 So this is a right orbit. They frequently ask like what borders the optic canal or the superior orbital fissure. So you want to be thinking of your sphenoid bones. The one little tidbit is at the front of ethmoidal suture marks the inferior extent of the anterior cranial fossa. So if you go above that line and you go through the bone, then you'll be in the anterior cranial. So it's a surgical landmark and they like to ask the bones of the orbit. So there's lots of mnemonics out there for those. This is my little chart for the fissures. You want to know which things go through what and that's, I'm not going to go too much in the detail here, but just as a refresher, that's some of that there. This little diagram here of the blood flow, particularly the anterior part is what they ask about. So the short postures that are arteries or carotidals are for the pre-laminar, the circle of syn and the laminar space, and the rest has different distributions of the central artery, the branch of the thymic artery and feel vessels. You may remember that the intercranial optic nerve is the anterior carotid and the anterior communicating. And the posterior circulation with the skull of willis goes back to some old anatomy from step one and step two, but that does have some clinical importance. There is some nice dual supply things and the optic tract is one of those and a lot of nucleus. So you may remember the anterior carotidal and the posterior lateral carotidal arteries for their specific visual fields that injuries from those would result in. I'm going to skip this question. There'll be some questions here, so we'll have some feedback. So you guys don't fall asleep on me, but the expected deficit of optic tract injury, this one's too easy. You'll have a contralateral hematopoeia, contralatal RAPD, contralatal band atrophy of the optic nerve hidden. As you can see on this diagram here, venous flow, maybe you more see this on neuroimaging, but there's some specific carotid optic cellular joint vessels, which you want to have a little differential for. These are the most common ones to your view. Neurofeet meningioma, glaucoma, chronic papillodina. Good old sympathetic autonomic system. You'll want to have a picture of this in your head, and you can find it up into the three different nerve chains, but I feel like it doesn't get asked too much on OCAPs. You may remember that the sympathetics get to the orbit through the nasoaciliary and long-cellar nerves, and that's a little tidbit that isn't so fresh to them or isn't so easily brought to memory. Similarly with the parasympathetics, you're primarily thinking finger Westfall, fortceary nerve from the cellular ganglion, but there's also the lacrimation component of it, so that has a different path, of course. These will end up going through the inferior orbital fissures as well, the things in the inferior orbital fissures, the parasympathetics. Two, I think everyone gets this one pretty well. Three, it does have many nuclei, so everything's lateral except this superior rectus, so we'll think of that in your nuclear creditor of three lesions. The levator is bilateral, and then there's this proportion that goes for accommodation, and then for the light reflex, which I thought I edited here, but ten times many fibers for accommodation, and that's one of the anatomic bases for light-neared association. Under four, the one we all know and love has a little décusation, it does décusate approximately, and it exists along the dorsal surface. We'll get more in the creditor four a little later. Under five, V1 and V2 go through the cavernous sinus, and you might recall the standing room only thing for the foramen that those go through. Under six, remember this one's, this is the one that's in the substance of the cavernous sinus, so it's more vulnerable to compression, and it initiates horizontal gaze through the medial longitudinal fizziculus. Under seven, we'll get into that a little bit later too, and this is why the efferent exam in neurophthalmology is so complicated because there's a lot of cortical input from many different areas, so it's poorly localizing, unfortunately. But in general, you can think of vertical movements being the midbrain and horizontal movements being controlled by the pumps. That's not as too frequently on OCAPs, so we won't get much detail for that. Okay, so you'll get lots of photos for your OCAPs, and does someone want to interpret this photo here on your left? Let's go with Cole. How did I know you're going to pick me? The last one that spoke. Photo of the left optic nerve. Did the fields go with the photo? No, no, no, sorry. Okay. I'm maybe a little power-less, but I don't see a whole lot else. Yeah, it's normal. Great job. Thanks, man. Recognizing normal, you'll usually get four pictures. One will be normal. One will be, you know, you're going to have three pathologic nerves, and you've got to figure out which one they're describing in the stem. That's a very typical question. So there's your normal one. I only have this one here because they have the sizes for the lights. Just remember one