Guest: Dr. Jennifer Robblee

View the recording from our Migraine Clinician Masterclass, developed in partnership with IVPN Neuropsychiatry. In this webinar, we hear from Dr. Jennifer Robblee, who discusses practical tips and effective strategies for managing patients with severe symptoms. Please note that this video is intended for healthcare providers.

TRANSCRIPT

Dr. Jennifer Robblee: I’m Dr. Jennifer Robblee, and I work at Barrow, which is in Phoenix, Arizona, and I’m going to be talking about how to manage patients with a lot of different severe symptoms in migraine. There’s a lot of different approaches that I could have taken with this. 

Here are my disclosures, just so you know, and I will mention some things that are off label. And of course, some of the availability of certain medications are going to vary globally, so I apologize if I’m talking about something that you don’t have access to. 

So I’m going to give some example cases as we go through the different steps of the talk and also talk about some of the spectrum of symptoms in migraine. And part of what I wanted to do today is talk about not just how we manage migraine, but when someone’s coming in and their severe symptom is something other than headache, what do we do in those cases? So that’s where I’m going to be focusing today.

 

So first off, let’s just talk about the spectrum of migraine symptoms. So, migraine actually has four phases. We often just assume that we’re talking about the headache part when we’re talking about migraine, but there’s four possible phases.

Now not everyone is going to have all of these phases, and really any of these phases could theoretically happen on their own. We obviously know the most about the headache in the aura phase, and we’re starting to know quite a bit about the premonitory phase, which is sometimes also referred to as the prodrome. We know a little bit less about the postdrome phase, however.

So, you may see someone who has just an aura. An aura is seen in about a third of patients with migraine, so remember you do not need to have aura for it to be migraine. The premonitory phase is an interesting phase, so we’re going to get a little bit more into that one in detail too.

 

But first off, just to give you an example case of someone who has all four of these phases. So envision that you have a 25-year-old in your office. She’s been having headache for about two years. She tells you she has attacks that are happening about twice a month. But when she has an attack, it’s really taking a good period of time.

So her typical attack course is that for the first 24 hours, she starts to feel just really fatigued. She feels irritable. As the day goes on, she starts noticing that she yawns a whole bunch. And then the next morning when she wakes up, she often will start to experience an aura.

Her aura is a pretty classic one. She’ll get a scintillating scotoma that’ll go on for about 5 to 10 minutes, and then she gets into the headache, and if she doesn’t catch that headache early enough, it’s going on for 36 hours. It’s your classic sort of 8 out of 10 headache. It’s pulsating. She has it on both sides. It’s a little bit worse to that left side for her, and she gets a bunch of photophobia and nausea, and she just feels unwell during the whole thing.

As the headache starts to dissipate, she’s still left with just this postdrome phase where she feels exhausted and just completely worn out, and that can go on for an additional day. So even though the headache itself is 36 hours, she’s basically got an additional day that she’s adding on to the start and the end of the attack. This is unfortunately common, and we don’t talk about it a lot when we talk about our diagnostic criteria. And we don’t really talk about it much when we’re talking about how to treat headache.

 

So first off, let’s get into this premonitory phase. So this can even be days before you have your actual headache phase start. And it’s interesting because often these are mistaken as symptoms that might be a trigger for headache; when, in fact, what they’re telling you is it’s a warning sign before you have the headache start. So for instance, you could have poor concentration and fatigue.

You might start to notice changes in your mood, so you could have depression or irritability, but you can also have an increase in your mood. I’ve had patients tell me that they suddenly feel this really excited, happy feeling, and for them, weirdly, that means that they’re about to get a migraine attack. Classic symptoms that you can get during the headache – like photophobia, monophobia, osmophobia – all of those can start to precede the migraine attack itself.

Often neck pain or stiffness starts to begin before the actual headache. You can start to have a lot of just poor sleep. You might have insomnia. You might be extra tired. And yawning is a classic symptom that can actually start to happen. You can get food cravings, often this is sweet cravings.

