 Good morning. Good morning. So this morning we have Dr. Hansen, our neuro-optimology fellow. It's coming to talk to us about the visual quality of life in migraine patients. And she did her training at the University of Cincinnati and then joined us and has been here for well. It'll be a year in July, I guess. Feel welcome her and she'll have some time for questions. Alright, thanks for having me. This, originally there was going to be two presenters, but now it's just me. So I added this talk on which is pretty brief, but I'm also going to be presenting an interesting patient that we saw in clinic. So this is a project that we're doing in the neuro-optimology department looking at the visual quality of life in patients with migraine. So just as a quick update on the background, as everybody knows migraine is a neurovascular clinical syndrome. In which patients get recurrent episodes of head pain that do not serve any warning purpose. It's very common, globally at least 11 percent of the population, but in some populations it's up to 20 percent. As everybody knows, frequently patients get light, sound and odor sensitivity and up to 30 percent of patients get an aura. Most patients are photophobic during an acute attack, but there were two really important papers that showed that patients with migraine are actually more light sensitive than the average person in between the acute attacks. So the IIH TT looked at visual quality of life in patients with IIH and they used two different questionnaires, the NEIVFQ 25, which is the National Eye Institute visual functioning questionnaire. There's 25 questions and the neuro-optomic supplement to the NEIVFQ 25. And interestingly, the scores were actually pretty similar to scores that patients had at MS and optic neuritis. And they found that patients with worse visual acuties and worse pain symptoms also had worse visual quality of life. Not that surprising, but one of the reviewers questions and one of their biggest critiques were that we couldn't say how much of the decreased visual quality of life was related to migraine because there's a huge overlap of migraine in IIH. And essentially that answer just wasn't known, hadn't been looked at. So we decided to use four different questionnaires and the first two on the list look at the visual quality of life and the second two look at the impact of headaches and the headache severity. And I'll just show you a screenshot of each one to give you an idea of what they're like. So this is from the NEIVFQ 25. As I said, there's 25 questions. They're all Likert scale questions, but they ask things like how much trouble do you have driving because of your vision and how much trouble do you have finding something on a crowded shelf, that sort of thing. And this is a screenshot from the neuro-optomic supplement. It's 10 questions. Again, they're all Likert scale questions. They ask things, questions about double vision and blurred vision and pain with eye movements and lip position, things like that. This is the migraine specific quality of life questionnaire. So all of the questions are asked relative to how much migraine has affected them in the past four weeks. And it asks things like, you know, how much have migraines interfered with your ability to do your daily work activities, stuff like that. And this is the hit six questionnaire, six questions. Again, all Likert scale designed to see how much of an impact the headache has on their daily life. So we separated participants into three groups, those with chronic migraine, those with episodic migraine and a control group. So our inclusion criteria were patients who had migraine headaches that fulfilled the ICHD third edition criteria. And if they had migraine headaches for at least 15 days out of the month, they were put into the chronic migraine subset and we just did adults. So we excluded patients that had a history of other neurologic disorders and those who had a history of eye problems causing vision loss. So, of course, dry eye does affect visual quality of life. But if we excluded any patient with dry eye in Utah, we would have zero patients in the study. So we just excluded patients who are actually under a physician's care for it. So this is just a table of the results in terms of the demographics of the groups. So there were 29 participants in the chronic migraine group, 37 in the episodic and 32 in the controls. There were more women than men in the migraine group. And I have the average age listed of the patients there. So this slide I know is a little bit busy. The table at the top shows what the average of the composite scores were for the NEI VFQ25 and the 10 items supplement for each group. So in these questionnaires, greater scores indicate a better quality of life. So what you can see from the table is that the controls had the highest scores than episodics than chronics. And these two tables here are just showing what the results of the unpaired T tests were. So there was a significant difference in terms of the scores of the chronic migraine compared to controls, the chronic migraine compared to episodics, and the episodics compared to the controls. So the chronic migraineurs had significantly worse scores than episodics who were worse than controls. And this was true for both questionnaires. And this is showing what the scores of the hit six questionnaire were. And in this questionnaire, a greater score, a higher score means that they had greater impact of the headaches on their life. So as you would expect, patients with chronic migraines had the greatest impact on their life. And again, this