Guest: Maria Machala, MS, NP

View the recording from our Migraine Clinician Masterclass, developed in partnership with IVPN Neuropsychiatry. In this webinar, we hear from Maria Machala, MS, NP, who talks about Vestibular Migraine. Please note that this video is intended for healthcare providers.

TRANSCRIPT

Maria Machala, MS, NP: So vestibular migraine, really the symptoms were first described in the Huangdi Neijing, it’s the Chinese medicine, some of the earliest writings there, and then by Aretaeus of Cappadocia, well-known Greek physicians. They described these disorders of episodic vertigo with ringing in the ears and headache, visual changes. 

There are a lot of different terms that we use or that have been used, like migraine-associated vertigo. The term vestibular migraine was first introduced in the early 1900s, and that’s what we use now. That’s the official term. 

It is a very, very common cause, if not the most common cause, of episodic vertigo. So BPPV is the other one. I would say in practice I tend to see vestibular migraine just as much, if not more, than BPPV, and then a lot of the other inner ear disorder causes of dizziness. It affects up to 2.7% of the population. Like I said, the most common cause of episodic or spontaneous vertigo, up there with BPPV or benign paroxysmal positional vertigo. Even though it is the most common or one of the most common causes, it is under-recognized, under-diagnosed, and under-treated, unfortunately. 

So let’s go over a little bit of the anatomy and the physiology of the inner ear. We have the three semicircular canals, and then we have the utricle and the saccule. That makes up the vestibular part of the inner ear. The cochlea here is for hearing.

The three semicircular canals detect rotation in all the different planes. Then the utricle and the saccule think of them as like gravity sensors. They detect where your head is in relation to gravity, as well as any kind of linear movement.

The inner ear will send signals to the brain via the eighth cranial nerve, which is the vestibulocochlear nerve. The end cells are the hair cells, and they have these little hair-like projections called cilia. The cilia move with the fluid movement of the inner ear with any kind of head movement. The movement causes excitation or inhibition depending on the direction. That’s what will send those signals via the vestibulocochlear nerve. 

Then we’ll go on to the central pathways here. From the eighth cranial nerve, it goes to the vestibular nuclei within the pons, the pons and medulla junction, in the brainstem. That is also where we receive visual and proprioceptive input. The brain uses all of these, so visual input, and then proprioceptive and tactile input. If you think of the stretch of the muscles and pressure on the footbed, things like that, that tells us where we are in space. From there, we have projections into the cerebellum, mainly, but also the cerebral cortex. 

Then the efferent pathways, so a strong connection between the inner ear and the eye muscles, especially with the semicircular canals. That’s what enables us to keep focused when our head is moving, so gaze stabilization or the vestibulo-ocular reflex. Then postural, and that is closely connected to the utricle and the saccule, so our gravity sensors and keeping our body upright. 

What do we think is going on with vestibular migraine? Probably similar to that of migraine headaches and a lot of the other migraine symptoms. So, sensitization and activation of the trigeminovascular system. So the trigeminal nerve, the fifth cranial nerve, the largest one, it innervates the face, mainly sensory input. When this is activated, there’s a release of these inflammatory peptides. These are just a couple of them, substance P for pain, CGRP, serotonin, one of the neurotransmitters involved. And these are all involved in pain, so nociception, and then also they activate the vestibular cortices. 

The trigeminal nerve also innervates the inner ear, which is interesting. So that’s why we might get some of those peripheral symptoms in migraine. So you can actually have hearing loss and loss of balance function in the inner ear with migraines on occasion. 

And then also these receptors, so the CGRP receptors and others are found in the inner ear. It might have to do with fluid balance. So we know there’s this connection between Ménière’s disease and migraine, and this might be one of the reasons why. But again, not fully understood. 

So key points here, the central vestibular pathways are really complex. They go to many different parts of the brain, so different areas can be affected, and that’s why patients will get all different kinds of symptoms. So it can be a spinning sensation, just more of a vague sense of disequilibrium. And then because you can have multiple different areas of the brain affected at the same time, you can get a lot of different symptoms in addition to dizziness. So it makes it really challenging to diagnose. 

So simplified, this is how I explain it to my patients. You have this brain hypersensitivity, so that trigeminal vascular system is activated a little too easily, usually genetic, and then you get this perfect storm of triggers, which we’ll talk about in a little bit, and then it causes, like I said, that activation and release of those inflammatory peptides.