You can start to have other GI symptoms like nausea, diarrhea, constipation. You can also have urinary symptoms where you start to get urinary frequency, or you may notice that you’re excessively thirsty. Now you can envision that, let’s say someone comes into your office and they say, every time I eat chocolate within like, you know, six to eight hours, I get a migraine attack. I think I need to stop eating chocolate. 

And you’ve got to pause and stop. And do you really tell that person that they’re not allowed to have chocolate now for the rest of their life that they’re still having migraine? The answer is probably not. We don’t have good evidence, actually, that it’s actually a migraine trigger. And what they may be having is a premonitory phase where they’re having sweet craving, and for them that sweet craving is the chocolate. So that’s actually their warning sign that the migraine attack is about to start, not that they actually are causing a migraine attack by having the chocolate.

Same thing, I’ll have many patients tell me that, oh my goodness, I went out into the bright sunlight and all of a sudden I had a migraine attack. Well it wasn’t that the sunlight caused the migraine attack, it’s that they were already photophobic. And they went outside, they noted that photophobia, and then soon after the headache started.

So it starts to change how you might approach counseling someone on trigger avoidance, because what you might be trying to do is tell them to avoid something that’s not actually a trigger at all, but rather it’s just part of that warning sign for migraine. So it does start to change how you might approach managing these patients with these symptoms. 

 

Now the aura phase, as I mentioned, happens in about a third of patients. We have typical aura, which 90% of the time is going to be visual, but we’ve also got sensory aura and language aura. And then there’s less common types of aura that include brainstem aura, hemiplegic migraine, and retinal migraine. And these are caused by cortical spreading depression that happens across the cortex, where you get this change in a wave of electrical activity that’s followed by a change in blood flow.

The way that you try to decipher whether or not you think this is aura versus something else like a TIA or like a seizure is you use the ICHD-3 criteria. And so aura should have at least three of. The symptoms should evolve over five minutes. So you can imagine if it’s a visual aura, it’s sort of like this expanding scotoma. You can have successive types of aura. So it starts with one and then moves into the next.

You can have an aura that lasts anywhere from 5 to 60 minutes. That’s the classic duration. You can have it be unilateral. And a language aura, by the way, does count as a unilateral aura. You can have positive symptoms. So you can imagine if you have a scintillating scotoma, you may have the scotoma, which is a negative symptom. 

So a lack of vision in a certain area, but around it, you have all those scintillations. That’s positive. That’s something that’s been added in. That’s something additional that you’re seeing. Or if you have numbness – it’s that tingling on top of the numbness – that’s your positive symptom. And then if it comes with an associated headache. So you should have at least three of those to feel pretty comfortable that it’s an aura.

 

And then we’ve got the headache phase. So, the headache phase is what we know best, but remember, it can come with so many other symptoms. As part of the criteria, we know it can have nausea, vomiting, photophobia, phonophobia. Don’t forget about osmophobia. That’s pretty common in migraine, and it’s pretty specific for migraine. You can have kinesiophobia where it’s that you have this issue with any sort of movement. Movement just makes you feel worse.

Dizziness is very common. That might be vertigo, but sometimes it’s just a vague dizziness. Brain fog where you have problems thinking. Neck pain is a really common part of it. And people will assume that it means that their headache is actually from the neck, but sometimes it’s actually the neck pain is actually from migraine. Remember all those pathways. If you look at this picture here, you have all of that going down into the trigeminal cervical complex. So remember we do have cervical as part of the migraine pathway. 

You can also have autonomic symptoms. So some patients may start to experience gastroparesis. They might have, you know, just in general, a lot of more GI symptoms, urinary symptoms. They have cranial autonomic symptoms. So you’re allowed to have something like myositis. You’re allowed to have some of those more mid-phase symptoms like congestion, rhinorrhea, your eyes might water. They’re going to be often milder than what you’d see an attack – and usually they’re going to be bilateral – but you can definitely have them as part of migraine. 

