Hi, thank you for listening to our session today. We will be discussing subspecialty-based pearls to help team physiatry manage headache. Hi, I am Monica Rodisco-Gutierrez. I'm from UT Health San Antonio, and I got to put together this amazing team of physicians and a nurse practitioner who manage headache in different aspects of PM&R, and I'm really excited to work with this group. Those are my own disclosures, which I will not be discussing today. Objectives, we are gonna talk about pathophysiology of headache in different diagnoses that physiatrists deal with. We're going to delineate strategies to manage headaches in different patient populations and hear what these leaders are doing in their own settings. We're gonna learn about evidence-based medicine. Across the board for different headache types and describe and build comfort in listening to amazing interventional treatments of headaches as well. So, the who's who in the PM&R headache world. I got to put together this team of amazing women in the PM&R world, and first we have Dr. Nicole Spare. Then we'll be hearing from Laurel Short, who's a nurse practitioner. Dr. Alexis Iaccarino, Dr. Molly Timmerman, and Dr. Katherine Travnicek. So, very excited, and you will be hearing from more of them today. I am going to just do the introductions as well as just briefly talk about, since right now the big topic is COVID, and I've set up a COVID recovery clinic, and I've been seeing patients who've been dealing with COVID. So, I'm just gonna touch briefly upon some pearls for headaches related to COVID. So, one of the most common neurologic complaints that patients have who have COVID is related to headache. Anywhere, you'll see in the literature, there's also narrative reviews that are out already, anywhere from six to 71% of complaints of COVID patients, the symptoms is gonna be related to headache. What features do these patients have? It's really differing, but kind of what's been studied so far is maybe almost half of them will have hemicranial pain. Mostly, I'm seeing a lot of holocranial pain, and then also then there's maybe a fifth of patients who have occipital headaches, and they seem to be really having, the ones that do have that, it seems to be a true kind of occipital neuralgia type of headache that they're getting. And then how is it being described? Pressing, stabbing, pulsating, it depends. Everyone's different. Some people, it's hard to describe it. They just feel head fullness or just headachy or migraine-y. So why are people getting COVID headaches? So we know the SARS-CoV-2, the virus that's causing COVID-19, it has a spike, the ACE2 receptors is where it attacks due to its spike proteins. ACE2, you have ACE2 in different parts of your body, including in your brain, and you have it also in vessels. And also it causes direct effects. It causes indirect effects, which is inflammation, and it starts an inflammatory cascade. And that inflammatory cascade can cause effects in vasculature, which we know is related to headaches. And then there's also immune effects. So immune effects and the immune system and causing changes in the immune system. So again, you can directly have infection of the central nervous system. There's neuroinflammation secondary to cytokine storm, which we know in other headache situations that patients with high neuroinflammatory markers like IL-6, TNF-alpha, they're more likely to have headaches. So that's something that's related. The coagulopathy itself and the hypoxemia. So these are some of the things that are related to the COVID headache. So diagnosis and treatment, you have to make sure, rule out a secondary etiology of a headache. Is it a primary headache or is it secondary? In those patients where you're concerned, it might be a secondary headache, then they would need an MRI with and without contrast to consider. A lot of patients are just having kind of run-of-the-mill headaches. And then you do symptomatic management based on the phenotype of the headache. Once things are ruled out, secondary etiologies, they're not having a stroke, they're not having venous sinus thrombosis, then just treat the headache like you would a headache according to the phenotype, which you're gonna hear a little bit about later. So if it's tension-related, acetaminophen, NSAIDs, I'm ordering a lot of myofascial treatments, trigger points, that sort of thing. If it's migraine, then you treat like a migraine. Do they need triptans? Making sure it's not a stroke-related one and they're safe to be on a triptan, then yes, give them a triptan or some of even the new medication class. Some patients I've had to send for IV treatments, magnesium, dopamine receptor antagonists, and then also getting them peripheral nerve blocks as well as SPG blocks. So if you have any questions, you can tweet at me later or send me an email. And thank you very much for being here. Hello, my name is Dr. Nicole Spehr. I'm an attending physician at the Jefferson Headache Center in Philadelphia, Pennsylvania. I'm excited to talk to you today about the emerging treatment for migraine using monoclonal antibody technology. These are my relevant financial disclosures. I will be speaking about the FDA-approved therapies today. In the past two years, we have entered a new era for the treatment of migraines. My goal today is to provide you with an overview of the biology describing CGRP calcitonin gene-related peptide and its role in the trigeminovascular system. The monoclonal antibodies against CGRP or its receptor have emerged as promising targets for migraine treatment. And at the same time, this has further established the strong involvement Migraine is a strongly disabling neurovascular pain syndrome. Over a billion people worldwide have migraine, including 40 million people in this country alone. Globally, headache disorders, including migraine, are the second leading cause for years lived with disability. To better define what is migraine, you can use the International Classification of Headache Disorders. Proper diagnosis enables the initiation of treatment, which can improve functional status and quality of life. Before we get started, let's quickly review how we characterize the two primary causes of migraine and headache. A clear distinction between these two headache disorders is that migraine is often worse with physical activity. Otherwise, you may see an overlap between features such as nausea, vomiting, sensitivity to light, sound, or smell. Migraine is more than just a headache. Pay attention to the associated symptoms that accompany a migraine attack. Migraine can be characterized by over-excitability in different areas of the brain. The attack most likely originates in the hypothalamus, which can explain the early symptoms such as yawning and cravings. Aura, cortical spreading depression, is a wave of electrical activity that spreads across the cortex of the brain. The average duration of aura can last anywhere between five and 60 minutes. Patients can have aura without migraine. The headache phase itself is anywhere between four to 72 hours. The postdrome, or as some patients liken to a hangover sensation, where they feel brain fog, cognitive slowing, fatigue, even mood changes. So who shares the burden of migraine headache? The patient has the physical symptoms, but family and friends are also impacted. The patient may not be as present, and employers also may, and fellow workers may also notice substantial costs due to work absenteeism and reduced productivity. In addition to lost productivity at home and work, the risk of comorbid conditions is higher in patients with migraine. Be sure to evaluate mental health thoroughly. Depression, anxiety, insomnia, irritable bowel syndrome, including fibromyalgia can all sensitize the central nervous system. Meta-analyses indicate that migraine with aura is associated with approximately a twofold significant variability between studies. Migraine may be underdiagnosed and undertreated. In one study of more than 80% of patients diagnosed with a non-migraine headache were actually found to have features of migraine. Of this number, almost 40% required preventive therapy, but only three to 13% of this large number were given an appropriate treatment. The success of older and current drugs in migraine prevention and rescue therapy have been limited by inadequate efficacy, tolerability, cost. And after cycling through multiple drug options, the use of opioids is an unfortunate method to combat this pain syndrome. The OVERCOME study revealed higher healthcare costs for patients with migraine, a higher risk of progression from episodic to chronic migraine. Chronic migraine is more than 15 headache days per month, eight of which meet the