In this episode of Spotlight on Migraine, host Molly O’Brien talks with neurologist and headache medicine specialist Dr. Barbara Nye about the original acute migraine treatments: ergotamine, dihydroergotamine (DHE), and triptans (such as sumatriptan, rizatriptan, etc.). Dr. Nye shares the history and evolution of these treatments, including the formulations, delivery methods, how they work to break an attack, and who may benefit from adding them to their migraine toolbox.

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In this video:

• How ergotamines (such as DHE) and Triptans (such as sumatriptan and rizatriptan) work
• Why treatment formulation matters
• Which treatments may help in treating prolonged attacks 
• Why one ineffective triptan doesn’t mean others won’t work either
• The safety profiles and side effects of these treatments

Learn About Preventive Options:

• Migraine Prevention Explained: When to Start, Why It Matters & What Success Looks Like
• Breaking Down Your Migraine Preventive Options: Medications, Vitamins & Devices

Dr. Barbara Nye is a paid consultant for a sponsor of the Association of Migraine Disorders.

TRANSCRIPT

Molly O’Brien: Research has led to huge breakthroughs in migraine treatment over the past few years. We’ve seen newer classes of medication come to market, not to mention revisiting and reformulating some older therapies. Hi, I’m Molly O’Brien, and this is Spotlight on Migraine.

We talk a lot about these newer classes of medication in today’s migraine landscape, so today we thought we’d revisit these older, well-established acute migraine treatment options. Again, we’re talking about acute treatment options today, but if you want to learn more about your preventive options, I hope you’ll check out our podcast series, all about prevention. We’ll put the link in the transcript and the caption.

I’d like to welcome our guest to talk all about well-established acute treatments, Dr. Barbara Nye. Dr. Barbara Nye is a board-certified neurologist and headache medicine specialist. She is associate professor of neurology at Wake Forest University School of Medicine, a headache specialist with Atrium Health Wake Forest Baptist, and director of Headache Medicine Fellowship. Dr. Nye is vice president of the Alliance for Headache Disorders Advocacy and serves on the board of the Southern Headache Society. So excited to have you to the podcast, Dr. Barbara Nye. Thanks so much for being here today.

Dr. Barbara Nye: Thanks for having me. 

O’Brien: So today, we’re going to talk about ergots, triptans, and some combination treatments. So let’s start off with ergots. We have ergotamine and dihydroergotamine, or DHE. Some people call it that for short. And ergotamine, I realize, came about 100 years ago. That’s when it was first used for migraine treatment, which is way old. So can you tell us a little bit about what ergots are, how they work, and we’ll start with that.

Nye: And ergotamines, as compared to triptans, are going to be less specific for migraine attacks. And they’re actually triggering multiple receptors. So that’s going to make it a bit unique, but it also allows us to hit multiple receptors. And for some patients, that’s a really great benefit. Interestingly, in the 1940s, it got derived from a rye mold and scientists actually started using it in postpartum hemorrhage. So it was actually used in the OB world before it was found to have migraine therapeutics and then started being used for migraine headache in the 1940s.

Ergotamine itself is not as clean of a drug. It has stronger vasoactive properties, and unfortunately, also comes with an increased side effect profile. So a lot of nausea and vomiting with that particular formulation. It’s usually available in orals, and I would say that you don’t see a lot of headache specialists using it. They also end up getting combined with caffeine, which if we’re having episodic migraine, which we define in the headache community as having less than 15 headache-days per month, then sometimes we use these combination treatments. But we worry about patients who have more than 15 headache-days per month of getting into medication overuse with some of these agents.

Dihydroergotamine, though, that was compounded, gives us a synthetic version and weaker in the arterial constriction. It still ends up binding serotonin, noradrenergic receptors, and dopaminergic receptors. So we end up getting multiple target areas. Sometimes that allows us to hit multiple targets can be a positive thing for some of our patients. And then we’ve also found that dihydroergotamine is helpful anywhere in the headache cycle, which makes it a unique molecule. It’s got this faster onset time but then gets metabolized slowly through the liver. So it has kind of this biphasic bioavailability. And so some of our patients can get a benefit from multiple doses of inpatient DHE, for example, for a month or more, even when it’s out of patients’ systems. So it’s a really great molecule that has been leveraged in multiple formulations.

O’Brien: Can you explain a little bit more on that, how it can work well throughout different phases of the migraine cycle, just to kind of help our audience understand really what that means?