of them, and then divide by four for each number. So the five sides is 64 square millimeters. We usually use the three, which is 16. So hopefully you can remember one of those, and use a rule of four from there. You won't ever interpret these visual evoked potentials, but they may mention that it's quite helpful that knowing that the latency is prolonged in emulation. And if it's the amplitude, that's more of the ischemic or compressive optic neuropathies. Right. So we're going to dig into a little more specifics. So they love to ask about the super rare things in OCAPs as well as in boards. So sometimes you have a pretty normal examination, but they're having either visual acuity loss or phytopsias, more phopsias, and you're trying to determine what they're describing. So be aware of your white dot syndromes as well as some of the other more retinopathy type of things that can be confusing in the question stem. So I think I... So that's just a little reminder to don't forget your retinopathy that can be the pretty normal on this examination. You'll have a broad differential. Of course, this is more clinical, I guess, than OCAP related. Let's get this one. And we're all very used to acute papillodema. I think from your call days we get plenty of those. You see it quite frequently, but these are some of the signs that they may show in pictures that you can or have written in the question stem that should make you think of an acute process. All right, we have another photo. Brandon. Yeah. So it looks like there is swelling of the nerve. You can see patterned lines circumferentially. I would say minimal vessel obscuration. And then you also have paler. I don't appreciate any drusen. That being said, without vessel obscuration, I'd be somewhat concerned for pseudo drusen. I mean, pseudo papillodema. This is an example of pseudo papillodema. This is actually from the BSG. These lines here would have fooled me as well, but you may think more of a hyperemic disc if you're having drudema or some vessel obscuration with what looks to be a lot of swelling if you're looking at the disc margin, but those are pretty clear. So this is pseudo papillodema, probably from drusen. I think I saw Allie. Yeah, Allie, what you got on this second one? This is a disc. It looks almost like the appearance that you would get with maybe like chronic edema where it's kind of got this fibrosis at the disc margin, or it could be myelinated because the disc itself doesn't look like it has paler, but it also could be obscuring. I don't know. Yeah. There's another pseudo papillodema. I think those are good two things that you brought up. This is, I'm pretty sure this is supposed to be myelinated in neurofibroliter. It is kind of broad. It's covering like, you know, more than six o'clock hours, which I think would be a little a-typical, but yeah, good job. Sorry. Let's give this. There's your differential for papillodema. Sure. So yeah, chronic papillodema has its own little fine beans and maybe Marshall, you want to describe or what do you think this one is here? Obviously it's chronic papillodema, but what are some of the findings that were? Yeah. So here you can definitely see still a little bit blurring of the disc margin, and then you can see some of the gliosis that's happening. Yeah. Yeah. So this is what does look pretty similar to that last one. Nice job. Hi, H. I thought you don't get many questions on this one, but obviously it has a lot of clinical importance. You may try to remember or be tipped off with some of these associations for pseudo tumor cerebri. I think that's an easy one. If they ask you a question about that, there are some findings. Again, I don't think they'll ask you much about it, because it's too easy for OCCAPs. You need more esoteric things. Yep. I don't want to ask you much about treatment either, and I don't think that'll be a question. There are some box of factors that they list in the BCSC, which are these five things, which I try to remember, but I don't think that'll be a question either. Optic neuritis is a good one. There's, of course, many different flavors of object neuritis, but the typical is the MS associated one, all this data is coming from the optic neuritis treatment trial. So most of those patients had or were evaluated for multiple sclerosis. It was kind of pre-mog and inov pain, of course, being a big tip-off and a normal funnest exam. And there's many atypical features here that should make you think of other things. So, yeah, if you're having funnest findings, then maybe you don't think multiple sclerosis thinks something else. Treatment, optic neuritis treatment trial, they might ask you about this. Basically, that oral is not used anymore. Sometimes there's old questions that are pretty straightforward, but yeah, oral prednisone, prednisone, increased risk of recurrence. And they won't ask you about any of the MS drugs like in particular. There's pretty classic rules, 25, 90, 50, 75 rule with risk inversion of MS. And so that is if they have no lesions, they have 25% to convert to MS in 15 years. And if they do, they have 75 for