 So we did a study not too long ago looking at the most common causes of eye pain in our department, as well as an ophthalmology department in Switzerland. And then we looked at the causes of, you know, when people were presenting with a primary complaint of eye pain in our neurology clinic here at Utah and then also at the neurology clinics at the University of Switzerland. And so, in the neurology clinic, the most common root cause of people presenting with eye pain was headache and migraine, no surprise there, optic neuritis, a distant second, and then these other, you know, miscellaneous causes like trigeminal neuralgia, and then some ophthalmic things like dry eye and blepharitis but, you know, far and away it was migraine and headache. In the ophthalmology clinic, we usually, you know, if somebody comes in and says their eye hurts, we really depend on the eye exam to tell us, you know, what's wrong. You know, we can look in there and we can see that they have blepharitis or that they have a corneal abrasion or that they have anterior chamber cell or whatever. But, you know, I feel like 80% of the time, we're able to make a diagnosis just based on our exam without asking any questions of the patient. But we're all really stuck when the eye is quiet and the patient is complaining of eye pain. And so, in my comprehensive eye clinic, just from my personal experience, not my neuro clinic but my general ophthalmology clinic, the most common cause, again, for me is migraine and it's, you know, and I think that's because of the wiring of the trigeminal nerve. I also see a fair number of people who have cervical paraspinal muscle spasm like from a whiplash injury that have referred pain into their eye. And then, you know, you know, way, way, way out in third place is myositis and surface issues like, you know, dry eye and blepharitis and junk like that. And then that's in people with a, you know, with a quiet eye. So then what do you do. Well, it turns out that, you know, the nerve that's supposedly irritated in migraine, the trigeminal nerve is also the nerve that supplies sensation to the eye and the eye socket and the eye muscles and the periorbital structures. You know, so it's all connected. And so I don't think it's surprising that some people with migraine, you know, have it manifest as eye pain instead of a usual, the usual headache. And if you stimulate different parts of the dura, which is also, which are also innervated by the trigeminal nerve, you can get referred pain to all these wacky places on your scalp and face. And so you can see again how, you know, if you irritate the trigeminal nerve in a certain region, it can be perceived by the patient as pain in or around the eye. And remember migraine is incredibly common, almost 20% of women. So like, you know, five women walk into your general clinic like on average, you know, one of them's going to have migraine, 6% of men. So, you know, a lot of people wonder if they maybe have migraines and so they're usually characterized by a unilateral throbbing headache. The headaches are usually characterized by light sensitivity and sound sensitivity and nausea, but not always. There's often a family history, but you have to really go digging for it. Many people are often misdiagnosed with some other headache syndrome or they're undiagnosed completely. Sometimes there's a childhood history of car sickness or unexplained episodic belly pain. And those people are sometimes thought to be, that's thought to be like a childhood manifestation of migraine that in adulthood presents, you know, more of a typical headache that we think of. Some people call this episodic belly pain in childhood an abdominal migraine like the visceral nervous system, you know, somehow gets caught up in the migraine pathophysiology. If you want a quick way to figure out if somebody in your office has migraine, you can use the three question ID migraine questionnaire. And then you can ask, has a headache limited your activities for a day or more in the last three months? Are you ever nauseated or sick to your stomach when you have a headache? Does light ever bother you when you have a headache? If somebody answers yes to one of these, there's a pretty good chance they have migraine. If they answer yes to two, there's a very, very good chance they have migraine. And if they say yes to all three, they almost for sure have migraine. Okay, so now what do you do? The patient has migraine and they've got eye pain, you've made the diagnosis, their eye is quiet, it's not an ocular thing. So sometimes you can go above and beyond the call of duty and you can actually initiate treatment. If you want to, like, sometimes, you know, people that, you know, don't have the time or the knowledge to do this, you can refer them back to their primary care physician. Or you can help them find a neurologist to treat them. You don't have to treat the migraine necessarily. But if you want to, there's some really quick, easy things that you can do while the patient is waiting because they're suffering, right? If they have eye pain, you want to help them with their pain. So you can at least initiate treatment. You don't have to be in charge of taking care of their migraines. So the most common causes, you know, that I see in my comprehensive clinic is going to be, you know, one of the most common causes of eye pain is analgesic rebounds. So these are people that have been taking Tylenol or Advil or something every day or almost every day for weeks and weeks. And that's sort of, their pain gets in this vicious cycle where they can't get out of it. Opioids are especially bad actors in this instance. You can recommend some over-the-counter analgesics. Alka-seltzer is kind of an old remedy, but it's, you know, it's kind of nice because it has bicarbonate of soda in it so it can settle your stomach. And nausea with a headache, it's nice for that. And because the aspirin is kind of dissolved in water, you can absorb it more quickly. You can use Excedrin migraine, which is a combination of Tylenol, aspirin and caffeine. There's usually generic available, you know, in every store. You can get into rebound with these as well. So you just have to warn people about that, not to use them more than like 10 or 12 times a month. You can also use prescription migraine meds. You know, Sumitriptan has been around a million years. It's really safe. The only real serious contraindication is if somebody has ischemic cardiac disease. You can give them some metaclopramide, which in addition to treating the nausea kind of supports gastric motility and can also help resolve the migraine. And then, you know, anymore, you know, in my clinics, both neuro and general, a lot of people are just adverse to taking any kind of medication, even over the counter stuff. And so that's fine, you know, you can usually people will tell you that, or you can ask them that, like, you know, are you the kind of person would rather take a medication or would you rather try to find something non, you know, non-visceral and they'll they'll tell you you can recommend physical therapy for their head and neck. Some people get benefit from seeing a chiropractor. You can recommend massage therapy and acupuncture all these things can can be helpful in alleviating migraine in somebody who specifically doesn't want to use medical therapy. I also talk about lifestyle stuff. You know, the big things that I see in my clinic that people are bad about is not getting enough sleep. They're too stressed out, and they're maybe drinking too much caffeine, or all three. So you can, you know, you can talk to them a little bit about sleep hygiene, you can talk to them a little bit about stress reduction with mindfulness or meditation. You can talk to them about moderating their caffeine intake. These are all some easy common sense quick and dirty things you can do while the patient is waiting to get back into their primary care physician or, you know, waiting for a neurologist these days is like, you know, 10 years in the distance. So, just real quickly, why does cervical paraspinal muscle spasm manifest as eye pain. And, you know, this is not something I think you'll find in any paper or textbook. It's something I learned from Dr. Diggory, but you might remember that one of the nucleus caudalus of the trigeminal nerve, you know, the trigeminal nerve is a gigantic nerve, right, and the nucleus, the nuclear parts of that nerve are all up and down the brainstem from the pons to the medulla. But