 So, here's question number one. Okay, number two. Number three. Read about this one. Alright. Number four. Okay. And then, last one. Number six. Okay. Uh, what's that? Uh, just my treat. Okay. There's no rush. Take your time. Back to one and two. No, you're late. No time. Strav, this might be our strategy to figure out how to get pie. I'm not even trying. Yeah, you are. Strav's too cool to try. That's right. Is that gonna be able to say good evening, Strav? Yeah, good evening, Strav. I'm a nice guy, so we'll take it back. You got that, Strav? One of you, Strav. It's okay. We're a family here, right? Alright, we'll go over these at the end. So, we did. One of you, Strav. You're gonna get that book from me, right? Sure. Shimmering black areas in the vision of both eyes, they last about 30 seconds each time. Um, in terms of his eye history, he's had some almyopia. He wears glasses. He's recently diagnosed with ocular hypertension, and so he's on the TANAPROS. No real significant medical history. Sometimes it takes artificial tears. So, what do you want to know about this guy? What questions would you ask in my clinic? How long has this been going on, and how frequently does it happen? Yeah, so it's been going on for a few months now. And it happens probably every day, maybe a couple of times a day, but not necessarily. How do you associate it sometimes? You know, Disney has no vertigo, no pain, or anything like that. It's really black, or is the shimmering color white? It's black. He thinks it's black. What he notices is that it's got like a shine to it. How do you treat it? He used to get a headache like once a year. Well, he gets a headache like once a year now. He used to have headaches when he was a teenager, but no longer gets frequent headaches. Do you ever get a warrant for headaches? He used to get a warrant for headaches. Can I draw what? A picture of his shimmering black spots. I know, he says that once, like if you ask him specifics, he'll say that once he was weakening, and he then like moved his head into a weird position, and he saw like these splotches of black. He's not sure if it was in one or both eyes, but at that point they lasted for a little bit longer, and then it went away like a few seconds, and then it went away. What is he doing when these come about? Well, that was one time he was weakening, but it's not necessarily associated with that. Okay, so he could be sitting down? He could be sitting down. Well, we'll get to an exam in a second. But that's okay. Okay, so he's 2020 in both eyes. He has some APD in the right eye, but his pupils are normally sized. His pressure is 18 in both eyes, and his ankles are open. I'm going to ask if they know that they should know evidence of BAS. No DIDs. So let's dial in. Can you ask him an exam now? Oh, yes, yes, you can. He's going to have a field later. This is what his optic nerves look like. How do people describe his nerves? It's like double mask. Very red. It looks normal, but maybe anomalous vessels in the disk. He does seem to have... He's a healthy guy. He does have a bunch of vessels, and that left eye doesn't look kind of like a little anomalous in the configuration of the vessels. He's got a little bit of a sheen. He's young. I don't know if this is right, but I was thinking about this. It looks like there's blurred margins, and so you always think, okay, blurred margins. Oh, is this papillodema? And so thinking of things that are pseudo-papillodema. So I was just saying, it looks like maybe he has some trusen, optic nerve head trusen. Oh, yeah. Like... Oh, here. Anything over here? Not as much. So, he had an auditory license, and he definitely did have trusen on an auditory license. So yes, very good. And let's see, I think... Oh yeah, he had also told someone else that he'd had visual field defects to leave out an MRI, because the MRI was pretty darn normal. This was a case where the guy had had transient vision loss initially, and then started having visual field defects later on. But just to talk about optic disk trusen for a second in terms of how it can cause transient vision loss, disk trusen is thought to be due to impaired axonal transport, and then the cells kind of die and extrude their contents, and they get stuck and calcify. I think that's a theory, but I think that's a well-established theory. And the trusen are mostly bilateral, but in this case, they were asymmetric, so he did have an APD really well with regard to that. And it's most often in white section of rare and non-white people. So you can get an ultrasound to see if they're calcified trusen. Autofluorescence was what worked for him. You could also get an OCT EDI to see if they're buried trusen. He didn't have that. And then, as you said, we want to distinguish this that disc leakage on fluorescent angiography that a true optic discidema would have, there's none of that in optic trusen. And I didn't know until recently that optic trusen is associated with a few other ocular conditions. Does anyone know a couple of what those might be? Not that they're always found in these cases just so they can be associated with it. So I didn't... Yes, it is, because in rare cases they can go on and it is kind of like a risk factor for developing an ION. I wasn't thinking of that one, but yes, you're absolutely right. So actually