was statistically significant. Chronic migraines were the worst, worst, and then episodics and then controls. And then these are the results of the migraine specific quality of life. And it's broken down into three sub-scales. The role function restrictive are questions that assess how the migraines limit their social and work related activities. The role function preventative questions assess how migraines prevent the activities and the emotional function questions assess the emotions associated with migraine. And again, these are not surprising results that the chronics were the worst and then episodics and then controls. But they're really important results. So, and these were all statistically significant. And one thing that we thought was very interesting, the scores for the visual quality of life, questionnaires in patients with chronic migraine were similar. They were not different than published values for patients who had other neurophthalmic disorders, like ischemic optic neuropathy and ocular myosthenia and thyroid eye disease. So diseases that you would expect would really have a significant impact. Patients with chronic migraine were just as bad. So we're still in the process of analyzing the data. And so we want to find out whether or not there's a correlation between decreased or a greater impact of headaches and their visual quality of life. We expect that there will be. But the biggest conclusion that we are taking from it right now is that migraine has really significant effects on the visual quality of life. And if you see patients with migraines in an eye clinic, you know that that's true. But this is just kind of proving it to everybody. And their quality of life has really decreased. So we understand a little bit about why that happens, but we really need to look further into what actually causes the decreased visual quality of life. And the other important issue is that when clinicians are assessing the overall disease burden of migraine, they really need to include what their visual quality of life is in that. So that's it for that part. These are the references. Which items on the EFQ-25 were they lower on? Was it across the board or were there specific ones? That's a really good question. It was across the board. I think the worst, the most decreased scores were actually with driving and near activities. I think were the most significantly decreased, but they actually were all the way across the board. But that's a really good question. So last week, the trick that I learned from Eileen is that if you want people to pay attention to your presentation, you should show them a picture of your brother. So I thought, oh, I could probably find a nice one from my wedding this past year. But what I found out is that I cannot, and there are actually only three pictures of him from the entire wedding. And he also might be a little bit insane. So I thought, oh, so this is my brother, Caleb. And this is the second picture that I found. That's Caleb eating dinner. And the third. That's literally the only picture that was from the wedding. Okay, let me switch over. All right, so this is about a patient that we saw in the clinic. He was a 53-year-old man that presented with double vision. He'd been seen by an outside ophthalmologist and referred in. He'd had three months of constant double vision that started fairly abruptly. He was on a long drive through Wyoming at night. And he had noticed since the time of onset that it was constant vertical binocular depopia. He reported that it was progressively worse as the day went on and a little bit better after a nap. So when the double vision would get really bad, he would go rest his eyes for a little bit or go take a nap for a little bit. And he would notice that his left lid appeared to be drooping when he got really tired. He wasn't having any trouble swallowing or breathing. So he really had no past medical history to speak of, but he also didn't follow regularly with a primary care physician. His neighbor is an instacare doctor, so if he would have problems, he would just kind of like pop over there and he would help him out. So he didn't really find the need to go see anybody. He also had no past ocular history and he'd already had an MRI of the brain and orbit, which was read as normal other than some sinusitis. And so he went to his neighbor's house and they talked about it and they decided to do a course of antibiotics and prednisone to see if it would help. It did not and he had just finished the course at the time of his visit in the clinic. So on examination, his acuity was normal with some correction. His pupils were normal, his fields were normal, his color vision was normal, his pressure was normal. He had some asymmetry in terms of the positioning of his lids. His MRD1 was 5 on the right and 4 on the left. And other than that, his slit lamp exam and his dilated fundus exam were very unremarkable. And this was his motility and alignment exam. So what I'll point out is that he had a left hyper that seemed to be worse in right gaze and worse in left head tilt. He also appeared to have some up-shoot in adduction of the left eye and wasn't quite able to get the right eye elevated fully. So I will just throw that out to the group if anyone wants to throw out the answer. What typically will give you a left hyper that's worse in right gaze and worse in left head tilt? Yes, good job. Yeah, a left one. Okay, so I'll let you think just for a second about what would be in the differential for that. And I came up with some ideas myself. So probably most commonly top of the list would