 So, for a lot of today, we'll be using the audience response. So if you're feeling very confident today, you can answer and then put your name after it because it's all going to be free texting, but if you want to be anonymous, that's quite fine as well. So just to quickly review, I think Dr. Cron did Monday the visual anatomy. So just so we're all on the same page real quick. So vision or light comes in the eye, goes to the retina, back down the optic nerves, decussates at the chiasm, temporal fibers stay on the same side, nasal fibers decussate to the opposite side. So retrochiasm all you've got input from both eyes. And then light goes down the optic tract, synapses on the lateral geniculate nucleus, which is in the thalamus, and then radiations go through the parietal, temporal lobe, back to the occipital lobe. And visual fields, as you know, hopefully, are not perfect circles. We've got more temporal field than we do nasal, so it's more of an oval, so that's something important to keep in mind. And then our blind spots are around 15 degrees temporally. So let's just start verbal, we'll not audience responses. So you're walking down the hall, you pick up a piece of paper and it's a visual field and you see this. What do you think that that patient had? You just shout it out whenever you have any ideas. So what's the visual field defect? You know, secocentral scatoma. So it's central extending over to the blind spots. That's secocentral scatoma. And which eye is it? Left eye. So this would be where a normal blind spot would be. And this is the secocentral scatoma. So what's your differential diagnosis? So could be, so we don't know anything about the right eye, but it could be normal. It could also be like this. So you're thinking correct along the lines of optic neuropathy, potentially glaucoma could look like this. So that's all good. And then so secocentral scatoma is affecting this papillomacular bundle in here. And this area in particular is very sensitive to oxidative stress. So things like metabolic deficiencies or medications like ethanbutol is one to think of can cause significant stress to this area and cause a secocentral scatoma. So here's the case, and we'll use the audience's response with this. So 55-year-old man, progressive visual decline in the left eye for two to three months. He felt like his right eye was normal. No significant past melchohistory, no other ocular history. And these are his visual fields. So let's use audience response. And it's just free text. So what's first name, what the visual field effect is? If you want to in the same response, you could localize it too. So we got two junctional scatomas. Okay. It's a pretty smart functional person. So chiasm effecting some right eye temporal fibers as well. So that's correct that this is a junctional scatoma. So what we have is basically diffuse depression of the left eye, but a vertical meridian respecting temporal defect in the right eye. So you're correct with chiasmal is localizing to the chiasm. But why is it causing more vision loss on the left side? So it's affecting the chiasm, but it's more affecting the left optic nerve. So this is more of a left optic neuropathy in addition to a chiasm compression. So you know it's at the chiasm or behind because you're getting this vertical meridian respecting temporal defect in the right eye, but you're getting this diffuse depression of the left eye. So that's more anterior to the chiasm. So as a definition of junctional scatomas at the junction of the optic nerve and the chiasm affecting in this case more of the left optic nerve, but catching those fibers in the chiasm that gives you the temporal defect in the right eye. So what kind of lesions might be causing this? What's the differential diagnosis for chiasm? So pituitary macronoma, what other tumors could be there? Prenuopryngiomas, apoplexy, what other tumor? Meningioma, what other aneurysm, how about in the autoimmune category? Optic neuritis or chiasmitis, which could be aquaporn4, MOG, could be MS optic neuritis. So this was this particular patient with a very large pituitary macronoma. And so one of the interesting things in this patient was that he really just felt like his left eye was a little bit blurry. He didn't notice anything in his right eye. So this is why our testing brings out often more information than just what they tell you and your exam. If you had done ready saturation, you probably would have picked up this visual field. So he got that removed and had really good recovery with this. So next case, 19-year-old man, painless loss of vision, a left eye that's been progressive over three days. Three weeks later, he had no improvement in that eye and now has developed painless vision loss in his right eye. So what's top on your differential? And let's