features of migraine, and more severe disability. The translation of therapies has been a long journey of discovery. If we go back to the 1930s, the vascular theory dominated. Here, vasodilation of blood vessels activated trigeminal sensory nerves, which led to the experience of pain. In the 1940s, cortical spreading depression was discovered. It is accepted as a possible generator for migraine and its associate symptoms, as I have previously mentioned. In the following 30 years, the serotonergic receptors were targeted. Triptans have been the mainstay for acute treatment of migraine. These drugs are partial agonists of the serotonergic receptor 5-HT1B and 1-D. Triptans block the release of CGRP. They were originally thought to relieve migraine through vasoconstriction. The pathophysiology was reexamined in the following years. In 1993, Sumatriptan was tested, and it was found to prevent the extracranial plasma level increase of CGRP. And at the same time, it scored the role of the CGRP in the treatment of migraine. In the following years, the CGRP was found to be the mainstay for acute treatment of migraine. And it scored the role of the CGRP in the treatment of migraine. Currently, the neurovascular theory dominates. Migraine is a complex disorder that activates, that involves the activation sensitization of pathways within the trigeminovascular system. In 2019, October last year, a third type of the serotonergic receptor 5-HT1F was identified as a target of interest. The acute therapy, the DITAN class, was FDA approved. And this particular medication does not vasoconstrict the vasculature. Therefore, something more is going on than just a vascular theory. Calcitonin gene-related peptide is a 37-amino acid neuropeptide. It is the most potent vasodilator It exists in peripheral sensory neurons in two forms, the alpha form and the beta form. The beta form is less well-studied. The alpha form is what has been focused on for the development of the monoclonal therapies. CGRP is expressed in C-fibers and its receptor is expressed in A-delta fibers. To recap the proposed mechanism of action, the trigeminal ganglion is thought to be a migraine pain amplifier. The trigeminal ganglion and the dura are not behind the blood-brain barrier. Therefore, when we look at the anti-CGRP antibodies or the anti-CGRP receptor antibody, if we can block CGRP transmission, could we prevent a more severe migraine attack? This timeline shows the discovery of CGRP in 1982 to the development of the therapies that were FDA approved in the past two years. This was a long road. The remainder of this presentation serves to address an identified unmet educational need among physiatrists and related specialties in the area of immunology as it pertains to migraine. Antibody structure and function can be engineered. To date, from 2018 to 2020, there are four monoclonal antibody therapies, three against CGRP itself, one against CGRP receptor. In addition to circulating half-life, most therapeutic antibodies and related technical discoveries have focused on IgG. We now know that antibodies, also known as immunoglobulins, are large glycoproteins, 150 kilodalton. If you compare this to insulin, five kilodalton, that's a large size difference. The FC region and FAB fragments form the backbone of all therapeutic monoclonal antibodies. The FC fragment interacts with the immune system. It can be engineered, and that's what's responsible for the half-life of these new drugs. The FAB fragment, the variable region, interacts with the CGRP target. The vast majority of monoclonal antibodies are eliminated by catabolism through the reticuloendothelial system. The neonatal receptor was originally studied as an antibody transporter between mother and fetus. Neonatal receptor can be engineered for faster or slower removal of circulation of these antibodies from circulation. Understanding the mechanisms behind migraine and migraine pain, particularly on a molecular level, provides hints about areas where potential new targets can be found. This is a really neat slide from Edvinson's landmark Nature paper in 2018, where you see the trigeminal nerve releasing the blue dot CGRP. CGRP then binds to its receptor here on a cerebrovascular cell or other trigeminal neurons. Once that CGRP is bound, it activates the cliquant AMP, ultimately leading to vasodilation. The upside-down Y in red, the anti-CGRP receptor antibody, can sit on that receptor to block CGRP from binding. That is a renumab. And the other upside-down Y, the other three, fremanizumab, galconizumab, or eptinizumab, target CGRP. Therapeutic antibodies must be delivered either through IV, subcutaneous, or intramuscular injection. They are very large. They cannot be taken orally. They would be natured. Be aware that no class of biopharmaceuticals is free of immunogenicity. What this simply means is that anti-drug antibodies bind to the drug that is being introduced to the body and may alter the drug in some way. Clinically, you would see this in terms of maybe no effect at all, which would be a good thing, or altered form of kinetics, hypersensitivity reactions such as itching or erythema edema at the injection site, this is a safety concern. So in summary, if there are three things that you can take away from today's lecture is that to pin the diagnosis of migraine, ask these three questions when you're speaking with your patient. Does light bother you when you have a headache? Does your headache impact your ability to complete your normal daily tasks, your job, both personally or professionally? Are you nauseous or sick to your stomach when you have a headache? Pin. This is a simple way to have an accurate diagnosis as if this is migraine. Help people with migraine meet their treatment goals. You can do this through biobehavioral approaches, acute pharmacologic or preventive therapies. Consider using a monoclonal antibody as a preventive therapy if you have a frequent headache, but even if if somebody does not have a frequent headache, ask questions such as how many times per month are you unable to go on with the rest of your day, that you have to change your plans unexpectedly, or if you have young children at home, are you able to eat dinner with them or prepare things for the next day? Sometimes, just even if the headache is not as frequent, the severity of it can be just as impactful and therefore warrants a good migraine preventive. If there is any overuse of acute therapy such as barbiturates or opiates, again this can increase the risk of progression from episodic to chronic migraine. This would be a good consideration again to start a migraine preventive. And again, always recalling any medical or psychiatric comorbidities. Important characteristics of these therapeutic monoclonal antibodies are that they confer high specificity to a single target, they break down to amino acids, there is a low risk of drug-drug interactions, they have low off-target toxicity, and the pharmacokinetics support a less frequent dosing interval. These are the four monoclonal antibodies available that you can prescribe to patients with migraine. Firminezumab is a subcutaneous injection. It can be administered on a monthly or quarterly basis. Irenumab is a subcutaneous injection administered on a monthly basis. This is the unique one that it targets the CGRP receptor itself. Galconizumab is a subcutaneous monthly injection. This one is unique in that the first dose is a loading dose, which would be two injections, and every month thereafter would be one injection per month. Eptinezumab was FDA approved in February of 2020. This is unique in that it is administered via an IV infusion on a quarterly basis. In this graph, we are not comparing each drug to each other. What I'm trying to show you that is each drug had the ability to reduce migraine days by half. This is dramatic. So in summary, our treatment goals for treating people with migraine are to restore their ability to function, reduce disability caused by migraine, and improve their quality of life. When we can relieve pain and headache frequency, this is a or delay disease progression. Thank you for your attention. Migraine is a challenging lifelong neurologic disorder, and I'm happy to answer any further questions. This is my email. Enjoy the rest of the conference. Take care. Thanks, Dr. Spear. Hi, welcome, and virtual greetings from Kansas City. My name is Laurel Short, and I've worked in physiatry for about 10 years as a nurse practitioner in the outpatient setting. I've become very interested and passionate about working with patients who have headache and migraine, and I completely agree with Dr. Spear. It's completely rewarding to see patients feeling back in control of their lives as