two other ones are like retinitis pigmentosa and suizanthoma elastica are both associated with disc trusen. So in his case, to answer your question about the field strap, he did have a pretty large peripheral archaeo-defect in his right eye based on the the trusen that was there. Any questions about that case? Back to that photo again. Which one? So I agree, his are not immediately obviously do look like his nerves are kind of weird and they look like normal, but you can kind of see that on the edge, if you correlate it with where the trusen is on autofluorescence along this edge here, then you can kind of see that that's where a little bit of the margin is blurred and it does look a little bit more nodular and bumpy there. I think it's a little harder to see on disc photos too, rather than undersolding. Looking at it, probably too. Okay, case two. So this is a 60-year-old woman. She calls the page response line intermittent blurry vision in her right eye. She says that she sees this like wax paper over her right eye and it's associated with this achiness. It's happened every night for the past four nights in the evening time and it lasts for about one or two hours at a time. So she sees a glaucoma doctor for asymmetric cupping. She's on Latina breast for that. Her pressures were recently checked like a week ago as 22 in the right eye and 14 in the left eye. She has a history of hypertension and hypothyroidism. What are two questions that you'd want to ask her? No diabetes. Is she faking? She is. Has been on other glaucoma drops in the past and they've all caused this horrible irritation to her eyes and so, yeah, her eyes are not at, your coordinates are not in pristine condition. So right now she's kind of just on Latina breast and only been able to tolerate that one. Good question. What's the achiness like? It feels like it's on her brow. Like she has this like brow ache. She sometimes does rarely. Not that she can tell. No, not terry. She has noticed that her pupils sometimes dilated when this happens though. We call her to come in for an exam. She's 20, she's still having an episode of wax paper over her right eye when she comes in. She's 20, 80 in that eye. Her pressure is 40. She has no ABD, but she's got microcystic edema in the central cornea of her right eye with one plus cell. Her angles are open on the right eye and she has moderately kept nerves more on the right than on the left. So this is kind of an interesting case. It's not the classic ankle closure that can cause intermittent transient vision loss, but in her case the glaucoma team thinks she has this weird inflammatory glaucoma and when she has an episode of inflammation or pressure spikes and she was off everything, but the Latina process at that time and so her pressure just kept on going up. So eventually she, this is what she had this RNF also just a little bit of thinning and then kind of an unreliable visual field on that right eye but they thought maybe that she has some losses that could be associated with glaucoma but her pressure was uncontrolled off of drops and she couldn't tolerate the drops so she just got an Ahmed valve recently. Did she have an episode of wax? She didn't now. I don't know if they have a reason for why she has this so it's kind of an unusual one, but ankle drops can do this and inflammation can do this. So the other one is 81 year old woman comes to clinic because she's been having black out vision on both eyes she notices this when she gets up in the night to go to the bathroom and she turns on the light and she says I just can't see and she doesn't think it happens without turning on a light or going from a dark room to a light room. She had cataract surgery 17 years ago, she wears reading glasses, she has a history of heart failure and hypertension and her vision is 2060 2150. Any question that you want to ask her? She turns the light on and she's like I just can't see anything. Probably lasts five minutes or so and I think that's better. No eye pain. One question. No, no jumping. Did she feel like her vision has changed otherwise? Her visual acuity is not very good. She knows that her vision isn't really good but that hasn't changed in a long time. I did her cataract surgery. 17 years ago, that was impressive. So you dialied her and she looks like this. So she's got a lot of Druzen and then she's got a whole bunch of geographic atrophy in the left eye in particular but also in the right eye. So what do you want to do to try to explain her episodes of vision loss? Yeah, sounds like a good idea. How do you do a photo stress test? Shine a light in her eye and measure visual acuity afterwards. Yeah, what would you be expecting to be normal? So so you shine the light in their eye for I believe it's 10 seconds and then they should a normal response is gaining two lines at least two lines above their best corrected visual acuity in less than 90 seconds. I think it's 30. I think like over 90s for sure abnormal, right? Yeah. I think BCSE says 28. But I think you're right. I think they have to kind of have a visual acuity of like at least 20 or so for this to work because if it's too high then it's kind of a little bit harder to measure. But yeah, within like definitely normal less than 30 seconds they get down to it then a line or two of what their visual