audience response that. What's your numbers after your name and death? I think it was 474. The hereditary apid neuropathy, leavers, MS. So some MS, lots of leavers. Why is MS maybe less likely? Painless. So young man, vision loss, one eye, painless. Shortly after, vision loss, the other eye. Even without any other information, your leavers is high on your list. So this is his exam. He's count fingers in the right eye, 2400 in the left. Has no color vision, neither eye. There's no EPD. Full motility. His fund, this exam, has some peripapillary telangiectasia and some kind of acetylodema appearance. What would you expect his visual field to show? Just shout it out. Yep, so this is mitochondrial. So causes oxidative stress and that papillomacular bundle is very sensitive to oxidative stress. So you would expect bilateral secrocentral scatomas. So this is his visual field. So that was that case. So leavers, most commonly, but not only, clearly, younger man. Could be a family history, doesn't have to have a family history. Again, painless vision loss, one eye. Usually within a few months, painless vision loss in the other eye. Secrocentral scatomas would be classic. They can get kind of the pseudo edema appearance of their optic nerves like what this patient had in little peripapillary telangiectasia. So if you see something that looks like a full disc or kind of looks swollen with this history, then leavers is high in your differential. But don't rule out leavers in women or even older women. It can definitely happen in that scenario too, but this would be the classic kind of textbook leavers case. So next case, so audience response. Where's the lesion? And I wanted to point out that the foveal thresholds are 30 in the left eye, 39 in the right eye, and vision's 20-20 in both eyes. You seem to see your answer, Chris, or whoever's answer. So for this one, we've got glaucoma, love stroke, macular sparing. Yeah, so let me clear. So those that got in, most of them were thinking bilateral occipital sparing, the posterior poles of the occipital lobe, someone's like glaucoma, that could also be true because we really have no other history to know how quickly this came on. So someone tell me why this is bilateral occipital lobe. Three of you said it, so what made you say that? Yeah, so can someone tell me kind of the arrangement of vision in the occipital lobe? So I think you would know based on how you're describing it, but so why does the sparing of the posterior pole cause this? Yeah, so occipital lobe, the more posterior you go, that's where your central vision is, and the more anterior into the occipital lobe is your peripheral vision. And some people will have their posterior pole supplied by the MCA artery. So if they've got a bilateral PCA stroke, then they'll take out the anterior and cause a lot of peripheral vision loss in both eyes, but if it's bilateral, but if they've got blood supply from the MCA to the very posterior occipital lobe, so have macular sparing, which is exactly what this guy had. So this guy was a very unfortunate guy who was at work on Veterans Day a couple of years ago and fell off a ladder while hanging the American flag and had head trauma and then had complications with hemorrhage and then he kind of herniated and blocked off his bilateral PCAs. So he had strokes of the bilateral occipital lobes, but sparing the posterior poles, allowing him to have the central island of vision in both eyes. So again, kind of to localize people with central islands of vision in both eyes, it could be a retina problem, like retinitis pigmentosa causes a lot of peripheral vision, but spares central advanced glaucoma could look like that, or if it's cerebral, then it's bilateral occipital sparing the posterior poles. Any questions on that one? Maybe not. So this one's a bit tougher and I might say this for our neurology resident, because it's a CAT scan and things aren't as bright as MRIs. What do you see? Like describe it and what does that mean for all the ophthalmologists here? Probably. Probably several hours ago. So based on what she said, where would you guys think the visual field effect would be? So we've got left, primarily occipital involvement. So some kind of right homonymous. So hers was more involving the inferior left occipital lobe. And in the occipital lobe, there's a division, so there's a superior inferior. So you can get quadrantinopias from the occipital. So if you involve the inferior, then you get a contralateral superior quadrantinopia. And then vice versa. So here's the case. Twenty-seven-year-old woman, she was five and a half weeks pregnant, came with vision loss, both eyes and then a headache times one week. The QED is 2020, she had no HPD, normal color vision. So what are you going to do to send her home? Because you're concerned