S2:Ep2 – Testing and Treatment for Vestibular Migraine



Voice-over: Welcome to Spotlight on Migraine, the Professional Series, a podcast hosted by the Association of Migraine Disorders. In the Professional Series, we dive deeper into migraine-related topics with the help of guests from the medical field. The content of these episodes is intended for medical professionals but may be useful or interesting for patients as well.

This episode is brought to you in part by our generous sponsors, Amgen/Novartis.

In this episode, we hear neurotologist Dr. Michael Teixido’s lecture about Vestibular Migraine. He describes how our balance system works and what causes vestibular issues. He points out the problems with current testing options for diagnosing Vestibular Migraine as the cause of their dizziness and talks about current treatments.

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Dr. Michael Teixido: I can say that we are probably now in an era of increasing awareness of this group of patients who is migrating from clinic to clinic to clinic looking for a diagnosis, for someone who will champion their treatment and partner with them to help reduce their symptoms and improve their quality of life.


Let’s see. I don’t have any disclosures, and let’s just make sure that if we’re going to talk about how we evaluate balance disorders — well, this is a little bit of a complicated topic, and we need to understand for a moment what the vestibular system is. If we have a — we each have two inner ears. Each inner ear has hearing on one end that came second. First, evolutionarily, came the balance side of the inner ear.


And we have five little balance organs on each side. Three of these organs are for sensing rotation, and they are in the semicircular canals. And two of them are for sensing any motions that are not rotations; that means side to side, up and down, forward and back. 


So those are wired through our brainstem to our eyes and our eye muscles so that we can walk and move in the world and maintain stability of the image we are looking at very accurately on the most high-resolution portion of our retina, called the fovea. That is sort of our 10-megapixel camera. Everything outside of this 2-degree-wide circle of high resolution drops down to about 1 megapixel. So it’s very important that we are able to coordinate our eye movements and our head and body movements, and this is what the inner ear does. So this is done through a reflex which very generally can be called the vestibulo-ocular reflex. 


Now, we have these otolith organs, and these otolith organs have crystals. These are the ones that help us maintain our orientation to gravity, whereas the semicircular canals help me to focus my eyes by telling them how much to turn in the opposite direction when I am rotating my head up and down and side to side. The otolith organs are wired some to the eyes, but primarily to the muscles of my body so that when I am tilting extremely, I can adjust the muscle tone in my body to keep myself from falling over under my own weight.


There’s a problem with this second system, though, and that is that you can create a force by tilting your head that is identical to the force generated simply by moving in a linear direction. And how do we tell the difference? So there is an ambiguity that occurs at very low accelerations and tilts. And we’re going to come back to this problem because this becomes very important into what’s going on in a vestibular migraine patient.


So our body has 2 inner ears with 10 organs. We have the eye muscles. We have the input from our joints and our muscles giving us information about the position of our physical body in space. And all of these inputs are integrated in the cerebellum and the brainstem through the thalamus, and we become aware of our position in space at the cortex. Any dysfunction in any portion of this network can result in a sensation of dizziness, imbalance, disorientation in space.


Now, as far as vestibular testing, I can say quite safely that there are no disease-specific laboratory findings until recently that are easily accessible to any of us as practitioners that tells us, “Aha, this is a vestibular migraine patient.” We are left, then, with our clinical acumen and our practical advocacy for that patient and our willingness to work with them as a coach to help them to reduce their disease.


We do use laboratory testing to understand vestibular disorders and to see if one inner ear has been injured. Is it weaker than the other side? Have the necessary adjustments been made in the brain to allow a person — the twin-engine airplane, to take off and land and taxi without drifting to one side or another? Or is this imbalance new and uncompensated for, or are there other aberrations?


