Okay, so you guys all made it to the end of this meeting and you're the only ones who are left still here in San Francisco, so thank you for making it all the way to the end. Our talk today is going to be done partially virtually as one of our members was too sick to come and she recorded her slides. I'm Dr. Dennis Senko, I'm going to be doing the second part and Dr. Thiem is going to do the third part talking about military veterans. Just out of curiosity, how many people in the audience actually have bad headaches themselves? Oh, that's not, that's about a third. Okay, Dr. Mia Menon, who will be talking first, she is certified in neurology and also did fellowship training with dual certification in neuropsychiatry, behavioral neurology. She is the chief of headache research and associate professor at NYU in New York City. Myself, I'm Dr. Dennis Senko, I am certified in psychiatry consultation liaison psychiatry and headache medicine and I work on the one of the only inpatient headache units in the country at the Jefferson Headache Center in Philadelphia. And Melinda Thiem, she is a Army psychiatrist or former Army psychiatrist who works in Albuquerque, New Mexico. And you recently also got a certification in headache as well, I believe, right? In terms of disclosures, Dr. Menon receives research funding from the NIH. Some tables and figures are from the headache chapter of the Harvard neuropsychiatry textbook and press. She helped develop the RelaxAHead app, which has shared IP between NYU and IRODI. I have received speakers honorarium from TEVA in 2020, nothing more recently than that. I was also one of the primary investigators on a TEVA-sponsored research study that looked at fremenizabab for depression in patients with migraine and the results of that study will be in press this year. And Dr. Thiem has no disclosures. Furthermore, the opinions expressed in this presentation are those of the presenters alone and do not represent the views of the U.S. Department of Veterans Affairs or the U.S. government. This is a QR code. If any of you want to click on that QR code with their smartphones, you'll be having access to a larger set of our PowerPoint slides in PDF format. We're hoping that what we'll be able to do today is help identify the characteristics of migraine and we'll also talk a little bit about other headache disorders as well and how we can use evidence-based, non-pharmacologic treatments, including behavior therapy techniques for the treatment of migraine. Identify migraine and the comorbidities in other mental health disorders, as you will learn, is bidirectional. We'll share some of the biopsychosocial aspects of migraine and mental health comorbidity and how you can use this to approach treatment. And in the end, identify what psychiatrists can learn more about headache medicine and become involved in a headache as headache specialists. So before Dr. Minnan begins her talk, I'm going to do a brief introduction. Why psychiatry in headache medicine? Well, traditionally psychiatrists have been rather absent or left out of pain management and headache medicine as a whole. Psychology, not so much, and there are plenty of headache psychologists that provide a supportive role for the primary headache medicine providers. But migraine is extremely prevalent and disabling and psychiatrists need to know what their patients are experiencing and how this can impact their treatments as psychiatrists. The rate of psychiatric comorbidities is much higher in patients with migraine, and I will discuss this in slides later. And there are some treatment considerations as psychiatrists that you need to know when treating your patient for psychiatric illness who might also have a migraine or some other headache disorder. But here are the basics. Migraine is not a psychiatric disease. I don't know how much more I have to stress that. It is not the somatic expression of a psychodynamic defense. It is associated with significant stigma, and I will talk about that later. And there is data showing that addressing the behavioral health concerns of a patient with headache can improve the headache condition, and improving the migraine condition can improve some of the behavioral health symptoms as well. So without further ado, our first speaker is Mia Tova Minnan from NYU, and I'll sit back while she presents. Hi, thanks so much for attending our session today. I'm really sorry I'm not able to attend in person. I'm Mia Minnan. I'm a board certified neurologist with dual training in both headache medicine and neuropsychiatry, and I'm going to be speaking about headache, what psychiatrists need to know from the neurologist's perspective. In theory, headache classification is easy. We have the International Classification of Headache Disorders, the third edition. It's kind of like our Bible, like our DSM. But in practice, I know it's not so easy, and it's really important because lifetime headache prevalence is 99%. One of the things that drew me to the field of headache is that the differential diagnosis of headache is one of the longest in medicine, with over 300 different types and causes. So you never know who's going to walk into your office each day. Major categories of headache disorders include migraine, with over 47 million Americans, and it's actually the most common type of headache that presents in your office. There's also tension type headache, the most common headache type out there. There are other primary headache types like cholesterol, so oftentimes nicknamed that suicide headache, where patients are pacing in the emergency department. Other trigeminal autonomic syphalges, and other primary headaches like primary stabbing, cough, exertional, thunderclap, those associated with sexual activity, hypnic headaches, that alarm clock headache that wakes you up at 4 a.m. every day, hemicrania continua, or new daily persistent headache, where one day a headache starts and it doesn't stop for at least three months. It could have been after a stressful event, after waking up from a surgery, some illness, whether it was a virus that was diagnosed or not diagnosed. A headache attributed to trauma to the head or neck, such as a concussion. A headache from a vascular disorder, so for example, a venous sinus thrombosis, or a stroke, or hemorrhage, temporal arteritis. Also, a headache attributed to changes in the pressure in the head, whether they're high or low pressures, related to a tumor, or pseudotumor cerebrae, for example. A headache attributed to a substance, or it's withdrawal, like a caffeine withdrawal headache. A headache attributed to infection, like the flu, or COVID-19. A headache attributed to other medical conditions, dialysis, hypothyroidism, the list goes on. Headache or facial pain, so for example, there is headaches related to temporomandibular dysfunction, headaches also attributed to psychiatric disorders. And so, as you see, there are all different types of headaches out there. So, the point is that you will see many patients with headaches and need to be familiar with the different headache types and how to treat them. So, how do we approach a patient who presents to our office? Well, we differentiate headache types by taking a solid headache history. And what do I mean by that? Well, we ask about the temporal profile, the time of onset. Did it start in the teenage years or after age 50, which would be a red flag? What's the time to maximum intensity? So, does it start at the snap of the fingers, like a thunderclap headache, or is it gradually progressing over a period of four hours, untreated or unsuccessfully treated, more like a migraine? What is the frequency, so how many days a week, or times a day, or you know, month, year, time of day? So, is this a headache that is occurring on awakening? Does it wake you up at night? How long does the headache last? And ask about recurrence. We also ask about headache features. So, features before, during, and after the headache. So, for example, during the headache, is there any associated nausea or vomiting, photophobia or photophobia? And a lot of it is also about how you ask the question. Because if you say, well, does lighter sound bother you? People may say, well, no, not really. But if you say, well, when you have a headache, would you prefer to lie down in a dark, quiet room? And people say, well, sure, yeah, but I need to work through it, so I'm not able to. So, a lot of it, a lot of it is about how you freeze the question. It's also asking about the location of it. So, is it fixed on one side? In which case, that would warrant imaging. What's the quality of the pain? Is it throbbing, pulsating, sharp, dull? The severity of the pain on a scale of 1 to 10, 10 being the worst. And what aggravates it or makes it better? So, was there any trauma, any change in medical conditions? Did you start any new medications or stop any medications, any known triggers? And what could be making it better or worse in terms of pharmacologic or non-pharmacologic treatments? Oftentimes, patients have been to other providers before reporting these headaches to you. They may have seen an ophthalmologist thinking they have blurred vision and that they need their eyeglass prescription changed. They may have been to the ENT thinking it's a sinus issue. So, it's really important to ask them, or even, they may have been to the dentist and even had teeth extracted. It's important to get a psychosocial history. So, any substance abuse, any, you know, occupational history in terms of shift-wake disorders that could be interfering, and also ask them about personal life and stressors. It's important to ask about sleep. What patients think is going on? What is their own diagnosis in their head? And it's also important to get a complete medical, surgical, and family history. The physical exam is important. So, does the patient look like they're in a lot of distress? Are they overweight, making you think, okay, maybe there's something like pseudo-tumor cerebral going on or sleep apnea. It's important to also check out the optic discs, visual acuity. In the acute setting, for the example, the emergency department, is there a rash, making you think there's meningitis, any signs of endocrine dysfunction. And then also, as part of the exam, we check to see if there's a positive tunnel sign. So, we tap on the back of the head over here to see if that elicits any pain or tingling sensation that could radiate to the top of the head, down the neck, to the ear. We also assess for temporomandibular dysfunction. So, if we put our hands by the jaw and open and close the jaw wide, is there any popping or clicking sensation, which makes us think, okay, maybe there's a component of temporomandibular dysfunction and they should see the dentist. Oftentimes, the question of imaging comes up and patients may come to you and say, look, I'm so frustrated. My doctor won't order imaging. I have these headaches. I'm scared. I'm anxious. It turns out the yield of CT scan or MRI in patients with any headache and