there's also part of this trigeminal nucleus caudalus that goes into the upper part of the spinal cord. And so it's thought that, you know, maybe if there's irritation in that upper part of the neck, you know, from a whiplash injury or somebody that's cranked their neck jacked up their neck somehow that maybe that irritates that trigeminal nucleus caudalus and again causes referred pain into the eye and the eye socket or around the eye because of the, you know, the shared innervation of the eye and other parts of the of the face and brain and meninges. The trigeminal neuralgia does not come up that often in my clinic, but you have to know about it because the treatment is way different. And it's a way more severe condition. It's much more debilitating, it can be much more serious and debilitating even causing people to contemplate suicide sometimes. You know, there's some overlap there with other headache syndromes where, you know, the pain is just so severe because the trigeminal nerve is just so revved up. It's generally in people over age 50, there's women are overrepresented in trigeminal neuralgia as well as migraine. You know, it's not super common. It's going to again be unilateral pain in the distribution of the trigeminal nerve so it's going to be similar, you know, in distribution. And the character of the pain is what distinguishes it from other pain syndromes, sudden severe stabbing shock like you can see why people are really debilitated by it. But it can also be constant aching burning sensation so it's these neuropathic kind of symptoms, the stabbing electric burning kind of thing that's going to tip you off to trigeminal neuralgia. And it can coexist with migraine to which makes things even more confusing. Intense flashes of pain can be triggered by vibration or contact with a cheek. Sometimes the wind will set it off you know just being out in the wind shaving brushing your teeth or chewing anything that's you know, kind of stimulating the trigeminal nerve can set people off and again these are things that distinguish trigeminal neuralgia from migraine which can also be unilateral. The luster headache also shares some similarity with trigeminal neuralgia. It's part of a broader headache category called the trigeminal autonomic cephalalgias and what distinguishes these headache syndromes. Again from migraine is, you know, it's again unilateral head pain or eye pain. It's accompanied by ipsilateral autonomic symptoms which can be eyelid swelling or ptosis, tearing a horner syndrome, congenital injection or a runny stuff you know so these are things when somebody's coming in with sudden acute stabbing severe unilateral pain I asked them about these autonomic symptoms because the treatment of cluster and these trigeminal autonomic cephalalgias is different from that of migraine. I think in the history, you know, getting a personal or family history of migraine or headache is helpful, asking them about new medications that they might have changed that might be setting them off, asking them about social changes like it's anything going on at work or at home or they've been in a car wreck. You want to always keep in mind Giants Larderitis you know that's another possible headache syndrome and in the right, you know, demographic you want to ask them the usual Giants Larderitis questions. Does the pain follow a specific dermatome of the face because that could tell you that it's zoster coming on or about to come on. Oh, and then this is a tricky one or corneal erosions because just like these other headaches syndromes the patient comes in by the time the patient comes in the erosion is gone. You know and you look at their eye and you know and you can't find an abrasion or anything like that their eye just looks red and irritated and they're telling you the pain's getting better just something to keep in the back your mind, something to body with a basement membrane disease or a history of a corneal abrasion with an organic object. Something that I had a little trick that I use in clinic with somebody with eye pain is to put in a drop of properacane. And if that makes their pain go if you're lucky enough that they're symptomatic while they're in your chair. The pain goes away with topical properacane you know it's some sort of surface thing. And then also you want to, you know, remember shingles which you know this is a I think none of us would miss this, you know shingles case down here in this slide. But sometimes it can be really subtle or it can be under the hairline and you have to kind of look around a little bit more. So just always keep that in mind. That can be a common cause of eye pain or pain in and around the eye, again with a different treatment. You know we're really lucky to have Dr. Harry, you know, in our clinic, because he can use an orbital ultrasound to look for other rare causes of eye pain if you're really stumped like posterior scleritis is a, you know, one it doesn't come up very often but orbital ultrasound is like really almost the only way you can diagnose it. Orbital pseudotumor he can also look, you know he looks at the lacrimal gland if you ask him and, and the extra ocular muscles and he can tell you if any of them are inflamed. If you don't have a ultrasound person like Dr. Harry. And sometimes these things will come up on a CT scanner and MRI. Orbital pseudotumor you know you can see enlargement of the muscles that involves that the tendons. If you have sinus disease, especially sphenoid sinus disease next to the eye socket that can sometimes be present, present as eye pain or eye socket pain. It's just cheaper and faster to send them to a neuro ophthalmologist you know if you happen to be. If you're lucky enough again to be working in a clinic or a city where there's a neuro ophthalmologist nearby. You, you might get more information out of a referral to them than, you know, ordering an MRI the orbits not really sure what you're looking for. Okay, so this was where like I was hoping to break us up into. Little groups where we could, where y'all could discuss these different cases that I put together after the presentation. But I don't know that they're, let me see who we've gotten the gallery. I'm not sure that we have enough people to like even break up into, into groups. Yeah, there's really not enough of us. So let's just, let's see. Gee, Lydia, do you want to give this one ago just kind of talk about it out loud and and we'll kind of help you. Yeah, sure. So 48 year old male with known metastatic prostate cancer comes in with four weeks of right eye pain and decreased vision. On exam has decreased vision and APD, ptosis, mild up base down gaze and some adduction deficits. So if I was to see this patient. The most important thing is in my, my, should I go through this kind of in a oral boards type of like more all boards type of presentation. Just tell me what you're thinking like what you know what things are you worried about with this patient and what would you do next. I mean, what I would be worried about with anyone who has metastatic cancer any history of cancer would be that there is a spread to the orbit, or to the eye. But if he has decreased vision and APD, ptosis and the restricted restrictions, I would be nervous that there could be a met in his orbit. So the big important thing for me would be to, of course, also, I don't know we got the vision, get a scan. I think a MI of the orbits and brain would be my first go to with and without contrast, and potentially go further with an ultrasound or other testing but I think that would be the first thing to start off with. Of course, this could be also with the ptosis. I would make sure that this is not a horners, because horners we would have to think of also some vascular issues but I think that the MRI would be the first thing to start off with, as well as of course some testing for other common diseases that could cause decreased vision and kind of symptoms. So I would also think like make sure he doesn't have thyroid on my studio or like anything. And I think that would be the first, my first work up for him. Right. Yeah, so a patient with a known history of cancer. They deserve a more careful history in a lower threshold for obtaining imaging. Especially if somebody that has decreased vision or evidence of other cranial nerve involvement needs special attention like this person sort of kind of sounds like they might have a third nerve involvement because there's mild up gaze down gaze and adduction