almost 75% chance. And if you don't give them a ride, then they're like in the 50% range. In a mo, may have some spine photos, perhaps. Diagnostic criteria here. I don't think you'll be asking any specifics about this, but good clinical information to have in the back of your head. No retinitis is a good OCAP question. You'll typically will have more than acute vision loss and may have a normal macula in the early stages, which is what this one shows here. I only developed the macular star or those exudates on this side. There's many different organisms, which we're going to skip that question. But who else is here? Lydia, which layer will the exudates to chemally? I'm wondering if it would be endless layer, but I honestly don't know right now. Well done. Perfect. All right, perineuritis. I don't see this too much, but it's one of the other painful eye movement entities. You do typically get some visual field loss, but not to the degree of arthritis. And you definitely need to treat it with steroids. That's one of those things that if it's kind of, that's what they're showing you on MRI with the nerve, sorry, the dural sheath enhancement, you'll want to treat with steroids and it should respond quite rapidly. So this is a little comparison between arthritic and not arthritic. I don't think, I mean, I don't think this is too groundbreaking here. It's good to know that there are symptoms that are sometimes minimal, but the transient dyplopia and transverse obstrations are good orthologic things that hopefully will pick up in your review systems. This is a pretty typical setup for these questions. I'll go through these. I think we've done these before, but the top frame is the right and left eye. So now I'm in on the left eye, the disc at risk on the right eye, and the bottom to our typical arthritis edema. So the right side doesn't have a disc at risk, and the left side has this kind of yellowish chalky, like no blood is getting to that area appearance. Let's get through some of this. Meningeomas are meningeomas and gliomas are at least one question typically. So big tip off is age. So if you're having a meningeoma, you're typically the middle-aged women, and they have it, I believe it's supposed to be a triad, but optic atrophy and the optociliary shunt vessels. I think there was supposed to be the third thing there, but so that's something that if you see shunt vessels, you're going to have to image them, because they may have the narshithmeningeoma. And we'll get to the comparison here. So gliomas are typically younger, 90% by the second decade, and proptosis is quite common with it. The big thing is comparing the two. So we have a CT here, which can be used. Who else is out there? Sean, what do you see and what is the diagnosis? So it looks like in the right orbit, there's some enhancement of the optic nerve sheep. And I mean, when I'm thinking about that, it could be a perineuritis, could be glioma with sort of a fusiform enlargement. It also could be a meningeoma with more of a tram tracking appearance. Nice. Yeah. So this is a CT. And so it's like thickening of the narshith is what it's trying to display here. And there is, you can kind of have a tram tracking if it wasn't MRI. We'll get some MRIs too. So yeah, this is more of the glioma style. There's the donut sign for meningeoma, narshith meningeoma, this MRI. And this is the more globular shape of glioma. Not the best imaging to be honest, but I think pretty sure these are photos from the PCSC. So here's all that together. Some things to point out. The meningeoma has a few tubular enlargement classically. And you may have this tram tracking. That's what you'll typically find on your OCAS. The glioma has a kinkine or buckling or can be, but can be fusiform, which these can be fusiform. If it's fusiform glioma, then it can be challenging. But typically you can make out the nerve on narshith meningeoma and glioma. It's hard to distinguish like a distinct optic nerve because of the whole things and transit to that tissue. So they love labors. So this is more males and females, typically in the younger crowd. And it does have a mitochondrial inheritance, most typical, typically sequential within a few months and end up with central or papillomacular visual field loss. This one you can have some pseudo edema as well. Pericapillary tautectegias are a good thing to be careful and fund us for. And the mutations are for me, I feel like they do ask about these, but the 11778 is most common and the worst. And the 14484 is the best. So here's some of those photos. You can kind of see hyperemia, the disc here with the tortuosity pseudo edema. And then this is presumably going to be the next eye to deal with that. You can get some staining of the disc, not particularly with much leakage. All right. Next one. There's someone else. Tony. So you have optic this photos of both eyes and it looks to be temporal pallor. Do you think it is? It looks pallorous to me. Right. What's the diagnosis? Diagnosis could be some kind of optic neuropathy, maybe nutritional. We're in the hereditary. We're in the hereditary. Oh, we're