be congenital or traumatic fourth nerve palsy. You could get a microvascular fourth nerve palsy, although that's not very common. If you had a little schwannoma on the fourth nerve or another tumor pushing on it, he could get it. Maybe it doesn't have anything to do with the fourth nerve at all. Maybe it's myasthenia or thyroid eye disease. You could get a vertical deviation with a skew, although you probably expect that to be a little bit more comatent, or maybe demyelination or aneurysm. So we actually think that there should be another thing on the list that you might not initially think of. And I didn't want to give this away before, but I'm going to show you a photograph of him. So it's probably most obvious, or it's jumping out to everybody, is the asymmetry here. So he really has Halloween of the superior sulcus. And it's a little bit hard to tell in the picture, but this is actually much more full on the left eye than here. He also has some pseudo-retraction, and I'm sorry, the hooding with the dermatical aces really doesn't let you see it, but the lid margin is just a bit higher relative to its position to the limbis. And then I don't know how easy it is to appreciate, but he had about two to three millimeters of hypoglobis and two millimeters of enulfthalmos. So at this point, we thought this was very suspicious for silent sinus syndrome, so we really wanted to get a look at his images. So this is a coronal T1 fat-set image, which confirmed our suspicion. He's got an opacified and collapsed maxillary sinus here, and you can see that the orbital floor is depressed here. So his inferior rectus is just kind of hanging out there. And this is a slice from his CT that was ordered by the ENT after he saw us, and I'll point out a couple of other things on that later, but I thought it just kind of nicely showed the difference in the contour of the floor. So at this point, we were asking ourselves whether or not he had more than one problem causing the double vision. And, you know, we thought, is all of this related to the silent sinus? Is any of it related to the silent sinus? Could he have a congenital fourth that he no longer can control because of the hypoglobis and enulfthalmos? But if you look back at the image here, you can compare the size of the superior obliques, and if he had a congenital or a long-standing fourth, you would really expect the left to be smaller, but we thought it looked very symmetric. And in addition, his vertical-fusional amplitude was five prism diopters. So what we took from that is that he needed four to correct his deviation, and then he could fuse one additional prism diopter after that. So we thought that his vertical-fusional amplitudes were not increased, and essentially we did not think he had a congenital fourth going on. And we looked at the rest of his scan and didn't see anything like, you know, a tumor or other demyelinating lesions or something to suggest that he had something else going on. But we really couldn't say that he didn't also have something like miastinia or thyroid eye disease. So we did decide to test for that. And actually at this point, Dr. DeGree, she made me bet, like, place a monetary wager on whether or not I thought he also had miastinia. It's just like a little bit of a shark also. But yeah, she made a lot of money from that. It was illegal tenders, what that is. So the testing was negative. So at this point, we were pretty confident that all of his vertical-what's that? That's irrelevant. It's irrelevant. Yeah, I lost. I lost. But so we were pretty confident that it was all related to the silent sinus syndrome. So it is a progressive enophthalmos and hypoglobus due to collapse of the orbital floor in the presence of asymptomatic chronic maxillary sinusitis. So it was first described in 1964 by William Montgomery, who was an otolaryngologist. He described two cases of double vision and enophthalmos with maxillary sinus, a case of pacification and collapse. And after that, there were several more case reports, but the term silent sinus syndrome was coined by Charles So Parker and his group in 1994. And they described 19 cases of hypoglobus and enophthalmos with asymptomatic maxillary sinus disease, meaning they did not have symptoms of the chronic rhinosunusitis. And so it typically occurs in the fourth to fifth decade of life. The largest review of cases had 84 patients. The average age was 39 and there were slightly more males as compared to females. So the underlying pathophysiology involves hyperventilation of the maxillary sinus due to obstruction of the osteomyatocomplex. So the first thing that happens is that you obstruct the sinus osc. And in 62% of patients, they have a lateralized middle turbinate, which we'll come back to. It can also be triggered by a deviated septum, a mucosil, a polyp, or even just chronic secretions. And interestingly, the underlying pathophysiology of silent sinus syndrome is considered to be very analogous to the pathophysiology behind chronic eustachian tube dysfunction and the resultant tympanic membrane atolectasis. So this is just a little diagram describing what happens in the course of silent sinus syndrome. So as I said, the first thing that you get is occlusion of the sinus, which eventually leads to development of a negative pressure. And it's not really entirely understood why some people who block off the osc develop negative pressure and some people don't, but it's thought to lead to development of negative pressure because the gas that's within the hypoventilated sinus gets resorbed by the capillaries of the closed sinus. And so