acuity was before and if it's like 90 seconds to two minutes or something like that you're definitely in the abnormal range of that's more of a macular problem because if it were a nerve problem she could have a normal macular stress test. So the other thing I absolutely agree with you Mike, if she has having transient vision loss in both eyes and she has 80 and she has any GCA symptoms I would definitely get labs on her but if she doesn't then I feel like you can kind of explain this as with a positive macular stress test. Also maybe you want to think about like ocular scheming syndrome vessel imaging. Not that I think this looks like that but it could be a little tricky because you'd be having lots of hemorrhages but. Would you expect ocular scheming syndrome to have a abnormal or normal? Abnormal. Abnormal. Could write on the issue. Yeah, exactly. Okay, last case. 46 year old man comes to the ED because his left eye has been blurry since this morning. He had a kind of episodic bilateral blurry vision when he was exercising a few days ago. These are all exercising vision loss, sorry guys. But at this time his vision is not returned to normal. He occasionally wears reading glasses. We have MS that was diagnosed seven months ago. He's on copaxone but he was not sure that the copaxone was doing anything and so he's doing this experimental intranasal stem cell injections up his nose where they tried to get to his brain and the last one was four days ago. This is a true story. His case. His vision was 2020 on the right eye, 2030 in the left eye. Colour vision was down in the left. He has a left APD. This was before I knew how to measure APDs so I don't know what it was logarithmically. He has a painkillability but his pain and abduction of his left eye and his normal DFE. So you're seeing him in the ED on consults July. What do you want to do? His episode of MS was when the only one that he's had so far was when he had numbness and weakness of his hand and he was found to have cervical spinal cord lesion and some demyelination was in his brain at that time. That's the only time he's had an episode you said? That's the only time he's had an episode you said? I've already gone for these intranetist stem cell injections. Is that two of them? The stem cell things? No. What's the uterus phenomenon? It's an MS when they get overheated they can have various neurological deficits and weakness or even transit vision loss episodes. Yeah. So actually that's a good question. So when he had his first MS flare seven months ago he did say that he was very heat intolerant his weakness would get worse when he was a little bit, you know, warmer or trying to exercise and he did have some blurry vision occasionally like episodically during his previous episode of MS in both eyes. After that flare went away it went back. This time it always returned until right now. The left eye hasn't gone back. About eight hours or so this morning he found some hang time. Only when he moves his eye abducts his left eye but yes he does no double vision. He says my left eye has always been my better eye and now it's definitely my worst eye. The stem cells aren't there or what would you guys say this is? Yeah. So he had an MRI there wasn't a lot of enhancement of the orbital portion of the optic nerve but you can see on the canolecular and pre-chiasmal part that his left optic nerve was rightly lit up compared to his right. So he was admitted before salumedral and the stem cells were just why he came in because he thought that was what caused it. But he was then he had to work up for NMO which the aquaport for antibody was negative and then he was supposed to follow up an MS clinic and he never did. So I don't know what happened to him. In the coronal section on the left side there seems like a dark spot like underneath the vasculature is that just how it happens to look? Below that, inferior and medial and inferior and inferior and medial Yeah that's like this whole circle like inferior to rear. Do you know what I'm saying? Like you going down? Oh I see what you're talking about. I don't know how to interpret that. They don't know what that is. It's just normal. Can you point out the optic nerve? Oh sorry. So his right optic nerve is right here and his left optic nerve is right there. So just some brief things about optic neuritis, Utah's phenomenon staff already described that one. They think that it's because of these like weird funky sodium channels that are affected and kind of abnormal after demyelination. I don't know if that's proven though either. The other thing that optic neuritis patients can get are basically flashes and photisms where they hear noise like the doorbell rings and then they see a light in response to that. So this kind of strange wiring that can happen after an episode of optic neuritis. And it does happen in about three quarters of MS patients at some point in their disease course and sometimes as the presenting symptom in like a quarter to a third of a quarter to a fifth of the patients or something like that. I think that's all I have. Okay so let's start off with a case. I'll just read it out loud. So patient presented to his optometrist following an episode of transient vision loss in his left eye. He describes a slow blurring and darkening of the vision of the left eye