All right, so here are the criteria. This is the Bárány Society, the International Vestibular Society, and the International Classification of Headache Disorders. So to have vestibular migraine, you need to have at least five episodes of these vestibular symptoms, moderate to severe intensity, lasting five minutes to 72 hours. Usually there is some current or previous history of migraine headaches, can be with or without aura. 

And then also one or more of the typical migraine features with at least half of the episodes. So headache with at least two of the following: the one-sided location pulsating, moderate to severe pain, and then aggravation by routine physical activity, light and sound sensitivity, and then visual aura. So you need to have at least one of those with at least half the episodes, and then not accounted for by another vestibular diagnosis.

And then probable vestibular migraine, which I would say is far more common, only one of the criteria of BNC, so they might not have a history of migraine, or they do have migraine, but they don’t necessarily have those other migraine features with the episodes. 

So this can be really difficult to diagnose. Like I said, there can be many, many different symptoms, there are many different causes of dizziness, and then there’s a lack of objective findings. So usually the exam is normal, testing is normal, which we’ll get to in a little bit. And then you can also have other disorders that kind of clouds the picture, like Ménière’s disease. There’s a much higher incidence of migraine in patients with Ménière’s disease, and a lot of patients with Ménière’s disease will have vestibular migraine as well. And then lack of evidence-based treatments, which we’re going to get to in a little bit here. A lot of what we do is extrapolated from migraine headache studies. 

So a lot of people make the mistake of confusing vestibular migraine with aura, but aura by definition only lasts 5 to 60 minutes and is always followed by the migraine headache. But it’s different than the brainstem migraine, you have to have two additional posterior circulatory symptoms, and typically with vestibular migraine they’re lasting, I would say, seconds to days at a time.

And then there was a study looking at vestibular migraine, is the criteria too restrictive? And I would agree that yes, in practice it’s not very common to see patients who fit that definite diagnostic criteria. So it’s usually probable. Like I said, symptoms will often last seconds at a time, so not necessarily five minutes. And then you can also see a chronic daily dizziness in addition to the little episodes that kind of clouds it a little bit when you put that 72-hour limit.

And then a lot of times patients are unclear about their own history of migraine. It’s interesting, I’ll ask a patient, do you have a history of migraine? And they’ll say no. And then I ask, have you ever had a migraine? And they’ll say yes, well it was years ago and I used to get them all the time. So yes, they have that, the genetic predisposition to have this and all that, but because they’re not experiencing migraine headaches, they don’t think it’s related at all. So really important to get a good history about whether or not they’ve ever had a migraine headache. 

So there is a lot of symptom overlap, like I said, Ménière’s disease. So Ménière’s disease is, you can think of it like an inner ear swelling or distension of that endolymph within the inner ear. And it causes episodes of prolonged vertigo, hearing loss, and ringing in the ear tinnitus, and then pressure in the ear. And over time it will cause actually permanent damage to the hearing, to the balance of that affected ear.

And so there’s a lot of talk now, is Ménière’s disease a form of migraine? So like I said before, the trigeminal nerve innervates the inner ear. A lot of those neuroreceptors are in the inner ear and kind of deal with the fluid balance. A lot of the triggers are the same.

And then again, a lot of patients with Ménière’s disease also have a history of migraine. A lot of the triggers are the same. And a lot of times you can get these purely Ménière’s episodes that fit criteria, along with the migraine symptoms like light and sound sensitivity and sometimes a headache as well.

And then 3PD, this is persistent postural perceptual dizziness. So this is the term that we use now. It was formerly subjective dizziness, but now we have better understanding it’s actually like a brain processing disorder. So, you have the input from the inner ear, the eyes, proprioception, but the brain isn’t processing that information correctly. And that is often triggered by a true form of vertigo, spinning vertigo. So anything like Ménière’s disease, benign paroxysmal positional vertigo, vestibular migraine, and then it leads to this chronic feeling of dizziness.

And that’s often seen in vestibular migraine, which can again make it a little confusing because the patients have chronic daily dizziness in addition to these little episodes of vertigo. Mal de débarquement, that’s disembarkment syndrome as well. The feeling like you’re still moving usually after getting off of a boat or a long airplane ride, long car ride, and it can last for months or even years at a time.

Post-concussion syndrome, you can have headaches that are very similar to migraine or even trigger migraine headaches, same thing with dizziness. BPPV, benign paroxysmal positional vertigo, that’s where you have the little inner ear crystals, the calcium carbonate crystals that will get out of place. They’re supposed to be in the utricle, saccule, get out of place and go into the semicircular canals. And that causes vertigo just laying down, turning over in bed typically. So different than the spontaneous vertigo that we see with migraine or vestibular migraine. 