So, well, what do we do with vestibular testing? Well, we are currently using this information to add to a clinical picture that does become important in the management of individual patients. But in our emerging and evolving understanding of vestibular migraine, it is really helping us to segregate some of these distinct manifestations of vestibular migraine in this smorgasbord of possibilities so we can develop much more specific treatments for individual patients and get right to the root of the matter. Because some people, it starts in the inner ear, and the migraine activity is a secondary phenomenon. Others have a primary problem that is in the brain, perhaps. And others have, as their migraine, a headache pain as a strong manifestation; and in others, the headache may be nearly absent and certainly not placed in a cardinal position.


So what we learned early on in this group of patients is that when we sent patients for testing, it wasn’t some particular abnormality that we were finding. But what we really found out was when these patients came back after their testing to review the results, they said, “You know, we weren’t able to calculate whether one inner ear was weaker than the other because when we interrogated the inner ear with warm and cold air to drive the inner ears as hard and fast as they could go and then to slow them down as much as we could so we could compare the strength and weakness, they wouldn’t allow us to finish the four irrigations necessary.” 


So this was the most common finding in our vestibular migraine patients. And then we would also find that those patients said, “You know, after the testing, I was out of commission for the rest of the day.” This intense vestibular stimulation just brought on and provoked a migraine storm that was unrecoverable for them. 


We did find that some of these patients, surprisingly, had an actual weakness in one inner ear, and this was really curious. How, if we have a migraine problem, could an injury happen in one labyrinth? So this brought up questions. Once again, here is an example of what I was talking about: the testing brings up questions. But whether that inner ear injury was compensated for or not told us whether or not that weakness was important currently in the management of that individual patient. 


A lot of these patients, we found that the testing reinforced what we were hearing from them in their history, and that is that they could not tolerate a particular type of stimulation called optokinetic stimulation. And this is where we have bars moving across the screen. Many patients recoil from this, even if you hold it up on a phone in front of them. And this corresponds to the clinical complaint that they don’t like to walk down the aisles in the grocery stores and they don’t like driving over bridges where there’s nothing to look at except the passing stanchions on the sides of the bridge. 


And so this evokes an emotional as well as a vestibular response that’s difficult for them. And in the case of bridges, they know they’re on a high bridge, and they know something’s wrong, but they don’t have a good explanation in terms of vestibular physiology. And this is the seed of a phobia, and now we have that to deal with.


Another thing that came up quite frequently is that in some patients — we do this testing called smooth-pursuit testing, so this is a dot moving back and forth across the screen, like this cursor is moving back and forth. And the eyes move back and forth to follow it, and we see how well we can follow it. And as we get to higher frequencies, this tends to fall apart; and anyone over 65 or 60 years old, we start to fall apart at high frequencies. But when we have a 35-year-old woman in our clinic and their smooth pursuit is falling apart at high frequencies, seemingly prematurely, then we suspect that there must be something wrong with their central nervous system’s ability to process this visual vestibular information. So these are very general findings.


Recently, we’ve also noticed clinically that a lot of these patients have positioning nystagmus. So if they come in on a day when they are symptomatic, we will put them — we look at their eyes in the dark so that they can’t fix their gaze on anything, and we’re looking at their eyes with infrared lenses. We put them in different positions and see if they develop nystagmus. 


Well, occasionally, you’re thinking benign paroxysmal positional vertigo — crystals in the inner ear. Well, that can happen, but patients with vestibular migraine, when they’re symptomatic, often will have a positioning nystagmus that is not very symptomatic and does not follow any pattern that could be explained by crystals or something happening in the inner ear mechanically. So there’s a distortion happening that it’s difficult for us to explain. 


Sometimes, patients with vestibular migraine will have something that does refer to the inner ear, and it’s called a floating cupula, where there’s not crystals. There actually is a change in the buoyancy of the cupula in the inner ear, and it’s unique to vestibular migraine, we think.


So another thing that our patients tell us is they say, “I have these episodes of vertigo, and I take meclizine, which my primary care physician gave me, and it doesn’t help at all. It even makes it worse.” And in fact, only about 20% of patients respond to meclizine and the traditional vestibular suppressants because these anticholinergic vestibular suppressants primarily suppress input from the semicircular canals — the three semicircular canals. 