a normal neurologic exam is, look, it's only about 2%. And so, we will usually image if it's the first or worst headache, if it's a subacute headache with increasing frequency or severity, a progressive or new daily persistent headache, that headache that I told you starts one day and it's unremitting for at least three months, a chronic daily headache, headaches that are sidelocked, always on the same side, or headaches not responding to treatment. We'll also do imaging if it's a new onset headache in someone who has cancer or HIV positivity, a new onset headache after age 50, the patient has headache and seizure. And then also, we consider associated symptoms and signs, which can be a little bit tough at times because headaches with fever, stiff neck, nausea or vomiting, obviously some of these headache disorders that are primary are accompanied by nausea or vomiting. But headaches other than migraine with or associated with focal neurologic symptoms or signs, if there's any public demand exam, any cognitive impairment or personality changes, or if it's brought on by exertion. And the determination of whether or not to image is backed up by the Choosing Wisely campaign. So basically, they say to do neuroimaging if it's a sudden or explosive headache, if it's different from other headaches, especially if age 50 or greater, it's brought on by exertion or accompanied by fever, seizure, vomiting, loss of coordination, change in vision, speech or alertness. So most headaches that you're going to see in the office are primary headache disorders. I can't emphasize that enough. So 80 to 90 percent of all headaches out there are primary headaches. And again, the most common type of headache that usually presents for care is migraine. So attention type headache is the most common headache type out there. The patients just don't present for care. And another example of the primary headaches are cluster. And this diagram here to the right kind of depicts how some of the features do overlap between migraine and tension type headache. And I think that's also a reason for the underdiagnosis and undertreatment of migraine, is that so many people just think, oh, it's tension type headache, there's nothing to really do, just take an over-the-counter medication. But in fact, migraine is extremely disabling, extremely prevalent, as we're going to get into. So it's important to try to figure out, is this migraine, so that you can treat appropriately. So as you may recall, I said earlier that migraine affects over 47 million Americans. That's a staggering statistic. It's 18% of women and 6% of men in the United States. So 12% of the US population. That's like one in five women. And in fact, migraine without aura is the most common subtype of migraine. So many people think that they don't have migraine, because they'll say, oh, well, I don't get those flashing lights like my sister, or I'm not completely bed-bound with the severe nausea and vomiting. And so, you know, I don't have migraine because it's not as disabling as others. And so it's really important to figure out, how do we define migraine? How do we define aura? And again, that leads us back to the International Classification of Headache Disorders criteria. So let's talk about how we define migraine without aura. Well, you have to have at least five attacks in your lifetime. They have to last anywhere from 4 to 72 hours, untreated or unsuccessfully treated. The headache has to have at least two of the following characteristics. So it has to be either unilateral, pulsating or throbbing quality, moderate or severe pain intensity. Now that moderate actually starts at a 4 out of 10 in intensity. And aggravated by or causes avoidance of routine physical activity. In addition, you also have to have at least one of the following. Either nausea and or vomiting, or photophobia and phonophobia. And it shouldn't be attributed to another disorder. So basically, in sum, just to be clear, you can have a bilateral headache, that's a 5 out of 10 intensity, that causes a little bit of avoidance of routine physical activity and has some nausea, and that could be migraine, right? It does not need to be unilateral. It does not need to be that 8 or 10 out of 10 headache. Okay. And so I really want to emphasize that you should know the criteria so that we can all work together to improve migraine diagnosis. Now, what is aura that one third of people with migraine have? Well, typical aura consists of visual and or sensory and or speech symptoms. In fact, about 90% of people who have migraine with aura have had visual aura. It can be a mix of positive or negative symptoms. So it can be flashing lights, or loss of vision like tunnel vision. You could have numbness or tingling on one side. The key part is that it gradually develops over a period of 5 to 20 minutes and should last no more than 60 minutes. So oftentimes we'll get referrals for patients with some sparkles in their eyes lasting seconds, that's not aura, right? So technically speaking, it has to last at least five minutes. You know, sometimes if it's two or three minutes, we may be a little bit conservative and treat as if it is aura. But if it's lasting seconds, it does not aura. You need at least two attacks in your lifetime with aura to have migraine with aura. So let's talk about various treatment types for migraine. It's a really exciting time in headache medicine because there are so many different treatment options for our patients. These can be medications, both acute medications to take when you have an attack and preventive medications. There are behavioral therapies, there are supplements, and there are devices. So there's a lot of opportunity to help our patient population. Let's start off talking about medications. We have a variety of acute medications that we can use for our patients. There are obviously non-steroidal anti-inflammatory over-the-counter medications that patients may use for mild to moderate attack. There are also triptans. Those are from our moderate to severe ones. There are also a combination of NSAID and triptans. You can actually just do it generically. You don't even need to use a prescription one. There are anti-nausea medications to use. There are rescue medications to use. And now there are even other migraine-specific medications to use, like ditans, which basically affect just one serotonin receptor as opposed to three with the triptans. And then there's also the GPANS. So a lot of different options out there. For the purposes of today, I want you to become familiar with the various triptans that we have for migraine. Now they're all generic. They all range in terms of how quickly they work in terms of time to onset or stay in the body. They come in different formulations. So remember we were talking about nausea or vomiting. Some of them are injectable, like sumatriptan, or intranasal, like sumatriptan or zomatriptan. And other ones do have orally dissolving tablets, like zomatriptan and rizatriptan. So really important considerations. This is a chart that you can refer to. I sometimes like using the orally dissolving ones because people can just put them in their wallet, keep it on them, and pop it in their mouth. If people don't realize they're taking a medication, they don't necessarily need water, etc. And then there are also non-triptans. So there's dihydrogonamine, and there are even nasal spray forms now of dihydrogonamine. So important things to know about when you're using triptans, they're best if used at the time of onset. So some patients may say, oh doctor, it really didn't work. It may be because they delayed taking it, they didn't have it on them, they were afraid to take the medicine, etc. So you really want to encourage patients to take it right away. They're FDA approved to be taken two days a week. They can be combined with NSAIDs such as such as naprosyn to try to prevent headache recurrence. And in terms of side effects, most common side effects can be a funny sensation over here. I tell them like in their chest, their neck can feel like an elephant on them and not to panic or anything. We think it's related to esophageal spasm and just know hopefully it will help the headache. Let us know we can try a different triptan. The other important thing for you to know about is there is a warning from the FDA about serotonin syndrome. It was based on theoretical concern. It was not based on data. And headache specialists went back and examined whether there was a heightened risk of serotonin syndrome with a standard dose of an SSRI or SNRI and a triptan. So that's for a standard dose. All bets are off if you're using super therapeutic doses, etc. But for a standard dose, it was not an issue. And I put the reference there. Triptans are contraindicated if there's a history of stroke or MI or uncontrolled hypertension. They are not contraindicated if the hypertension is controlled with medication. And they are relatively contraindicated after age 65. I mentioned rescue medications previously. I'll oftentimes use promethazine at doses between 12.5 to 50 milligrams at night. If someone has an ongoing attack, other headache specialists will oftentimes use prochlorparazine. But just to realize, we do sometimes use these to break headache cycles. Other acute treatments for migraine, including for status micronosis, which is an attack that lasts for at least 72 hours, could be IV fluids, the prochlorparazine, metoclopramide, or ondansetron, NSAIDs. So you can use Keterlach. You can use ibuprofen, naproxen. You could also use indomethacin. You can even use that rectally. Sometimes we'll do a medical dose pack. We might use valproic acid or a DHE. So it could be IV DHE, but also now also available in nasal spray forms. Let's talk about when to use a migraine preventive agent. We think about starting a migraine preventive medication or other treatment when it's on average four or more headache days a month. That's why it's so important that patients maintain a headache diary so that we actually know the frequency at which these attacks are occurring, and then also to see whether the treatments we're implementing are effective. Now, if somebody has two attacks a month and they're really bothersome, really disabling, they're missing work, school, et cetera, we might start talking about migraine prevention. If somebody has six headache days a month, but they're responding really easily to an NSAID, we might say, okay, fine, but beyond that, we should start talking about migraine preventive and implement that. We also talk about migraine prevention in individuals at risk for medication overuse treatment, or really just are not responding to acute treatments or have so many contraindications to acute treatments. The American Academy of Neurology has migraine preventive treatment guidelines. Unfortunately, they were put out in 2012, so they're kind of old, and I'm actually on the author panel for redoing this, so there should be new guidelines coming out, but in terms of the old guidelines, there are