Nye: Let’s lay that foundation. So we’ve got the prodrome or the premonitory symptoms before a headache. Some patients get yawny, may start getting nauseated, neck might start being uncomfortable, may even get fatigue. And then we get into aura and possibly the head pain portion. All can be separated by minutes or hours and sometimes days, depending on the patient. And then we have the postdrome, which is kind of the aftereffects that often doesn’t include the headache pain, but often has things like fatigue and not feeling quite like yourself.

So we’ve got all of these phases. And as you know, migraines are very unpredictable. Some people wake up with them. Some people get them during the workday. And one of the cool parts about this molecule is that it’s actually been shown to be effective if you take it 30 minutes into a headache attack or two days into a headache attack. And some of this is thought to be because of this action of this biphasic elimination and two peaks of benefit, because it sticks around in the system. A lot of our therapeutics – we’ll be talking about triptans momentarily – but they’re fast-on and then they come off, they get metabolized. And so if that headache attack is lasting longer, this is an ideal medication.

O’Brien: That’s really helpful to understand. And like you said, it’s really interesting and why we wanted to revisit these types of therapies, because with the newer like gepants and monoclonal antibodies, we’re looking at a very specific receptor and even like PACAP coming down the pipeline, very specific. So kind of cool to hear about medications that it almost like, not necessarily throw it at the wall and see what sticks, but for some reason that just pops in my head.

Nye: That’s not a bad way of thinking about it. But I think, you know, we haven’t come up with the one final pathway that defines a migraine attack and each individual attack as well as each individual person is going to manifest slightly differently. And so there are super responders to all our therapeutics. We’ve seen this across the board, across the years. You know, some of our folks just, that is my miracle drug, right? That is the thing that takes all things away, but it may not help their cousin or their brother or their friend, right? So we’re not all wired the same way. And we have a lot of understanding about the migraine pathophysiology these days, but we don’t have the final connect, everything gets in line, if we disrupt this piece, it’s done. And it’s probably got some variation between individuals.

O’Brien: I’m curious, and we’ll get into a little bit more into the nitty-gritty here in a minute but say you’re in an attack that is just lasting and whether your status or refractory, you’ve been in it for a while. Can DHE be a good option if you are in this just really long-lasting attack that just isn’t breaking?

Nye: We can’t ever say yes with a blanket yes statement, but that is one of the places that I really like to use the DHE products. It’s in prolonged headache attacks in patients that are either in status or that just tend to get these headaches that last three days and they’ve tried other acute medications, and they can’t quite get that three days to be truly shorter despite treatment. It’s also helpful in wakeup headaches because wakeup headaches, a lot of our acute treatments are really geared towards the beginning of the headache cycle. And so when we say that at the beginning and onset of migraine headache, we know that the peripheral first-order neurons are the things that are starting that cascade. And once we get to second-order neurons, which are going up into the trigeminal nucleus caudalis, and then third-order neurons to the thalamus, we’re going into the central nervous system. And a lot of our therapeutics really work in the peripheral nervous system. And so we need to catch it as early as possible. And that’s why we say, treat early and quickly when we get a migraine attack. And if you know it’s a migraine, use that migraine-specific therapeutic if it’s available.

And so kind of thinking about attacks that last longer and when we can’t find the starting point, these wakeup attacks often are starting in the middle of the night. You don’t know if you’re 30 minutes in or three hours in. And so this is one of those areas where DHE can be very, very helpful. So I’d say prolonged headaches, wakeup migraines, and status migrainosus are my kind of top three areas. And then I’ll add patients with chronic migraine are often an excellent therapeutic class because again, they’re having more headache-days than not. So I want something that’s hanging around a little bit longer to break that headache cycle.

But I do think formulation matters. And when we say formulation, it’s how it’s delivered. So we talked about ergotamine being in an oral form and sometimes combined with caffeine. And so that’s a little bit more dangerous when we have more frequent headache-days, plus the nausea factor. And then there’s nasal spray formulations. There’s two out on the market. So there’s migranal nasal spray, which is a very traditional, it’s the nasal spray that just goes spritz up the nose as best we can. That one often doesn’t get very high in the nasal cavity. And sometimes patients really report a lot of dysgeusia or kind of tasting the medication afterwards. And so the goal when we use a nasal spray is actually to get it through our olfactory regions that are mucosal membranes and to get that absorption and bypass the GI tract. So we’re not looking for the medication to go into our throats. It’s kind of yucky. For a lot of reasons. And so that’s migranal. 