deficits. So yeah, this person needs needs an MRI the orbits just like you said great. Okay, so Tony, I'm going to ask you to take this one on. This is a 75 year old woman who used to get migraines, but she hasn't had them for years and recently she began to have headaches, some proximal muscle aching and pain when she choose her food a few weeks later. She suddenly went blind in her left eye. So I think this is a pretty classic presentation for giant cell arthritis given that she has symptoms of polymylogyramatica and some jaw claudication. And then on her fundus photo you can see that the nerve has a waxy paler with edema and or chalky white would be the best way to say it and that would make me concerned for GCA. Yeah, that's exactly right. And again, this is going to be like overall like thinking about all the people that are going to come into your clinic with eye pain. This is going to be an uncommon one, but a dangerous one and so that's why it's emphasized so strongly and the O caps and oral boards and stuff and it's, you know, and it's one that's still people still miss and so yeah, that's why I brought it up great job. Quick question. There's something significant on the photo of her external face there. No, it's just like, just like it's, yeah, I should probably delete it actually. Thank you for bringing it up. Okay, so we learned about some red flags, some people that had in addition to their pain they have some motility deficits or decreased vision, or they have a swollen nerve, you know anything like that as a red flag that means this is not the run of the mill. Eye pain patient that's migraine or cervical paraspinal muscle spasm or some other easy peasy thing. The more red flags, you know it would be worse headache of my life that's, you know, one that we all learn about even in medical school because it can be a sign of a subarachnoid hemorrhage. Also remember carotid or vertebral artery dissections can also cause head pain and pain in and around the face and eye. A sign of thrombosis would be a rare cause. And then there's these other, you know, rare things are reversible cerebral vasoconstriction syndrome, and posterior reversible encephalopathy syndrome, you know which kind of share some commonalities and maybe a common path of physiology but they can come on with decreased vision, and sudden severe head pain and, and those people, you know need a brain imaging right away. Shout out to intracranial hypotension we think a lot about hypertension but occasionally people will come in with headaches from hypotension because they have a CSF leak is the most common cause. And those the thing that's characteristic about that is that they're going to feel much, much better when they lie down and much, much worse when they get up and start moving. And these are all uncommon but serious and that's why we talk about them. Okay, let's see who's in the still in the gallery. Marshall, how about this one for you please. Sure. So, there's a 23 year old woman gets unilateral throbbing eye pain with light sensitivity and nausea. So, with a normal exam. So I would probably be most concerned about migraine in this case, given the light sensitivity and nausea with a unilateral throbbing eye pain is pretty classic, especially with the normal exam might think about other things like optic neuritis and in in this kind of patienting patient for the normal exam to be a lot less likely. Yeah, I agree. This is a classic case of migraine but you know they've gone. So why does somebody with migraine go to the eye doctor right it's it's a neurologic disease. The thing is their eye hurts, and you're an eye doctor and so they assume there's something wrong with their eye, right. And that's why they've gone to you so you don't have to fix it. I would say your eye is fine. I'm pretty sure this is migraine. I'm going to send you back to your primary care physician. You know, and then you can choose to or not to talk about some of the, you know, treatment things that we talked about earlier in the presentation. Perfect. But your main job is to make sure her eyes okay. Make sure she doesn't have one of those red flag diseases, and you can, you know, and then you can choose if you want to treat them yourself or send them back to their primary care physician. Oh man this is a complicated one. So we're back to, I think we're back to Lydia. This is a lot to read. So 24 years and presents for evaluation of intermittent vision loss. He reports episodes that last 30 minutes, starting with a blind spot in the center vision that expands into the periphery and then dissipates. This incapacitated during these spells. And if they occur while driving he has to pull his car over the blind spot has a colorful shimmering appearance. These spells occur about once every other month, and he said three to four spells over the last six months. So this sounds very typical for a migraine or that can happen without a headache. He doesn't complain of headaches. It sounds like a migraine or without a headache, but I mean he's 24 years old, so I'm less concerned for any, like, I'm a roses Fugax but I think that things that should be on the differential are, of course, especially in an older patient, things like I'm all this Fugax and then ocular ischemic syndrome, especially if it is light induced, but I think the presentation is very classic. So what other questions I mean, talking about a headache, going through kind of the headache questions risk factors family history. If like all the like different things but more targeting the migraine pathway. Photophobia, phono phobia, other associated symptoms. And then suppose the patient returns a day later a year later and reports that the spells have become more frequent, more intense and longer and duration. These spells are associated with weakness of the same side as the visual field defect and the recent MRI shot several areas of T2 hyper intensity. That would lead me more in into the scheme of like an MS type symptoms, or like an like demyelinating symptom syndrome, which of course is also on the differential for this. I don't think I asked if earlier if it's in both eyes or just in one I think that's important to ask. Yeah, you know, and also you know, I mean it's rare but young people can get like carotid disease or cardiac disease and so, you know if you're seeing a bunch of T2 hyper intensity you're absolutely right that could be multiple sclerosis but it also could be something like, you know, brain disease from, you know, from, from like a cardiac source or a carotid source so somebody like that you know you might want to have a stroke specialist. Look at them and make sure they're not having little strokes that are presenting as something that sounds more you know it sort of sounds like an aura so yeah. And then the last one's tricky. Suppose in another scenario. I mean early onset strokes and cognitive decline I would think in the hyper corgability scheme, like I would think of things like antiphospholipid syndrome, homocystine, I don't know the pronunciation of the word, but I would get kind of a correlation work up to make sure these are not like vascular strokes that like strokes in the brain that cause the decline, as well as of course like Alzheimer's or other like no logic conditions. Hey Marshall, do you, does that ring any bells for you. Family history of early onset stroke and cognitive decline. Oh, is it su sex. No. That's not that's usually not hereditary. Yeah, it's not. I'm not sure they make me think of like basket dementia but I'm not sure what it's pointing to. There's another one of those uncommon things that sometimes shows up on tests, it's mitochondrial encephalopathy like acidosis and stroke like yeah yeah. Yeah, or it could also be a catacil. You know, those are the two inherited. So me loss and catacil are kind of these two inherited syndromes that can can present with vision loss and and headaches. Yeah, so it's just it's one of those rare inherited symptoms that sometimes pops up because it has this, you know, because it has this distinctive set of, you know, the history is so distinctive. Okay, that was a hard one. Let's see what else I've got. Can't remember. Oh, yeah, this is just to remind me that if you're talking to somebody in clinic and you're thinking that what they're describing is a migraine aura but you're not exactly sure maybe they're able to articulate, you know, what they're seeing. You can just go on to Google images, you know, on your computer in the room