 

And then finally, we have the postdrome phase. Often that lasts for hours into a day or two.

And this is colloquially called the migraine hangover. This is just where you feel tired. You have an inability to concentrate. Your mood might be lower. You might have some of the residual symptoms like nausea and light sensitivity. You could have more of that ongoing brain fog and you just kind of feel awful. And so while your migraine attack is seemingly over, again, it takes time to recover from it. 

 

So generally the way that we approach treating all of these symptoms is using what we recommend, in general, for treating migraine. So we have our preventive treatments, we have our acute treatments, and then we have the neuromodulation devices, which overlap. So for preventive treatments – just as a quick overview – we’ve got our nonspecific pills. That could be things like topiramate, propranolol, amitriptyline. We’ve got a whole bunch of different medications that are actually antihypertensives like candesartan, lisinopril. Depending on where you are in the world, you might have flunarizine – I don’t have access to that – valproate. So we’ve got a lot of different options there.

You have the CGRP pills so the calcitonin gene-related pills. These are the gepants. So you have rimegepant, which is known as Nurtec, and then you have atogepant, which is known as Qulipta. Then you have the self-injections. These are the CGRP monoclonal antibodies. And these are the ones that are the subcutaneous injections. So you have erenumab, which is Aimovig; fremanezumab, which is Ajovy; galcanezumab, which is Emgality. 

And then there’s injections that you can do in clinic. So you have onabotulinum toxin A, and then there’s also nerve blocks, which the evidence is not as strong for, but it is something that’s very commonly used. And then finally, as an intravenous treatment, we’ve got eptinezumab, which is Vyepti. So I would recommend before you consider someone having no other options, they need to try basically everything on this list.

What you have for your nonspecific pills is going to vary by region and by which guideline you use. But generally, I recommend every single patient should go through basically all of these medications one-by-one. Usually it’s for a three-month trial, unless they just do not tolerate it. Start low and go slow. And when you’re using the medications, you can consider doing combinations. So for instance, there is some evidence that combining Botox with one of these CGRP medications may have a synergistic effect.

So do consider doing some combos, even though we don’t have a lot of evidence for it for the other medications, I do think that that is worthwhile. And then don’t forget that all patients need to have an acute treatment, and you can always consider the neuromodulation devices if you have access to them. And then once you’ve tried all of these things, that’s when you start to go outside of what we have good evidence for. And that’s a whole talk in itself that starts to get way beyond what we have good literature, and you start to get into a little bit more of that art of medicine. 

 

So let’s talk a little bit more about aura. So envision that you’ve got a 32-year-old female. She has a migraine attack about two to four times a month. Her attack usually starts with these sort of zigzags and checkerboard patterns. And often it starts on one side of her vision, but eventually it spreads and it encompasses the whole vision.

That goes on for about 20 minutes. As that starts to sort of wear away, she then gets numbness and tingling that goes into her face, into her tongue, and down into her hand on that left side. That goes on for about another 15 minutes, and then it may or may not be followed by a headache.

So this would be a pretty classic example of an aura. There’s positive symptoms, there’s unilaterality. They’re going on for that, you know, 5 to 60 minutes. They’re successive. Sometimes it’s followed by a headache. So you can see that this is very classic, very fitting with migraine aura.

And so these are the actual diagnostic criteria for how you diagnose an aura. And these are what I mentioned in that previous section. And so these come from the ICHD-3. So really you want to have some combination of B and C. It needs to be one of those six different types of aura that I’ve already mentioned. And then, as I mentioned, you want to have at least three of those symptoms that I mentioned. And of course, you need to feel pretty confident that you don’t think it’s some other disorder.

 

So there are some other types of aura. So you can have aura that’s called persistent aura without infarction. So that’s where you do have a migraine aura. It’s typical, but it’s now gone on for at least a week. You should have neuroimaging in that case that shows that it’s not an infarction. And of course, you need to feel pretty confident that you don’t have another diagnosis.