still there. Okay. Could be autosomal dominant optic artery. Yes, all done. So, yes, this is the OPAG, ocrumasal 3, also thought to be mitochondrial. It's nice to remember this one has that blue-yellow deficit. So tritoninopia. And that's a good question that they'll tend to ask. That temporal pallor in a young kid that failed a vision screening exam is a typical stem. So, yes. Drusen. Everyone loves Drusen. Remember retinitis genitosa and pseudo-exanthoma elastica as the commonly associated, very rare diseases. I think we can skip these. The photos are more important. So all of these photos are Drusen. So I won't test anyone on these. But just pick out these little small refractile bodies here, here, here. I've got peppered all over on this one. This one has somewhat irregular blurred margins as well. This one has very clear Drusen. It also has that blurred margin. You can have these little ILM things that will make it look like it's swollen. You have some really dramatic ones. This is supposed to point out this anomalous vascular branching, which can sometimes be associated. And then if you see this, maybe think of something else. Cole, we're back to you. What else? What is this? Like an astrocytic hamartoma. Very nice. Mulberry lesion. They love to ask about fecomatoses. I don't have that much in my presentation. But this is one of those. This can be with tuberculosis. Okay, genital, optic nerve hyperplasia. Fetal alcohol syndrome can be pointed out with this one. Let me show you a kid with telecanthus and that long enlarged or prolonged philtrum syndrome. With obturant nerve hyperplasia, you may have this double ring sign. Not super clear on this photo, but that's what that one's supposed to be. There is a spectrum of obturant nerve head anomalies, which include optic pit, coloboma, nerve dysplasia, and warning glory anomaly. And I'm thought to all be, to some extent, the same embryologic process. But optic pit, you're thinking infrotemporal. That's a nice one. And you can have these serious macular attachments in a good portion of them. Colobomas are infronasal. And typically associated with coriorectal colobomas as well. This has a very bright, not bright, but an egg white type of picture to it. It's pretty distinct. I'm sure you'll recognize that. This plastic nerve, you'll typically have central retinal vessel attenuation. And you may even have non-perfusion periphery. And this associated with this PAX2 papillorenal syndrome. Same with morning glory. Morning glory anomaly. You can also have peripheral non-perfusion, but you want to image these because if they're you're thinking of vascular anomalies like Moyamoya or baselow encephaloceles, which are an important thing to not excise. Transient vision loss. Sometimes they can help you with describing how the vision loss goes. So that may give you some inkling that this is a retinal emboli as opposed to some of the other things. Like bilateral vision loss be opposed to your circulation. Geometric qualities. I think you have occipital lobe dysfunction. So that could be a migraine, case evoked, or mass. So that may be helpful to really specific things on the exam. TIAs. I think the big thing here is you resend them to the stroke unit. So that's typically the management question is you have one of these retinal or emboli and it's now pretty well supported that we don't mess around with those. We send them for stroke. It's one of the things that you think of from giant salt arthritis, ocular hyperperfusion from CRBO, ocular chemic syndrome. And I personally like ocular chemic syndrome. So we'll go a little bit to this exposure to light will cause it and it can have positional qualities as well. You're typically going to have, you know, the like a typical veteran that has a lot of vascular factors to help you lead you to this diagnosis. Phytospazin is a diagnosis of exclusion and you may have some hyperviscosity that can lead to transubmission loss as well like polycythene. And so Coria does not equal any of the people that are defects. This is the effect. I think you've all seen this before because I think I've probably given you this before, but if you have a smaller and dim lighting, you have problem with dilation, that's sympathetic. You have greater in bright light, that's problem with constriction, that's parasympathetic. And you can use the cocaine test to distinguish for an arsyndrome and physiologic or apriclontidine test. And then use your lamp and pylocarpine on your other side here. Arsyndrome, a sensitive finding is dilation lag. And this is what she'll find with that. So apriclontidine, you'll have reversal of anisecoria. And with cocaine, you'll have a greater anisecoria, the normal pupil react in the abnormal. If you do the hydroxyamphetamine anymore, I think it's out of the questions as well. Can be some helpful systemic neurologic findings to help you localize it. And again, having this picture of the anatomy in your head can be helpful. For light near dissociation, another good one for anisecoria, dorsal midbrain syndrome is a typical or a classic one. So you'll have lopid