However, there is possibly an increased incidence of BPPV in patients with migraine. And sometimes migraine, you can have positional symptoms. So important to differentiate between the two. With BPPV, we can diagnose that with the Dix-Hallpike maneuver.

Superior semicircular canal dehiscence, kind of a lesser known, a rare type of dizziness. That’s dizziness caused by a change in pressure in the middle ear, so coughing, sneezing, things like that. And also loud sounds. And what SSCD is, is a missing bone over one of the semicircular canals in the inner ear. 

So our surgeons typically won’t operate on SSCD patients unless their migraines are managed well. A lot of patients with this condition also have migraine. And so the symptoms can kind of overlap there. You can get this phonophobia, a noise sensitivity with vestibular migraine, which is pretty similar to the noise-induced dizziness that we see in this condition. 

And then, you know, we do worry about some of the rare central nervous system causes of dizziness, multiple sclerosis, cerebellar ataxia, stroke, and things like that. So these patients, this can be a really, really difficult set of symptoms. Migraine itself is a risk factor for anxiety and depression. And then dizziness is also a separate risk factor for anxiety and depression.

And then because this is so challenging to diagnose, it’s not well known, kind of falls in between the different specialties. A lot of times these patients are taking a long time to get diagnosed. And so that diagnosis uncertainty can also cause anxiety and depression. And I do see that a lot. It really can take years to get the proper diagnosis and treatment. 

I had the pleasure of speaking with, she’s a nurse as well as a vestibular patient, Lindsey Mwesigwa, a few days ago. And you can see here, she provides these lectures to different healthcare specialists about vestibular migraine, and she shares her personal story. And you can see she’s seen numerous specialists, and it took quite a long time to get the actual diagnosis. So very, very challenging for these patients.

So the most important tool in assessing these patients is getting a good history. And because of that anxiety, depression, the numerous specialists, the lack of great treatment, it is very important to listen to these patients with compassion and really hear their story, because that’s what’s going to clue you into the diagnosis.

Typically, these patients have a normal neurologic and vestibular exam. Typically, they will have a normal VNG or videonystagmography, the vestibular testing that we do. Sometimes we see these exaggerated response to caloric stimulation of the inner ear. Sometimes they do have some positional nystagmus. But essentially, the VNG is going to be normal, unless of course, they have other diagnoses as well.  And typically, the MRI is going to be normal. We do see white matter hyperintensities. That’s a common finding in patients with migraine. 

So if a patient does have an abnormal neurologic exam, vestibular exam, the vestibular testing or imaging, does not necessarily mean they don’t have vestibular migraine. They might have something like Ménière’s disease. You can have BPPV and vestibular migraine. So just because we have an abnormal finding like a weaker ear on the VNG, one ear has vestibular loss, does not mean they’re not experiencing vestibular migraine.

You can have a vestibular loss from years ago, you can have something like a virus or something like that, that will knock out the balance function. But what do their symptoms fit with? So you have to look at the diagnostic criteria. And again, listen to the history.

So, moving on to treatment. Who is treating these patients? Usually, it’s a mix of ENT, particularly, neurotologists or those who specialize in hearing and balance, neurologists, and then primary care. 

When do we initiate treatment? Really, I go by what the patient is experiencing. If they are having these very frequent, very severe episodes, I will be a lot more aggressive than somebody who’s having episodes on occasion that they can kind of treat symptomatically. What we’ll get to in a little bit is preventative treatment versus abortive treatment. 

There’s not great abortive treatment for vestibular migraine, like there is for migraine headache. And so with migraine headache, to initiate prophylaxis, you have to have these frequent migraine headaches. I will initiate preventative medication for vestibular migraine a lot sooner because we don’t have that great abortive treatment. 

And then like I said, it’s rare for patients to come in with this definite picture of vestibular migraine. I will treat probable and even possible migraine. So when I say possible, I mean, they don’t really fit that criteria that I explained before, but they have no evidence of any other inner ear disorder and other central causes have been ruled out. So they might have really unusual symptoms again, dizziness lasting for just seconds at a time instead of the five minutes, no personal history of migraine, no family history of migraine, maybe no light sensitivity, sound sensitivity, headaches or anything, but we really have no other plausible cause for their symptoms.