we work with them, really using all the tools that we know work with other physical medicine and rehab conditions as well. I'm very avid about the power of self-management to impact severity and frequency of migraine symptoms. Based on my practice experience, I became interested in strategies for improving access to meaningful patient education. I feel that we need tools that we can easily blend with traditional clinic settings to help streamline our care, make it efficient and meaningful for patients. So this became a focus of my doctoral project. So today I would like to reiterate some of the disability associated with chronic migraine, some tips and strategies that you can use in your clinic for your headache history and treatment plans, and the results of my pilot project. I do have one disclosure that's not written on the slide, but I've done consulting and I'm on Speaker's Bureau for Allergan. So as Dr. Spear mentioned, we know that migraine is in the top 10 causes of disability worldwide. We know it's a chronic neurologic condition that causes both societal and individual impact. While people with chronic migraine aren't lying in a dark room all the time, we know that at least half of every month their daily lives are impacted by their migraine symptoms. We need to understand the disability associated with this condition. It affects all areas of their life, school work or paid employment, household tasks and leisure activities and family time. Average health care cost for someone with chronic migraine is over $3,000 over 12 months, and that's double because someone with episodic migraine has about $1,500 over a year specific to their migraine treatment. Even more significant is that decreased productivity for migraine costs a total of $13 billion per year in the United States. And a fact that really sticks with me is less than 5% of those with chronic migraine receive all three steps that we consider for optimal care. That includes access to care, a correct diagnosis and a comprehensive treatment plan with both preventive and acute strategies. I'd also like to point out that the supply of neurologists is expected to grow by about 11% by 2025, and demand is expected to grow by 16%. I think this really highlights how physiatry specialists can help meet this gap in access to care for those with migraine. I won't read word for word the definition. We went over that already a little bit with Dr. Spare, but just to reiterate that if someone is coming into the clinic with a chief complaint of headache, more often than not it is going to be migraine. And we have studies that show, we do chart reviews, many folks that have been diagnosed with tension type headache actually met the criteria for chronic migraine. That's why it's so important to get an accurate history, and we'll talk about some tips for that. As with any chronic condition, we have both modifiable and non-modifiable risk factors when it comes to chronic migraine. As we've stated, it's much more common in women, a three to one ratio. And while not all the factors, risk factors associated with migraine are modifiable, the more we can understand what's going on in our patients' lives, the better we can help them. So I'll just highlight a couple of things off this slide. One is sleep. If we have a patient who's not responding as well as we expect to treatment, and also at our initial intake, we need to be asking about morning headache, are they waking with headache, or do they feel well rested when they wake up? There's a large correlation between sleep apnea and daily headache, especially for someone who's waking with a morning headache. Actually just received a report back from a sleep study that I recommended for a male patient in his 30s. Even though he doesn't feel like he was snoring, he was waking, not feeling well rested, and he wasn't responding very well to the initial preventive therapies that we were trying. And his report did come back with a positive finding for sleep apnea. So I'm hoping that addressing this will be a game changer for him in addition to the other treatment that we're trying. Especially as Dr. Gutierrez pointed out, we have folks going through a lot of stress right now, related to COVID-19 and other societal factors. And I've seen this a lot in our clinic of patients coming in, feeling like their headaches and migraines are increased related to this stress. So moving into some assessment tools that I hope you can find helpful. I also have a slide on the migraine ID3, as Dr. Speer did, and some initial tools that you may find helpful and you can incorporate into your EMR even, for the migraine disability scale, or the impact tool. This could be helpful in making your initial diagnosis, and then also monitoring as you start treatment to see how patients are responding to different modalities. There's also many free apps that patients can use on their smartphone or a tablet to track their symptoms. And in addition to these apps, I'll also share a slide with a simple headache chart that I use with our patients in clinic. Establishing a diagnosis of chronic migraine is really based on a patient's history. What I would like to point out is patients with migraine tend to be very stoic. So for example, you ask a patient, how many migraine days do you have per month? Their initial reaction is to only tell you about their very worst days. So we want to establish open communication and reassure patients that we want to know about all of their headache days. We can often get to the information we want much more quickly by turning the question around and flipping it around. Instead of saying, how many headache days are you having per month? We can say, how many days are you headache-free? How many days are you crystal clear from the neck up? We know at least 70% of patients with migraine also have associated cervical spine, myofascial pain, and I count those as symptoms days for patients with migraine. So we want to make sure I count those as symptoms days for patients. Kind of tagging on the phases of migraine that Dr. Speer talked about, a patient often is not familiar with the terms prodrome and postdrome. So I find it helpful to take a few minutes, explain this to patients and count these as symptom days. Often they'll describe the postdrome as kind of a quote, hangover from the migraine. And so patients with chronic migraine are often just fluctuating in and out of all these phases of migraine, and they feel like they have no crystal clear days. They feel like their normal is to have a headache. I've had patients say that they push through their workday, the things they know they have to get done, and they have nothing left to give their family at the end of the day. We want to reassure patients there is a name and a diagnosis for their condition, and that there's treatment options available. And nothing feels better than having a patient leave the initial consultation just looking like a weight has been taken off their shoulders because someone has listened to them and is helping them develop a treatment plan. Migraine ID3 was already reviewed, but just as a reminder, this is a great tool to use in your clinic, and it's something that can be done by a nurse or even maybe even on the initial intake. I also really like this visual to remind us that migraine really is more than, quote, just a headache. Patients don't always understand that these other symptoms they're having are associated with the condition of migraine, and they may initially want to tell you about the different types of headaches that they have. And so the simple way I explain it to patients is the primary diagnosis I'm using is migraine. It doesn't mean that it feels the same way to you every day. And we want to really understand how the associated symptoms are affecting their life and knowing that we can treat some of those, for example, giving them ondansetron to help treat their nausea. I recently started working with a patient who shared with me her main challenge is bright lights and loud noises in her work environment, and she can't easily take a break from that when she feels a migraine coming on. So she's leaving work early and missing work very often. Another new patient I met this week was telling me how she perceived that every time she gets indigestion, it's followed by a migraine, feeling like her indigestion is causing the migraine. So this led to a really interesting discussion we had about GI symptoms that occur as part of the migraine attack, not causing the migraine attack. Like other chronic conditions, we know that those with chronic migraine really benefit from a toolkit approach of lifestyle interventions along with pharmacologic therapy. We have a lot of new, really