stagmus, retraction of stagmus, accommodative precess, and you may even have the up gaze palsy. There's some epinems that go with these that are I can't quite think of right now. Argol, robbers and pupils, think you're syphilis or some of these autonomic disorders, even heavy PRP can give you that. And aberrant regeneration is a good one to keep in mind as well. Because the near reflex typically either is sustained or regrows, but the light reflex is not as robust. But this is only with trauma or compression is not with ischemia. And edutonic pupil, which I had other slides on, but you can think of that with the previous slide with the algorithm. They do like to show these gaze position photos. So I'll have someone go through this one as well. Let's see. Sean. Sure. Walk us through your process with going through these. So I mean, I suppose the first thing I'm just looking at is, you know, primary gaze or they or though they are. And then I mean, really just quickly scanning through and seeing if there's any obvious, you know, misalignment or palsy, which I really don't notice in this set of photos. Yes, this is a normal one. My helpful to bid for you is to look at the lead position for these, especially in primary gaze. That's something that they like to try to sneak in is either have like a little ptosis or reverse ptosis in there, or there's like one lid doesn't or like the retraction down gaze, like those are usually don't have someone holding up there. That's for that, obviously. But remember to look at the position as well, not just eye movements when you see these nine, nine gaze photos. 50 year old man presents with Diplopia of line resuscitation for stroke, right head till left hyper tropia, Diplopia approach with right gaze. Allie, would you like to answer this one? She's still here. Brandon, you go. All right, give me one second here. Right head tilt. Left hyper. It improves with right gaze. So I'd be thinking left, fourth, then you can also have x-cycle torsion. Let's see, hold on. Yeah, let's go with that. Fourth. Yeah. Okay. This is a tricky one. And one of the last frequently, this is probably actually an ocular tilt reaction of which skew deviation is part of ocular tilt reaction. But this one here is showing in cyclic torsion on the left eye. That's your tip off. That's not fourth. It doesn't quite follow the fourth nerve pattern. And they always will on these ocabs. So if you're, we're going to get to that in just a moment of what the fourth nerve pattern is. But it's, if you're thinking in real world, it's important to think of restrictive causes as well. So thyroid eye disease being very common and predic being more common compared to restrictive, at least in their ophthalmology clinic. So you can determine these by looking at the scatic velocity, which will be slowed in policies, four sections if necessary. This is my little overview for this section. So they're super nuclear, intra nuclear, intra nuclear and intra nuclear causes of Diplopia. So we're going to touch mostly on these last two thirds, but these are you know, tough ones for in clinic, but not for okay. So hard to write questions about screening of three. Remember the anatomy a little bit. You'll have driving nuclear lesion. You'll have the contralateral spirectis involved. Otherwise, it's all it's lateral. For the fourth, always be on the lookout for bilateral fourths that can be tricky. But if you're having a trauma and you're in a fourth, you should always be checking for bilateral fourths. You may have a horn syndrome if you're having a lesion to the dorsal caudal midbrain. And creator of six is nuclear lesion is a gaze palsy, not isolated abduction precess. So frequently try to trick people up on that with nuclear compared to inframuclear lesion. So if you're having a nuclear lesion, you'll also have some seventh nerve signs, like this blot of fish weakness as that fasciculus wraps around the sixth nucleus. INOs named for their slow to adducting eye. So left INO will be on the, wait a second. Yes, will be on the left side. So of the MLF will be where your lesion is. Because sixth nerve has can do its thing fine. And then as that signal goes up the midbrain to the third nerve is where that MLF is. That's where that adduction is going to be, that transmission is going to be slow. You typically will have a scudiation with that. You're thinking de-boundation at young, stroke at an old person, but it can be other things as well. Syndrome with this as well. So one and a half syndrome INO plus horizontal gaze palsy. So basically you're including the sixth nerve in addition to the MLF, or sixth nucleus, I should say, in addition to the MLF. And then the eight and a half is that plus the seventh interaxial fasciculus. So you'll get a seventh nerve palsy. I've seen these a few times, I guess, INO caps. So we're not going to go into all of them, but just be aware. This is your time to look at it and maybe remember a couple of these eponyms because they're still out there. If we have time, we can go back to this. People involving thirds are your scary ones. So as you may