with a similarly gradual return to normal. The whole episode lasts 10 minutes. He described similar episodes every two to three months for the previous three years with no associated migranous aura or headache and exercise was not a trigger at this point. And so this is not meant to trick you at all so this is actually a really cool case report I found. So this is his fundus photo of the left eye before the episode and then they actually caught one during the episode here so you can see kind of diffuse retinal whitening along the inferior and superior arcades. And then this is 10 minutes after the episode. And so we're going to come back to this case so just kind of like keep that in mind. But to start off I'm kind of going to go over transient monocular vision loss secondary to more anatomical reasons and so I wanted to start off with just like the anatomy of just basic anatomy of the vasculature of the eye. So we have the internal carotid artery and of course that branches off to the ophthalmic artery and that further branches off to the posterior ciliary arteries and then the central retinal artery. The next slide I have a kind of a better picture here where we can see the central retinal artery coming from the ophthalmic artery and then the short posterior ciliary arteries coming to kind of feed the coroid. And then just remember that it's the central retinal artery that kind of gives off these collateral branches that feed the optic nerve and this becomes important in a couple of different disease states that we'll be talking about. So central retinal artery and posterior ciliary arteries are N arteries and reduced perfusion and either of these will affect the retina. So the territory is actually overlap which is a safety zone for the optic nerve head but it also creates a watershed zone in the retina. Does anybody know what layer in the retina this watershed zone is? So Rob I know you know inter nuclear. Yeah we talked about that like my intern here I think you taught it to me now I'm teaching it to you. So it's the inter nuclear layer that you have this watershed zone. So when you're evaluating somebody with transient monocular vision loss I think we can gauge a lot through history which I don't know about you guys but that's not necessarily why I went into ophthalmology but in neuro ophthalmology we do talk to the patients and it has a lot to do like how the vision loss occurs. And so the pattern of vision loss may give a clue to the diagnosis. So when you're talking about altitudinal vision loss so when they describe this kind of veil shutter shade or dimming this was actually a study that I read sorry I didn't reference it but these are the four most common symptoms or ways to describe people's symptoms when it is actually this altitudinal vision loss and that is strongly suggestive of vascular etiology so this is opposed to like a constrictive vision loss so when you have this altitudinal vision loss very very strongly suggestive of vascular etiology and then we talk about positive or negative symptoms so positive being scintillations or photopsias and then negative symptoms being black or gray this gray is kind of up for argument there's once again like this other paper that was all about gray being a positive versus negative symptom is very riveting but I think they kind of concluded that gray was maybe a negative symptom but nonetheless these negative symptoms are you know this isn't a hard and fast rule black and white but negative symptoms do often lead one to believe that it's more of a vascular etiology rather than you know a cerebral migraine kind of etiology for migraines what do people have do they have positive or negative symptoms generally positive exactly yeah okay so this is kind of a really cool drawing of patient that experienced transient monocular vision loss so he describes you know his whole vision going gray or let's just say that's black for the lack of we don't have you know black as a negative symptom and then this is kind of how his vision came back kind of like in these white blobs what what artery do you think was occluded to make I'm telling you that this is in fact caused by like an arterial occlusion what do you guys think actually caused this exactly yeah so that's yeah exactly what this is is because you got to remember the posterior artery kind of branches and has all of these tiny other branches that feed the coroid and so this is basically the coroid reperfusing and so I thought it was a really cool this was actually drawn by a patient when he was describing his visual loss and so you know people can also describe these like lobules blackout vision with these lobules of vision reappearing and then of course the valuation so looking at the patient's eyes this isn't as valuable in a lot of these transient monocular vision losses because unlike the photo yeah and especially like the reperfusion of it too it's going to be kind of like you know like whitening coming out not so much like these blobs appearing back in the vision yeah so they actually published a whole article about that I mean it's really hard because we don't catch these people in the act a lot of the times of these like transient monocular vision losses but at least with this with the posterior ciliary arteries I don't know about the central retinal