exciting medications coming out, but what I tell patients is we can have the best medication in the world, and if we don't also work on lifestyle and behavioral interventions, the medication can't work as well as we want it to. So I'm going to talk a little bit about self-management. Self-management involves patient education, but the goal is really to empower patients to manage their condition through problem-solving, community resources, and shared decision-making. Self-management completely matches with physiatry goals of partnership, empowerment, and optimizing health for our patients. So what I'd like to point out here is hopefully a resource for you. It's a website that I developed as a platform for my pilot project that I'll talk about now, YourMigraineToolkit.com. This is an open-access website with patient education that you can use in your practice. So to share a summary of my doctoral project that was completed in 2019, the purpose of my project was to determine if an outpatient self-management program for chronic migraine given over eight weeks could decrease migraine disability and improve their self-efficacy or their confidence in managing their condition and secondary outcome goals for decreased headache days and emergency department visits. So this was a small quasi-experimental single group design with pre-test and post-test evaluation, and it was really framed around an intervention of creative video and web-based modalities and education for adults with chronic migraine. I was initially targeting a sample size of 30 for more statistical power, but this was adjusted to a pilot size of 15 due to some time limitations that we all know can happen with IRB process. So really the hybrid idea of this was patients still had in-office education, but they also had online resources that they used at their own time. They used a migraine tracking chart, and after the first visit where we did the initial pre-test evaluation, they had eight weeks to practice self-management methods, and the specific behaviors I was asking them to work on were hydration, sleep hygiene, relaxation techniques, and looking at morning protein intake. We also emphasized early use of rescue medication rather than waiting until their symptoms were severe. They used a headache diary to track their symptoms, which is a common way to track outcomes in migraine studies. I also sent them a weekly text message through an online-based text system, and this was really neat. It was actually through our EMR. So this is something that you might have access to as well, and it allowed me to kind of pre-set up text messages that I could push out to them. So one example would be, have you made time to practice relaxation and deep breathing today? Keeping calm during a migraine can make pain less severe. Resources at yourmigrainetoolkit.com. So it was a reminder of them to go to the website and use it. So a second visit was completed eight weeks after the first visit. That's where I completed the post-test data and got some feedback on things. So now I'll move to the chart that they used, and this is still the chart that I'm using with patients now because I had such good feedback from the project. I know you can't see it up close, but it has your usual things, associated symptoms. Do they have a headache that day? Were they aware of a trigger? What acute medication did they use? But the difference in the scale they're using instead of a number scale, it's a traffic light model, and this is based on an article that Dr. Lay out of Canada and her group published, and it sounds simple, but it's so effective. It is kind of modeled off after looking at the severity of asthma symptoms and applying that to migraines. So green is a mild day, yellow is, you know, have to slow down, and red is their worst day. And after putting all this work into the online platform, I expected that to be really the highlight of the program, but interestingly, patients and the participants came back and said they really liked the simplicity of the scale and how it visually allowed them to track things over the eight weeks. As far as outcome measures, I used the MIDUS, the Migraine Disability Scale, commonly used in migraine studies, and I was also interested in self-efficacy because previous studies have shown that even without changing migraine severity and frequency, improving someone's self-efficacy helps them with their overall quality of life and just making them feel much more in control of their situation. And I did see that my outcomes, there was a correlation between decreasing the disability and improving the self-efficacy. There was also overall decrease in the disability scores and amount of acute medication use, which I was happy about, and total headache days. Certainly, there were limitations with this project given the small sample size and convenience sampling, but the outcomes were consistent with what we've seen in the literature. Many other studies have shown that both online and in-person education shows improved coping, reduction in migraine symptoms, and reducing intake of acute medications. So hopefully down the road, this can be repeated on a larger scale or working with other clinicians to show additional outcomes. So I'd like to share just a few additional resources to summarize here, and some of them, like DawnBuse.com, she is a very well-known PhD psychologist in the headache world who has great resources on her website, the yoga app, and podcasts. All of those are also linked through the migraine toolkit intervention that I created. But I also wanted to share a newly launched clinician website that you may find helpful through the American Headache Society. We know a vast majority of migraine patients initially seek care at their primary care office or in a non-headache specialist, non-neurologist clinic. And going back to how I stated in the beginning, we have many more patients who need access to care than we have neurologists and headache specialists. So this first connect was developed to give non-neurologists, clinicians, a lot of resources and tools that hopefully you can find helpful. And the headache certification, if you're interested in some more information on that with the National Headache Foundation, that's an exam that I've taken. I know at least one of our other presenters in our group has taken. It was really a great experience for me to improve my knowledge and confidence in working with these patients. So therapeutic education strategies should absolutely be emphasized when we're working with migraine patients so they can be active participants in their care. My intervention represented a self-management toolkit that hopefully is practical for your clinic just as it has been for mine. Using a hybrid model that incorporates in-person and web-based strategies really allows for individualized education and treatment. And doing this type of education is really the wheelhouse of nurse practitioners and nurses. And I know as a psychiatrist, you also enjoy educating your patients. So hopefully this is something that your whole team can incorporate in your clinic. So in my portion of the presentation, we've talked about how migraine is a significant condition with both direct and indirect consequences. Self-management model really does have the potential to improve patient quality of life and reduce the burden of disease associated with this condition. So I'm hopeful this intervention can be a tool for you in your practice. And I will turn it over to our next speaker, Dr. Aya Cunningham. Hi, everyone. Greetings from Boston. Thank you for joining our virtual session on headaches today. My name is Alexis Agarino. I'm a physiatrist at Spalding and Mass General, and I conduct clinical care and research in mild TBI. And today I'm going to be talking about exercise and support concussion as it relates to headache. I don't have any relevant disclosures for this presentation. I received some salary support, and I'm an independent neurotrauma consultant for the National Football League. Why are we talking about headache and MTBI? So it's the most commonly reported symptom after support concussion, and in most cases of mild TBI, and I'll be using those terms interchangeably during this talk. Headaches are commonly exacerbated when people are trying to return to play or do exercise. And also more recently, we've been using exercise as a potential treatment for the symptoms of support concussion. So it's relevant to understand how headache may factor into this. So there's a lot of reasons that athletes can develop a post-concussive exertional headache. These things can include things like whiplash or cervical dysfunction that lead to tension headache and may be exacerbated