level A medications. You see that we have valproic, we have topiramate, we have propanolol there. For level B, amitriptyline did get demoted because their dropout rate was greater than 20 percent in the studies, and so it got demoted from level A to level B in the 2012 guidelines. You can also see there's menlofaxine there. There was a Cochrane analysis which showed that menlofaxine is not effective for chronic migraine, but it did have level B evidence for migraine in general, so it might be something to use more for episodic. You'll see level C, there are ACE inhibitors like lisinopril and ARBs like candesartan. There are actually some well-designed studies out now that show evidence, and based on Canadian Headache Society guidelines, I frequently will use candesartan because it's pretty well tolerated. You should note that there are certain medications here that are listed as not having good evidence. We do not use limotrigine for migraine unless you're trying to deal with aura prevention. We don't use gabapentin. We don't really use verapamil, so things to see here. Also, these are old guidelines, so you don't see onobatulinum toxin mentioned, although the American Academy of Neurology does have a guideline on onobatulinum toxin for migraine. It does have top evidence for chronic migraine, so that's 15 or more headache days a month, and then also you see this does not talk about the calcitonin gene-related peptide antagonist medications, which are newer, and so those also do have pretty good efficacy, and those will be in the new guidelines. If you're trying to figure out which preventive treatment to use, the American Academy of Neurology guideline says that evidence is insufficient to establish how to choose an optimal therapy. Treatment regimens therefore need to be designed case by case, accounting for efficacy, adverse events, coexisting comorbid conditions, and personal considerations, often trial and error is needed. I would be remiss to not say why we don't use opioids in headache medicine. In addition to the whole opioid epidemic, opioids just don't work well. In terms of acute migraine, there was no randomized controlled trial which looked at pain-free as a primary endpoint that demonstrated that they worked, and in terms of chronic migraine, initially there was a 26 percent decrease in pain, but the improvement declined over time. Patients did not show objective signals of decreased disability in terms of the ability to return to work, they weren't able to stop other medications and rely only on opioids, and a lot of them, more than half, required increased doses during the five-year period. In addition, patients violate their contractual agreements, use medications inappropriately, multi-source scripts, and try to fill them early or claim to lose them and request more, and so it's really not appropriate treatment for migraine. In my patients with migraine and comorbid depression, I'll frequently try to use medications that could help them or could be neutral in terms of their mood. So, for example, I kind of like using ACEs and ARBs because I feel like they're mood neutral, and even a study showed that there's a 50 percent decrease in the risk of mood disorder admissions, suggesting a possible protective role. I'll also use CGRP antagonists or autobotulinum toxin, although that's just for chronic migraine. In terms of autobotulinum toxin specifically, so treatment with it leads to a significant reduction of disease severity of both chronic migraine and major depressive disorder in patients comorbid with both conditions, and migraine intensity is related to depression and can decrease in migraine. There can be a decrease in migraine intensity score, leading to a decrease in depression scores. So, for example, in one study, 38 percent of patients with migraine had improved HIT-6 scores, that's related to headache disability, after a second round of autobotulinum toxin, and saw an improvement by at least five points in their PHQ-9 scores. Only about 10 percent of patients that did not have meaningful improvement in the HIT-6 had a decrease in PHQ-9 scores. And regarding those calcitonin gene-related peptide antagonists, well, CGRP reduces headache frequency and intensity in patients with comorbid depression. So, for example, there was a decrease or reduction of about five headache days a month for a quarterly dose, and about 28 percent had at least a 50 percent reduction in migraine days. There was also that decrease in about five headache days a month for a monthly dose, and 33 percent had a greater than 50 percent reduction in migraine days, and yet only about a reduction of two headache days a month for placebo, and only 13 percent had at least a 50 percent reduction in migraine days. So, we know that the CGRPs can be effective for both migraine and for depression, or patients with comorbid depression. I provide here some additional references for studies for how autobotulinum toxin for migraine can help with comorbid psychiatric conditions. And similarly, here's another reference for how CGRP drugs for migraine can be helpful in patients with comorbid psychiatric conditions. This table here shows how various pharmacologic treatments can be used for both migraine prevention and psychiatric comorbidities. That said, I do want to caution you with the fact that oftentimes these medications are used at completely different doses for migraine prevention and psychiatric comorbidities. So, we used to think, oh, let's kill two birds with one stone and just use one medication, but now that's not as much the thinking. The thinking is, why don't we try to figure out what's best for each condition, even if it means two different medications, and if it's one medication, great, all the better. But you can see there is a lot of overlap in terms of the treatments used. So, we use tricyclic antidepressants. We can use SNRIs. We don't really use SSRIs. The Cochrane review showed that SSRIs were not better than placebo for migraine prevention. We do use beta blockers like propanolol, which can be helpful sometimes for anxiety, and we do also use topiramate and dibalproic sodium. There are also supplements that are evidence-based. So, the American Academy of Neurology used to have a guideline showing evidence for these supplements. However, it got retired because we do not recommend Butterbur anymore. There was concern for liver toxicity, and so they retired the guidelines. But I do, in clinical practice, still use a lot of magnesium and riboflavin. The dosing is key. So, magnesium and riboflavin are both 400 milligrams. If I'm not mistaken, they're both 400. I tell patients that because what you get in a multivitamin or B-complex vitamin is not the 400 milligrams that the patients would need. There's also studies for CoQ10, also for fever funeralness, melatonin, and so forth. But I do use a lot of magnesium and riboflavin, particularly magnesium for aura prevention. I think it's extremely important to talk about non-pharmacologic treatment of migraine. So, first of all, there are various trigger factors. It could be missed meals, not eating on schedule, or drinking on schedule, like hydrating. Changes in sleep patterns, so going to bed at different times during the week and weekend, waking up at different times. So, really trying to maintain good sleep hygiene. There are other sensory stimuli, hormonal changes. So, for example, there's menstrually related migraine and menstrual migraine. So, changes in estrogen levels, but also changes in cortisol levels, alcohol, and stress. This slide shows some complementary therapies for migraine prevention, but I really want to emphasize today that we have grade A evidence-based behavioral therapies for migraine prevention. They're grade A, first-line treatments that can work alone without preventive medications, and they are cognitive behavioral therapy, relaxation, and biofeedback. And I want you to know that there are CBT manuals available for migraine that you can either use or offer to psychologists that you work with. And if someone is trained in CBT for other conditions, they can easily do CBT for migraine. So, there's a book you can buy online by Dr. Todd Smitherman and colleagues. That's Todd Smitherman, and he basically and his colleagues explain how you can do CBT for migraine. And then there's also a free manual that the VA has developed for how to do CBT for migraine. So, I think this is really integral. Studies have shown in pediatrics that the CBT actually yields better results than medications. And I'm a big believer in this, and as you see, I do a lot of research in this area. Really, the best treatment involves accommodation of medication and behavioral therapy. Both of the other speakers today are going to be talking a lot about migraine and headache and stigma. And so many patients say to me when I refer to them for behavioral therapy like CBT doctor, you don't believe me. You think it's all in my head. And I will say to them, well, it's one brain, one organ, so same neurotransmitters. And I will actually talk about this study here that basically looked at patients' brains, the neurocircuitry, pre and post-CBT for migraine. And so, they found that there were changes in brain structure pre and post-CBT. So, headache frequency decreased from 15 headache days a month before CBT to 10 after CBT. After CBT, there was greater brain activations in frontal regions involved in cognitive regulation of pain. And they found that CBT increased connectivity between the amygdala and frontal regions. And also, there were associations between brain activation and amygdala connectivity with a reduction in headache frequency observed. I also want to speak a few moments about emerging non-pharmacologic treatments for migraine because I think a lot of providers are practicing these, the third wave ones and others that we're going to be talking about. But I do want to emphasize these are emerging. There's research being done, but they're not the grade A evidence-based ones I just mentioned. And those are cognitive behavioral therapy, biofeedback, and relaxation. So, some in the audience may have heard of MBCT. So, that's mindfulness-based cognitive therapy for migraine. And it was initially developed to prevent depression relapse. And we've studied MBCT for migraine. It does reduce migraine-related disability. So, in a study of MBCT for migraine versus usual care for migraine patients, Dr. Singh, one of my colleagues, I was on the team, found that headache disability mean scores decreased more from month zero to month four in the MBCT group than the waitlist treatment as usual group. And severe disability category fell significantly from 88% at month zero to about 67% at month four for the MBCT group. So, MBCT may be more effective in patients with episodic migraine than those with chronic migraine. And there's currently an NIH study investigating this. Some of you also may have heard of MBSR, mindfulness-based stress reduction. It's usually group-based. It doesn't need to be done