artery if it's been like evidence proven or not well yeah that's that's the point of this is this is not like this is what patients say and how it can help like us further evaluate what the patient has you know like they're we'll talk about that yeah yeah and then evaluating the anterior segment and the posterior segment can be really helpful too I spoke about this just last week because I don't want to go too much into depth about ocular ischemic syndrome but that's one cause of transient monocular vision loss that can actually have physical exam findings so we can have iris neovascularization we could have anterior chamber inflammation and can someone describe the anterior chamber inflammation seen in ocular ischemic syndrome in terms of like the cell and flare so it's flare at a proportion to cell definitely an ocular ischemic syndrome and then the posterior segment evaluation so let's see Marshall what do you see here in this fun this photograph the peripheral hemorrhages yeah exactly so that's kind of like the classic physical exam finding for ocular ischemic finding ocular ischemic syndrome you could also have cotton wool spots you could also have flame hemorrhages as well but these kind of mid peripheral Dopplot hemorrhages are kind of classic for ocular ischemic syndrome and then I don't want to sound like a broken record but you know with ocular ischemic syndrome as I talked about in FA last week you have dilated but not tortuous veins because the tortuous veins are found in which type of etiology CRBO exactly yeah so you have dilated non-tortuous veins and then kind of attenuated arteries and then trigger factors is a big key that patients with transient monocular vision loss can kind of lead you to the diagnosis so gaze of voc transient monocular vision loss is a tumor in the orbit until proven otherwise and so in this article Pezzel et al. described that optic nerve sheath meningioma are actually the most common cause of gaze to voc transient monocular vision loss and then bright lights leading to vision loss think of ipsilateral internal crowded artery occlusion and I wanted to put this in here because I misspoke last week and my explanation for bright lights leading to vision loss in ocular ischemic syndrome was that it requires more blood flow to kind of feed those photo receptors which then cause this is ischemia which then causes these dimm outs but in this article the physiological mechanism underlying this observation is not entirely clear because in diabetes it has been shown that dark and not light causes hypoxia in the retina leading to the suggestion that sleeping with lights on may have a neuro-protective effect on eyes with diabetic retinopathy so can you comment on that Dr. C? I have not heard of that yeah it's crazy I mean I've never heard of any retina doctor recommending a patient to sleep with their lights on but just something to think about what's that yeah exactly so diagnostic workup so most patients are not observed during the attack the rare situation with the case that I talked about in the beginning this patient happened to be so you really have to dig deep talk about the onset talk about the way their vision went away the way it came back aggravating factors of course EKG is really important ESR CRP super important especially in individuals over the age of 60 remember that ESR is normal 30% of individuals with GCA and then of course in DFE you know looking for visible emboli disc edema disc pallor attenuated retinal arteries cotton wool spots and attenuated veins this is kind of an old-fashioned technique just something I think we should know about so when you're applying digital pressure and the transient monocular vision loss is due to hypoprefusion you expect that the arteries are going to collapse whereas if they normally wouldn't collapse but there's one other etiology that actually has this same physical exam finding that is not hypoprefusion does anyone know what that is when you apply digital pressure seeing the arteries collapse so like high IOP so like well but it's just tricky because if the patient has already high IOP and you apply digital pressure and you see the arteries collapse you can like think of that to be like hypoprefusion from another source as opposed to from glaucoma like high pressure so just be aware of that if they have high pressures and you apply digital pressure it might collapse so ESR is normal in 5 to 30% people with GCA test like how do you rule out GCA well that's never how you rule it out no that's just a screen test if you're suspicious you start on steroids and schedule them for a temporal artery biopsy sometimes I'm asked to just like order ESR like labs for GCA where we're not really suspicious at all just because they're old well it's it's kind of like the sensitivity and specificity right so it's got a high sensitivity but low specificity so if you're actually that concerned that a patient has GCA then you like you should but it sounds like it's low sensitivity also I mean so he's right though it's all about pre-test probability so depending on your level of suspicion you know be smart about ordering this test because you're right you can open up a can of worms if you have a really low suspicion someone doesn't you know have GCA if you order this then when you do you're stuck