about what are those things? What else is on the differential? Yeah. How does that cause vision loss? What do you say, cavernous sinus? What are the kind of thrombosis? Or just, yeah, venous sinus in general. And how does that cause vision loss? So venous sinus thrombosis causing elevated intracranial pressure, causing optic discidema, causing peripheral vision loss. So she's got 2020 vision. So unless you're a really non-thorough doctor, you might not know what's going on. But then you look in her eyes and you see this. So highest on differential now. So elevated intracranial pressure because she's got bilateral optic discidema with preserved visual acuity. So vision's 2020 both eyes, significant edema both eyes. These are her visual fields. So what are you, what's your thought process? What are your next steps at this point? So you're still in Moran Clinic. It's your second day as an attending. What kind of imaging? Eye of the abdomen. So you're looking for? Thrombus. It's high on your differential because she's pregnant. Yep. So you went relative mass. In general, contrast from MRI is kind of controversial in pregnancy. So some places won't do it, other places will. So without a real indication for contrast like this case, you could probably do it without contrast. So she had a brain MRI which was normal. I'm pretty sure it was without contrast. I don't remember. Did have findings of elevated intracranial pressure, which include, shout out those findings. Finding in the globes. Empty cellar. Yep. And had a lumbar puncture opening pressure of 56, but otherwise normal CSF. So what's your next step at this point? So these are her visual fields. So you want to relieve pressure. So yeah, she got admitted for a lumbar drain to relieve pressure. And then our general kind of protocol is to admit for lumbar drain and then evaluate them after a few days. And if their visual fields are getting better, then that's reassuring and you can treat them medically. If not, then we start pursuing most commonly optic nerve sheath fenestration, but some places do shunts more often than we do. So she got drained and started on acetazolamide. So acetazolamide in pregnancy, just so you know, is Category C. So we use it when we have to because there's really no evidence in humans that it's geratogenic. So we use this when we need to. And so this was her over time. She actually did quite well. And her visual fields got better with the drain, so we did not have to do any procedures on her. And so it ended up basically here. And this is where she actually is now. So she did well, fortunately. Now her optic discidema is resolved. She's got powder-aseptic nerves, though, but doing well and delivered. So that's audience response, this one. So name the visual field defects and then localize it. So right, homonymous hemianopia with right and temporal sparing, some left occipital temporal crescent. Well, that was mostly correct. So right, homonymous hemianopia because this space is missing, but you've got this thing over here in the right eye, in the very far periphery. So this is called the temporal crescent. And so as we talked about, the occipital lobe is arranged. So central macular vision is posterior. Then the more anterior you go is your peripheral vision. So we know that this is the left occipital lobe because you have a right homonymous hemianopia. And then because we're picking up this temporal crescent, we know that the anterior portion of the occipital lobe on the left is spared. So this would be an example of a lesion kind of sparing the anterior occipital but affecting the rest, giving you that temporal crescent. So if you just get a Humphrey visual field, you're not going to pick that up because this is out here between like 60 and 90 degrees and Humphrey's not going to pick that up, but a Goldman should or on confrontation, you can often pick that up. And I think that was Chris. You had that guy with me who had a, I think a right homonymous hemianopia, but he's like, but I can see way out here. And so that's exactly this going on. So he spared his anterior occipital lobe. So here's kind of a schematic again, just to point that out that the posterior occipital lobe does the macula, whereas the anterior does the peripheral retina. And again, superior occipital does inferior and vice versa. And again, so if you overlap your visual fields, you've got more of a temporal field that's not covered at all by the contralateral eye. So it is possible to have a lesion in the brain, retrochiasmal causing just unilateral vision loss, but it's very out temporarily in the field that is not even possible to be covered with the contralateral eye. So another case, so 33 year old woman, she came in reporting trouble finding birds in the sky, reading the first parts of words, seeing the mouse