by psychologists and so forth. And my colleague, Dr. Rebecca Wells at Wake Forest, who's been studying MBSR for some time, she's had NIH grants on this, and she found that MBSR demonstrated significant benefits on headache duration. There was also a 27% reduction in migraine days per month, and found that MBSR is more effective than simple stress management. And so, she's doing ongoing studies for this. Acceptance and commitment therapy has also been studied by my colleague, Dr. Grazzi, in Italy, and in the paper that she published down below, they found that in patients who were treated with it, there was a decrease in monthly headache days in the ACT group, with a reduction of three and a half days a month, no change in the control. And then, there was also a decrease in monthly medication intake in the ACT group, with no change in the control. We also emerged on how acupuncture can be helpful for migraine prevention. I personally still prefer the behavioral therapies, those grade A evidence ones. I really want you to remember the cognitive behavioral therapy, the biofeedback, and the relaxation, compared to acupuncture, because those are grade A. And also, in terms of self-advocacy, patients can do those on their own. They're not dependent on going for acupuncture appointments, but I do want to bring this to your attention, because it is a valuable treatment for some of our patients. Treatments, as you're well aware in psychiatry, if patients don't take medications, they're not going to see the benefits. If patients have hypertension or diabetes, and they don't take the medications, they're not going to see benefits. And if they don't go to the psychologist for behavioral treatment, they're not going to see benefits. Well, similarly, unfortunately, in a lot of our patients, we may prefer them for behavioral therapy, but there are a lot of issues we have in terms of initiation and adherence to our recommendations for behavioral therapy. Access to behavioral treatment is limited. Few patients with severe headaches and migraine, less than 1% of the population, report using biofeedback. They are using deep breathing exercises more, and they are using mind-body interventions more, which is why it's exciting to understand MBSR and things like that that are more accessible for our patients. But there are still many questions unanswered, and we really need to improve access to behavioral therapies that are evidence-based for our patients. So my team has really looked at how can we improve initiation? How can we improve access? So we've studied motivational interviewing to try to get patients to go for behavioral therapy. We've also done a lot of work on smartphone technologies, including using the HeartMath Interbalance, a little thing over here that you put on your earlobe that connects to your phone to really learn how to do some heart rate variability biofeedback. We also developed an app that is called Relaxahead that has a headache diary and progressive muscle relaxation therapy. And these are just some of the publications that we've published using Relaxahead. All of this to say that we really do want to try to have more scalable, accessible forms of behavioral therapy available for our patients. And in the meantime, you can still Google and find links for relaxation on various sites, including in different languages, so that you can offer these, you know, your patients some behavioral therapies. So I'm going to conclude by talking about some devices that we have for migraine. I just mentioned a minute ago about some heart rate variability biofeedback apps and wearables. So in Norway, they developed the CereBreathe, which is basically an app that also has body measurements for physiologic data capture with wireless sensors, teaches patients how to relax and breathe and how to then adapt their relaxation so that they can gain the most with the heart rate variability biofeedback. And this is another one that was developed called Juva from Migraine. The video camera was tracking heart rate, heart rate variability, blood volume, pulse, respiratory rate. They were also trying to capture the skin's galvanic response and oxygen saturation. And this is the reference here for the HeartMath Interbalance study that we did. It was a randomized controlled trial looking at the interbalance versus usual care. And we found that of those who did use the interbalance sensor, they did actually have improvements in their quality of life. So either you can help to deliver the cognitive behavioral therapy relaxation or biofeedback, or you can turn to some of these devices that are now starting to offer it or sensors and smartphones and wearables and so forth. But again, the great aid treatments are the cognitive behavioral therapy, biofeedback and relaxation. And then finally, there are FDA approved modulatory devices that can also be used for the acute treatment or preventive treatment of migraine. And again, these are FDA approved devices. Unfortunately, insurance is not covering them at this time. We had even had other devices out and unfortunately now we're insurance coverage issues and so forth. But I think, as I mentioned before, it's a really exciting time in headache medicine because we have so many different options. We have medications, we have behavioral therapies, we have devices. And so I would encourage you to learn about these devices, offer them to patients, because I think that there's really low risk in terms of using them with our patients with psychiatric comorbidities and other comorbidities in general. Thank you again for attending our session. I hope that you will continue to learn more from the other speakers. And please feel free to reach out to me with any questions. Again, I'm so sorry I could not be there with you today. Thanks again, bye bye. Thanks to Dr. Minnan and yeah, she is not available to come today, but we do have her on the phone for the Q&A after if there's any particular questions you wanna ask her about her talk. I'm now going to talk about what you as a psychiatrist need to know about treating a patient with migraine. And this is going to be from the perspective of a headache medicine psychiatrist myself. I work in a quaternary care setting where we have an inpatient headache unit where we infuse people with ketamine, lidocaine and high dose neuroleptics, DHE, magnesium and attempt to lyse their headaches. And I'm not gonna be talking about that because I think that's way beyond the scope of what I want you guys to know today. But what I will talk about is what do you do when you have a case coming to your office? So let's say in our imaginations that you do have a woman who comes in with depression and anxiety and you treat her for medication management psychotherapy. She's wearing sunglasses and asks you to turn down the lights because it's hurting her head. And this is going to be one of those facetious examples, but all of these answer choices have been provided to me in real life by other providers. Do you refuse her request because it stems from a desire to be accommodated by the therapist? Do you demand that she remove her sunglasses during the session as she's using them as a form of resistance to psychotherapy? Do you want to explore deeper for the presence of a fictitious disorder? Or do you want to spend a couple of minutes gathering more history regarding her photophobia and the possibility of the presence of migraine? Unfortunately, I've had a lot of patients that have described to me that their therapist and psychiatrist have given A, B and C as actual things that they were demanded of during sessions. Migraine has a, associated with it, a tremendous amount of stigma. And this stigma comes in many different forms. A lot of the stigma for migraine might have been developed only in the last 200 years or so as men became the primary medicine providers for the population in the form of medical doctors. And we're trying to figure out how to deal with that stigma and we're trying to really still deal with a lot of the stigma that was developed during Victorian era. And that included that the patient with migraine might be a whiner, maybe they're hysterical, they're lazy, they're being weak. Being effeminate is a major barrier for why men with migraine don't seek care or that they're incapable of handling their stress and their problems. There is definitely a dichotomy between men and women in how they are viewed with migraine, where men are almost kind of congratulated for having migraine for working so hard and being so detailed, oriented, and ambitious, while men are considered to be neurotic, unnecessarily stressed, and nagging their husbands. This stigma also goes to a professional realm as well. I've had many of my own colleagues almost disparage me for working with patients with migraine, saying, well, aren't they all borderline? Aren't they all somatoform-preoccupied? Aren't they hypochondriac neurotics who are drug-seeking? Are they malingers? And the stigma also continues into research as well. Despite the fact that migraine is one of the top diseases in the entire world in terms of disability, it is not extremely well-funded in comparison to its level of disability. And even when we see pharmaceutical stock photos of people with migraine, this is the typical photo that you'll get, an extremely well-dressed woman with makeup holding her temples together. Or perhaps they'll show some children in the background as the possible cause of their migraine, or perhaps suggesting that this patient with migraine is unable to take care of children. When we do an epidemiologic study of people with migraine, about a third believe that people who use their migraine as a way to get out of work or school commitments, almost half feel that they should be easily being able to take care of migraine. After all, they've had headaches in their life as well. And a third might feel that migraine is a result of their unhealthy behaviors. We get inadequate education in medical school. We probably learn maybe one lecture about the top three migraine disorders in medical school. And I think by our intern year, we're told that if you have someone with headache, provide them a Furoset. Similar to maybe we talk about dizziness, we just provide meclizine, and that's all we need to learn about dizziness. When we talk about constipation, we have about five different dozen medications that we wanna give for that. The reduced funding, as I mentioned before, it's the worst ratio of NIH funding to disease impact. And as a result, there can be internalized stigma as well. A patient might experience shame, poor self-esteem, poor engagement in treatment, and reluctance to seek care. When you look at the Venn diagram, migraine, anxiety, and depression all contribute together. Migraine associated with a decreased chance of remission depression. Depression is associated with a poor response to migraine medications. And anxiety increases with migraine frequency. And when you put stress on top of all of this, a stress-causing