and, and you can just say migraine aura and you pop up with stuff like this and you can say does it look like this does it look like this, you know and something like this. Oh my God, it looks exactly what it looks like, you know, and then you know that you're, you're home free. There's also some really good pictures on the internet of people's impression of visual snow, which is, you know, usually a benign condition that's more common in migraine people that there's usually a history that goes all the way back into having this, you know, static in their, in their vision. But there are some rare serious causes of, you know, late onset snow but almost all of it's benign. Yes, we already talked about that they perceive this as an eye problem or vision problem so they go to the vision doctor or the eye doctor. Oh just really briefly I want to mention these CGRP. So calcium. Oh God, I'm spacing calcium calcitonin. Calcitonin G related peptide. I'm trying to remember what CGRP stands for. You're right calcitonin gene related peptide. Thank you. I'm not, I'm not going crazy. Okay, so there's a lot that thank you Kathleen there's a new group of medications that target CGRP and its receptors for migraine and so I just wanted you to be aware of them because they're now very they're on the market I'm sure you've seen ads for them. So CGRP is a neuro peptide that's why it's a target of interest in susceptible individuals, you get CGRP release. Pro inflammatory mediators so that's why it was chosen as a possible target for headache or migraine treatment. You get and then when you get these pro inflammatory mediators you get further release of CGRP synthesis and release of turns into this vicious cycle that can last you know hours to days, you know, similar to you the duration of a typical untreated migraine. And so that's why CGRP was was studied for migraine and found to be a good target for migraine treatment. It's a potent dilator of peripheral and cerebral blood vessels. So that's another reason you because it's thought that cerebral blood vessel dilation might be part of the pathophysiology of migraine pain. CGRP is widely distributed throughout the body, you know it's not just in the brain it's in the respiratory endocrine gastrointestinal immune and cardiovascular system so it's a widely dispersed molecule. Interestingly, Sumitriptan and botulinum reduce CGRP levels in a dose dependent fashion and cell culture so that's all kind of stuff pointed to CGRP as a possible target for you know migraine pathophysiology. So, you know, it's thought that in a normal person light smell and sound somatosensory inputs lead to, you know, normal releases of CGRP in the brain. But in a person with a predisposition toward migraine. It's thought that the same stimuli which are normally not noxious to people causes a markedly increased release of CGRP and that's what leads to the light and sound sensitivity nausea and pain of migraine that's the kind of the hand waving theory. CGRP levels are elevated during a migraine attack and CGRP is released after nerve activation. It appears to be involved in pain transmission and interestingly you can infuse CGRP into migraine people and it'll induce a migraine attack. There's a there are a group of CGRP antagonists on the market. They're intended for both prevention and abortive therapy. There's injectables and intravenous molecules were the first to come out but now there's some oral oral medications. They target either the CGRP molecular receptor. And these are some of the, you know, there's, there's more of them coming out all the time but these are some of the ones you might see advertised on TV I know I see a lot of nerve tech ads personally, but these are all preventatives and acute and trained and drugs for acute treatment of migraine that you might see. Let's just make a comment. The, you know, optimism ab, feminism ab, Yelkin is a map. And anyway, all of those are in a map are all monoclonal antibodies. And then as the G pants, Ubrojapant and remidjapant are small molecule antagonists. And then there's one more G pant that the Ubrojapant and remidjapant are for acute headache and remidjapant can be used every other day for prevention. And then there's a third one called a tojapant, which is a daily medication which is prevention. And the good thing about these G pants is we don't think they have any cardiovascular factors so in people who might have heart disease or some cardiovascular problems these small molecules may be something that could be used. Yeah, so I'm, I'm, you know, I'm certainly, I'm not bringing this up because I expect you all to know how to prescribe these drugs and you know and they're extremely expensive and insurance companies are very hesitant to approve them unless somebody's been has failed other medications I just brought it up so that you're aware of what these drugs are what they're called how they work, you know because your patients are some of your patients are going to be using them. You know, we showed in a study that we did with one of our former residents and fellows Christa Canard that chronic migraine is associated with reduced corneal nerve fiber density and symptoms of dry eye so I can't remember I think she had like a cohort of like 20 or some patients with chronic migraine that she did a confocal microscopy on and they had these distinctive you know changes in their corneal innovation and we're not sure if that's what's causing their migraines or if it's a effective migraines or at some sort of biomarker of migraines, but it was it was pretty it was a pretty striking difference and so again there's it's just showing that there's some connection between eyes and migraines and the trigeminal nerve. And then the other thing that was striking was that, even though all of them in this particular cohort had normal Schermer's testing and normal tear breakup time and, you know they didn't have like a bunch of pigment epithelia erosions, I'm sorry, punctate epithelia erosions in their cornea. They all all of them, every single one of them of these pages with chronic migraine had symptoms of dry eye, you know as as shown on a dry eye questionnaire. We don't know. Again, if that's a biomarker if dry eyes like a biomarker of chronic migraine, or chronic migraine causes you to have dry eye symptoms or dry eye symptoms cause migraine like we have no idea which way the arrow is pointing, or if it's pointing in multiple directions but patients, it does seem that if you have a patient with chronic migraine sometimes treating their dry eye symptoms can make some of their pain better and it reduces some of the stimulus to the trigeminal nerve. And I've been preaching to the neurologists, you know because I think they're hesitant to prescribe eye drops, you know even though they're over the counter and, but it's an easy peasy way that you can sometimes make people at least a little bit better with regard to their eye pain. Now we've also shown that patients with migraine have substantial reductions in their measures of visual quality of life, so there are these quality of life measures that are, you know, validated by and are part of the National Eye Institute questionnaire. And it turns out that these patients with migraine, what's driving their reduced, well their perception that their visual quality of life is poor, it seems to be dry eye symptoms. Let's see. Okay this is another tough one, but Tony I think it's your turn we'll help you. So a 42 year old man reports periods of intense unilateral period orbital pain lasting 30 to 60 minutes. He's had a spell almost every day for the last week. Spells are accompanied by tearing he has a selfie of his face from a spell in which he has mild ipsilateral ptosis. This is an episode of similar spells about a year ago, and but then had no spells to last week. What is most likely diagnosis and I think this is a cluster headache. Yeah, and reason for that is because it's unilateral one side is per orbital pain pretty severe. So it's a three day, but still clustered in like a certain timeframe within the year like in a week or so. And then he also has tearing and swelling and toses you can have like a horny syndrome like picture with that, you can have some issues with like tearing and rhinorrhea and even congenitival injection, even eyelid swelling treatments, most effective for this order in the acute phase think you can use like 100% oxygen. And outside of that I am unsure, but I think you can also use some of the preventative