's a debilondative picture. If it's an older patient, it's going to be a stroke picture, but mycenae gravisan millerfisher can mimic it, including like with the nystagmus in lateral gaze, so keep that in mind. This is a picture of a midbrain INL. So, this is DWI, but I'm just trying to show you where it is. If it's in the pons, it's going to be a little bit more dorsal, so kind of like in that area of the pons there. But that's another one that's so easy to ask because it's so localizing, so I would definitely know that. CPEO, chronic progressive external ophthalmoplegia is an inherited mitochondrial myopathy, which can be inherited either through the maternal mitochondrial DNA, autosomal or sporadic. So you get slowly progressive symmetric lack of movement of the eyes, usually with ptosis, sometimes without. It can be out that you can have a nuclear DNA mutation that drives a mitochondrial protein issue, so it can either be nuclear or mitochondrial in nature. So this is the picture, you know, diagram showing representative findings. So this is what it looks like ptosis. They usually have a little bit of a chin-up position and they're going to have symmetric ophthalmoplegia to varying degrees. So because of that they're usually not depopic, but they do have a hard time reading and they're bothered by the ptosis. That's usually like, it's usually about it in terms of the visual complaints. They're not usually that bothered by the lack of eye movement. And then some people have generalized proximal muscle weakness. So in order to diagnose it you can do genetic testing and you get a muscle biopsy looking for the ragged red fiber. So this is the comory trichrome stain in a current seer. So this you definitely have to know current seer is the syndrome that's associated with CPO and the cardiac conduction abnormalities can't kill them. Does anybody know what the finding is in EKG? Like what are you actually looking for? Prolonged PR. They get heart block. But everybody with CPO should have a hearing test, an EKG and an LP. This I thought was kind of helpful. I'm not going to go into like thyroid eye stuff because I think it'll be covered well elsewhere. But I thought it was a helpful thing to show. What does it look like if it's tendon involving versus tendon sparing? So this is the tendon involved, tendon involving and tendon sparing. Thyroid orbitopathy is tendon sparing. I'll say this, it's not. Okay these are some of Anna's slides. It's too much, it's too much to go over. So aesthetic pupil is generally idiopathic and we don't really know why. It involves loss of innervation through the short posterior and the ciliary ganglion. That's usually a unilateral initially but a significant number becomes bilateral. It's usually a woman and she's younger and she'll have a big pupil that doesn't respond well to light but it responds better to accommodative effort and the pupil will sometimes get small over time. That's the little old 80s and they have loss of accommodation that usually gets better. So when you look at them under the slit lab you look for the verbiform movements of the iris. Why do they get the light near dissociation? Because 90% of the fibers are innervating the ciliary body, 3% are doing the iris sphincter, so they actually get aberrant regeneration of the iris sphincter by those remaining ciliary body fibers. That gives you the slow air reflex. So usually you don't have to work it up but if they present with kind of acute bilateral 80s think about other causes. Usually it's going to be like a simplest question. Ideologies of light near dissociation, you do want to be just kind of generally familiar with it. Yeah, so you do have to know the localizing types of nystagmus. They'll probably ask you about, if they're going to ask you about one, it's probably downbeat and then the next most common is probably seesaw or obsoclonus. So downbeat nystagmus, you want to know that it is pathology at the cervical medullary junction but also medication induced like lithium and some of the other anti-seizure medications. Obsoclonus can be perineoplastic, you want to know that. Neuroblastoma, you're going to cover this elsewhere too, but if they talk about a kid that has sudden onset proptosis or eyelid swelling or eyelid bruising, especially if they're describing any type of nystagmus picture then it should immediately make you think of neuroblastoma. And they may have errors with it but you diagnose it with looking for catecholamines in the urine, you can biopsy it, a mean age of presentation is two. These are pathological features of metastatic neuroblastoma to the orbit so the Homer right rosettes are the typical thing unless it's metastatic and then they may not be as differentiated. These are the poor prognostic factors in your life. Okay, that's it. Does anybody have any questions?