on a computer screen. It's been slowly progressive probably over years, but she was unsure, felt like it was in both eyes, no family history, no personal history any vision problems. So her visual cutie was scanning, was 2020 in both eyes, color was reduced in both eyes, pupils were normal, no APD eye movements were full. And these are her funnest photos. Someone just quickly tell me what you see. Well, I'll just say it's normal. So normal funnest photos. These are her visual fields. What do you guys think about these? Yeah, so if you just look up here, you wouldn't pick it up, but looking down here at the pattern deviation, you can see, and just with her history, you could correlate these with what she's describing to you, very central, peri-central subtle points that she's not seeing. And then you get a gold mon, kind of definitely in the left eye will confirm that. So local eye is this. So this is left eye here, right eye, and you can see here with this eye software, she's got this central scatoma. It's not really picked up on the right eye, but if you go to the Humphrey, you can see it a bit there on the left eye. You can see some spots there right in the center on the right eye. So she's got bilateral really small central scatomas. So bilateral small central scatomas, her history was progressive over a few years. And again, just based on her history, it's really small, like just trouble tracking really small things reduced in both eyes. What do you guys, just localize it first. So bilateral macula and just in general, bilateral central scatomas could be bilateral optic nerve, bilateral posterior pole problems in the occipital lobes. So you get more testing on her. This is her RNFL OCT, which is pretty normal. And then someone described this macula OCT. Yeah, which again correlates with her visual field, correlates with what she's telling you. So she got zentiretna and she had an ERG, which was actually normal. And I don't remember her name, but I know that they sent Dr. Bernstein-Sarr and was concerned about a cone dystrophy and sent off genetic testing. But I don't know her name, so I don't know how that turned out. But so example of bilateral central scatomas from a retinal problem with basically really subtle findings. And you have to be really pay attention to their history, especially when you're reviewing their visual field, because those were pretty subtle. And then do testing to look specifically like this macula OCT. So this is a 15-year-old girl, was in a car accident one month, and then she came in complaining of blurry vision in the distance and the pulpy at nearer. She had headaches and nausea. She had some neck pain. She went to her eye doctor and was told she had peripheral vision loss. What are your thoughts at this point? Could be. So concussion can cause convergence and sufficiency, double vision at nearer. What about our blurry vision? That could be coming from double. What? Is that it could also be the double vision that she's experienced? Right. So some people can describe double vision as blurry. So her visual acuity is 20-20 both eyes. Basically everything is normal, but she has an XT at nearer with a remote near point of convergence going with convergence and sufficiency. And these are her fundus photos, which are normal. And this is her Humphrey visual field. Describe. Yeah, so they're very constricted. And so are these reals? And then you don't believe her because she just got a car accident. She has to be faking. So you get a gold mon and it's the same. And so what are some techniques you can do just in the office to see if tunnel vision is non-physiologic or not? Tangent screen. And what you do at the tangent screen? Yep. If you don't have a tangent screen, you can do a similar thing just with confrontation. And same thing, you just back up and their visual field should expand. But if it's staying the same, a lot of times it's getting smaller, then that's concerning for non-physiologic. So this one, I sent her for more testing. So when we've got this kind of visual field loss, it could be retina, but her retina looked fine on exam. Could be brain, but less likely. I think she'd already had a normal MRI. So, but I was uncomfortable with her. So I sent her for more retina testing and actually had a quite abnormal ERG and also got sent to Bernstein. And he was concerned for a genetic type of retinitis pigmentos in her. So don't just dismiss people that you know that. That really, I mean, conversion is tough. It's probably my least favorite thing. So I tend to do a lot of testing in these people. Not too much inappropriate, I don't think, but I give them the benefit of it out most of the time and look for things like this. So just kind of conversion can fool you a lot. So don't immediately dismiss them. So here's an audience