then you get this negative pressure. So Eric Cass and his group proved that there was a negative pressure. They took an 18-gauge needle with a transducer attached, stuck it in there, and showed that they had sub-atmospheric pressures on the affected side. So then they get an accumulation of secretions within the sinus. So what happens is the aqueous component of the secretions gets resorbed back in and you're left with this transcellular exudate and it really thick mucus. And that leads to chronic subclinical inflammation, which kind of like continues this loop, and eventually you get maxillary sinus atolectasis. So all patients will have enough thalamus, usually two to six millimeters. About half patients will get hypoglobis, usually one to six millimeters. Most have double vision. The most common late abnormality is pseudo-retraction, but you can also get pseudo-tosis. And radiographs are an essential part of the diagnosis. You must have maxillary sinus shrinkage and a pacification. You'll get a depressed orbital floor. And then you may see areas of bone demineralization of the orbital floor. It's a little bit controversial because it's not always seen. And in fact there are some case reports where the maxillary walls actually were thickened after. But a lot of people think that the demineralization, as a result of the chronic inflammation, predisposes you to collapsing the floor. So this was an interesting case series where they described the radiographic findings. And there were only five patients, but they all had an enlarged middle miatus and all had varying degrees of lateralization of the middle turbinate. So this is the CT scan from our patient, so I thought I would point out you can see how lateralized his middle turbinate is. And you know, it's sort of all, now all of this anatomy is like a big thickening mess. And you can use CT or MRI to diagnose it, but a CT scan outlines the anatomy a little bit better and can, from what I read, help you differentiate other possible causes better. So this is a list of some, most, but not even all of the items that would be in a differential diagnosis for silent sinus syndrome. So I'll point out a couple of things that are really important to consider. Like a malignancy can cause chronic obstruction of the ass, so you'd want to rule that out when they have a procedure. I'll talk about that a little bit. Sometimes it's just congenital asymmetry. Sometimes it's orbital fat atrophy or bone growth arrest if they've had external beam radiation. So this was a really important retrospective observational case series. And this group included 19 patients that have been sent to them with the diagnosis of silent sinus syndrome, but they didn't actually have silent sinus syndrome. They did have spontaneous asymptomatic enabthalmos, like asymptomatic meaning other than the double vision and that. So this is a list of what it actually turned out to be. So in the majority of patients, they'd had unrecognized orbital floor fractures. A large amount actually had Perry-Romberg syndrome or linear scleroderma, they're on the spectrum. It's hemifacial atrophy. And three of them, it was congenital facial asymmetry. Two of them actually had thyroid eye disease. One of them had HIV-related lipodystrophy and one had an asymmetric facial atrophy from Barakir Simmons, which is a rare acquired lipodystrophy syndrome. And one had metastatic breast cancer in the orbit. So just some important things to think about that may not be as obvious as it seems. So there are two main goals of treatment. The first is to relieve the obstruction and improve maxillary sinus drainage. And the second is to restore normal orbital anatomy. So the first goal is accomplished with a sinus procedure. The Caldwell Luke involves fenestration of the anterior maxillary wall, so they actually go up under the lip. But that's an older procedure and has fallen out of favor and people primarily use FESS now. So the two aims are to reestablish normal drainage of the maxillary sinus and then to aspirate in culture secretions and you can also do a biopsy if you're concerned about malignancy. Functional endoscopic sinus surgery. So this involves using an endoscope to go up through the nose. So they may or may not start with a septoplasty to improve access. Then they remove the unsonant process so that they can have access to the osteomyatocomplex and then they do an antrostomy to enlarge the ass. So the need for and timing of reconstruction of the orbital floor is in some ways, some people think it's a little controversial. In this series of patients, 22 out of 23 of them had resolution of their symptoms after just FESS alone. But not everybody resolved with FESS alone. So there are a couple of different timing options. You can do a single stage procedure with the FESS or you can do it two to six months after the FESS or not at all. The implant choices, implants that have been used successfully are varied. So you can do titanium plates. You can do implants. You can do the septal or castor cartilage. Another interesting option is using hyaluronic acid gel. So this is a group out of Greece and they injected like two CCs into the intracronal and extracronal spaces and had good, they had improvement of the patient's enaphthalmos for about six months. But this wouldn't be expected to really do anything for hypoglobis. But it's an option. And I thought very interestingly you could also do an inferior oblique myectomy on the contralateral side. So David Geithen wrote this up in 2010 a patient who's a 41 year old man who presented with double vision and he was found to have