So this, for instance, would be someone where they have that scintillating scotoma that starts – it’s seemingly their usual – but that scotoma just doesn’t go away, and it’s now been a week or more. And it’s still there. You’ve done imaging. There’s no stroke. And so that’s what we’re talking about in this case. 

And then there’s also what’s called migraine aura status. This is an appendix diagnosis. And so this is where you have a migraine aura – so it’s filling the typical diagnostic criteria for it – but within at least three days, you’ve had at least three auras. So they just keep happening in more rapid succession than what you would expect. And again, this is a time when you should be getting some sort of imaging. You want to make sure that you’re not seeing that there’s stroke. You want to make sure that there’s not something odd like a vasculitis, etc.

Especially in an older adult, you want to make sure that there’s nothing like an amyloidosis type process happening. 

 

Now what do you do to treat aura other than just treating the underlying migraine disorder, which would involve all those things that we’ve just talked about in the previous section? So we don’t have a lot of good evidence for it. There is a good consensus from the American Headache Society that magnesium can help with treating aura.

So if you’re doing that acutely, you can use IV magnesium, 1 g to 2 g of magnesium sulfate. There’s a little bit of evidence to suggest that divalproex may also help with migraine aura in addition to the headache. And then otherwise, you’re using a little bit more anecdotal or low-level evidence.

Ketamine has been looked at being used that way. You can use ketamine as a compounded nasal spray or as an IV medication. You can actually make it into troches as well, which are like lozenges. With ketamine, the data is pretty variable and it’s inconsistent. It has been studied specifically for hemiplegic migraine. And we do sometimes try it. But again, it’s hit or miss and we don’t have great data on it.

You can try the neuroleptics. Again, whether or not they’re going to help, it’s always hard to know, but it’s something that often you’re going to try acutely for migraine anyway. So something like prochlorperazine, chlorpromazine, that type of thing. You could always give some IV methylprednisolone. So using the steroids may help, but again, evidence there is low. There’s a great review article, from 2015, that was done by Rozen and Continuum, and he made some recommendations of trying things like acetazolamide and IV furosemide.

And again, those are more based on theoretical evidence than good evidence. But I have to say, I’ve tried it and sometimes I’ve had a little bit of success with them. And then if you have a patient where they just tend to be really prone to aura and that’s a really disabling symptom, one thing that I’ve tried is using lamotrigine orally for these patients. Obviously, this is not something that’s going to work in the acute setting because you’ve got to actually build up the dose, but it is something that I’ve tried with some success.

 

So let’s talk next about what you do when patients are really having bad GI symptoms. So let’s say we’ve got a 25-year-old female. She has migraine attacks about eight days a month. And every time she has an attack, she’s got really severe nausea and lots of vomiting. It’s hard to keep her medications down.

And when you probe a little bit more, you find that she’s prone to early satiety. So in addition to having all that nausea and vomiting, even in between the migraine attacks, it sounds like she’s having some GI symptoms where it may be consistent with something like a gastroparesis. And we do know that patients with migraine are more prone to gastroparesis.

So again, when you’re considering all of these medications – particularly for the acute treatments, which is what we’re really going to get into – you want to consider how you should be choosing your medication when a patient has a lot of GI symptoms. You may also want to consider it for the preventive, especially if they have GI symptoms in between the migraine attacks.

So this might be where you go more for rimegepant, because it’s an orally dissolving tab, or a self-injection, clinic injection, or IV medication, because all of those are going to avoid having to go through the gastric process. And a neuromodulation device might be another nice option here. 

 

So nausea is really common. We see it in about 73% of patients. So first off, you want to look into what they’re using as their acute treatment. Is it working? Are they keeping the medication down? How quickly does it work? A good goal is if the medication isn’t working in one to two hours, then you want to try something different. That’s usually how I decide whether or not to move on. Now for those really difficult refractory patients, you’re going to get the best that you can get. But for most patients, that’s a good goal to have.