medications that you do for migraines typically also and then for food and beverage known precipitate spells. I actually forgot that one I'm not too sure. It's alcohol. Oh, okay. Okay, be a precipitate. Yeah. And does this patient need neuroimaging and I do not think so. Yeah, I don't know. Yeah, and I think you could, you could, you know, you could interview 10 neurologists and they might. I don't know. I think most of them would image. You know, so I'd say it's a it's a toss up, but I'd say probably just because it clusters kind of kind of rare, you know, it's not super common. And I think he, you know, he probably deserves one MRI. Can this Kathleen absolutely image the first attack. It's one of the headache syndromes that's the highest secondary causes pituitary tumors, cavernous sinus lesions, etc. You know, in migraine, if it's a normal exam, you never image because there's, you're not going to find anything, but in any of the trigeminal autonomic spell just the first time you would image. Another condition that can kind of mimic cluster that can come into ophthalmology is carotid dissection, and it can look because they get a little Horners red eye unilateral eye pain, and it can be very painful. So, so I would say, most headache specialist most neurologists would say on the first time you see somebody with attack you image. And remember attack is a trigeminal autonomic cephalalgia, you know, we brought that and that's something that does come up occasionally on. And again, it's not because you're expected to know necessarily how to treat these people, but you have to, you know, you need to be aware of them so you can at least make the diagnosis get them to the right person to help them. You know, get the right treatment. And again, they have eye symptoms that's why they go to the eye doctor, even though it's a neurologic disease. Oh my God, another case. Marshall your turn please. I'm 60 year old woman reports a continuous right sided headache for the past three months, occasional stabbing pain around the right eye lasting just under a minute. Instead of tearing shares nausea and photophobia shares a selfie showing right sided TOSIS. So, this kind of sounds like hemicrania continua. Excellent. And the continuous nature and the stabbing pain and the autonomic symptoms. I think you can use like NSAIDs like in the medicine as a possible treatment for this. And I think for the same reasons that Dr. degree talked about we should get at least one for him. Yeah, yeah, I think I think that's probably true. No, you're right. It's not any NSAIDs though it's it's it's exquisitely and specifically sensitive to into medicine. I don't know why. But, but it, but actually that helps it's into medicine is not only therapeutic it's diagnostic, you know, somebody responds to into medicine, then that sort of helps nail down the diagnosis of hemicrania. Excellent job Marshall. Way to go. So this is a, and an abbreviation notes on abbreviation it's a, it's not an eponym is a acronym. Thank you. The snoop acronym is one that they're real big on and neurology so if somebody's having headaches you're supposed to remember this acronym to help you decide if this is you know something serious and scary that needs imaging and other, you know, maybe some work up or something that's probably benign. And so this is what snoop stands for I have a person I have a terrible time remembering what snoop stands for which is why I've got it written down on this slide but if this works for you, then, you know, more power to you but again this helps you know helps you ferret out some of the things that we've talked about earlier like giant solar arthritis or a subarachnoid hemorrhage, or, you know, a pituitary tumor or being a science rhombosis or some other, you know, scary bad thing that, you know, can be that can lead to serious morbidity and mortality. That's the end of that, that's the end of that lecture with three minutes to spare. So, let's take a 10 minute break. Everybody can mute and turn off their video and then when we come back we're going to talk about functional vision loss. Thank you. This was great. You're welcome. Let's talk about non organic visual disorders. If you find the BC SC somewhat lacking in terms of its description of functional vision loss and what causes it and how to distinguish, you know, malinguers from people that are just suggestible. This is a short article written by one of the neuro ophthalmologists who was at Iowa when I was resident Stan Thompson. And it's just it's a very easy read it's it's it's written in a very conversational matter it kind of gives you some background on the history of functional vision loss and sort of the spectrum of different kinds of patients that you see in functional vision loss and some of the things you can do, you know, making observations in clinic and other tricks you can play in clinic to try to ferret out, you know, functional vision loss or distinguish it from, you know, organic vision loss and it's in our file cabinet I think it's also in the packet that everybody gets and it's, I would just highly recommend it I found it a really fascinating read when I was a resident. And here's a tough case. And I'm going to have, see I think it's just Lydia and Tony that are left me at the gallery here. And I defer to Tony because I may have to take over consoles I'm just trying to figure that out right now. Okay. Yeah. Yeah, Tony, I guess you're up. Okay, so differential diagnosis for these visual fields can have glaucoma you can have maybe pituitary issues since there's it's by temporal. It could be like some sort of bilateral optic nerve issue. Like a like something toxic or metabolic. Let's see. What tests would you order to determine whether visual field loss is organic or non organic. So we did the visual field also look at the RFL to see if there's any thinning of the nerve. That's the OCT to see if there's, of course, there could be like macular issues since these appear to be secocentral. So you can look at like an OCT make sure it's not something in the retina. You can do a MRI orbits and brain without contrast to see if there's anything along the optic nerve optic track, or if there's something more posterior to with the presence of normal people are reflexes including the lack of a RPD effectively rule out the probability of organic vision loss. Let me think about this real quick so no it does not because again it could be in the retina could be something just in the macula and if you don't have extensive retina disease you might not have a RPD and then if there is symmetric optic nerve issues on both sides and there might not be a relative effort people are defect and then if I'm just trying to think of there's anything post LG and it can look like this and not. That's my knowledge so I'm not sure there's anything cortical related that would that could look like this though. So what's the different you know you're exactly right these are secocentral scatomas because remember this lady has 2040 best corrected vision. So what's the differential diagnosis for a secocentral scatoma. So you can think of things affecting the was it called the papillomacular bundle. And in that case is the those fibers are very active and so anything that affects metabolic activity so you can think of things like metabolic issues, toxic exposures. So you can think of things like LHO and good. I wonder if autosomal dominant optic atrophy also looks like this to something in the center. It could. That's not at the top of my list but yeah good sure. And then that's what I got for now I mean also. I can imagine glaucoma can have central related defects to. How about in a patient who's undergoing cancer for Michael plasma avium complex. Yeah, family tall toxicity can give you a secocentral scatoma. Yeah, those are good things to think about the other things that might go on that list you know you talked a little bit about a cone dystrophy could also be like car or Mars you want to ask the patient about a cancer history and about cancer which are pretty typical. Yeah so that's no that's a great, great job. You're right you know you pointed out that the defects look by temporal which kind of makes you think chiasm, but that's actually an artifact of testing because the Humphrey perimeter does not the particular 24-2 or 30-2 that we use doesn't test the midline points and and doesn't test like the points directly over the midline so it can kind of make something that secocentral look more by