remember, the pupa fibers are superficial. And on the medial aspect, so it's right next to where the PCOM and ICA come together. So that's where the aneurysms can affect that. So non-traumatic thirds are aneurysm until proof otherwise. Complete thirds without people involvement, however, are almost always benign and microvascular because that's, if you think of like the inner substance of cranial nerve three being affected, but the pupa fibers are superficial, so they're still getting some blood supply. So your pupil will be fine, but your movements and your ptosis will be complete. But you can have a partial without people involvement that is still scary as it may evolve to include the pupillary fibers. This is a little chart that I made for that. So again, partial thirds, whether the pupil is involved or not, you need to roll out an aneurysm or compressive lesion. You have a complete third. If the pupil is fine, then you can probably relax a little bit, but you may consider GCA in the right setting. Who's next? Marshall, you still there? Yep, still there. Describe these. Well, describe what's happening in the photo on the right. The photo on the right, you see a left-sided ptosis primarily. Hard to really make out much more than that. Maybe the opposite actually. This is down gaze and this is retraction on the right. Oh, yeah. This is a good one. What process is this? I guess that's like a down and out with a blown pupil on the right. There is a lot of people on the right. Ignore that. This is average generation down gaze. You're having a third nerve palsy that now you're having activation of the inferior rectus and the levator at the same time. So that's your average generation there. So this is, yeah, the synkinesis. Dramatopressin, definitely not microvascular if you see average generation. So back to fourth nerve palsy. You have the combination of the tropia, the tilt, and then you may have a chin position as well as being improved in a certain gaze. So do I remember this? Oh, dang it. Yeah, remember these muscle actions as well? The one thing that you review quickly before you take the test is for the obliques, the primary action is the torsion component. So superior in torsion. And then the cortical action introduction and then AB detection for the obliques. This is my way of remembering it. Everyone has something a little different. If you're having a fourth and you almost certainly will get one of these questions where you're supposed to do this, three step test is to do the, my way to remember it is boot and woog. For me, that's easy to remember, but better on opposite tilt or opposite gaze. So you can just, if it's that pattern with the appropriate side, then it's going to be a fourth in these testing situations. So you can not write down your HHS and circles and all that stuff. Because sometimes time is an issue, but this is a quick way to identify a fourth from it. Yeah, so you'll have that torsional component. They talk about a double man X rod. They may have this lines converging towards the lesion. That's kind of your exact which I don't know. Yeah. So this right eye here is exactly toward it. You can see the macula is kind of too high in relation to the object nerve. Yes. Six nerves. I don't think I have too much to say on this other than this is kind of the gaze center here. So you have to do lesion. Again, you'll have gaze policy as opposed to reduced abduction or just reduced abduction. You always think of the six nerves anatomy and think of other processes that could be causing a six nerve, especially if it's congenital, you'll have that Dwayne syndrome, which can be reduction abduction, adduction or both. And you also have globe retraction with Dwayne syndrome. These are just some things out there. All these super nuclear motor systems don't remember these here, but they're going to come up in just a moment so I include this slide. Skiu deviation is an important one to distinguish from the fourth nerve. Use boot and woog. You'll typically be A, but sometimes skiu deviation can do this in real life, but in OCAPS, the in torsion, the x-cycle torsion is going to be the distinction. This is what ocular tilt reaction is. It's the head tilt, skiu deviation and cycle torsion rotation. We've been talking about it indirectly this whole time, but you're typically thinking of otoliths in the peripheral, but it can be central as well. It's midbrain syndrome. Discuss this a little bit already, but this is where basically you're going to have all these different systems affected as they kind of go through this dorsal midbrain. Yeah, I don't think that is too important. Let's get this one. You want to rule out a pineal base tumor if you're having dorsal midbrain syndrome, but it can also be more common things like a stroke or multiple sclerosis and newborns that has a little different presentation with that setting sun sign, and they'll be stuck in down gaze. Stagnance is a good one. I think there's a video here, but I'm, ah, dang it. Well, the fastest new dance has ocular oscillations that have arming into our cause. Who's next? Tony, are you