when the neck stabilizes during exercise. They can be vestibular and ocular dysfunction, which is common after a concussion and can be exacerbated by motion, gaze stabilization required during exercise, and there are a host of other factors, dehydration, deconditioning, and autonomic dysfunction that can occur as a result of concussion. But we're going to focus on cerebrovascular etiologies that may underlie the post-concussive headache and the physiology that may cause exercise to exacerbate these symptoms as well as how exercise may be used as a therapeutic. Before moving on to, it's important to review that the brain is a greedy organ when it comes to blood flow. It demands a steady and constant flow of blood and it's relatively intolerant to even minor blood flow perturbations. There are three important mechanisms that underlie and are used by the brain to ensure maintenance of appropriate cerebral blood flow and they're listed here. The first is cerebral autoregulation, which refers to the ability of the cerebrovasculature to counteract the fluctuations in systemic arterial pressures that occur in everyday activities, including exercise. The second is neurovascular coupling, which refers to the idea that blood flow changes in response to metabolic demand and that cerebral blood flow and metabolic demand are coupled. For example, there's increase in flow to the whole brain or to specific regions in response to increased neuronal activity and metabolic demand. And the third is cerebrovascular vasoreactivity, which refers to the sensitivity of the cerebrovascular to change in arterial oxygen and carbon dioxide partial pressures and the ability to alter flow with changes in CO2. So for example, hypercapnia leads to vasodilation and increases in flow, whereas hypocapnia can lead to constriction and decreases in flow. Following a mild TBI or concussion, optimal cerebral blood flow is needed to meet the metabolic demands to facilitate recovery of the injured brain. However, research in animal models suggests that global cerebral blood flow is reduced following a cerebral injury and there can be interhemispheric asymmetries in blood flow as well. Cerebral blood flow can remain reduced for extended periods, leading to blunted responses of the cerebral blood flow to changes in carbon dioxide and neurovascular uncoupling. Consistent with the animal research, global cerebral blood flow has been shown to be reduced even after mild TBI in humans. Mike McCray's group in 2015 did a nice study where they found changes in cerebral blood flow globally and regionally, immediately following sport concussion and persistence to some extent after one week from injury. This reduction has been shown to correlate with symptoms. As well, if you look at the primary migraine literature, individuals with migraine demonstrate excessive increases and decreases in cerebral blood flow in response to both hyper and hypocapnic states. And this is associated with the development or persistence of headache. Regarding cerebral autoregulation, within 48 hours of injury, Youngberg's group found that almost 30% of patients with a mild injury had impairments or absent autoregulation. In addition, autoregulation was found to be impaired chronically in boxers due to repetitive subconcussive blows during sparring. And this impairment not only can be associated with headaches, but also was found to be associated with neurocognitive dysfunction. Basal reactivity has also been shown to be reduced in athletes who had acute concussion. And in a study of adolescents with prolonged post-concussive symptoms, basal reactivity was strong, really related to post-concussive symptom burden. Taken together, all of this work raises concerns that dysfunction in one or more of the mechanisms that regulates cerebral blood flow may prolong neurophysiologic recovery and contribute to underlying clinical sequela of concussion. So now that we understand cerebral blood flow and how it changes by concussion, how might exercise impact these hemodynamic mechanisms? The answer is that exercise generates demands on each of the mechanisms. While it might be thought that blood flow increases in response to exercise, the relationship is actually not linear. As we can see here on this diagram, cerebral blood flow will go up with mild to moderate exercise and then actually begin to reduce with heavy exercise. The reason for this is partially related to CO2 partial pressures, whereas with early exercise, our respiratory rate keeps up with changes in CO2. As we begin to move to heavy exercise and begin to blow off more CO2, we actually see the inverse effect on cerebral blood flow. We can use exercise to better understand symptoms such as headache in the context of concussion recovery. When headaches are produced with exercise, one underlying mechanism is the disruption of brain blood flow responses to metabolic demand, changes in arterial CO2, and cerebral auto regulation that are needed to maintain homeostasis with exercise. Thus, exercise can be used as a probe to understand headache and other symptoms in concussion, most commonly dizziness and cognitive dysfunction. It's the understanding of these physiologic mechanisms and their disruption in concussion that leads us to use exercise as a potential treatment. Going back to our drawing on the effects of exercise on blood flow, which is reproduced here and is similar to the one on the prior slide, aerobic exercise engages multiple mechanisms of cerebrovascular control. During exercise, there are increases in systemic pressure with even low intensity exercise. This tempered by auto regulation to prevent over-perfusion. Similar, the exercise induced increases in carbon dioxide production is accompanied by vasodilation to regulate flow. Finally, sustained muscle engagement leads to cortical activation in motor and sensory areas, increasing cerebral metabolism, and engaging neurovascular coupling. Therefore, mild to moderate intensity exercise can engage these mechanisms and may actually condition the cerebrovascular function by engaging all three. Thus, maintaining a moderate sub-symptom threshold level of exercise in likely the subacute phase of concussion might be ideal for improving cerebrovascular function while avoiding the difficulties that are associated with intense Exercise is becoming more and more commonly a successful treatment in acute and subacute phases of concussion. The most well-described paradigm is a modified Belkey protocol or a Buffalo concussion treadmill test is also very commonly described. The most well-described paradigm is a modified Belkey protocol or a Buffalo concussion treadmill test is also very commonly described, which utilizes walking at a progressive incline to slowly increase exercise intensity. Heart rate, rate of perceived exertion, and symptoms are all monitored during this exercise and the development or increase of symptoms is thought to represent that inflection point at which there's a perturbation in the appropriate cerebrovascular responses. Patients are then recommended to exercise at a heart rate or rate of perceived exertion that is below that which causes symptoms, utilizing again light to moderate intensity exercise to help improve or condition cerebral blood flow mechanisms. Over time, exercise intensity is increased and patients have been shown to tolerate it a little bit better. There are also bike-based exercise protocols which we use commonly in our program, thinking that being able to stabilize the head a little bit better on a bike than a treadmill may help reduce some of the confounding variables around cervicogenic contributors to headache and vestibular ocular contributions to headache. The use of exercise to help with concussion symptoms such as headache is not fully understood. There are some caveats, so we used to think it was most appropriate in a sub-acute phase. We now better understand that it might have an important role in the acute phase of concussion within the first week. The mode of exercise, so treadmills versus bikes at an incline, how much resistance, is also not perfectly well understood. Duration and intensity also not fully understood. However, most of the work around aerobic exercise at a sub-symptom threshold level has been shown to help reduce concussion symptoms and potentially hasten recovery. So in conclusion, headaches are very common after concussion and there's a variety of reasons for that. One of them may be a link to cerebrovascular blood flow changes in the post-concussive state. Some of this is drawn from understanding of the migraine and other primary headache types. Exercise may be a really good probe and provocation of headache may be due to alterations in cerebral