And then there’s DHE in the Trudhesa form that uses precision olfactory delivery technology that actually propels the medication much higher and gets it absorbed up where the olfactory nerves are, in that nasal mucosa that’s ready to absorb things. So that’s a one-up on the migraine all in some ways, and gets it into the system faster, less complaints about that kind of dysgeusia and tasting it a lot. There’s a third nasal formulation that is not on the market yet. It’s called Atzumi. It’s a nasal powder. So that’s a totally different thing. Unless you were in the clinical trials, you haven’t experienced it yet. Hoping to see that come to market. It was approved last year. So hopefully we’ve got a new product coming.

And then we get into injections. And so for years, we’ve been able as physicians to prescribe it as an ampule. And that brings up a little bit of kind of a challenge, right? Because I’m telling you in a migraine attack, you have to take an ampule, which is the container for it, break it, and then draw it up yourself and inject yourself. And now more recently, Brekiya has come out with an autoinjector so that you don’t have to go through that process. And then finally, we move into the emergency or inpatient setting where it can be delivered IV as well. And the IV formulation is actually approved for kids six and up, believe it or not. So there’s a pediatric indication there. I don’t believe any of the nasal sprays have yet gone to the lower age groups. I think everything else is 18 and up. And so again, just this broad spectrum of formulation.

So we’ve got to think about where patients are in their attack, what they’re willing to do when we ask the question of who do we recommend this for? Because there’s certainly people that look at me like I have four eyeballs, possibly more, when I say, what do you think about giving yourself an injection? They’re like, I don’t think so. But I get the same reaction for nasal sprays, interestingly. So with this formulation of medication, it does have this long half-life and benefit either really early on in the headache attack or later in the headache attack. But you have to be willing to take a nasal spray or an injection. As I said, you get a lot of nausea with that oral formulation, and we don’t tend to use that. So that makes a difference in who do we have this discussion with.

O’Brien: Anyone else that should just, it’s a straight up no for DHE or should have deeper conversations with their doctor?

Nye: Hypertension, I would say, is the softer call in all of these. The terminology that we use is uncontrolled hypertension. So is that one blood pressure reading that’s abnormal? It depends on who your provider is. There might be a lack of comfort level if you’re meeting someone for the first time and they don’t have a history and your first blood pressure is out of the normal range, they may be less comfortable with it. But with the severe peripheral vascular disease, if you’ve had a stroke, heart attack, or have coronary artery disease or an aneurysm, that’s a no-fly zone and definitely something you want to disclose to patients.

O’Brien: What about pregnancy or postpartum?

Nye: We also avoid ergotamines in pregnancy because of the vasoconstrictive properties. And so we don’t want to contribute to any premature rupture of membranes. That’s the concern when we’re late in the pregnancy. Postpartum, we also tend to be very careful with it. We don’t have good lactation data. I’d say that that’s unfortunately a challenging area across the board that most of the studies, if we have them available in women that are lactating, it’s two to eight women are usually what is studied to give us our safety data. So this is one of my pie-in-the-sky goals. Eventually, I would like to create a model that we can be studying some of this, maybe even after people are done breastfeeding their babies, but studying some of these in actively lactating women to get a better understanding of what are we delivering to our babies? Is it safe? Is it something that we can consider? As of right now, we don’t have good data that says, yes, it’s safe. So we shouldn’t be doing it.

O’Brien: As we kind of wrap up our conversation on ergots, did we miss anything? I feel like we’ve covered a lot.

Nye: Often medication overuse headache, which we want to call medication adaptation headache these days, is a result of overusing short-acting medications is the most common culprit. But DHE actually falls into one of these areas where we are concerned about what happens if you’re using it more than two days a week as an outpatient. The exception to this, I will say, is something we call the modified Raskin protocol, which we can use to stop status migrainosus. It’s an inpatient protocol under doctor monitoring where we actually administer the drug with some other medications three times a day for three to five days. And actually Raskin – oh yeah, we used to call it the Terminator at Dartmouth. So it really gets rid of the headache, but that requires some medical monitoring. That’s not the way that we do it in an outpatient setting without having those extra monitoring parameters in space. Medication adaptation headache can happen with ergotamines, so we want to limit them to two days per week. Most of the doses can be taken twice in a setting so you have an opportunity to dose more than once at a time, but again, limiting to two days per week.

O’Brien: Right. So let’s move on to triptans. Triptans, a lot of people call them tried and true. They’ve been around a while, but actually not that long. Triptans became available in the 90s. And again, they were a huge, huge, huge breakthrough for people living with migraine. I’m sure for providers as well. There are seven different FDA approved triptans. So again, that’s US based. These are for acute treatment. So tell us a little bit about triptans. What are they? How do they work? And thankfully, they’re here.