Then you want to consider what you’re using for an antinauseant. So you don’t want to just give them a triptan, but what are you doing to help actually control their nausea? So ondansetron, which is Zofran, can be quite effective for patients. However, some patients will have a side effect where they actually get headache as part of the side effect so that can be counterproductive, obviously. 

Metoclopramide is another great option that I use all the time. You can use 5 to 10 mg for that. And then there’s other medications that are also anti-dopamine, like the neuroleptics. So again, that’s going to be things like promethazine, prochlorperazine, chlorpromazine. And we don’t have this in the US, but domperidone can be quite effective. And then finally, you want to consider if it’s a prolonged attack or if they’re having a lot of vomiting with it, are they getting sufficiently hydrated? And that might be when you want to get someone into urgent care or the emergency room to make sure that they’re getting rehydrated. 

So consider the route. If they’re having vomiting, then we want to avoid oral. You may want to avoid the orally dissolving tablet, just depending on how they tolerate it. It might be just putting anything in their mouth is going to be enough to trigger the vomiting. And you might be able to get it in and then get it absorbed before they actually vomit. But you’ll want to base that on the patient and how quickly they’re vomiting. Nasal injection and rectal are all great options in these patients when they’re vomiting. 

 

If they have gastroparesis – and a good sign of that is if they have a lot of vomiting or they have a lot of early satiety – then again, you want to try to avoid oral medications. And I would advocate for oral being avoided as much as possible for both your acute as well as for your preventive medications.

Here, the orally dissolving tablet might be a good option, so you could consider it in these patients. And then nasal injection and rectal, of course, are all going to be great options as it bypasses the issue with gastroparesis.

 

So basically, to summarize, if you have a patient with nausea, you can try oral. But if they’re going to vomit it back up or they’re going to not tolerate it, then you may want to go more for the nonoral. And you want to make sure that they have an option for an antiemetic.

And again, that antiemetic could be oral or nonoral. Now if that nausea comes with vomiting, that’s when you should try to avoid the oral more consistently and make sure, again, that they have a nonoral antiemetic. And of course, if the patient gets admitted, then we’re going to do parenteral treatments, and we maybe want to consider some IV hydration if there’s been a lot of vomiting. 

 

So here’s an example of some of the medications that I’ve mentioned with some of their dosing. And this will be posted so you can always steal these slides later. But these are the spectrum of things that I use except for the domperidone, which we just don’t have access to in the US. 

 

Let’s talk about sensory sensitivities next. So envision that you’ve got a 45-year-old male. He’s got a history of chronic migraine that’s been going on for years. And while the headache is painful and he has headache basically every day, his most bothersome symptom is that he’s got severe photophobia. He basically lives in the dark. If he has go out into the light, he’s wearing sunglasses. And he doesn’t know what to do. It’s just completely debilitating for him. 

So how do you manage it when headache is not the most bothersome symptom for a patient? 

So we’ve got a lot of different examples of what I mean when I say a sensory sensitivity. So photophobia would be what this person’s experiencing. But some people are very prone to noise. I have one patient where basically he just goes around wearing noise-blocking headphones all the time. Some patients are extremely smell-sensitive. So it’s hard for them to go out in public because any little smell, any perfume, soap, food is just nauseating and headache-inducing for them. And then some people are very prone to feeling worse headache by movement. 

So it’s like a kinesiophobia. So activity is very limited for them, and they can get very sedentary. So how do you manage these things? And so first off, for photophobia, a lot patients will first try the blue-blocking glasses. There are companies out there that make these. And if you go to an optometrist, they can often add a tint basically that’s blue-blocking into the actual lens itself. For phonophobia, a lot of patients are going to try things like earplugs. Osmophobia, that’s a tough one. I mean, basically they end up doing trigger avoidance. 

And then for the kinesiophobia, usually I try to send these patients to a physical therapist who knows how to just slowly get this person basically some exposure therapy to movement and see how we can get their brain to rehabilitate itself to tolerate movement better. In all of these patients, you want to make sure that they’re on preventive treatment, and you want to try to optimize that preventive treatment.