And so I’ll go ahead and initiate treatment. And it’s really interesting to see how many of these patients respond to migraine medication. And so I think that’s a really important key. When I see patients who have seen a lot of other specialists and providers, you know, they don’t fit the criteria. And so they’re nervous about missing another diagnosis. But really, when you’ve exhausted all the testing and you know that there’s really nothing else going on, then go ahead and treat these patients.

So treatment, a lot of it is the same as treating migraine headaches. So trigger avoidance is very important. Usually, it’s a combination of triggers that will give rise to these episodes. So it might not be one trigger all the time. Sometimes the patient will be able to, you know, eat chocolate and nothing happens. But when you combine the chocolate with the change in weather or stress, then you can have an episode. So it is important to know, to be familiar with the triggers, dietary changes, there are supplements that we’ll get to, the medication, neuromodulation, and physical therapy. 

So these are the common triggers. I definitely focus on stress and sleep disturbances. I think those are the two, those are two of the main ones. Some of these other ones you can’t really avoid, like weather changes. You can’t always control the environment that you’re going to be in. But when patients know that these things might happen, they can preemptively treat. So it is important. Dietary triggers are also very important. I do not like for my patients to necessarily do a very, very strict diet. Sometimes that can be, that can cause stress, right? It’s hard to control your diet all of the time, socializing, going out to eat, things like that. And sometimes focusing so much on diet, like I said, you’re going to cause a lot of stress and then you can miss a lot of nutrients that you actually need.

So some of the common groups, I’ll have them cut out, like MSG, you know, that’s one of the main ones, a lot of patients cut out right away, tyramine, nitrates. And you want to cut them out for at least a month or so at a time. And then you can slowly add things back in and see if it makes a difference. 

Not everybody has the same trigger. So you don’t want someone to be super restrictive when it might not be a trigger of theirs.  This is where keeping journals can help. But again, you don’t want the patient to be so fixated on it because some of these things are so hard to control and that can cause a lot of anxiety and stress. 

Here are the supplements. So this is the American Headache Society and the American Academy of Neurology, 2012. My practice, we use the top three the most, just because of the level of evidence, the efficacy, fewer side effects, especially compared to the feverfew and butterbur. And a lot of patients do really well on these. Not many concerns, magnesium can cause some stomach upset, diarrhea. And so a lot of times we’ll have to start on a lower dose or try different formulations, but typically these are tolerated really well, and they do seem very effective. 

So if a patient, you know, if they’re not really ready to start a preventative medication or their symptoms aren’t happening as frequently enough to warrant that, then I will definitely just start on these with trigger avoidance. 

Here’s a list of the medications. This is a review done by Smyth published last year. You can see on the left side, these are likely effective. I will use all of these really, aside from Depakote at the very bottom there, the sodium valproate, just because that one is teratogenic. And so we want to avoid that in women of childbearing age, which a lot of these patients are. But otherwise, these are all great medications. They do seem to be effective. 

And then interestingly, likely ineffective nortriptyline, even though it works very similar to amitriptyline, the study showed that it wasn’t as effective. I will use it on occasion, especially if the amitriptyline is kind of working, but a little too sedating, nortriptyline is less sedating. And then Botox and CGRP inhibitors, there aren’t a ton of studies on these, so we don’t really know. 

I was just at the headache symposium this last weekend, so the American Headache Society, and I did my own personal poll of a lot of the neurologists there to see how they treat their dizzy patients. Because again, there’s not great evidence out there for vestibular migraine, not a ton of studies. The studies that we do have are usually small, so lower quality. And it was interesting to hear how many of the providers do see improvement in their dizzy patients with Botox and the CGRP inhibitors.

And then also I had some who use cyproheptadine, which is an antihistamine, using that as a preventative. We know that this is effective in children. We don’t really see it in adults, but some of them are using it in everybody and they seem happy with it.

So I think the important takeaway here is you can try a lot of these different things. And if none of the ones on the left are working, then go ahead and try some of these other ones that haven’t been studied very much, because we know they can be effective in migraine headaches. And if it’s really the last resort for your patient, I think it’s worth trying.

There are some safety concerns that we think about with these medications. So antidepressants, if you’re on, you know, a couple of them, or if you’re on triptans too, then we worry about serotonin syndrome. Fortunately, this is very rare. And usually the doses that we need for antidepressants are a lot lower than what would cause serotonin syndrome. 

Propranolol, it is a beta-blocker. You would avoid it in patients with asthma or severe hypotension. I will still use this in patients who have normal or even blood pressure that typically runs low. Again, these doses are lower. I typically don’t see problems with hypotension on this, but you want to educate the patient and if they can, you know, have them check their blood pressure at home.