Nye: Yeah, thankfully they are here. And I mean, can you imagine the validation to both the patients and the providers treating patients with migraine in the 90s that having a drug that stopped this in its tracks? I mean, it’s mind blowing, but also changed the paradigm. It legitimized us in so many ways. And I mean, we’re still fighting the stigma battle, right? But the use of the triptans and now the CGRP medications that actually target the migraine mechanism go a long way to say, this is a biological condition. This is a chronic neurological condition that has a biologic basis. And I think that’s important for all of you to hear that are listening to this. This is real. And anyone that doesn’t tell you that, please leave them in your rear view and don’t listen to them. I hear so many of my patients that just feel not believed. And so the journey with these medications has also helped validate what you’re experiencing in so many ways.

So as we were talking about triptans, they are serotonin 1B/1D receptor agonists. That’s all technical speak. They’re serotonin receptor binding. And 1B, for blood vessel, that is the binding mechanism on the blood vessels that causes the vasoconstriction. And the 1D is in the other areas. And so these medications also have some vasoconstrictive properties, a little bit different and a little less aggressive than what we saw on ergotamine. So it makes them a bit safer. But still, we’re going to have the caution talk later about who do we avoid these therapeutics in. It’s going to be very similar to what we talked about with ergotamines. So these have a peripheral nerve binding but then have a central effect in inhibiting the pain signal. Remember, we talked about those first-order neurons, we’re stopping it progressing to the second order, which is why it’s so important to use these early. These are an early target medication. 

Now, that doesn’t mean you shouldn’t use them if you’re two hours out. Some patients do get a benefit from it, but the best benefit possible is early at onset for those migraine attacks. And if you’re new to the migraine space, remember access is key here with triptans. And so I like to tell my patients, there’s a jewelry that you can buy to put a triptan tablet into to have access to it. So, I mean, you know, you can get this little cute pill necklace. Think about your purses, ladies, you know, but have access. Access is important. And that’s not just with this drug class, it’s with others. But just want to emphasize that if you have access, you will give yourself the best leg up. That is not to blame you if you don’t. But really just kind of thinking about those pieces, especially if you’re one of those folks that get them infrequently or once a week or once every few weeks, sometimes that habit of having it with you is more of a challenge. 

So with these triptan medications, we have these serotonin binders and inhibitory signals that are created centrally. That’s the primary mode and mechanism of action for these therapeutics. As we said, optimizing them with the earliest action possible. If you try and fail one of them, it doesn’t mean you’ve tried and had the medication fail you as a class. When we talk about a class of medications, that’s all those seven triptans that Molly mentioned. So just because your doctor gave you one doesn’t mean the second one won’t work. So don’t lose faith. There’s an art and a science to how we distribute them. And sometimes there’s an insurance factor in the mix, as far as which ones are selected in which order. But it is worth trying more than one, and I would argue up to three or four different ones.

O’Brien: Some of these drugs are available to use in different ways. So talk to us a little bit about what’s available out there and why we have these different methods.

Nye: Fabulous question. And that is probably the most common change that I make for a patient with episodic migraine that comes to see me is actually changing the formulation of their triptan in the clinic. So formulation comes back to, is it oral? Is it a nasal spray? Is it injectable? Now, orals come in oral dissolving. There’s a couple of the triptans that come in dissolving wafers or dissolving formulations. Unfortunately, their mechanism of action doesn’t work until it gets into the small intestine. It doesn’t have buccal absorption in the mouth. But sometimes just getting that into the system that way makes it more rapid just because it’s already dissolved and can get through the intestines. 

Why is it important to think about formulation? When you’re in a migraine attack, we have a phenomenon called gastroparesis. That’s another big medical term. That basically means your stomach’s slowing down. You’re not emptying things at the same rate. And sometimes gastroparesis actually manifests with that nausea feeling, right, because you’re not emptying your stomach or just flat out vomiting is the most extreme. So we’re not going anywhere. So we can imagine that if we put a tablet in our mouths and we have gastroparesis present, we’re not getting it to target. Target is in the small intestines. That’s where our medications get absorbed. And so if we don’t get there, then that’s why medication can be inconsistent. 