temporal. You brought that's a really I'm glad you brought that up to great point. So in terms of some of the different tricks that are described in you know Dr Thompson's manuscript or in the BC SC. You know there are a lot many of them help you determine that the patient's not blind like you know like using a rotating okay and drama rotating a mirror in front of the patient. But that doesn't really tell you how good the vision is and because you can have functional vision loss on top of organic vision loss, you really want. I think to use a test that's going to tell you exactly how good the patient's potential vision is. You know my favorite is the bottom up refraction, where you put the patient behind the foreopter and start them on the 2010 line and you have to really encourage them and coax them and how many letters do you see and can you just take give me your best guess that helps me, you know, run the dials back and forth to figure out how to make your vision better. Another good trick is using the red green glasses which is why I have this slide up so. Our. Acuity charts in clinic you can put up, you can make them red and green like this. And then if you're wearing the red and green glasses, it will, you know, cause the vision and one I to be black for, you know, one half of the chart and they'll be able to read the other half and if they can read the tell if somebody's doesn't really have vision loss and one I, I always have to put the red green glasses on myself before I hand them to the patient to make sure I don't, you know, mix up which, which I am trying to test. The visual acuity screens in our clinics are polarized to reduce glare. And then if you have if you take the stereo vision glasses that we use to test of stereo acuity with the fly the flybook. And it also will turn because those the polarization and those lenses are 90 degrees to each other. It'll turn the vision one I black like if you put them on and try to look at the eye chart. One eye is completely blacked out, and the other eye looks normal because the polarization is the same angle as the, as the screen. And again I have to I can never remember which one is which I always have to put the glasses on myself before I hand them to the patient to make sure I'm handing them the glasses, either right side up or upside down, depending on which eye they're claiming vision loss and testing their stereo acuity actually is another clever way, because you know in order to have a certain level of stereo acuity requires a certain level of vision. And that's something you can look up there's a, there's a I think it's on the internet you can just Google it. Because I can, again, I can never remember, you know, what level of stereo acuity corresponds to what level of visual acuity. So there's, there's lots of test there's lots of different tricks out there. The important thing is just to find one that you're comfortable with, and that you can do smoothly you don't want the patient to think that you're doing something unusual, or weird, or that you don't want to, you want to, you want in their mind, you want them to think that you're just doing your normal thing your normal routine the thing you do with everybody and so it's got to look effortless and smooth. In order to get the best cooperation from the patient. So just pick something and stick with it. Here's a trick that I don't think is in the BCSE that you can use. If a patient is claiming a visual field defect in one eye so in this case this patient is claiming a right. You know, Hemianopia and their right eye. You know, you don't have to worry about something, you know, behind the eye like a by temporal lesion or, or, or, you know, like simple lobe lesion because it's only in one eye. What you can do is you can ask your perimetrist to repeat the test with both eyes open. And if they map. So, if this was an organic lesion with both eyes open since the left is normal. So the bottom visual field should be full. So if they map that blind spot from their supposedly bad eye into the visual field that they obtained that you obtained with both eyes open. That that tells you that it's non organic or organic, you know, if the visual field defect disappears and you're like well gosh, I was wrong you there's really something wrong here. You know another trick you can do if somebody's just claiming a little central islands of vision. This is talked about in the BCSE you can, you know, I mean it's almost a it's not. It's not easy to get a Goldman visual field these days here it is we're lucky but you know outside of an academic eye center their heart it's hard to find a Goldman perimeter and someone who knows how to run it. So the classic thing and functional vision loss with Goldman perimetry are spiraling fields are crossing of the eyesopters. But you can also use a tangent visual field. If you don't have a Goldman perimeter and so the idea here is that if somebody has a central island of vision that's x degrees wide. When you back them up from one meter from the wall to two meters, the angle of the of their vision should double to two x degrees. But people with functional visual field constriction will usually not expand their visual field when you back them up from one to two meters. It's just a characteristic of non organic vision loss. And so that's another quick and dirty way that you can do in just about any clinic. If you suspect a patient's visual field constriction is is functional. And that's something that I think we demoed at our residents when they're in clinic, or at least try to. So this is just a reminder that it can be really frustrating to take care of patients with non organic vision loss because we're as ophthalmologist we're really trained to take care of organic vision loss. And so we find non organic vision loss frustrating. I just feel like the patient is wasting our time that they don't have an actual problem with their eyes and that they, you know, and the important thing to remember is that the vast majority of these people are not malingers, you know, like I'd say, 100 patients with functional vision loss I've seen, you know, over 20 years, one of them was a malingerer, you know, these are usually people that have some other psychological thing going on they're stressed out at work they're stressed out at home. They're not getting any attention from their parents because they have a sibling that's sick and that's getting all the attention. They have a minor thing wrong with their eye and they think that if they come in and tell you what their minor thing is, you'll blow them off because it's so minor so they, you know, sort of amplify the symptoms to try to, you know, get your attention. The thing to remember is these all these people all have something wrong. It's just not necessarily an eye problem. Oh, actually the most common cause in my clinic, I would say is chronic headache. You know, so these patients have chronic headache and for whatever reason I have no idea why they come in with functional vision loss and I think it's because nobody's treating their chronic headache and they're which is leading to anxiety and depression, which is making their headaches worse which you know it becomes this vicious cycle. And so then their psychological problems manifest as a physical problem so these people all deserve care they all deserve treatment as an ophthalmologist your number one job is to make sure there's not an organic cause for their vision loss like in the first case we looked at, or that it's not organic vision loss on top I'm sorry non organic vision loss on top of an organic problem. That's your number one job is to make sure nothing's wrong, which can be, you know, time consuming. And then the next thing is, you know, is that you have to, you know, take off your ophthalmologist coat and put on your doctor coat and you have to address some of these things like get them into a neurologist to treat their chronic headaches or get them into a mental health therapist to help with their depression or their anxiety or things that are going on at home or at school or at work. So these people do have an actual problem it's just not an eye problem. I have a quick question on this one. So, exactly like you were saying, and I've learned in the previous to Iowa to that there's a lot of times in underlying psychiatric issue but I thought I just saw in the Stanley paper that you show that there is not really a psychiatric issue and would not recommend referral to a psychiatrist. I'm not