like you back yourself into a corner so I'm not sure if you're saying like I feel like this test is not super useful I guess you know yeah no systemic symptoms and you get a normal ESR CRP that's really reassuring but if for some reason that comes back elevated you can totally have it all without any systemic symptoms so if this comes back elevated then that would probably push you to do a temporary biopsy in the absence of systemic symptoms or an ultrasound to hide your biopsy okay shoot I forgot to pull this up I think this is this thing it's really cool because once again you're kind of caught so this is actually you can see ret like emboli in the retina which is like super cool it look like so look down here and up here that's where I saw them the most yeah you see that one down there they go really fast yeah you see that one it's like shooting stars whoa like we never see that but be pretty cool whoa yeah it's really cool video to watch when you guys have free time yeah I watched it a lot yesterday okay so back to our case so what's on the differential for that guy that I talked about so yeah what do you guys think how old was he I thought you no he was young I took that out on purpose actually it was in the case but he was young he was like 22 years old yeah I would have just given it away what's on the differential yeah perfect okay awesome what else definitely sure well yeah I mean yes that's why I took out the age because I wanted us to kind of expand the differential likely not in a 22 year old but definitely sometime yeah yeah exactly so embolism retinal vein occlusion gca not in a 22 year old hyper perfusion migraine aura without headache or retinal vasospasm and I want to spend just like the last two minutes talking about retinal vasospasm because I feel like for me this is the one out of all of these that I don't know a lot about and it's I think it's oh yeah this was some other test here he did get this like whole work up so nlp during the episode were covered to 2030 no visual field abnormality no hematological abnormality and crowded cardiac investigations were normal so retinal migraine so the term was introduced in 1970 maybe by doctor degree who knows but so the definition the international headache society stipulated in 1987 that in retinal migraine a headache follows visual symptoms with a free interval of less than 60 minutes but may precede them so essentially headache can go before or after the visual symptoms and then obviously the diagnostic criteria for retinal migraine you must rule out any other etiology you can't just call something a retinal migraine because it could actually be something that can kill them very quickly and I thought this was really cool so systematic review they said in 142 patients that were diagnosed with retinal migraine and they concluded the diagnosis was probably wrong in the majority with convincing evidence in only 16 cases importantly all of these suffered from headaches and the absence of a personal or family history of headaches suggested of migraine caution should be exercised before making a diagnosis of retinal migraine and the reason why I put this up there is for the main reason is because you have to understand that the pathophysiology behind a retinal migraine is actually vasospasm of the retinal arteries but the incidence of migraines and retinal vasospasm is highly, highly correlated they're not really sure why but those are very much correlated so without that history you need to rethink your diagnosis so facts about retinal migraine monocular vision loss for 10 to 20 minutes it's a diffuser unilateral headache exercises generally precipitates the attack so that's something different about our case and it's caused by vasospasm of the retinal circulation or ophthalmic artery treatment is propranol and nephetapine of rapamil patients are having this all the time you could prophylactically treat them with aspirin and nephetapine to prevent these exercise induced attacks and then I had a couple other things about GCA but I'm not going to we're running out of time so just one thing I wanted to mention about GCA is that although most of them present with arteritic anterior schemic optic neuropathy remember that this can also include posterior schemic optic neuropathy, CRAO, BRAO, choroidal infarction, CNS stroke or diplopia the pathophysiology is exactly the same in all of these so vasculitis within the elastin of this small or medium to large arteries but they can present like this normal fundus finding but then you look here and this patient had a choroidal infarction secondary to GCA so just because the fundus looks okay it doesn't completely rule out GCA so in this sorry but in this one you're saying that this would have been like a posterior choroidal artery problem? Yes. So how come in the case that you're talking about at first like that guy had retinal whitening during his first I mean it would have to have been more than just the posterior choroidal artery? Yeah definitely it was probably like a branch of the central retinal or maybe it wasn't even the CRAO they didn't talk about which artery it was but yeah no that's a good point they say that most of the time like GCA doesn't only affect one vessel right like if you have symptoms of GCA you're having a lot of medium to large size