What seems to be more effective for these patients are GABAergic vestibular suppressants like benzodiazepines — diazepam and clonazepam — which have more activity in the utricle and saccule, these otolith organs. Now, these are the organs that — and that’s the reason we give benzodiazepines to astronauts, because they get sick for the first day in space when their otoliths are floating. Their semicircular canals work fine, but they lose the gravitational vector, and they get space sick. And we give them usually lorazepam at low doses so that they can remain functional and not waste a valuable day of space time. I don’t know what the cost per minute of having an astronaut in space is, but it’s quite a lot.


So we know that something is going on, and maybe there’s something going on especially with the utricle and saccule in these patients. So, well, we have a new — recently, a new test for the utricle and saccule. So there’s a test called the vestibular evoked myogenic potential. We call it a VEMP, a cervical VEMP. And what we do is we bombard the saccule in the inner ear with big pulses of sound, and then we measure — remember, those are wired to your body’s muscles — we put electrodes on the muscles in the neck and we measure how much the muscles relax in response to those big sound bursts. And it seems that in one study, there was a tendency to having a little bit lower amplitude on these.


That’s an interesting finding because it seemed consistent in this study, but we couldn’t explain how that really fit into the clinical picture that we were seeing. And in fact, it seems to be not supported by any of the other VEMP studies, and none of these were very high-quality studies. So we did have — you can get a VEMP from the saccule called a cervical VEMP or an oVEMP that comes from measurements and responses mediated through the utricle. And so we found that there was no real difference in the sensitivity of the utricle and saccule to linear motion. It wasn’t the amplitudes, but the latencies that were reduced. 


Well, maybe this reduced latency suggests maybe a little hyperactivity. We liked that. We said, “Aha, yeah, there’s more hyperactivity in this system.” But once again, we didn’t see it in any — haven’t seen it in any other studies yet.


So we have another study in which vestibular migraine patients had a higher tendency to have abnormal cervical VEMPs, but in this case, the abnormalities had to do with differences in the amplitudes between the two sides or the fact that we couldn’t even get responses in a high number. And this suggests that VEMPs are so finicky that it’s really hard to compare results from laboratory to laboratory. And so we’re really foundering a little bit.


The traditional and the gold-standard testing in the vestibular system comes from the VNG, and this is where we put the warm and cold air in the ears and we measure some basic eye motor movements and eye tracking abilities. And when we did that — and we also did something called vHIT, a new test which allows us to stimulate each of the six semicircular canals individually and to compare the eye movement and the head movement. We found that a lot of patients with vestibular migraine had some deterioration in their oculomotor coordination, and this is what I was talking about when I said we see young patients with pursuit abnormalities at higher frequencies.


We also noticed that a lot of patients had this positioning nystagmus that was not accountable for by crystals. But overall, there wasn’t really a very significant difference between the overall basket of findings in the vestibular migraine patients and the control patients. So we’re just not really getting anywhere.


Now, this study demonstrated that if you take all of the patients with vestibular migraine and you do balance testing and they do have a weakness in one labyrinth that can be demonstrated with this caloric test or a weakness in a labyrinth that can be demonstrated with this head impulse test called vHIT, which measures each canal response individually, then they are much less likely to respond to treatment. So there’s something about having an abnormally matched pair of inner ears that will prevent you from responding to treatment very well.


Now, the biggest advance we found was — came from Richard Lewis a few years ago, and he demonstrated that — and remember, we were talking about — he demonstrated that the problem may have to do with not the sensitivity of the otolith organs or the sensitivity of the semicircular canals — which is the same in vestibular migraine patients as in normals — but in the ability to coordinate the input between the two. 


So we have this complex — remember, we mentioned that the otolith organs have this problem. It can’t tell the difference between accelerating and tilting at very low accelerations, and the way it tells is by borrowing information from the semicircular canals.