With topiramate and acetazolamide, there is an increased risk of kidney stones. You know, if they have a history of kidney stones, I might not use it as first choice, but it’s not a contraindication. You just want to educate the patient, you know, make sure they’re drinking lots of water, avoiding things like grapefruit juice.

And then valproic acid, like I said, it’s teratogenic. So you want to avoid it in women of childbearing age unless you do have strict precautions and education. But there are so many other medications that you can use.

So then how do you choose the medication? You know, we don’t have a guideline on how to do this. Sometimes it’s just picking one randomly and seeing how the patient responds. But if they have any underlying conditions, you can kind of go off that. So patients who don’t sleep well, who have insomnia, amitriptyline is sedating, like do you take it at night? So that’s my go-to for that. A lot of patients have anxiety and depression, like I said before. And so we have, you know, antidepressants that can help.

Propranolol actually helps with the physical symptoms of anxiety. So it can slow the heart rate and the breathing, which can be helpful. If the patient is overweight and they’re concerned about the possible weight gain with some of the antidepressants, topiramate can actually reduce appetite and help with weight loss. If the patient is underweight, venlafaxine can help with that. And it’s also effective in perimenopausal women experiencing hot flashes. 

Another key point that I like to educate my patients on is that patients with migraine tend to be a little more sensitive to side effects of medications. Again, it’s a brain hypersensitivity issue. And so, a lot of patients right up, right off the bat are nervous about starting a medication. So I explain, that’s very common. We can still use the medication. We start at a super low dose. So lower than a typical starting dose, usually like half, we start really low and you can go really slowly, as slowly as you need to. 

And then, you know, side effects, while they can happen, it doesn’t necessarily mean that it’s dangerous or that it’s not going to work. So a lot of patients they’re nervous. As soon as they start experiencing side effects, they’re concerned, you know, it’s a safety issue. So really good education about that. And then a lot of the side effects will decrease over time and then they’ll start noticing improvement once they get up to the correct dose.

Medication adherence is a big problem in migraine. So I think spending some time educating these patients about this is very important. And then also about how long it’s going to take. It might take four weeks to get up to the normal dose. So it’s already a month where they might not notice any improvement and getting up to that target dose. And then you want to give it about four to six weeks after that to see if it’s going to be effective. So I tell patients, you know, let’s just plan about a two-month trial for each medication.

And then if it’s not effective, you can go ahead and start another medication and wean off the initial one. Or if it’s partially effective, you can try and add on a different medication. 

So abortive medication, like I alluded to before, just unfortunately, not a lot of great options for vestibular migraine. Antihistamines, like meclizine, are often used or benzodiazepines, like diazepam. I think these can be effective, especially when the patient is experiencing like a true vertigo, so a real spinning sensation, because it suppresses that vestibular system and kind of calm the spinning. 

Antihistamines you want to be careful with because if taken too frequently, they can actually suppress the balance system so much that you can actually develop this 3PD or the persistent postural perceptual disorder. So I see that a lot in patients. They’ll have this chronic daily dizziness because they’ve been using these medications inappropriately. So I try not to use meclizine for that reason, or if I use a diazepine or another benzo, then I make sure they’re only taking it on occasion. So maybe once or twice a week, if that, but usually if they’re having episodes that frequently that we need to be a little more aggressive with the preventive treatment. 

Antiemetics, like ondansetron, and a lot of the others are effective. You know, a lot of these patients do have nausea and so important to treat that as well. We will try oral steroids. If somebody is in just a really vicious cycle of vertigo, you can try oral steroids, dexamethasone, prednisone, to try and break that cycle. 

And then triptans are likely not helpful. So, this was published back a year ago, but then there was also a Cochrane review published earlier this year that again, they’re likely not helpful. And we really don’t know the safety of triptans in vestibular migraine. 

Neuromodulation. So I have a couple listed here. I know there are a lot more than this. There are some studies, some smaller studies that show that it may be effective as both abortive and preventative treatment. So I think it’s, you know, something to consider. You have to talk to the patient about it. You know, some downsides, it can be expensive, but if they’re not tolerating the other medications, things like that. And again, because we don’t have good abortive treatment, it might be really good option. 

Sleep. I think sleep is a really important thing to focus on. We know that poor sleep can trigger, can contribute to migraines. There was a study done in vestibular migraine, you know, earlier this year that patients with vestibular migraine do have poor sleep quality, fragmented sleep, disrupted circadian rhythm. You know, I will oftentimes check my patients for sleep apnea, or at least evaluate, you know, symptoms and then underlying anxiety and depression can contribute to poor sleep.