blood flow. And then exercise at a mild to moderate intensity may be a good actually help to improve cerebrovascular dysfunction and thus reduce symptoms. Thank you very much. Hello everyone. I'm very happy to be here with you virtually. My name is Molly Timmerman. I'm the medical director at the TBI Outpatient Clinic and the co-lead of the Headache Centers of Excellence in Palo Alto. I'm also affiliated with the Stanford Residency Program in PM&R. I'm going to talk a little bit today about my experience working with veterans and active duty service members with TBI and post-traumatic headaches and the relatively recent designation of several nationwide Headache Centers of Excellence and the role PM&R and the interdisciplinary team is playing within these centers. So no disclosures. As far as disclaimers, I will be discussing some off-label uses of medications and devices as there's currently no FDA-approved medications or devices specifically for post-traumatic headaches. So we know that since 2001 there have been over 400,000 documented head injuries of U.S. service members largely attributed to blast injuries in Iraq and Afghanistan. As such, TBI has been considered the signature injury of the wars in Iraq and Afghanistan. The majority of these, over 80%, would be classified as mild, which as we know can mean anything up to momentary altered level of consciousness to loss of consciousness up to 30 minutes. We also know that while mild TBI generally has a good prognosis for complete recovery, a minority develop persistent post-concussive symptoms, the most common of which is headache. Head injuries that occur during military deployment are also complicated by blast nature of the injuries, oftentimes multiple concussions, sometimes in close temporal proximity, and oftentimes without treatment or rest after the injuries. And they're further complicated by the fact that these are occurring in life-threatening situations often, which increase the likelihood of post-traumatic stress, sleep disturbance, and other injuries. This is a typical injury history we'll get in clinics. So this is a veteran reporting multiple concussive events due to hard landings from parachute jumps, combatives training, multiple combat blast exposures where he was fearing for his life and the life of fellow soldiers. In these cases, often months, years after, they are still having significant difficulties. On the right, you see a typical problem list, headaches, dizziness, hearing problems, multiple psychiatric diagnoses, and multiple chronic pain complaints, often including headaches. This is a study done out of Boston VA where they coined this term polytrauma clinical triad, which describes a high prevalence of post-concussive symptoms, post-traumatic stress disorder, and chronic pain in service members with TBI, headache being one of the most common pain complaints. This is a poster presentation done by one of our residents a few years ago. She looked at a continuous sample of 829 patients seen in our clinic who had been diagnosed with combat-related blast injury, and 75% of those were reporting headaches to be a clinically significant problem for them. And I won't go too much into this slide just to say that multiple studies have demonstrated the high prevalence of headache disorders after combat head injuries. And headaches due to TBIs are tricky because they are considered a secondary headache disorder. As such, they are excluded from a lot of studies on headaches. Post-traumatic headache is defined by the International Headache Society as a headache that starts within seven days of the head injury or regaining consciousness. And clinical features aren't described by these classification systems, but they tend to present most similar to either tension type or migraine type, some evidence suggesting that military blast-related tend to be more migraineous. Again, I won't go too much into this slide. This is describing primary headache types, just to say characteristic feature of migraines is the severity, the light and sound sensitivity, and the exacerbation by activity, which makes them especially disabling. So how do we treat post-traumatic headaches? Unfortunately, we don't have great data. This is a systematic review published in 2012, and then another one published in 2019. And the conclusions are essentially the same. There's no strong evidence from clinical trials to direct the treatment of post-traumatic headaches. And recommending basically to look at the primary headache disorder it most resembles and treat accordingly. But is this the best way to go about things? Unfortunately, we don't have great data and evidence doesn't support a lot of the medical management. And as I said before, especially in studies for migraines, they often exclude secondary headache disorders or post-traumatic headaches. Additionally, many of the traditional medications indicated for the prevention of primary headache disorders, such as beta blockers, anti-seizure medications, antidepressants, can worsen other post-concussive symptoms, such as dizziness or cognitive slowing. So in 2018, the Senate Appropriations Committee recognized the impact of head injury and post-traumatic headaches as a major issue causing disability in veterans and charged seven sites around the nation with developing headache centers of excellence. And these seven original sites were Richmond, Tampa, San Antonio, Palo Alto, Minneapolis, Cleveland, and New Haven, Connecticut. And the direction behind this was really develop a system of care that utilizes interdisciplinary team and maximizes non-pharmacologic options. And truthfully, knowing our complex patient population and understanding biopsychosocial aspects of pain, this type of treatment really makes the most sense. And there's fairly good evidence for non-pharmacologic treatment, specifically for headache, including level A evidence for biofeedback, cognitive behavioral therapy, and relaxation training, as well as good evidence for these interdisciplinary treatment programs. So protocols vary, but in general, these programs incorporate medical treatment, education, psychological intervention, oftentimes cognitive behavioral therapy, mindfulness, and some type of physical therapy and exercise. And these studies show not only improvement pain function and mood at the end of treatment measures, but tend to have sustained improvements after follow-up at one year. So we developed our own protocol, which fit nicely within the scope of practice of our already established interdisciplinary team. One thing we really wanted to focus on was patient empowerment and awareness of headache triggers and how to manage them. We were seeing a huge lifestyle component, especially medication overuse headaches, complicating our clinical picture. So almost 50% of our patients, when they come in, are overusing abortives. Oftentimes this is making their headache situation much worse. Many of our patients have disrupted sleep patterns associated with postpartum depression, many of our patients have disrupted sleep patterns associated with post-traumatic stress subsequent to deployment. So many of our patients are fairly young and tech savvy. So we thought, let's build an app-based headache diary, allowing patients to be more aware of their headache patterns and triggers. Also allowing us as providers to better characterize their headaches and even allowing us to track data from wearables, including sleep and activity. Also allowing us to push surveys such as HIT-6 and Midas and provide educational material from our eight-week program. So I was also asked to talk briefly about neuromodulation devices. In our clinic, we have a lot of interest in neuromodulation devices, and there are several devices that have been FDA-approved for migraine and cluster headache, not specifically for post-traumatic headache, however, generally well-tolerated and without side effects, which makes them an attractive option for somebody who's having other post-concussive symptoms. Supraorbital TENS, or a cephaly device, was the first device to receive FDA approval for migraine prevention in 2014, so now it is approved both for abortive and preventative treatment in migraine. So the idea behind mechanism of action is you're stimulating the supraorbital branch of the trigeminal nerve and modulating that hypersensitivity of the trigeminal nerve complex. For prevention, it's recommended for 20 minutes a day of aware, and for abortive, it's one hour during an acute attack. So minimal side effects, some patients report paresthesias kind of in that forehead supraorbital nerve area. If the migraine is progressed to the point of aledinia, this can be painful for people. Vagus nerve stimulator, or