I will say, just like sometimes I’ve tried lamotrigine in patients with aura, patients with really severe versions of these symptoms, I will sometimes try the lamotrigine here as well. Completely off-label, completely anecdotal, but it is something that I will try. These patients are often quite debilitated by the symptoms. And so doing something like a cognitive behavioral therapy or mindfulness to help with some of the mood changes that can come along with this and the stress of it can be quite helpful because often these patients are going to have concurrent anxiety or depression.

And then one thing that, again, it hasn’t been studied – I don’t think I have any good study to refer you to for it – but something that I’ll try is a gradual exposure. So for instance, if you have this patient with severe photophobia, you know, them hanging out in the dark every single day, wearing their sunglasses with any light, they’re actually reinforcing this photophobia, right? And so what you might do is have them start with something as simple as in the morning before the sun comes up, go outside without your glasses, let the sun come up, and see how long you’re able to tolerate it for.

Do it right to the point where you’re at the max of your tolerance. And then keep doing that until you can tolerate more. And then maybe eventually it’s that you’re going to start with the lowest watt light bulb that you can find, and you’re going to slowly see if you can get higher and higher watt light bulbs that you can sit by for longer and longer durations. And you just have them work with a very gradual exposure to rehabilitate their brain to be able to tolerate it.

It’s one thing I’ve found that can help, but you need a patient who’s very engaged, who’s willing to do that. Our physical therapists and our pain psychologist, at Barrow, are great, and they can help us with that. But otherwise, it’s something that you’re doing and can be quite difficult and a lot of work. And they really need a lot of guidance because they can get frustrated because this is not a quick process, it’s slow.

 

All right, let’s talk about dizziness next. So imagine you’ve got a 39-year-old male who’s got a history of episodic migraine. But in addition, there’s episodes of this rotational vertigo that can last 20 to 30 minutes. Sometimes the attacks of migraine and the vertigo co-occur, but they can both occur separately.

So this patient probably has vestibular migraine. So to be diagnosed with vestibular migraine, you need to have had at least five episodes. You need a history of migraine, be it with or without aura. And usually the vestibular symptoms are pretty moderate to severe. They’re debilitating, and they last anywhere from five minutes up to three days. And they should be associated with some of these following features.

So if you have the headache, it should be a headache that’s pretty typical of migraine. So you need at least two of unilateral, pulsating, moderate to severe, or aggravated by routine activity. That comes from the ICD-3 actual criteria.

Headache associated with photophobia and phonophobia. They don’t have nausea listed since often you’re going to get nausea with vertigo anyway, or visual aura. So they want you to have at least one of those headache features that are with at least 50% of the episodes. And then it shouldn’t be better accounted for by another diagnosis, be it a headache diagnosis or a vestibular disorder. 

So now some of the vestibular symptoms that you’re going to see in these patients is an internal vertigo. And that’s where you feel like you’re moving. Remember vertigo is basically an illusion of movement. You can also have external vertigo. That’s where you may not feel like you’re moving, but you feel like the world is moving around you.

The vertigo may be positional. So it’s when you get up from bed or stand from sitting, those types of things. Visual vertigo is a really classic symptom that we see with this. And so complex patterns or seeing a lot of movement will induce the vertigo. And then finally, head motion. So turning your head, looking up, those types of things might be vertigo inducing.

First off, you want to make sure that they don’t have another disorder. So rule out something like Meniere’s disease, BPPV. And then usually for prevention, you’re going to use your typical options. But one thing that I really like in these patients has been the vaccine. I find it helps with the vertigo. I also find that it helps with some of the anxiety that comes with it because vertigo tends to be very anxiety inducing.

Some off-label things that I sometimes will try is gabapentin and acetazolamide. I’ve even had them use acetazolamide as a PRN medication for this type of thing. And there’s actually a study that’s looking at using galcanezumab for vestibular migraine.