So some folks may have experienced that, you know, if I get really early in my attack and I’m not nauseated at the time I take my triptan orally, no problem. It’s gone in 30 minutes, 45 minutes. I can go on with my day. Other times it runs up on me and same kind of timing, but I’m nauseous at the time. And it doesn’t work the same way. It may take two hours to get the benefit that I would have gotten otherwise. So that’s that gastroparesis part of the equation. So thinking about bioavailability, how do we bypass the GI system? Well, we take a nasal spray or we inject ourselves. And so there are nasal sprays. This is sumatriptan, or Imitrex, tends to have the most kind of formulation types with it. It was the first to market. It was the first injectable available. Injectables were available actually before the orals in this category. So providers were injecting their patients with their first sumatriptan doses in the 90s. 

But the nasal sprays can be nasal powders or nasal like droplet formulations, depending on what products you are using. And then the injection is also the sumatriptan injection, and it comes in autoinjectors as well as vials so that you would draw up how much you want to use. And that can be helpful in other disease states like cluster headache disorder. That’s where we often see people parsing out a little bit more because they’re more sensitive to the dosing. Migraineurs tend to need the six-milligram dose when they’re injecting themselves.

O’Brien: Such a great history and reminder for our friends who maybe used triptans a while ago or are just getting back to them for the first time. Talk to us about who is a good candidate to use a triptan in their acute medications, acute treatments, and then who should really just avoid these? It might just not be the safest bet or the best bet.

Nye: I think patients who have those faster-onset headaches, this is a nice medication to take right when you feel it. Take that medication in any formulation. That’s super helpful when you can kind of see it coming. I don’t think it’s as good for the wakeup headaches. Sometimes we use the injection formulation to avoid the time that it takes for other absorption methods to get into the system, and sometimes that can be successful. But if you can kind of see when it starts, that is super helpful. You’re going to be limited to two days per week. One of the therapeutics can be used up to three days per week, but for the most part triptans you think of, again, two doses in a day, two days per week. That’s the limit because then we get into that medication adaptation headache thing again.  And then we should be thinking about prevention. That’s my provider hat back on of going, we need to be talking about other things, but that’s not the focus of this podcast. So if you are using more than what I’m talking about, then that means you should be having a conversation with your provider about prevention as well. 

And then who do we avoid this in? So again, kind of repeating myself, patients with a history of vascular disease, peripheral vascular disease, hypertension, coronary artery disease, having a heart attack, stroke, or an aneurysm, those should be avoided. I will note that there are warnings that pop up about risks for serotonin syndrome. So for patients who are taking an antidepressant, a tricyclic antidepressant, an SSRI, or an SNRI, sometimes we get those warnings. In general, most patients are not on high enough doses of serotonergic agents for anxiety and depression that we are worried about serotonin syndrome. It does come up, as I said, in a formulation piece of the warning, maybe with your pharmacist, but as long as you’re not taking high doses of serotonin-blocking medications, if you’re taking multiple antidepressants, if you’re requiring that kind of treatment, then you might want to ask those questions. But I would say, as a general rule of thumb, we don’t worry about it much when a patient is taking a single medication and often two medications for depression or anxiety.

O’Brien: Talk to us a little bit about potential side effects or complications. We talked about contraindications. But talk to us a little bit about potential side effects from triptan use.

Nye: Because they’re fast-onset medications, they can give us a flush-rush sensation. A small handful of patients actually get worsening of the headache before it melts away. Some people, again, a small percentage of people just get worsening of headache, unfortunately, which I hate for them, but it’s very rare.

O’Brien: That’s terrible.

Nye: I would say I really don’t get that many patients that tell me that they’re out of commission and it’s not great, but there’s always a small group. We worry about chest pain, and some people can get chest discomfort. That’s a reason to talk to your provider because maybe you have an undiagnosed condition. So you may not know you have coronary artery disease, and you may need a screening EKG or something like that. If you’re starting as a young individual, often we don’t do a ton of cardiac testing because your risk factors are low. But if you have a strong family history, that’s certainly something to talk to your providers about, making sure that they screen for that cardiovascular history. Chest pain can be kind of completely benign for some folks. We usually don’t tend to continue that particular medication. And then we don’t also throw out the entire class, yet again, kind of thinking about the class, if you get discomfort with one of the therapeutics because they are not all as fast. 

So when I kind of line up my triptans, sumatriptan is the fastest in onset. My rizatriptan, zolmitriptan, almotriptan are kind of in the middle. And then our frovatriptan and naratriptan are longer-acting therapeutics. And so for my patients that have prolonged headaches, so kind of like I was talking about earlier with ergotamines, I may use a prescription of naratriptan because it’s a longer acting triptan. And most people don’t get any side effects with that medication. It’s also slower. And so that also means that people can’t feel the benefit in the 20 minutes the same way they can with the rizatriptan or eletriptan or almotriptan or zolmitriptan. So just kind of thinking about that. And so as a provider, I tend to pick a rizatriptan/Almo-type medication in the middle ground as the first trial for a patient.