increased inflammatory response, you see that all three of these are comorbid and working and playing against each other. When we talk about migraine, I think we all think about migraine as being an attack, a pain attack to the head. But migraine disease is actually a cycle. And there's a lot of psychiatric comorbidity that occurs interictally outside of the migraine attack. Patients who experience migraine and have periods where there's less migraine severity, they might have anxiety about when their next migraine attack occurs. My headache right now is a four out of 10, but if it goes to five out of 10, do I need to cancel today's plans? Do I need to take my medication? Which medication did my doctor tell me I should have taken first? And then if that one doesn't work, I go to the next one. And all that can really increase anxiety. There also can be avoidance behavior, kind of similar to what you might see in someone who's got social anxiety or social phobia, or agoraphobia. And there can be a compulsive use of acute abortive drugs in trying to prevent the next pain cycle from occurring. Before headache pain occurs, we talk about a prodrome of symptoms. And the prodrome of symptoms, in the hour preceding can include aura, but in the hours before the migraine, you might experience more depressive symptoms, more drowsiness. Some patients even experience euphoria and hyperactivity and irritability. There may be increased talkativeness. Concentration might be decreased. Yawning might occur. As you can see, a lot of these symptoms sound very psychiatric, but some patients do recognize that this is the beginnings of their headache coming on. There might also be behavioral changes, including a desire to not eat, increased thirst, some food cravings, as well as GI symptoms. A lot of patients feel that chocolate, for example, causes their migraine. And in fact, what we now know is that a craving for chocolate is actually a physiologic response to the migraine. It's just that your body's thinking that it's the chocolate that causes the migraine and the migraine is happening because you were craving chocolate. And then after the migraine attack, there might be a symptom of lack of energy, a tiredness, somnolence. There might be unhappiness as well as relief and concentration difficulties. The number one mood disorder that is most common in migraine is major depression. It is about two to four times higher than in the general population. But I wanna make an important case here about bipolar disorder. There is a strong concordance of bipolarity with migraine. About one third of patients with bipolar disorder will have migraine. And a family history of bipolar disorder will actually increase the risk of migraine four times in offspring. We don't know why there is this concordance. Perhaps the two disorders just live on the same chromosome. But there's people trying to study this. And as a result of that, when we're actually using these medications as preventives, including tricyclics or SNRIs, we wanna be cognizant of the fact that there might be bipolarity present in our patients. Anxiety, as I mentioned, is very high in patients with migraine. Personality disorders, there is a slight increase. Although I think that a lot of personality disorder that develops with migraine is very common to the kind of personality structures that occur in other people who have chronic disease during their adolescent and teen years. Think of sickle cell disease or type one diabetes, where having that kind of disease really changes in the way that there's an outlook about caregivers and providers and what kind of medication works best for them. ADHD does have an increased correlation in migraine. And substance use disorders, which is a tricky one because I will talk about medication overuse headache. And then there's a kind of a spectrum between where medication overuse headache ends and where substance use disorder might begin. There's a lot of other comorbidities that can occur in migraine. Stroke, for example. And we know that in someone who has migraine disorder, we wanna avoid estrogen-containing compounds. Cardiovascular disease as well. Crohn's disease can cause extra GI side effects, including tension type or migraine headache. Sleep apnea causes headache as well as depression. Restless leg syndrome is often co-associated with depression and there's an increased sensitivity to dopamine antagonists, which we might use for the treatment of migraine. Fibromyalgia is also very commonly seen in our patients. I bracket here these three more rare disorders, including iliodendrose postural ophiostatic tachycardia, which is POTS, and mast cell activation syndrome. I'm not gonna talk about these in great detail, but you will encounter a patient once in a while. At Jefferson, we'll see about five of these per year, who have this tetrad of disorders. When you see one, you think, oh my God, one person couldn't have all these possible diseases with a list of 20 potential allergies or intolerances in their EMR. But when you see five of them every single year, you start realizing that there is some small population that do have all these disorders together. And being able to recognize that this is something that does occur would be very helpful for your patients. Compared to bipolar disorder, bipolar disorder with migraine patients are more likely to have an earlier onset of their bipolarity, greater psychosocial impairment, higher rates of suicide, and more severe and more frequent mood episodes. And this is interesting because migraine is more common in bipolar disorder type two than bipolar disorder type one. And because bipolar disorder with migraine are more likely to have rapid cycling, we wanna be careful when using antidepressants in patients with potential bipolar spectrum to reduce the chance of any mood exacerbation due to the antidepressant. Now, while we talked about how those guidelines are over 10 years old, and they do need to be redone, valproic acid does have evidence that it might help patients with migraine. I think when they reach our level at Jefferson, we find it's not nearly as helpful as we would like it to be. But since valproic acid is so good for bipolarity, one could consider it perhaps above others. While lamotrigine does not have very good evidence at this time to be helpful for migraine, we have noticed anecdotally that in some of our patients who have vertiginous migraine, that's migraine with a lot of dizziness, that lamotrigine may be potentially more helpful in those cases. While lithium has no apparent benefit in migraine, it might help with other headache disorders, particularly cluster headache, and it can be used at the same kind of doses that we would use lithium for bipolarity. We do use dopamine antagonists for aborting a headache, and that can be often in the ER setting with medications such as droperidol, haloperidol, chlorpromazine, prochlorperazine, metoclopramide, and phenazine. But among the atypical second-generation antipsychotics, the only one that we have seen to be potentially helpful to abort a headache is olanzapine, and maybe that's because it is the dirtiest atypical that we have, and it works in some way that we don't yet know why. We might use five milligrams of olanzapine nightly or twice a day for several days, and it can abort a headache and potentially even avoid a hospitalization. But we have no data suggesting that taking it daily provides any greater benefit for most patients, and I think I would worry particularly about the metabolic risk factors of doing something like that. I have no real good data to support this apart from my own anecdotal experience, but the partial dopamine agonist antagonist that includes aripiprazole and brexpiprazole, I have had patients say that they felt that it made some of their headaches worse, and perhaps that might be a dose response effect depending on the particular agent and what particular dose has more preferential dopamine agonistic effects. I think the dopamine agonistic effects might make some people's headache worse, and when you get to a dopamine antagonistic effect, potentially maybe that goes away. But I try to generally avoid these for patients that might need an atypical antipsychotic. So among the tricyclic antidepressants, the one that has the most evidence is amitriptyline. Amitriptyline is typically used as a headache preventive at doses of 10, 25, 50, maybe rarely going up to 75 or 100. And nortriptyline we might also use with those low doses as well. There is very little data supporting the use of using a tricyclic with another serotonergic antidepressant, either in the psychiatric literature or in the headache literature. This is the only study with only 88 patients in it. And in this one they used, oh I don't have the, I don't have the footnote on it. But in this study they used citalopram with amitriptyline and versus either one of those agents alone. And they did find that that particular combination afforded greater benefit for both the depression symptoms and the headache prevention symptoms than either agent alone. That being said, with very little evidence, we have a lot of patients who are on both agents. They might be on an SNRI with a TCA or an SSRI with a TCA. And one has to kind of try to weigh the pros and cons and on examination of the patient, whether or not there might be too much serotonergic involvement. I've had plenty of patients that seem to do fine on high doses of multiple serotonergics and they require additional education, avoid additional serotonergic such as tramadol. But I have others that have been started on multiple serotonergic and they're showing signs of tremor and irritability and GI upset. I'm like maybe we need to kind of reduce some of these serotonin agents. Among the SNRIs, most of the data is with venlafaxine and duloxetine and most of it is with migraine with aura. But since migraine without aura is a lot more common, we do try to use these medications as headache preventives. When it comes to using the SNRIs, venlafaxine and duloxetine we go to high doses, over 150 milligrams of venlafaxine to 25 or 300 if possible. And with duloxetine we might go up to 120 milligrams. It's unbelievable how patients with headache are able to tolerate the side effects of duloxetine at those doses when none of my patients who have depression without headache are able to tolerate anything about 60. Regarding milnasopran and levomilnasopran, since these are newer medications that are still brand name, we don't have much evidence that they help with headache. There is only one small retrospective study looking at milnasapirin, and it seemed to have improvement in migraine symptoms at average doses that would be used for depression. So potentially these could be heartening in the future, and I have noticed that patients do find that these can be very helpful for them, and they have a different side effect profile than some of those older S-centerized, which could be potentially beneficial for your patient. But