sure if I saw that correctly so I'm a little confused why he's saying that. So I'd say that most, most of the patients that I see with functional vision loss don't have an underlying psychological problem it's usually like I said chronic headache, or you know, but it can be or I pain, it can be. Gee, I'd have to go back and look at the paper and see exactly what Stan Thompson said. It just depends on the situation. I'd say that most of the time these patients just need treatment of their chronic headache, but then like sometimes like when a kid comes in with functional vision loss, you know, then I'll take the kid out of the room and just talk to the parents and say, you know, I really don't think there's anything wrong with your child in terms of an eye problem. You know because of some of the tests I did we're very reassuring but you know sometimes, you know, kids can get a like what I would describe as a mental block you know they can't they can't access the vision that they have. And then the parents will say, often they'll say yeah, you know, we kind of thought there wasn't anything wrong with their vision either because their behavior, their visual behaviors are normal. And it turns out that parents are getting divorced, or there's another kid in the family that's sick or, you know, or there's, you know, three families living in one house or some something like that and so then, then you just kind of have to put it back in their way or to do what they can to help solve the problem, you know, but sometimes it is depression or anxiety or some others are an actual psychiatric disease and they do need to see a mental health professional. So it just depends on the situation and you just have to ask a few probing questions. So I'd say if that's what it says in Stan Thompson's paper, I'd have to go back and look at it but yeah it just depends on the situation. So now what I was going to do is I'm going to stop screen sharing and I'm going to bring up some videos to look at. We can talk about me stop my share for a minute. Okay, so this is a video from the novel collection that Dr. degree did with her partner in crime Dan Jacobson when she was a fellow at Iowa. This is somebody who's reporting difficulty with focusing and eye movements and tracking. Did we lose Lydia to consults. Yes, I believe so. Okay, Brandon is sick. So she has to. So are you the sole survivor. I am. But I'm all for it. I'm here. Okay. So what do you think of this patients video. So there's some I, I fluttering and associated with eyelid fluttering to as well as some, can you play one more time I think there might have been some pair orbital, like, I don't know if there's some grimacing but muscles. Let me see if there's anything else. Yeah, the thing that really trips me up is the, the eyelids and so that all points towards a more voluntary type of an astagmus, which I actually have seen myself before too. Oh, cool. From what I understand this is more along the line of a functional issue rather than a organic problem. Yeah, exactly. Okay, good. Thank you up the next note on that patient that was a resident and ophthalmology resident when I was a fellow who could do this at will anytime he wanted to. And at the end of the video, his eye really, I mean, I even know his name, but, but he was a, he was a I resident when I was a fellow at Iowa, and it was really fun that he could do that a party. I have a quick question on that one. Can a commonive spasm look anything like that at all, almost like, I don't know if borders align between voluntary and not when they're just trying so hard to focus on something that it produces this voluntary and astagmus book. I don't think so. I mean, convergence spasm, which we're going to talk about in a minute can be, you know, can be organic but usually not, but accommodative spasm. I meant convergent spasm. Yeah, yeah. I think that people that can do that voluntarily do sort of use convergence somehow some way to induce the fluttery movements but I don't, I don't think that. At least in my experience, somebody with like asthenopia, you know, like somebody that's having difficulty reading, you know, doesn't end up going into a flutter like that. No, I don't think so. The only reason I ask is because I saw this one patient on call who was reporting like dramatic vision decrease young male who's denying any stressors but his parents as he was having some and that was the only finding that I saw where he was having these fluttering eye movements but with eyelids also he came back into neuro clinic Eric and I saw him. At the end we decided that it was most consistent with convergence spasm and along with accommodative spasm so we gave him some recycled bleach to many actually made him way better and he was super happy with that. Oh. Oh wow that's cool. Yeah, and so that's what we had him on he was very happy to see that his vision got better that he wasn't accommodating so much he was just eating up there. When we're trying to refractive you're just eating up the power just kept accommodating over it. Huh. So were they was it a latent hyper or. He was not actually. Okay, he was amatropic. But felt better after psych. Yeah, oh well no that's something I've never seen so yeah I that's great I guess that's part of the differential. When you see somebody doing that you know is that they're going into an accommodative spasm interesting. Cool. Okay, now we're going to go. So this is a different this from Shirley Ray, who's a neuro ophthalmologist at mass iron here, Harvard. And it's similar to the last case but there are some important differences. So for this, I'm seeing these horizontal. Flutter movements, and they don't seem to have a particular pattern in them. They seem to come go and then there's like pauses in between them that make me think that they are it's not doesn't seem to be sustained. Right, or some eyelid. There's some blinking associate with them to a couple of times. But that's the most I can pick up. Yeah, so the things yeah I agree with you the things are like differentiate that video from the prior one are. It's not continuous or these little bursts of back to back saccades it's like the eyes go right left right left right left and then they stop. You don't see that spasmy squinty eyelid movement like we saw in the first video. And so when you see those little, you know, very intermittent back to back saccades without any accompanying eyelid movement or, or, you know, any of that squinty converging kind of movement that can be that actually can be an organic problem, like a perineoplastic disorder so I just brought up those two videos to kind of show the difference between what a voluntary nice dagmas looks like and then a similar ocular flutter, which can actually be something more serious and you know in need, you know further work up and it's involuntary. Okay, so those those blinks that I saw probably just her blinking normally. I think so, whereas like in the first video the guy is kind of like squinty and his eye movements were kind of fluttery when he's doing that's almost like his eyelid movements are synchronous with the buzzy back to back and forth movements of his eyes. That makes sense. Okay, last video. This is a, this is another film from novel from Shirley Ray's collection at mass pioneer and Harvard. And this is a 17 year old kid who's also complaining of eye pain difficulty focusing and difficulty moving his eyes. He saw an outside ophthalmologist who diagnosed him with bilateral six nerve policies. And you can see that he does seem to have trouble abducting each eye. It's a combination of depression or normal, but it's weird because like sometimes his eyes look like they're moving normally as here when they, when one eyes covered. You can see that the left eye can clearly abduct and here you can see that the right eye can clearly abduct when that when each eye is covered individually but when he has both eyes open he just can't seem to abduct or has a lot of trouble abducting. And also it's a little hard to see in the video but there's some, the pupils are constricting to sometimes when he's asked to makes these weird movements like you can like move the eyes like independent of each other. Like as well. Yeah. What did you think of that video Tony spasm your third or new try it. Yes, conversion spasm. Yeah. Yeah, so what's happening is when, you know, whether or not it's voluntary involuntary that's, you know, not for us to decide but. But when he's being asked to move his eyes to