So for these patients, you know, amitriptyline might be a good choice, but again, you want to be careful if the patient does have sleep apnea, you don’t want really sedating medications that can worsen that. So if I start amitriptyline, I try and make sure they don’t have underlying sleep apnea or make sure it’s well-treated. 

So, physical therapy. Physical therapy can be effective in these patients. It does not help with the acute episodes. So it’s not going to help prevent the spinning episodes that occur. But it can help with that chronic daily dizziness that a lot of vestibular migraine patients have, that three PD. So again, that’s a central processing disorder. The inner ears are working fine. The eyes are working fine, proprioception, all that. But usually the brain is relying too much on vision as opposed to the inner ear vestibular input. And so vestibular therapists can help kind of retrain the brain to use the inner ears for balance.

So my patients with chronic daily dizziness, I’ll always send to physical therapy. It can also help with that motion and visual sensitivity. And then, you want to consider, especially in older patients who might have other comorbidities, they can also have a chronic feeling of dizziness. It’s not necessarily three PD, and this is going to be more imbalanced when they’re up walking around. So when you combine imbalance with vestibular migraine, that’s really going to increase your risk of falling.

So important to treat, especially, like I said, the older patients who might have peripheral neuropathy or arthritis, all of this can contribute to proprioceptive disorders. Patients who wear bifocal or progressive lenses, what that’s doing is it’s kind of blurring the peripheral vision, which we still need for good balance. So, sometimes patients will switch to actually two different pairs of glasses, one for distance and one for reading, and they do a lot better.

And then if there is any underlying peripheral vestibular disorder. So these patients respond well to physical therapy as well. 

Anxiety and depression can’t stress this enough. It’s very important to address. You want to reassure the patient, you know, you can’t always see what’s going on. The patient’s feeling dizzy, but everything looks normal on the outside. And so that’s really, really challenging. You want to reassure the patient that this isn’t a psychiatric disorder. So that’s, you know, we see what is happening in migraine headaches, the same kind of thing that’s happening with vestibular migraines. So reassurance is important.

Treating the anxiety and depression can also treat the vestibular migraines, the amitriptyline, venlafaxine, propranolol. Making sure they’re getting restorative sleep and then cognitive behavioral therapy. 

So again, treatment is very holistic. You want to look at the whole patient. You want to get the whole picture. What seems to be their main triggers? Use medication when needed. You want to look at the diet. So having the patients keep a journal can be really helpful, decreasing stress, possibly treating allergies can help. 

And don’t give up. So lack of response to even several migraine medications does not mean that the patient doesn’t have vestibular migraine. And you can see there are so many different things to try.

So I think we might be out of time for this. I was going to go through a few of the other disorders. I’ll just go through it really quickly here.

We already talked about Ménière’s. Is it possible that it’s a form of migraine? I know we are starting to treat Ménière’s patients with migraine medications, even if they don’t necessarily have a personal or family history of migraine. Before we consider any of those ablative procedures, we’ll treat them with migraine prophylaxis. 

3PD. like I said, it’s like chronic daily dizziness. I like to use venlafaxine in this. So 3PD is treated with physical therapy, SSRIs or SNRIs, and cognitive behavioral therapy. Of the SSRIs and SNRIs, venlafaxine seems to be the most effective in migraine. And so that’s why I like it in these combination patients. 

Mal de débarquement, is it a form of migraine? We do see there’s a higher incidence of migraine in patients who have this disorder. So if nothing else, if they’re not responding to physical therapy, I go ahead and try and treat them with some of the migraine medications.

And then you can have a lot of other ENT manifestations of migraine. So, patients who come in with chronic sinusitis, but their sinuses look totally clear, usually a form of migraine. You can have isolated ear pain and ear fullness with migraine, middle ear myoclonus or tensor tympani spasm. And then, you know, some of these smaller like case studies, recurrent facial nerve palsy. 

So in practice, because there are so many different ways you can treat vestibular migraine, it’s important to focus on just a few things at a time and seeing these patients frequently until you can get things stabilized. It’s important to have a lot of educational handouts, you know, because there’s so much information. you can’t cover everything in clinic, having a way to get this information to the patients.

And then if the patient is symptom-free, then, you know, consider trying to come off the medication if they’re open to it. You can always go back on. And then referring to the other providers, neurology, ENT, physical therapy, and all that. So that is all I have.

Thank you very much.

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