like Dr. Minnan mentioned before, the data regarding SSRIs is very conflicted or negative. I might turn to an SSRI only in the patient who has not seen any benefit on high doses of tricyclics or high doses of S-centerized, and yet they have a lot of anxiety and depressive symptoms. And I say, well, maybe it's time for us to kind of try to stop trying to kill two birds with one stone. Your anxiety might be much better suitable with sertraline with a lot fewer side effects. And then I will transition back onto an SSRI. Bupropion is a difficult one to answer. When you look at the manufacturer's label, 27% of people report headache on bupropion. And I've had patients that have noticed bupropion make their headaches worse, and I have others that have been on bupropion without any apparent exacerbation of their headache disorder. But I do avoid the azidones, trazidone and valazidone, I'll talk about that more in a minute. Buspirone is usually very well tolerated as one would expect from buspirone. Mirtazapine might have some benefit for tension-type headache. Vortioxetine, perhaps, if you wanna use it for depression, but I see no particular benefit from a migraine perspective. Nearly every antidepressant lists headache as a side effect. Telang et al. are the only ones that actually performed a meta-analysis looking at the risk of headache in patients who are put on an antidepressant. And what they found was that, yes, when compared to placebo, SSRIs appear to significantly increase the risk of headache. SNRI appears to have a decreased risk of headache, although they did not find that to be statistically significant. And when they compared the SSRI to the SNRI, there was no evidence for any significant difference in risk. In fact, they went on further to say that from what they were able to statistically determine, it seemed that the risk of getting a headache when starting an antidepressant seems no different than the risk of getting a headache regardless of whether or not that antidepressant would have been started, meaning it could have been just due to chance. But this is the graph that looks at that particular study, and the line is the confidence intervertebral crossing one. We see that escitalopramine on the SSRIs might have slightly increased risk of headache, and bupropion both seem to have a greater than one risk ratio. I want to call your attention down to the bottom with trazodone and velazodone. Now, these meta-analyses were in people with depression. These were not meta-analyses in people with migraine. And in both of these papirazine derivatives, trazodone and velazodone cross one in terms of their risk with causing headache. I think that if this study were repeated among patients with migraine, we would see a lot more positive significance. And that is because of the metabolite that trazodone and velazodone all share. These agents are papirazine derivatives, and they get converted in the body into M-chlorophenolpapirazine, or MCPP. We use MCPP, and we feed it to mice to give mice migraine so we can study migraine in mice. The dose that would achieve the same plasma-level concentration of causing a migraine-like headache in a human is probably about 100 to 150 milligrams of trazodone. I don't have enough data to suggest what would be the appropriate velazodone dose to achieve that. What would happen in patients, and we've actually known this for many years, but our use of trazodone has really reduced since the 1980s, that migraine-sensitive patients do get migraine headaches from trazodone, possibly three hours after the dose. So I have plenty of patients that say, yeah, trazodone helps me get to sleep, but then about three hours later, I wake up with nightmares, anxiety, and a headache. So while it might not be causing your migraine, it might be definitely perpetuating part of the cycle. I try to avoid using them at all costs. And there's more information, I'm gonna keep going. As I've mentioned already, what causes serotonin syndrome is still a main source. That's me. So I wanna talk about serotonin syndrome briefly because of what causes serotonin syndrome. Dr. Stahl was partially correct in his MAOI lecture earlier this week that serotonin 2A is the primary subtype of the serotonin receptor associated with severe serotonin syndrome, the one that gets you to the ICU. But there is a possible mild to moderate contribution of the 5-HT1A receptor. And because these two receptors are co-located, it's possible that in some cases you might get patients who report a kind of more mild jitteriness, an upset stomach, that one could call on the, let's say, spectrum of serotonin syndrome. And there are other genetic factors that we are still trying to identify. One of the theories is 5-HT2A shunting. And in this situation, you might have an atypical antipsychotic that works as a serotonin 2A antagonist. And by doing so, you're shuttling the SSRI or the SNRI to the co-located 1A receptors. Now, this can be beneficial. This is why we think that atypical antipsychotics are helpful to improve depression because you're getting more of the effects on the 1A receptor. But it could also cause some mild serotonin toxicity. Now, the ERGOT derivatives like dihydroergotamine, which we also use, do have affinity for all receptor subtypes, just like the serotonin reuptake inhibitors. And while they do happen to have a 20-fold less affinity for the 2A receptor, there could be potentially a therapeutic window above which you might see some signs of serotonin toxicity. To reiterate from before, when the FDA put their 2006 advisory, this was based on case reports and theoretical ideas. A position paper done by the American Headache Society showed that there was insufficient evidence to limit the use of triptans with SSRIs and SNRIs. More recently, the JAMA Neurology, they published a retrospective review of prescriptions in the greater Boston area. And with this rather impressive end, they were only able to find two credible cases of serotonin syndrome among 48,000 prescriptions. Right now, as we speak, there is somebody, probably hundreds of people, who are taking a triptan while they're on an SNRI and they're not dying. There is one possible explanation based on animal models that I do want to include, which showed that chronic treatment of triptan, which is not the way that we prescribe triptans used for headache, might lead to a downregulation or desensitization of the 5-HT autoreceptors and perhaps increases serotonin synthesis rate. And if there's more increased serotonin synthesis rate, then maybe there's a diminished neurofeedback signal for serotonin synthesis, which means that repeated exposure to triptans on a daily or multiple daily basis could resort to a serotonin syndrome development. But we're not supposed to be prescribing more than 10 doses of triptans per month because of the development of rebound headaches that can occur from that. Medication overuse headache, which some people find to be controversial, but it is a real situation. And this can occur from multiple different abortive substances that are used in migraine. When using a migraine abortive and it works, you wanna use it again. But what happens is over time, and the agent that is used differs in how quickly it can happen, you can get a secondary, almost baseline headache, like a kind of four out of 10 headache that will always be there. So your abortive might get your headache from a 10 out of 10 back down to a zero in the beginning, but then over time, it only brings it down to a four. It keeps working, but you're continually having a secondary headache, and that's what we call medication overuse or medication adaptation headache. And overuse is probably a bad misnomer on it because these patients don't think that they're overusing medications. We're not using these doses at high levels. We're talking about 15 days a month of using an NSAID, more than 10 of a opiate or a triptan. So by no means are these doses, with a patient saying, I'm not really using it, I'm not using it every day, but it's enough to actually create this syndrome to occur. And as a result, when we have patients who might be in the hospital for a headache treatment, we might have to detoxify them from certain substances. While NSAIDs do not require any detoxification, opioids would. I don't, we would use the same methods that one would be normally accustomed to in detoxing opioids. With combination analgesics that include butalbitol, so that would include furoset, which is a combination of acetaminophen, caffeine, and butalbitol, we have patients that might be using 10 or more of these tablets per day, and they're kind of stuck in a cycle. Butalbitol withdrawal can occur. In patients with, who need butalbitol detoxification, we don't have very good data on how to do it. There's theories and ways of doing it. One would be loading a patient with phenobarbital until there is sedation, but I think this leads to a rather high barbiturate burden. We don't know if this is the safest option to go, but unfortunately, there is a study that show that patients don't reliably report the amount of butalbitol use. So it might be better to have a loading dose protocol such as that in case your patient is using much more furoset than they are telling you. Conversely, though, you could use a fixed dose taper. We feel that 100 milligrams of butalbitol is equal to 30 milligrams of phenobarbital, and one furoset tablet has 50 milligrams of butalbitol in it. So you can use that conversion ratio to figure out how much phenobarbital someone might use. We typically will make our own decisions based on a variety of other factors whether or not we want to give the full equivalent dose of phenobarbital or maybe less than the full equivalent dose, and then 50% decrease every day or two. Finally, I want to talk briefly about headache and ECT and transcranial magnetic stimulation because it is true that I think about a third of patients who get ECT will report a significant headache from the treatment. And while migraine and other primary headache disorders are not a contraindication for ECT or TMS, our patients might be worried that their headaches might get worse from the treatment. It seems that both ECT and transcranial magnetic stimulation do release calcitonin gene-related peptide, which is the inflammatory compound that causes migraine. We don't have any clinical data suggesting that using a CGRP antagonist prior to ECT or TMS would reduce the risk of developing headache from ECT. So if anybody out there is interested in doing a study with me, you can let me know. We do have some evidence that either tryptan or acetaminophen or ibuprofen is enough to reduce the incidence of ECT-induced headache. And regarding transcranial magnetic stimulation, we do have a device that works on transcranial magnetic stimulation. Unlike TMS for depression, which is dual-phased and applied to the dorsal prefrontal cortex, single-pulse TMS for migraine is applied to the occipital area. This can be effective for both