arteries affected so most of the time we do see not most but you know something on exam some dyskidema anything like that okay Teresa you're up. Really quick here diagnosis migraine. Okay good why tell me how do patients subscribe to these whenever they have them based on the pictures flashing lights in their peripherals so scintillation that's like where that comes from right the scintillation and then the scatoma which you can see kind of in the middle picture so what about this like I was wondering I was like what's this like fortification spectra if you guys read this like so that is like the picture on the right so kind of like there's some zigzagging lines there and it was thought to resemble like the wall outside of an old medieval city and the like battlements up on the top and so that's like a long historically where that name comes from so migraine this is probably the most common thing that's going to cause a transient binocular vision loss however most patients are probably going to see it as just unilateral even though it affects both eyes and so you can see these you know with the eyes open and with the eyes closed classically so usually linear geometric and then the classic migraine aura is like I said that fortification spectra it tends to be black, white, or monochromatic and it will enlarge over several minutes so Dr. Degree in her headache lecture last week talked to us about how do you tell the difference between a TIA and a migraine do you guys remember what she said with vision changes yeah absolutely and then there was one more thing particularly with timing do you guys remember what she said and then the onset so the onset sorry I should say onset so the onset with the TIA is sudden whereas the onset with a migraine is going to gradually kind of come on and build and build and build and build so that can be helpful in distinguishing TIA versus migraine in the history so they can also describe heat waves or tunnel vision and they can't have micropsia, sorry that's in micropsia so small and big vision kind of the Alice in Wonderland effect as well so they're always usually at an hour if they're more than an hour you should be suspicious that something else is going on it's rare that they're outside of that and then they associated symptoms headache, nausea, vomiting sound and light sensitivity okay what's your diagnosis here okay so positive or negative positive what about the characteristics of the picture there's a pinwheel right and then what do you notice about the there's like stars formed is it black, white or colorful colorful what does that make you think of brain stuff good thanks John Brad so occipital seizures so these are typically unformed positive visual phenomenon so there's a whole other section on hallucinations for patients where they can have formed visual hallucinations and a lot of different diseases and that's in a completely different chapter in the BCSE that we're not covering today but classically these are colored swirling lights, a white out of vision can also be described with bubbles or a flash bulb going off circles and spherical patterns so that was actually a patient that just wrote through a picture of what he saw when he was having his occipital seizure generally these are very rare motion tends to be a frequent characteristic with them and then they can't have visual distortion and classically they're going to be in the contralateral visual field to the side of the seizure and they can have negative visual symptoms so these are going to grow over seconds in contrast to migraine aura which grows over minutes and of course they're more vivid and you can think of it this way so a post-ictal headache is actually a common feature of occipital epilepsy so just because a patient has a very vivid migraine aura and has a headache afterward you need to be thinking about occipital seizure instead and then their insights usually always intact to this but then your associated symptoms are a little bit different than a migraine so deja vu, somatosensory phenomenon, head and eye deviation motor activity and impaired consciousness and so here you want to get an EEG and neuroimaging is indicated so adults with this usually harbor a structural lesion whereas children it's usually benign diagnosis patient come to describe the visual loss to me is it positive or negative so negative sometimes you always want to think about occipital ischemia so complete binocular transient vision loss may represent a TIA that involves the occipital lobes so I think this is kind of another thing that maybe requires a little bit more explanation so a lot of blood vessels and our visual cortex takes up like our visual system takes up so much of our brains that there's a lot of different blood vessels that can supply it and so obviously you can think about the PCA territory with the occipital lobes but also the basilar artery is also intimately involved in supplying the system so if a patient had vertebral basilar system disease you're going to see more complex deficits so what kind of symptoms do you see in a patient that has like a vertebral basilar symptom or vertebral basilar stroke instability so ataxia imbalance staggering what about other symptoms nystagmus so ocular motor disturbances so gaze palsies INOs, SKUs, cranial nerve