the left or right he's converging his eyes and that's sticking them in, you know, so that one eye goes in towards his nose, and then the other eye doesn't seem to be able to abduct but you know the really compelling thing is that when you cover one eye and ask him to move each eye individually, you know the eye moves fully so you know it's not a six nerve palsy. And then the other thing that's, you know can be difficult to look for, especially if somebody has brown eyes is, you know, the pupils constricting when you're asking them to move their eyes back and forth and, and that's the tip off. You will not, you know that will differentiate that from something more serious so there are some organic. There are some causes of convergence spasm. It's like Wernicke's I think you can see it. Some like space of the skull things you know at the junction between the brainstem and the, you know, the upper spine. You know, the same place like where you would see a Chiari or other things that cause downbeat nystagmus can also cause convergence spasm, the Lamoc hemorrhage you know weird stuff like that it's really rare. But the thing that's going to differentiate those organic causes from non organic plain old convergence spasm is the pupillary constriction, you know, and, and the lack of other neurologic signs and symptoms. You know, convergence spasm that's a whole another kettle of fish that can be difficult sometimes using dilating drops like you were describing Tony with the patient that you saw with Eric. Sometimes that can be helpful. Sometimes it's just an asthenopia thing and they need reading glasses or they're a late in hyper open they need prescription glasses. But sometimes it can be really tough to treat sometimes it's a psychological thing. And they're stressed out they're drinking too much caffeine not getting enough sleep so there's there's a bunch of different things that can cause it, and different ways to try to get rid of it but it can be difficult, especially if somebody's been doing it for a long time. Well, it looks like we're done early. I had, I don't think let me look but I don't think I had anything else in my presentation. So it was very popular topic. I really enjoy non physiologic vision loss and non physiologic eye movements and I've seen some people with non physiologic TOSIS and obviously there's occasional person who puts drops in their eyes and stuff. You know, there's all kinds of all kinds of stuff I think it's always important to start to think about that you know you want to assume physiologic and you know prove non physiologic and that's the one of the huge advantages that we have and neuro ophthalmology is that we're not just, you know, well that doesn't look right to me, and just saying that the person is crazy but you know like with seizures or movement disorders, but we can actually prove. I think one of the really tricky ones for me is the flutter and the convergence spasm kind of stuff. And I think it's really, really important to make sure that you've looked carefully at vertical eye movements, because you know you don't want to miss a pineal tumor or something like that. Some people will actually have convergence spasm with medical issues like calcium disorders and hyperventilation, you know, pulmonary disorders. So sometimes it's a, it can be a physical manifestation of an actual medical disorder but I think as Brad pointed out those are those are really, really rare so. Judith, what would you say to Tony's question about referral to a mental health professional professional. Well, that's a really, really great question. And I don't know if you went to the whole session on non physiologic. They've actually decided they, you know, they have decided that functional functional disorders are a real thing, which is a little bit tricky because functional was sort of in the physical therapy where the world's kind of used as a description of this is the functional disorder. You mean like the functioning disorder but they decided to use the term functional disorder, meaning that it's that kind of sort of brain neurological disorder. And it was actually a very, very controversial session because the psychologist, Dr. Stubb from Mayo was basically saying that it's all physiologic. And that, that you that that, how was he putting it Kathleen it was really it was really difficult and you know, the all of the neurophemologists in the audience were basically saying like, you know, because somebody gave a talk on, you know, non physiologic stuff and the audience was just going nuts of like, well, but it's not real. Yeah, but we are the keepers of real, you know, I know but his point was that there is some kind of brain pathway that allows for these kinds of things to happen like the convergence phasm or whatever. Let's, let's say it's non physiologic. I mean we like to turn non physiologic because it tells us that it's not based in some pathway but his point was that all of this is based on some pathway. It's just an aberrant way of demonstrating the path pathway or the for the person. So it was it was very unsatisfactory for for many neuro ophthalmologists because it started to disturb their world view. Very much so but anyway the answer to your actual question is, I definitely have the talk with the parents with the associated people. I think that in some cases you really can identify a clear secondary gain, in which case, you know, I can be quite blunt with them. But most of the time I think the vast majority of the time, people are either innocently suggestible or that this is a physical manifestation of a psychological disorder and I feel like I am not doing my job as a physician if I just just say, oh, it's okay dear pat on the hand I feel like it's really important to get them into a mental health professional. And, you know, I think it's I think that's important to have a one or two mental health professionals that you can work with and I've had really good luck with that. My, my most recent really severe conversion spasm, I think I might have even sicked her on you at one case Brad, but she was just terrible terrible. And I just looked in on her psych notes and she is, she's doing so much better. And, you know, they identified some really, really significant stressors that had kind of been blown off by patient and mom. But I think, I think that, you know, as a, as a professional and making this kind of diagnosis it is, it is your obligation to, to refer to a mental health professional be you know a counselor or a psychologist or a psychiatrist usually psychiatrists not much use, I would be much happier with a cognitive behavioral psychologist. CBT is I think probably going to turn out to be if it's ever studied probably the best route for these folks CBT is because it's not all sort of, you know, let's talk about your mother's stuff it's more like okay how are we going to do a practical thing this week, report back to me how you did, and you know that we're going to work on the next thing. And, you know, but at the same time an incredibly supportive environment for them. Yeah, and I would just say that follow up is important to you know you don't want to discharge the patient from your clinic if you, when you make a diagnosis of functional vision loss you want to make sure they get better, and then you're not missing something organic. Kathleen any, any final thoughts before we sign off. I think functional visual loss is one of the most challenging things we do. And, and I like, I think it's, I think your point that we follow them until they're better as a good one. Okay. Tony thanks so much so much for doing all those cases with us it was a lot of fun and I hope you have a great weekend. Sometimes they don't get better they just choose a different non physiologic thing to work with. They move they move from your blurred vision to unexplained abdominal pain and you know, then they're seeing somebody else. Yeah, but you know, and I want to underscore Judas comment about CBT that has been studied in migraine, not so much chronic migraine but episodic migraine. And compared people doing and also this showed up in kids. In that big study, the champ study that cognitive behavioral therapy was as efficacious as preventative migraine medication. Yeah, yeah. And we do I think that's an important point just a quick plug for the Utah Center for evidence based treatment this is a good way to get people plugged in with a CBT therapist. It's a good resource for the patient. Okay, thanks again Tony.