migraine, abortive, and preventive benefits. It is unfortunate that it is probably the most expensive device that you can purchase. It's over $1,500, I believe, and it's not covered by insurance in any state but Utah, I think. The symptoms, side effects are rather low. And you can't, of course, wear metal or anything else that you would attribute to an MRI, for example, that shouldn't be used in patients for this device. It did go, the company did go bankrupt, but is now back online, and this device is available. So I wanna circle back, you know, in the images of migraine that I showed you regarding stigma, this is actually probably the most common example or image of someone with migraine. These patients are very sick. They have photophobia and phonophobia, and they can't get out of bed. So with that image left, I will take you to our final provider, speaker today, which is Dr. Thiem. I am, hang on, I am Dr. Chom, I am a, let's see, hang on a second, oop, how do I go forward? There we go. All right, so I am presenting, I wanted to talk specifically about veterans in the military population. I am a prior Army psychiatrist. Just by a show of hands, anybody here a veteran or a military provider, anybody? Yay, okay, anybody here work with veterans or military? All right, so this one is actually for you. So I started off my career in the military medical school with uniformed services, and so this is one reason why I wanted to really talk about this. So this is one of the things, so why are we here today? Past president of the American Headache Society was a psychiatrist. One of the things in the American Headache Society, we have a behavioral section that is composed of psychologists and psychiatrists and neuropsychologists. And so we also want to be able to empower all of you and healthcare professionals to improve headache and migraine care. So I say that I'm just a regular psychiatrist. I work in the VA system, and I also work in a, when I got out of the military, I actually worked in a private practice section, and I saw that many of my patients struggled with headaches, especially with veterans. So again, I don't have a specialized headache center. I'm not a neurologist, so I see that patients are struggling with both mental health disorders and migraine, and it's a huge challenge working with access to care. How many people here have patients who have migraines or who have headaches? Anybody? How many patients have difficulty getting into care? And that's a huge struggle. And the same thing is, there's a challenge with patients getting into accessing us, with only 55% of psychiatrists take health insurance, so you can imagine this challenge with neurologists and headache specialists. So by the time they see us, they've already struggled with getting access to care. And so trying to see another specialty for headache is even a harder time. Not all neurologists and medical care providers, not all primary care providers understand headache. So the likelihood of them seeing a neurologist or a primary care provider who understands headache is necessarily helpful. And I've had patients who've gone to primary care and they are told, oh, go see your mental health provider. Especially if they have a mental health disorder, they are automatically referred to us. And so let me go here. So having been, and when I got out of the military, I've worked in community mental health and private practice and then the veterans. I have a tale of three different ones. So in community mental health, I've had a case where this is a female patient, she presents with a severe headache, slurred speech. And she goes to her community neurologist because she has movement problems. And the community neurologist tells her, oh no, just go see your psychiatrist for psychotherapy for your, or no, for hypnotherapy for your past trauma. And so I had a word with that neurologist and she didn't back down. But again, that just kind of goes with the stigma because that neurologist happened to be biased against, she thought that patient had a conversion disorder and didn't want to see her. Private practice, I had a severely depressed patient who had treatment resistant depression and she figured that she already had headaches but she thought they were normal because she would sit in her home with lights out and she said, well, it's not as bad as my regular depression. You know, I just figured it was normal sitting with the lights out all the time and since I could get out of bed and walk around and it wasn't as severe as my severe depression so therefore it was normal. That's why I hear a lot with my veterans where they learn to think that the migraine is normal and to them, a migraine isn't a migraine as long as it's not debilitating in bed, in the dark room and they can get out of bed. So especially for those who lived with severe depression, to them, being able to operate and be out of bed, that's good to them. In the words of Monty Python, the famous, it's just a flesh wound for them. So to them, that's not that bad as a migraine. So migraine, it's not incapacitating so therefore it's not a headache. And it's the same thing with a lot of veterans. I had that where another female who was seen in her pregnancy and she had to stop for Botox treatment and so many times in pregnancy you'll see is estrogen is very similar to depression and so a lot of migraines will go especially women with migraines the migraines will follow along with the depression because estrogen migraines will also follow estrogen and so what will happen is their depression and the migraines will follow along together so it might be better during pregnancy and then in the postpartum period the depression and the migraines hit like a like a vengeance and so that's what happened with her and so we tried to find her a neurologist and unfortunately that didn't we weren't able to find her one very easily because they decided that she was but seen by a that that got denied because of logistical ones because no one wanted to see her because she was breastfeeding and so in community mental health this is really difficult because even in the cases like a red flag they happen a lot of times they don't don't even access to regular primary care anybody here working community mental health no so you probably seen this where people might not even have access to regular primary care so you're it if they're looking enough to see a neurologist or even looking up to have primary care especially if they're sick enough you are oftentimes the primary care provider for that patient pretty much have little to nothing to treat them with and so trying to find that any kind of treatment is based off of whatever fee based options they have private practice is a little bit easier because if they have money to see you you know they have money to see other ones so and then veteran clinic is a little bit easier but depending on what VA you're at depends on what access you have because the primary cares might be swamped on oftentimes the veterans might be hesitant to open up with primary care and oftentimes they are more open up to see you because once you've established a treatment plan with them they may be more open with you and so I'm gonna skip this part and so this is one of the quotes ahead with one of my veterans says I don't know what we're supposed to do if we show that we are in pain we are accused of embellishing exaggerating symptoms and told to go away but if we stay calm and we maintain our military bearing despite very bad pain they think we are faking and send us to mental health we can't win for those of you who work in the VA is anybody familiar with this and really a rings true because it's the military bearing so we do have headache centers of excellence so I'll let you see this slide we do have copies of the slides will be able to send out now fortunately there's only 14 of these in the in the military in the DOD or in the VA system so we while we have these we don't have enough of them and we're developing more regions of them and so one of the big things we see in the military or head injuries if you have treated a veteran most likely they've had head trauma even if they don't realize this and oftentimes because of the head head injuries a challenge with this is that has become very political just like the diagnosis of PTSD and so oftentimes if it's and they can't even necessarily even admit that they've had head trauma because depending on the politics behind it they may not have been diagnosed with this and so oftentimes it may not have been disclosed or reported one example of this was in 2020 after January 6 there were a lot of retaliatory strikes from that and if it was declared that no injuries occurred nobody can report it then so if some kind of political incident happened and they were told no injuries occurred any sailor marine airman's not going to be able to report that if their commander told them you cannot declare a TBI how then are they supposed to go and report a TBI so there's a lot of catch-22 with this in the military so just because they didn't report it it may not have been their fault in that sense that they may have had injuries that did not get reported but again so that becomes a very difficult situation in this so this goes again a lot of times they'll stop mentioning headaches or treatment in the military because they give up they had him I had one history I went back and looked in the chart and one soldier he was reporting headaches but then every time he started talking about a headache he was told oh well you're just depressed you have a headache so it's all due to your mental health so I had one who every time he started talking about his depression and trauma he had a headache so attributed to his mental health so it's a high comorbidity with a lot of other mental health many have struggled with treatment and so this is where oftentimes in mental health where are the ones that often they can develop alliance with and so I'm gonna try to get this so one of the time so oftentimes we kind of develop a dual diagnosis approach and so like you've seen before with that prodrome a lot of times I've seen we see a lot of high comorbidity with PTSD even though it's not necessarily diagnosed in the sense with the headaches and and the headaches and the dual diagnosis so oftentimes you see that prodrome that your ability cognitive dysfunction like to say the body remembers trauma and you can see this I'm going to go through here we've talked about the risk of suicide is there's a lot of risk of suicide along with migraines it's one of the pain conditions that have the higher risk here and so if you familiar with dr. Gallagher's work on suicide crisis syndrome one of the thing I like about this with migraines if you look at this the premise of the suicide crisis checklist is the frantic entrapment affective instability loss of cognitive control disturbance and arousal and social withdrawal which actually are all parts of the vagal nerve and so one of the things I like to do with the