still there? Yep, still here. Let me just read that real quick. Yes, 18-year-old. Oh, dang it. I hope you didn't see that. 18-year-old woman. Right nystagmus with left eyes covered, left nystagmus, and the right eye is covered. You get some tracings. What do you expect to see in this latent nystagmus? Well, I did see the answers. All right. Well, this one's decelerating. And that's opposed to congenital or infantilitis nystagmus. This one has the especially increasing slow phase. So to go back to this here, that's what these are, especially increasing slow phase and then a rapid correcting saccade, increasing velocity, slow phase, breaking saccade. And this is the light nystagmus where it's getting slower on the slow phase. I felt like I was always confused by that, but because they always would put fast phase on there, but like you can't have an accelerating or decelerating fast phase. It's just fast no matter what. So like the answer is always one of the slow phase ones. You just have to remember which one is which. Yeah. Good point. Fast phase is fast. Can't mess with them. Oh man, we only have five minutes left. So let's see. For the congenital of the stagmus, you're thinking of a pregeniculate vision loss. So foveal hypoplasia, retinal dystrophy, cataracts, emotional hamster business involved as well. But some that are quite frequent to be idiopathic as well. But you especially want to be thinking of pregeniculate causes of vision loss. Light nystagmus, this is any condition that disrupts binocular development early on, especially infantile exotropia. So we'll get some DVDs with this. Strabismus is common. Spasmus Newtans does tend to resolve later on, but you're mostly thinking of cellar, paracellar tumors as the cause for this. So that's something to check for. Stereolurnus stagmus. I wish I had more time to go through these, but remember the periodic one. I think that's one that's actually has really good treatment for it is baclyphine. So that may be something that comes up. This is their chart in DCSC for localizing the lesion. You'll get asked this on your neuro biology rotation. One bit about opsoclonus. One thing they like to ask about is neuroblastoma in kids. So one of the presenting signs is opsoclonus. And sometimes it's an early science was actually good prognostication if they have opsoclonus. Because it's more outwardly visible. It can be discovered. And one thing that you'll check is the urine for those metabolites of the catecholamines. Because it's actually pretty sensitive, like 96% or something like that. When adults, you may think of one or two antibodies and these cancers that tend to have those perineoplastic syndromes. They almost always ask about Whipple disease in some fashion. So remember Whipple disease as a cause for misdiagnosis. Mystena, I think we're all pretty familiar with that. Sarcoid. TPEO is another rare one. They like to ask about is mitochondrial, but sporadic is actually the most common. You tend to have ptosis, but Diplopia is actually fairly rare because there tends to be pretty symmetric involvement. You have the buzzword, aggregate fibers, and you want to do cardiac evaluation for conduction deficits. OPD is not a cause of aphthalmoplegia as well as ptosis. You have the French Canadian ancestry for that. And there is a mutation that I used to remember, but I don't remember anymore. I have been one PABN one. Thank you. I know we looked at that from clinic one time. You would know that. It's the only reason why. That's the only reason why, no. My type of dystrophy is osomal dominant. If they ask that for some reason, you'll have a lot of systemic signs, but you also want to do a cardiac evaluation for these people. Immersion hallucinations, not much for this one. Maybe this will be the last thing. So let's see. Who has time to do this one? Brandon, you have time? Sure. Which one's Gertzman syndrome? That's when you ignore the other half. No, that's semi-special like that. Gertzman is Alexia Grafiae, Calcula Fingregnosia. Which one's Anton? Anton's the Denial, because I ain't blind. Yeah. Which one's Blint? That's the optic ataxiac, the motor praxiae, and the cymultingnosiae. Yep. Bridac is motion, and you can be special neglect for the rest of your life. Let's see when we miss. We didn't get to talk much about ptosis or seventh nerve in its oddities. So we almost made it. That's like usually people may get through like a quarter of their slides. That's pretty good. Well, I hope, you know, it's hard on these reviews to delve into many details. So it is kind of a rapid fire, you know, one more time for your subconscious to see these entities. I hope this was helpful for you. There's, I think you get a really good neurothemology exposure here. So at least compared to what I've experienced, what other people experience. So I hope neurothemology is something to score well on. And I hope if you have any questions, you'll feel free to ask me. I'm happy to help. Eric, could you send up the slides? The PowerPoint? For sure. Just don't distribute them widely. Got it. Thanks. Thanks, Eric. Thanks for coming, guys.