response. Match the image, so just send in a number for the visual field that this lesion would cause. So one other thing about that previous case is that she came in not really complaining of peripheral vision loss. That was one of the things that took me off to that. It was more blurry, double, but it was incidentally found her visual field defect. And she was like, I've always seen like this. I don't know why it looks like that. So that was a big clue as well. So this one, let's go back. So we've got some 1's and 3's. So this is, where is this lesion located? Oh, this is all one. Which one? It's all one. And two. Wait, are they all one lesion? I mean, it's all the same. Oh, yeah, they're all the same person, just different sequences on the left. So we just, this is just passing for a number, not too bad. That's why I was like, sorry. It's a little choice, not magic. Yeah. Yeah. Oh. Yeah. That's the way it's supposed to be. That's the way it's supposed to be. That was a positive, yeah. That was confusing. So this is anterior left occipital lobe. So this would be an example of something that can, a retrochiasmal lesion that can cause just monocular vision loss very temporally. So anterior left occipital lobe could cause a right temporal crescent loss. So that would be number one. Sorry, that was confusing. I didn't predict that. So just for a couple minutes, let's do a few of these and just shout them out. So what's the defect? Not central scudoma. So missing this. So inferior altitudinal in both eyes. Some lesions that could cause that. So this would be the field to the brightest, biggest eyesopter out here. And we can see that the furthest out, then as you, the eyesopters become dimmer as you go in. And so they can see this eyesopter here appropriately, but it's missing down here. And it respects the horizontal meridian here. So inferior altitudinal defect, both eyes. So bilateral optic neuropathy, such as bilateral schemic optic neuropathy, could be, or bilateral superior occipital lobe. Let's do this one. So we've got this visual field defect. So all of this is intact, respecting the vertical meridian and then not seeing that eyesopter over here. Either eye. So in addition to that, we have a right APD, left optic tract. So the visual field is a right haemonomous heminopia. And explain why you get an APD with an optic tract lesion and why is it on the right side. So left optic tract is the lesion. Why is the APD on the right side? Yeah, more, you're correct, the more nasal fibers that see the temporal field. So in the tract, there's, it's very slight, but a little bit of overrepresentation of the contralateral eye due to us having more nasal fibers because our temporal fields are bigger. So in the tract, there's a little bit of overrepresentation of the contralateral eye. And APDs are caused by asymmetric lesion, asymmetric vision loss anterior to the LGN. So in the optic tract, you can get asymmetric involvement, involving a bit more of the contralateral eye. So these APDs are not big, they're really small. So if you see subtle APD on the same side as the haemonomous heminopia, then you're thinking tract lesion. Let's do one more. This was part of, oh, let's go over your quiz actually. Don't change anything because I want to see your answers. So first one, right central scatoma could be macular problem, could be optic neuritis, any kind of optic neuropathy, basically anything anterior to the optic chiasm on the right side. So second one, left haemonomous heminopia. So we know we're retro chiasmal. So could be right occipital, could be right parietal and temporal, could be right optic tract, if they have a left APD. Third one, left superior partial quadrantenopia, thinking right temporal lobe with that one could potentially be right inferior occipital, but I expect that to be bigger. Fourth one we just talked about is the right temporal crescent, which should be anterior left occipital lobe. Next, left superior quadrantenopia, haemonomous. So right temporal, right inferior occipital lobe. Next, what's the next one? Rings chitomas. They look like rings. What causes a rings chitoma? Retina, this is a retina thing. Yeah, but localizing this is a retina and then that differential. Next, bilateral central scatomas or kind of secocentral scatomas. So could be macula as well. Could be bilateral optic nerve like Lieber's or other metabolic or toxic or optic neuritis. Next is, what's this one? Go with that. What does that look like? Posterior pole, right occipital lobe. What's the artery that supplies that in several people? MCA versus rest of occipital, which is PCA. Any questions? I would just say left homonomous central scatoma. Yeah, it might have a fancy name, but what? Posterior pole, the right occipital lobe. So the macular area. Any questions? Thank you.