When you’re using acute treatments, again, you’re going to use the typical things, but there have been some small RCTs that were done specifically with zolmitriptan and rizatriptan. So you may default to using those first, but really any of the rescue medications would be appropriate. And the most important thing for these patients is to get them in with physical therapy, and they need to have vestibular rehabilitation to help them learn how to cope and how to manage with these symptoms.

And they need to not just do the physical therapy when they’re with the physical therapist, but they need to also continue doing their home exercises. And they need to know that this is going to be a long path. This is not going to get better in a few weeks. So you need to help them set expectations. 

 

So now you’ve got this patient, and he was lost to follow-up. He comes back five years later, and now he says that he’s got daily dizziness. It’s a little bit more vague now. He just kind of constantly feels like he’s on a boat and he’s moving. And he’s wondering, what do I do? Like, what happened? Why did this get worse? And so this is something that you should be aware of because it’s often going to co-occur in patients with vestibular migraine or with any other cause of vertigo. And this is something called persistent postural-perceptual dizziness, PPPD or triple PD. 

So here they’ve had persistent dizziness for at least three months. The symptoms are going to be on most days. The severity can definitely fluctuate, but it’s impairing. It’s very debilitating. It’s often worse with upright posture, with movement and visually complex patterns, so they get a lot of that visual vertigo. But it’s not truly vertigo that they’re having now. It tends to be more vague.

I find the most common description I hear is that they feel like they’re on a boat or like there’s just kind of this vague on steadiness, wavering. Often when you watch their gait, you know, they can do things like tandem, etc. but they’re just very cautious. They need a lot of prompting.

They’re very uncomfortable with it. So these patients need a lot of vestibular physical therapy, and they may benefit from some cognitive behavioral therapy as well. This is basically like a functional neurological disorder of dizziness as best we understand it.

Basically, you can imagine that they were experiencing vertigo. And instead of their brain sort of improving and getting used to it and getting better – especially if they were lost to follow-up and didn’t get good treatment – now their brain has sort of, you know, rehabilitated itself in the wrong direction. So now any movement is just not tolerated, and it’s become a pervasive symptom.

So these patients are going to need a lot of rehabilitation to help with these symptoms. And it’s not uncommon for it to coexist in patients with vestibular migraine. And the hint is going to be that their dizziness is more vague and it’s more constant.

And often it seems more disabling than what you would expect for what you’re seeing on your physical exam. And it’s going to come with a lot of that visual vertigo. They’re just very intolerant of looking at things. They often have a lot of other things like light sensitivities I find very common in these patients. 

 

All right, let’s talk a little bit about brain fog. So for some patients, especially those patients with chronic migraine, headache is one thing, but they feel like they just can’t think. They feel like they’re just dumb. And so let’s say we’ve got a 34-year-old female. She’s had migraine for the past two years and she’s now got this background daily headache.

It’s about a 1 to 2 out of 10. So she feels like she’s never truly headache free. And eight days a month, she’s got a full blown migraine attack. And she feels like over the past couple of years, she’s had this increasing cognitive impairment. She feels like she’s got word finding difficulties. Her concentration is poor.

She feels like she just can’t remember people’s names. And it’s stressing for her because she’s worried am I getting a dementia? What’s happening? So you do something like a MoCA or an MMSE and she gets 30 out of 30. So there’s no latent evidence that she’s getting some sort of dementing process. So what is this? 

We know that you can have migraine-related cognitive impairment. There’s definitely been evidence of this. It seems to be particularly affecting attention and concentration. There might be some effect on language. And while you can definitely have it ictally so part of the migraine attack, there are patients who have it interictally.

And I find that’s particularly true for the patients with chronic migraine, where they have some degree of symptoms all the time. While it is more common, I find, if they have a mood disorder or a sleep disorder, it does not require that they have one of these. It can be purely from migraine itself.