palsies, nystagmus all those things within the system too they can also have gray out or white out of their vision that lasts seconds and can have positive flickering stars and then also hemiparesis hemiplegia and hematosensory deficits and then also the bulbar symptoms dysarthria and dysphagia so these will typically last minutes they're going to be an older patient with vascular risk factors then they have a sudden onset in contrast to migraine and then they can't even have a headache in the brow contralateral to their hemianopia so just because you have a headache afterwards doesn't mean all the automatically migraine okay and then really quick not a visual hallucination but this is actually a painting that's in the National Gallery of Art it's called The Faint so I was looking through and I was like I remember this painting from somewhere so really quick I just wanted to touch on hypoperfusion so anything associated with postural hypertension or basal-vego presyncope has anyone ever passed out before so I had passed out in the OR this year for like the first time and had the like which was really interesting and then Stokes-Adams attacks so that's where a patient has an underlying cardiac dysrhythmia and then doesn't like a heart block and doesn't perfuse their whole head and so most commonly these episodes are going to occur while standing if they're occurring while the patient's sitting then you can think about something else so with the basal-vego and postural hypertension okay and then last one thing that we kind of talked about was occipital mass lesions and so you can also have episodic headaches and bilateral transient vision loss with these so I think this is kind of another thing too where you would want to have a field to evaluate it but tumors and AVMs can also present in the back with transient vision loss so it's kind of the same pictures before all right Chris Bear let's just review our quiz real quick for the sake of time and then let's get to clinic so for the sake of time we'll just skip the rest of this stuff here we've talked about a lot of this history's important there's some questions to ask, exam's important test and we'll skip all of this this is a nice differential for transient vision loss I can send that to you if you're interested alright so our first question young woman some white dots for revision a little bit of discomfort when she has these what do you guys think the answer is the most appropriate next step so if two answers B and A exactly so I agree the most appropriate next step would be gonioscopy because we're concerned about intermittent angle closure and someone like this with these kind of presenting symptoms so gonioscopy is the next best step and then we can pursue other things as needed but gonioscopy is the appropriate next step number two so 6-5 year old guy hypertension, smoking transient vision loss most securities in brightly lit environments so most important test to perform so I agree magnet stress test wouldn't be a bad idea um maybe this is a poorly worded question but the most important test is vessel imaging because oops, that's wrong most of the test is vessel imaging because like Brad said we're concerned about this is light induced hemorosis we're concerned about vascular problems and specifically in the carotids so vascular imaging would be the most important thing most common causes of transient bilateral vision loss natural woman transient vision loss headaches worse with lying down as though she was nausea um and so she's been taking accutane and so what does she have first and then what would be the thing that's not consistent with her most likely diagnosis right so we think she has IH right and so which of these would not be consistent with the diagnosis of IH the exact as you can have papillodema, you can have MRI we have to sell and you can have a cranial or six palsy but cranial or four palsy would make us think about other things so we wouldn't expect that absolutely number five, a six year old woman hypertension, transient episode of vision loss she's at vertigo um and she's had these episodes when she's at her hair salon getting her hair done um she thinks it's monocular but she hasn't checked so what's the most likely source of her pathology? exactly exactly um so this is vertiborbasin insufficient since Rich was just talking about um and I put it there the thing about the hair salon because it's kind of in the literature you can hear as like beauty salon or beauty parlor thing because as you have extension of your neck while getting your hair done you can have episodes of hyperprofusion causing these symptoms so um ask about where they get their hair done um and then finally uh you have an 80 year old guy hypertension diabetes he's a new floater kind of black spot that comes and goes and he had this episode transient double vision a few weeks ago um he's got a PVD with multiple floaters so what's the most appropriate next step for this guy? D I agree so even though he's got vitreous floaters he's got what he describes as a spot um you know his symptoms are concerning for um potentially GCA we need to make sure we pull that out and so um getting me a salon CRP would be the most appropriate next step um out of all these options here any questions on any of these? okay great let's go to clinic