GammaCore, also was approved initially for treatment of cluster headaches for abortion and prevention, now approved for abortive and prevention treatment of migraine as well. So similar mechanism of action as cephaly, essentially using the peripheral modulation of the trigeminal nerve complex, as far as use, a patient will apply to their neck in the area of the vagus nerve, give themselves two two-minute treatments on each side during a migraine attack, or for prevention three times a day. So again, generally well-tolerated. As far as STMS, I won't talk about that too much as my understanding that it's no longer available, but it was approved for prevention and abortive treatment of migraine headaches. The mechanism of action for this is a little bit different. Magnetic pulse to the occipital lobe, the idea is that this is disrupting the cortical spreading depression that's been implicated as part of migraine. And repetitive transcranial stimulation, I won't talk too much about this, but we are using this a lot based on some evidence in our patient population. So a study out of Leong at the VA in San Diego looked at patients with history of head injury and post-traumatic headaches and found a fairly good response with this. It is already FDA approved for depression and obsessive compulsive disorder. Thank you very much. Hi, my name is Dr. Katherine Travnacek. I'll be talking about interventional therapies for headaches today. Disclosures, I'd like to give a shout out to my dear friend and mentor, Miles Day. He's a program director at Texas Tech. Some of the slides today are from him. So I don't have too much time, so I will only be discussing interventional therapies for cluster headaches, cervicogenic headaches, and occipital neuralgia. Using the ICHD-3 classification, cluster headaches are primary headache, cervicogenic headaches are secondary headaches, and occipital neuralgia is in the other headache category. So these are the procedures I'll be discussing today for each of the headaches. So cluster headache, most of us know about cluster. It happens the same time of year, same time of day. The interesting thing, though, is that not all patients get parasympathetic and sympathetic overflow. You will have patients with cluster bout headaches with no parasympathetic or sympathetic findings, but they do have a sense of restlessness or severe agitation. So it can be difficult to diagnose. I work closely with board-certified headache specialists. These patients typically come to me after they've had the correct diagnosis, but if I'm concerned, if they come from primary care, I'll get them back because there are patients that get misdiagnosed with chronic migraines that actually have cluster headache. Chronic cluster headache, it's about 10% to 15% of patients, very severe, the bouts don't remit, and they can last longer than a year. So what's the pathophysiology? I think we're still learning this. There are interactions between the central and peripheral nervous system. The hypothalamus gets activated, and the hypothalamus controls the parasympathetic, sympathetic, and the trigeminal cervical complexes, which then in turn stimulate the sphenopalatine ganglion, the trigeminal ganglion, where you can get the sympathetic and parasympathetic findings on exam from. However, this isn't the full story. We used to think it was a trigeminally-mediated headache, but this was published in Cephalogen 2013. We actually think the parasympathetics have more, are thought to now be more relevant than in the past. So this was a small study where they, it was about seven patients, where they did a low frequency stimulation of the sphenopalatine ganglion, and that actually stimulated autonomic features in a cluster-like headaches. And they subsequently treated that with high frequency stimulation of the ganglion. So the question is, how many of these patients have their headaches that are initiated by the sphenopalatine ganglion? So this is just a review slide, just to remember that there is rich innervation in the sphenopalatine ganglion, which is also called the pterygopalatine ganglion. It has rich innervations or contributions from the sympathetic and the parasympathetic systems. So the anatomy quickly. The pterygopalatine fossa is behind the posterior wall of the maxillary sinus. And then the posterior wall is the sphenoid bone. And then above it is the inferior wall of the orbit, which is important. This is an anterior view of X-ray. The blue arrow is going to the middle nasal turbinate. This is where we direct our needles for these blocks and radiofrequency procedures. The red line is typically where this sphenopalatine ganglion lies, and where our needle point needs to end. So there are different types of block techniques. Intranasal, typically patients have had this and failed when they get to my office. So the procedures I'm doing are through the infrazygomatic approach, where the RFs and neurostimulation type procedures. There are two types of approach. You can do the lateral approach through the coronoid process, or you can do an anterior approach. The anterior approach is much more comfortable for patients, because when you do the lateral approach, you have to walk off the lateral pterygoid plate, which is quite painful. So here's a picture on the right is where the needles in the sphenopalatine ganglion or the pterygopalatine fossa. And that is a lateral approach. And here's the needle placement in AP view here. So RFA, typically people are using thermal RFA. Some people do use pulsed, but we don't have any evidence for pulse. So we have some small studies looking at thermal RFA. So this is a very small study that was done. This is 1997, where they only looked at, it was 50, let's see, they looked at episodic cluster headache and then chronic cluster headache. And 56 patients total in the episodic group, and about 60% of those got pretty good relief with RFA. They didn't have enough group, enough patients in the chronic cluster group, so you can't really make any conclusions from that. Another study was done by Dr. Naruse, this is out in Cleveland. And this is a perspective study, only 15 patients, they used thermal RF, and these patients did reports, or the study did report statistically significant improvement, although pain returns in these types of procedures, so you have to repeat them. There was one study found on alcohol percutaneous neurolysis. There were about 42 patients. Unfortunately, the effectiveness was defined as greater than 50% or equal pain relief that lasts a month, which isn't ideal for a procedure that you're probably going to have to repeat. These patients did have significant improvement. This is a review published by Miles Day in 2008. Most of the data that we have for RFA or neurolysis are for these various types of headaches with cluster trigeminal neuralgia. They are very small studies, case reports, case series, and we basically have the same level of evidence today, which is level C. So what's new? This is an interesting new thing that's come out. This group in Europe had done a previous study showing the presence of SNAP25 and SV2A receptors in a rat trigeminal ganglion. So they wanted to know if it actually was located in the sphenopalatine ganglion, which they did find in rat and human subjects. So then the question becomes, can we use Botox for SPG ganglion-type pain or cluster headache? There was a pilot study done, and there were only 10 patients. They were looking at safety of Botox, but they did find that over 50% of the patients had greater than 50% pain relief and reduction of their headaches at the six-month mark. So that's promising, and there are random controlled trials looking at this now. Neuromodulation. This is a potential therapeutic modality. There's a lot of small studies. They're high quality, but they do have a small amount of patients and different stimulation settings. But the best random controlled trial was done by Schoen, and that was a sham study that they did with 28 patients, but the response was quite good. Here is the stimulator that they used. So that has a six-contact lead. They implant it along the sphenopalatine ganglia, and then they fixate the anchor to the maxillary sinus there. And what they did is they had the controller, which had high-frequency stem, submax stem, and then no stem. So there was a sham part of the trial. And even with that, patients, 25% of patients, or 68% of patients had significant improvement. 25% had greater than 50% of relief of their treated attacks. 