And the good news is there is at least some evidence that it can improve with treatment. So again, you want to look at preventive treatment. So you want to go through all of those different options and try different things. Now they may be less tolerant of some of the medications that are sedating or something like topiramate, where they’re going to have some cognitive side effects, but that doesn’t mean you can’t try them. Because at the end of the day, this is from migraine and not from something like a dementia. 

So you can try those, just go slow and be gentle with it. And then make sure you screen for depression, anxiety, sleep disorders, including sleep apnea, and that those are also getting treated, because if those are not treated, then you may have ongoing sort of that pseudo-dementia type picture.

 

And then finally, I want to talk about allodynia. So envision that you have a 32-year-old male. He’s had episodic migraine for the past eight years. And he started noticing over the past year or so that migraine attacks have increased. They’ve gone from maybe three to four days a month, and slowly over the past year or so has gotten up to eight days a month.

And now he’s having this new head tenderness in between the attacks. And so if he just kind of touches his head, he said it feels like his hair hurts. It’s harder for him to wear his glasses, like right around the ears. It hurts to have any pressure there. So this is allodynia. 

So when we talk about central sensitization in migraine, often the correlate to that is allodynia, and then also you can have hyperalgesia. When we talk about peripheral sensitization, that’s more thought to be that throbbing pain that we feel in migraine. And so it’s really whether or not the sensitization is happening out in the periphery or happening centrally in the brain. 

So the official definition from the IASP is that central sensitization is increased responsiveness of nociceptive neurons in the CNS to their normal or subthreshold afferent input. So translation –nociceptive neurons, those are basically your neurons that sense pain. They’re becoming hyperresponsive, and it no longer just needs their normal sort of stimulus that turns them on. Now even a subthreshold stimulus is going to be able to turn them on.

So remember, normally a nociceptive neuron is going to turn on in response to something that’s painful. Well now it can get turned on by something that’s not painful, like touch, i.e., allodynia. So allodynia, by definition, is pain caused by a nonpainful stimulus. While the hyperalgesia, that’s still that you have a painful stimulus, but it hurts more than you would expect it to hurt. So for instance, that little pinprick that you might do on exam is now suddenly very painful. 

So what does central sensitization do to migraine? Well we think it might help make that chronification more likely to happen. So you’re more likely to have more frequent headache. You might start to get that background headache. You might start to get just overall worsening symptoms.

We think some of those cranial autonomic symptoms may relate to central sensitization, worsening of your sensory sensitivity. So things like photophobia and phonophobia may worsen. And then having allodynia is a sign that there’s central sensitization.

And so again, these are patients where you definitely want to have them on a preventive. And any of the types of preventives would be appropriate. And really, the goal is that when a patient has about three to four migraine days in a month, that’s when you should be starting treatment.

If you’re like at two to three days and they’re already having allodynia, especially if some of it’s interictal, that’s when you may want to start a preventive even earlier because that patient is going to be higher risk for progressing to more frequent migraine attacks and even to chronic migraine. So allodynia is a good sign that you may want to be more aggressive with your treatment early on. 

 

All right, so we’ve talked about a lot of different things. We talked about the phases of migraine and all the different treatments that can come along with it. We’ve talked about the different types of aura and some of the ways that we can try to treat it. We’ve talked about dizziness via vestibular migraine or something that often comes alongside of it, triple PD.

We’ve talked about allodynia. We’ve talked about GI symptoms, including nausea, vomiting, as well as gastroparesis, the different sensory sensitivities. And then cognitive symptoms and all the different ways that you can try to treat these when you’re focusing not just on the headache but all the other symptoms that can make migraine disabling. And that can be for patients sometimes, they’re more a disabling symptom than the headache.

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*The contents of this video are intended for general informational purposes only and does not constitute professional medical advice, diagnosis, or treatment. Always seek the advice of a physician or other qualified health provider with any questions you may have regarding a medical condition. AMD and the speaker do not recommend or endorse any specific course of treatment, products, procedures, opinions, or other information that may be mentioned. Reliance on any information provided by this content is solely at your own risk.