You’d ask kind of how do I pick that? Part of that is insurance will cover those. So that’s good. But I also don’t want to turn someone off that has never tried a medication. And if I give them something like the sumatriptan as first line and they do not feel well, then sometimes depending on the provider they get, they’ll say, oh, I’m allergic to them all. And that’s not really an allergy. And I don’t want to close the door on that entire class. So my recommendation, and as I teach my fellowship, I tend to stick with the middle ground, see how people react and what they feel like, and then decide, do I want to go faster or do I want to go slower as I’m working my way through that class of medication.

O’Brien: So what do you think our audience should know about stroke risk and triptan or stroke risk and ergot use as well? Like how do we factor all of this in? Maybe some people are scared because they just hear stroke risk and think, no way, I’m not taking these medications. So, how do you talk to patients about this?

Nye: That’s a really great question. Data is a really important guide here. Now, what we know is patients who have high blood pressure, diabetes, and high cholesterol you’re at an increased risk of stroke, right? Those are what we call modifiable risk factors. Getting older, we can’t do anything about. Men are at a higher risk than women, so yay women. So those are non-modifiable risk factors. Having migraine with aura, so having either visual, sensory, or motor aura can increase that stroke risk and it’s an independent risk factor in the migraine space. It it’s about two-fold over your age-matched population. And so if you are young, healthy, don’t have cholesterol issues, those numbers are pretty low. And there is no contraindication to taking an ergotamine or a triptan medication when you have migraine with aura. 

The contraindication comes in if you have these other risk factors. If you’ve had a stroke or heart attack if you’ve had an aneurysm, those are the things that we worry about. Then there are estrogens, which is kind of a whole different topic. But the use of estrogens increases some of that risk in patients that have migraine with aura. And so there is good data out there. I actually provide a summary table to my patients. The original data was done in the Women’s Health Study, where we were using 50 micrograms of estrogen in our supplements. These days in birth control, most of them are in the 15 to 20 microgram range. So we’re at much lower doses. And so with the 50 micrograms, we would get about up to a six-fold increased risk of stroke when we were taking these estrogens. Currently, the odds ratios are in the 1 or 2.0 range with 20 and 30 micrograms of estrogen. So there is a dose response curve. 

And so if you are someone that has migraine with aura, you should definitely have a conversation with both your OB and your neurologist about what is your risk. It has nothing and I mean nothing to do with any risks associated with taking triptans or ergotamines. So they’re two separate issues. And so patients with migraine with aura should not be denied treatment with a migraine-specific therapeutic like a triptan unless you have those other risk factors in the background. But migraine with aura is not the thing that should shut the door for you.

O’Brien: And I appreciate you spelling all of that out clearly. It really does boil down to having these ongoing discussions. So we appreciate it. Thank you so much. This was really incredible. I love getting a chance to speak with you and to connect and learn so much and help our audience out. Is there anything else before we wrap up that you want to make sure we touch on?

Nye: I think just a general statement to all of you guys that are listening out there. Thank you for tuning in, number one. Number two, I want to validate the fact that this thing is real. And I hope that no one has ever told you that it’s not, but I think odds are sadly that they have. And I really encourage you to find the people that will be in your corner. There’s lots of wonderful support out there, whether that’s in support groups through these programs or your local providers. Find the people that fit with you and have them support you. We are here. We are a growing network. I’m excited to say I’m a fellowship director and get to train a fellow a year. And so we’re trying to grow this community and make sure you have the providers out there to care for you.

O’Brien: It gets a little emotional, you know, because it is real. 

Nye: It is real. Yeah. And too often do I hear people not feeling validated and not being listened to. And it hurts my soul.

O’Brien: It really does. Well, thank you for caring. Thank you for caring about all of it. Not just your patients, but all of us, and really giving so much of your time to helping people and for giving your time for us today. We really appreciate the conversation. 

Nye: Thank you. Really appreciate you, Molly. Thanks for the invitation. 

O’Brien: And that wraps up this episode of Spotlight on Migraine. With the Association of Migraine Disorders, I’m Molly O’Brien. We’ll see you next time.

*The contents of this podcast are intended for general informational purposes only and do 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.