36% had reduced frequency, and 7% had both. So this is a promising thing. We don't have it in the States. This was done in Europe. Another option available to patients, although a little bit more invasive, is traditional stem. So they put a stem lead, put it in the sphenopalatine ganglia, and those leads have been tunneled over and through the neck, and then the impulse generators in the chest. So this is for patients who have failed a lot of things with cluster headache, and they're completely miserable, and they're willing to do something like this. So when you look at the evidence for sphenopalatine blocks, radiofrequency, and neurostimulation, the evidence is good, and the studies were controlled, but we need more larger trials that are randomized control and that need to be replicated. Another interesting thing is deep brain stimulation for chronic cluster headache. Cluster is related to your circadian rhythms annually or a certain time of the day, and this is regulated by the hypothalamus. So there are people doing this for severe refractory cases, but again, this is case studies and case series. And the other reason they thought to do the, they figured to do the posterior hypothalamus, but they're also putting stimulation in the ventral tegmental area. When you look at various MRI scan or functional MRI scan imaging, as well as PET scanning, these are the areas of the brain that are activated during cluster attacks or in between them, enterically or in between cluster bouts. So we have a complex set of events going on here, which can make cluster headache difficult to treat. So occipital nerve stimulation, this has the best evidence for migraine. Cluster headache, it is anecdotal. Occipital nerve stimulation has suffered from some problems. Insurances typically don't pay for it, and you really do need an expert implanter for this, and I'll show why in a minute. A lead placement is controversial. I've seen it placed across the base of the skull. People try to put the leads on the third occipital nerve and the greater occipital nerve in a, going up the back of the head. The random control trials are equivocal at this point, and migraine really only has one. The importance of sending someone to an advanced implanter. This was published in Neuromodulation, where they analyzed adverse events in management of chronic migraine with peripheral nerve stimulation. And as you can see at the top, the patient, up to 90%, well it's 88.9, but 90% of patients had peripheral nerve implant related additional surgeries and problems. And down at the bottom right, the NPPIP, that's basically the interventional pain physician, how many implants they've done. So if they've done five or less, your complication rate is quite high. And what are the complications? So patients will have lead migration, lead breakage, and lead fracture. So I highly recommend if you really think your patient is a candidate for occipital nerve stim, get them to an expert implanter. Cervicogenic headaches, I'll briefly go through this. Basically, it's a headache that is coming from some pain generator in the neck. There's a wide differential for this. Typically, we think of the upper cervical spine as the pain generator, so C1, 2, through C3, whether it's the facet joints, the discs, the ligaments, the muscles. But you can get cervicogenic headache from lower cervical disc herniations. I do see in my clinic where a patient has a C5, 6, C6, 7 disc herniation, they have radicular symptoms, and they have a headache. And the headache goes away or gets better with the epidural injections or as the cervical radiculitis improves. And I've seen headaches go away even after spine surgery for these types of discs. So the biggest thing with cervicogenic headache is finding a diagnosis, and this is what we use our injections for. These are the various types of injections we can do or interventional therapies, but I don't have time to go through all of them. So we'll just go through some pain patterns and the most common ones. So, or the rare ones, AO joint pain is actually rare. You get the suboccipital pain here. There are only three studies that have been published on this type of pain with injections. It's typically similar to AA joint pain. The joint injections provide up to about six months relief, but you do need to repeat them. If you look at the AA joint pain referral patterns, it's very similar to third occipital nerve or the C2, 3 facet joint. AA joint pain is actually much more rare, and third occipital pain is much more common. This study was done by Dyer where he looked at, I think he probably used some medical students and injected facet joints and looked at pain referral patterns. You can see the C2, 3 joint and the C3, 4 facet will go up into the head. And this study was done by Cooper where he looked at patients who had neck pain and headaches. And if you look at the pain referral patterns, you get the neck, the head, the top of the head, the ear, and even into the forehead and the eye. And why would you get facial pain with cervical spine? This is because the convergence of nociceptive sensory input from the upper cervical roots into the trigeminal nucleus, which is why you will see this. So if your patient says they have forehead pain, it still can be from the neck. So these are just some examples of injections. I won't go through in details, but here's an AO joint injection with the head down. That's a post-here approach. This is the AA joint. These injections tend to be more risky because the vascular anatomy. This is a lateral approach into the AA joint. For AA joint, again, there's only one study on this with a small amount of, well, 115 patients evaluated and only 26 of them out of 32 had greater than 50% pain relief, but the pain returns and you have to repeat the injection. Third occipital nerve. This is an interesting nerve. It goes, it has a superficial branch to the back of the neck, but the, it also travels to the dorsolateral surface of the C23 facet joint. And this is actually probably the most common procedure I do for cervogenic headaches. This is an interesting nerve. It's large and it's variable. So the picture on the left will show where we think the third occipital nerve may be, and you'll see people place one needle there and do a block or an RF. Generally, patients generally will fail that. So if you look on the right, the middle picture, when you see the C23 intervention, sorry, not interventional, intervertebral foramen, the length of that, and then the C23 facet joint, that nerve can lie anywhere in that area or even across the area. So the far right picture shows when you're doing an RF procedure that you need multiple needles and multiple burns, or you need to at least cover that area. So if a patient comes back to you and says, you know, I had a C23 RF and it didn't work, please get those images and review them because they may have not had it done appropriately. This is the evidence for cervogenic headache. The best evidence we have, which is level B, is for RFA of the cervical facet joints. And everything else either has no evidence or level C. Finally, really quick, occipital neuralgia. Here's a brief review of the anatomy. We all know that the entrapment theory is the most commonly accepted theory. Most people, they come in, you press on the back of the head, the pain radiates to the front, you do occipital nerve block, and where you're targeting the nerve is where it's accessible to you, not actually where the nerve may be entrapped or where the problem may be. And musculoskeletal ultrasound is advancing this type, these types of injections and this type of work currently. So finally, for occipital neuralgia, the interventions we have are really the steroid injections into the greater occipital nerve or around it, sorry. Depending on what you read, they'll say it's level A or level B evidence, it's pretty good. There are people injecting Botox, there's level C evidence for that. Others are doing cryoneural lysis, pulse RF, regular RF, but really the improvement with these procedures is about a third, and there is recurrence because the nerve regenerates. And then there are people doing occipital nerve stimulation, which has the same problems I discussed before. So to summarize, I hope that we understand there are lots of interventional treatment options for patients. Interventional therapies can provide a diagnosis and alleviate pain. Finding the pain generator can take time, it can be difficult, and even finding the most effective treatment can be frustrating for patients, we've got to hang in there. And for invasive procedures, please refer to an experienced interventional pain physician or a surgeon. Thank you.

headaches

COVID-19

ACE2 receptors

inflammation

migraines

triptans

monoclonal antibodies

self-management strategies

post-concussive exertional headaches

cerebrovascular function

exercise as a probe

concussion symptoms