a silent sinus syndrome on the right and causing an apparent left superior oblique palsy. So they felt that the depression of the orbital floor resulted in tightening of the ipsilateral inferior erectus and inferior oblique and then loosening of the ipsilateral superior erectus and superior oblique and then that mimics fourth nerve. But they actually also had the apparent inferior oblique overaction on the left side just like our patient had. And so the guy in the case had already undergone FESS and didn't have complete resolution of his double vision. So he was going to have reconstruction of the orbital floor but then somebody sent them to this clinic so they thought let's try an inferior oblique myectomy and it worked. So I thought that was very interesting. That's it. Any questions? Which MRI scan didn't show the sinus? It did. It just was an MRI scan. Yeah, that was the MRI that I showed was from the outside hospital. We just got it sent in. It's hard to know everything but it really depends on your fellow physicians with expertise like in radiology and your nose and throat to help you out when you're in a bind. So you really feel screwed when you send somebody for an MRI and they don't read it. And so sometimes you just have to do it yourself. In fairness, a lot of radiologists have never heard of the silent sinus and I've heard that a lot of you ENTs haven't either. How long does it take for resolution if they are adequately aerating that sinus and how long does it take for the orbital and the avenue to do it normalize and make the double region better? That's a really good question. I have no idea what the average amount of time is but I know that typically people will give it up to six months. Dr. Patel, do you have any more experience with that? Let's make it representative to the 22 out of 22 normalize of the silent sinus syndrome. If you look at it, we don't found most of it. We can double read the symptoms. So if there are patients who present with dryness and the common radiations, at least if they are medical products on that side. So it's a combination of pseudo-infection and pseudo-physicists. If you look behind the side of the eye, there's no major component of the mechanism. So that is a really controversial because you never rest along the aeration of the ability for developing the symptoms of the sinus with the natural normalization. So what do you do about six months and then you do a new product with the normalization? Sometimes you have a different measure to do that on the product and so on. So that's the one component of the mechanism. They only look at symptoms with the sinus. So I think the question of normalization is that if you look in this show you make a video of the sinusitis, which if you make a custom holiday you can show the sinusitis in a different way. It's the sort of normalize the normal. None of those videos show the sort of normalization. And our patient did have the fest and he felt like his double vision was a little better but it's not resolved. So he's actually good to see you and why he's so excited. So Any other questions? Yeah, good question. Are there any rotational aspects of the double vision? No. Yeah, no. There was not a cycloportical indication of any questions. So that brings to mind what to do with fixing. And you know, I have a lot of respect for doing a guide one. But if you recess the contralateral into your bleep you're probably going to give it some portion. So the thing to do is that we're going to discuss if it doesn't get better, which it may well do gradually. You want to check the worst actions in the operating room. If that gypsilateral inferior rectus is tight, I mean, keeping in mind you've got left eye higher than right, your options are either to bring left eye down, this is what you're going to accomplish with your bleep recession or bring right eye up, which is what you would do if you'd be inferior bleep. On the left, if you recess the right inferior rectus, you'll bring the eye up. You'll help normalize the position of the eye. And if that's tight, it'll turn out to have been the right thing to do. Probably a decision you can't really make in the operating room, but that issue of torsion is kind of key to do. If you do an inferior bleep recession and a patient that does not have torsion they're going to come back saying, yeah, things are kind of okay, but now this image is twisted like this doc and then you're kind of playing the catch-up trying to fix that by doing offsets on additional muscles you're operating on which won't be the best thing. So the smart thing would be for the patient to get better than I've ever had. The right-hand space was that the patient had not had a certain of the muscles served. Right. He had a FES. Yeah, so I think your steps should be your FES can be ordered to the natural rectum before you do FES. It's just like a thyroid disease. Absolutely. It's the old syndrome, if you go through a rectum surgery they'll fix you right away. It's a more common approach. It didn't come up in any of your in any of the articles you cited, but I've got a patient I've been following for about 10 years now who just doesn't want to take the time out of his schedule to do strobism surgery. So we've been managing him with prisms and he's been currently happy with that. That works too. Good. This guy's deviations probably works in common. Just don't look right. And he's slightly better already. Didn't you talk to him? Not entirely. But quite a bit better. And that's just, he's only close to like 6 weeks or something like that. Yeah. All right. Nice job. Thanks.