There’s a very complicated test where you roll a patient and tilt them at the same time. This is not something that you can do at home or in your office. You have to have NASA-style equipment to bundle patients and put them in total dark rooms and orient them in different ways in order to roll and tilt them at the same time. And then you can demonstrate that at very low rotation and tilts, which we’re not supposed to be able to feel, that vestibular migraine patients can still feel things. 


Our system protects us against feeling this mismatched information by shutting it down or by substituting extra information that it makes up, called velocity storage, and this happens in the brainstem. So you can see that here are the normal patients. Here are the migraine patients; they tend a little bit more to the more-sensitive side. But the vestibular migraine patients seem to be in a world of their own in terms of this sensitivity.


So what is the implication of this, and what does this tell us about vestibular migraine and where we might be going? What it tells us is that although there’s no increase in sensitivity, that there’s a problem of integration. And where does that integration happen? Well, it happens in the vermis of the cerebellum, right in the midline of the cerebellum, a part that you can’t see very well. 


Or there’s another possibility. We don’t become aware that we’re dizzy until our sensations get processed through the thalamus and go to the cortex, and some of these integrated fibers do go up into the cortex. And that’s an interesting idea, because know that patients with vestibular migraine, when they get challenged by extra motion, they can also sometimes have increased pain, just the way that we have increased pain with light. 


Well, Rami Burstein demonstrated that there is a convergence of trigeminal fibers and optic fibers that results in increased firing in the trigeminal fibers when light comes that corresponds to an increase in pain. And this same phenomenon may be happening in the thalamus and cortex in some of our vestibular migraine patients. So we don’t know for sure whether it is here in the cerebellum or at the cortex and in the thalamus that vestibular migraineurs are having this abnormal processing, but we think that this is where we should be focusing our attention in the future.


So how do we treat these patients? In short, we don’t have any specific treatments for vestibular migraine. We treat them like chronic migraine patients. What we really need to do when these patients are here is to convince them and enroll them in the idea that migraine is the underlying pathophysiologic mechanism that is likely to respond to treatment — that nothing else is working. These patients have been to rehab and physical therapy and have taken vestibular suppressants and sometimes have had ablative procedures, which have made things worse; and that even if their headache isn’t a prominent feature, it may be present, and this is likely where the money is in terms of treating them.


Now, we don’t know because we haven’t parceled these patients down into subgroups well enough in our categorization system for study, the way Brian mentioned — which treatment to start with — and we don’t have the right pharmacogenetic information on these patients. We can’t take a cheek swab yet and say, “Aha, you’re going to respond to topiramate. You’re going to respond to nortriptyline. You’re going to respond to propranolol.” But at least we know that we can work with them in a very general way and enhance their quality of life. 


So we are going to — so what we do is we know that these patients are living over their threshold that was part of their genetic substrate, but we can use medications to elevate the threshold, and then we can use lifestyle modification to reduce triggers. And this can take many different forms in many different patients depending on the problems they bring to the table and result in big improvements in their well-being. 


So all of the studies in vestibular migraine treatment involve tests of calcium channel blockers, beta blockers, tricyclic antidepressants, and sodium channel blockers — the same categories of drugs we use for chronic migraine. They all show varying degrees of efficacy. The quality of those studies, however, is not very great, and it is undermined even more greatly by the fact that this diagnosis is still a wastebasket term. They’re lots of patients with different entities being thrown into the same basket.


So what do we do? We treat patients as if they have chronic migraine, and we try all of these medications. Vestibular therapy — can it help? It can help a few patients, but I am frequently releasing people from the burden of their vestibular therapy because they’re wiped out every day after their vestibular therapy appointment, just like they are after their VNG. So vestibular therapy can be helpful, but it’s important to work with someone who understands that many patients can only tolerate a small dose of this type of treatment, maybe even a few minutes at first.


So if we follow this simple paradigm, then we’re going to make the greatest gains on behalf of our patients while the scientific world works this whole problem out in more specific ways and finds out who has a migraine-related inner ear disorder, who has a primary inner ear disorder, who has a primary brain disorder, and who has the whole ball of wax. 


So thank you very much.




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