military service members anybody's familiar with polyvagal theory this is what I did for the military guys and so we made the yellow is kind of this polyvagal theory where a lot of them are kind of get stuck in the yellow mode which is the sympathetic nervous system where they get stuck in this where their priority there is safety and security where emotional regulation is not required cognitive flexibility is poor it's not needed because you're a mission focused because if you're downraging the military you don't need that you just need to fight your your primary goal is safety socially you're focused on looking for the enemy the vagal nerve at this point you're you're prying for high pitches and low pitches and which are those tones associated with danger the red this is the dorsal vagus this is the more immature vagus this is where you are this is where that's the I think of it as a thousand-yard stare this is the one where they're prone for survival and emotional regulation does not exist the homecoming one is the called rest and relaxation so parasympathetic nervous system and so what happens a lot of military the same thing with migraine they get stuck in the yellow or the red that little arrow there is what is the vagus nerve that's the balancing system what you want to do is have that be able to be balanced between the yellow and the green so what happens in the hyper arousal tend to get stuck there and so what happens is you want to be able to treat with the migraine the migraine as well as that frantic entrapment and as well as the sympathetic nervous system if that makes sense so oftentimes that we're doing with a lot of our militaries we're treating the migraine we're treating that hyper arousal and then also a lot of them are at risk for that suicide crisis syndrome and oftentimes we found that a lot of them what's really neat with the suicide crisis is none in that one there's no actual asking them if they're suicidal it looks at that biomarker or it looks at that that hyper arousal all that part of the vagal nerve in that part and so one of the things anything that helps act on that vagal nerve helps comb that and move that what we call move that vagus nerve towards green so one of the things that we've been doing at my VA at least is actually using the trigeminal or transcutaneous vagal nerve stimulation let me show you so you've heard of some of the neuromodulation devices so of these ones the one on the third one that's this one right here it's actually that tried transcutaneous vagal nerve one and then the one on the fourth one is the trigeminal nerve stimulation and the occipital nerve stimulation and so we haven't been able to use that one because the VA doesn't have that one but all the three devices on the first three the VA actually approves and has and so for those of you who work at the VA they actually have those and the third one is a dual diagnosis one of the first one I also look at that one there are some proof that trigeminal nerve stimulation might help with ADHD as well as PTSD and major depression disorder but the big one for PTSD I look at this one back here it looks back towards this one where it helps move that I call it the yellow towards the green so we actually did that with one of our actually studied that and actually have done a poster and a write-up on that because Amory has actually done that with looking at PTSD so we actually had that this morning or one of our posters so I don't want to I know we're kind of rushed right now so since we're out of time I'll just go straight to questions we did have a couple cases that we could run through but it's one minute to three o'clock so if there was anyone who had any particular questions for either of us or dr. Minnan who is still on the phone here here's again the QR code I just had a quick question you didn't mention it so much directly but is there many cases around comorbid tinnitus and how you guys generally approach that tinnitus yeah go ahead use the microphone there's been some research on comorbid tinnitus and the vagal nerve stimulation most of its been auricular I've actually been using that on some of the vets who've been having comorbid tinnitus I'll use that with the gamma core device even though it's usually the auricular one but I'll use it off label for my veterans it is tough to because the serotonergic agents can actually worsen tinnitus in some patients and sometimes you do have to keep that in the back of your head and just ask okay did your tinnitus get worse when we started this SSRI or the center I some will say yes and some will say no any other questions I struggle with my patients that get we call analgesic rebound headaches because they just will not believe me that if you try to cut back do you have any suggestions you know people who are taking Tylenol or ibuprofen every single day because if they don't the headache yeah I mean I think dr. Minnan would probably want to add a little bit on that but it's very human nature to want to stop something with an abortive and to get someone to really conceptualize going from an abortive perspective to a preventive perspective it's a very similar discussion that you have about using benzodiazepines to treat your anxiety and we want you to switch over to using an SSRI especially in the first couple of months when someone tries to get off of some of these abortives they will report more headaches during those couple of months and at some if there isn't any good you know way of kind of you know having the ability to recognize that that will occur and this is what we can do instead of going back to your old habits they will revert and that can be quite problematic. Dr. Minnan, does Dr. Minnan have anything to add? Can you repeat the question? I couldn't hear all of it. Sure, so the question is you know what do you do for someone who is using an abortive like a Tylenol or if you're a set every single day and you like what do you do what's the challenges to getting them off of using an abortive and trying to reduce the medication adaptation headache. Sure, so first of all huge issue like you say you don't want to stop acutely with a furoset or furanol because of the butalbatol you don't want to send someone into a seizure so you would continue some of that part without the caffeine and taper that part down and it depends on how many tablets a day and you would gradually taper but you would want to start a preventive medication. One of the preventives that were discussed today there isn't really great evidence to say one over another there was a MOTS trial out of Mayo that was looking at medication overuse if you want to refer to that but really the key would be to start prevention really to educate about the role of just you know five to eight tablets of a furoset or furanol potentially causing medication overuse and so slowly titrating and if patients have been on it for years this may be a very long taper so you really don't want to stop it abruptly but happy to answer any more specific questions if you need to message me. Right, so the really long taper I think is really for the psychological dependence on the abortive because with all of them the half-life is extremely short the the actual physiologic taper should doesn't need to be as as but we find that sometimes it is just more beneficial to have a I'm gonna be here for you we're gonna go through this together and it's not that we're just stopping all your medicines today and you have no nothing that you can turn to tomorrow. I'm gonna say if they're able to use it one of the neuromodulation devices might be an option too if it's an affordable option depends on what kind of place that you work at and they're affordable places. Sure I mean topiramate is a fine medicine as a preventive you worry about the 1% suicide risk and that some people just you know can't handle the cognitive a lot of people can't handle the cognitive effects. We have plenty of patients that you know are on 200 milligrams or even more of topiramate in a long-acting form and do very well and then there's you know the patients that just can't do it. Yeah I mean I think that the key is to just become comfortable with using at least two to three preventive medications and you know your role as a psychiatrist that's also what we tell primary care providers as well we obviously don't expect you to be comfortable using all of the different medications and if you've tried you know at least two of the preventive medications and it's not working that really is an appropriate referral to neurology right so but with topiramate you know it's FDA approved has you know level 8 evidence per the American Academy of Neurology guidelines we use it all the time for migraine prevention. Okay I think we got one more question. I have a patient with chronic migraines like you know greater than 15 days a month and bipolar 2 diagnosed by a prior psychiatrist. I was just curious with your graph there with like the circle of the prodrome and just diagnostically like you know do you have any tips in sort of distinguishing bipolar 2 and sort of these cycles of migraines in which some of the symptoms might be you know impulsivity acute fluctuations of mood. Right so I mean I think that trying to diagnose bipolar spectrum is tricky and I mean again you know unipolar depression is the most common thing and while bipolar is four times more common it is still you know proportionally a smaller percentage of our patients so we always just try to keep it in the back of our minds and if we do achieve better control of their bipolarity reduce the number of hospitalizations there will be better compliance with their other medications as well. Yeah you know I've had patients that were started on lamotrigine for example by their neurologists and they're like yeah I don't think this is helping my headache. I'm like okay but coincidentally you've also had much better improvement with your mood so maybe we shouldn't necessarily reduce it today. It can be very challenging to have both. I was going to say for patients with PTSD actually the propranolol can actually be a beneficial one. For those of you are familiar with propranolol and PTSD study about using propranolol prior to therapy. It was one of the articles for ABPN in the pilot journal or the pilot mock trial about using propranolol prior to therapy for fear extinction. So I think I've used that for several dual diagnosis ones with migraine as well as PTSD because that's been beneficial for like a twofer for many of my patients who have that extreme activation because oftentimes it's thought it was traditionally thought not to be ideal but especially with a lot of patients extreme arousal that's actually been beneficial for PTSD. Thank you so much for staying to the end. Anybody else has any questions you guys can come up.

headaches

migraines

psychiatry

mental health

treatment options

migraine impact

psychiatric comorbidities

behavioral therapies

stigma

military veterans

PTSD

headache management

patient outcomes