All right, let's go ahead and get started. Welcome back to another AAP Virtual Didactic Lecture. This is the second one this morning, so we'll kind of speed through some of the front matter here. I think we're familiar with the goals from this morning. Again, housekeeping stuff. We're going to keep everybody video and audio muted, both for bandwidth and for decreasing distraction for those who are participating. If you have any questions, find me by clicking your participant list. My name is Sterling Herring. I should be up near the top of the list. You can double-click my name and send me some questions during the course of the lecture, and as appropriate, I will ask them when time allows. If you have any general questions, suggestions, or concerns, there's an email address for Candice at AAP, and you can track us down on Twitter as well. Without further ado, we're excited to have Dr. Kelly Heath with us today from the University of Pennsylvania. Dr. Heath, welcome. Thank you. I am going to try to share my screen. This is not what we use as our forum, so I am new to this. I apologize. I'll share my screen. Give me a second. All right. Hopefully everyone can see that. Yes. Okay. So today, I usually use Poll Everywhere to ask a couple of questions. This gives you a sense of kind of the course objectives. If you text that number, 37607, you can access my poll, and my first question is a very simple just to make sure everyone can get into the system of what you think of when you hear the word headache. So I will give you a couple minutes. You can do this by your phone just to text into that poll what you think of, and then I have two more actual questions, and then we'll get started with the lecture. So if anyone wants to participate in the poll, text that 37607. and some people are getting it to work because there are definitely things coming in. So thank you. Okay, so now that I know it works, I'm going to give you our first real question, and that is, which symptom is the most prevalent in the eye of the following? A, difficulty falling asleep, B, hearing difficulty, C, poor concentration, or D, headache. Again, you just text that 37607, and you put in A, B, C, or D. Okay, we seem to be going between headache and poor concentration. I'll give you another 30 seconds and then I'll go to the last question before we start the lecture. So, our last question and hopefully you'll learn these throughout the lecture. Which of the following is an FDA-approved medication for the prophylaxis of migraine? A, sumatriptan, B, propranolol, D, lisinopril, or C, lisinopril, or D, fluoxetine. FDA-approved for prophylaxis of migraine. Okay, most people are between propranolol and sumatriptan. So hopefully those two questions will be answered throughout this lecture. Quickly, the objectives of this lecture will be a brief review of concussion of valve since this is a post-traumatic headache. We're gonna define what post-traumatic headache means, and then we're gonna go over the different types of treatment plans for different post-traumatic headache patterns, including migraine, tension, and cervicogenic. So briefly, traumatic brain injury. Overall, there's roughly 2 1⁄2 million cases a year, and 80 to 90% are mild TBI. So the vast majority are mild TBI, and the majority of those are also considered concussion. Headache is the most prevalent symptom of all severity, including mild to severe TBI. Concussion, considering mild TBIs, you have some red flags in which you immediately seek medical attention. These include a loss of consciousness in greater than five minutes, a Glasgow Coma Scale of less than 15. If your patient is declining in mental status, you see a seizure associated with it, or any motor or sensory deficits, so neurological deficits that go along with the concussion. So this is saying concussion as a mild TBI. There's the Canadian CT head rule, which is one of the numerous rules that help emergency departments determine if they should be imaging. This categorizes into high risk. So these people feel we should be getting a CT head right away if they have a concussion, and that is that GCS less than 15 at two hours, a suspected open or depressed skull fracture, any sign of basal skull fracture, more than or equal to two episodes of vomiting, and age greater than or equal to 65. So the consensus was these should, or were high risk, would possibly need neurosurgical intervention, so should get a CT. Also, medium risk, might not need neurosurgical intervention, but still highly likely to need a CT of the head would be amnesia before the impact. So retrograde amnesia greater than 30 minutes, and to look at the mechanism. So head strikes, if they were ejected far from their vehicle, or fell from a far elevation, those would be reasons to get a CT. Now this is not applicable to non-trauma cases, or anything less than mild, and this was not looked at pediatrics, and obviously open skull fractures and cumulonimbus disorders are exempt from this rule, and would go on to having a CT immediately, regardless of their clinical picture. What do we do when we're looking at a mild TBI patient? Of course, taking the history to get the circumstances of the injury. A symptom inventory. There are three available ones that tend to be used. This is the neurobehavioral symptom inventory, or the NSI-22. Also the post-concussion grading scale is used often, and the river mead, which is often seen in research. If you look at the different colors, it's generally organized in different clusters of symptoms. The red here being the physical symptoms of concussion, the yellow being the concentration or memory, the blue subset of sleep, which is sometimes put in the cohort of physical symptoms, and then green, the subset of the emotional or psychological symptoms. It's good to get a sense of what the symptoms are. These inventories break it down in the patient ratings as to how they feel. They're good at tracking over time, but the reliability per patient is good. It's good to get a good sense of all their medications, especially if you're going to prescribe medications, and also looking for medications that could be worsening their concussion or their cognitive symptoms. And your physical exam, especially your neurological physical exam, key things you should be looking at is all their cranial nerves, their motor and sensory function, including their reflexes. A good neck exam, especially dependent on their mechanism of action, including range of motion, looking for radicular signs like spurling, and for trigger and tender points. A balance exam, the BESS, or the Balance Error Scoring System, is one example of a balance exam that's used widely. And you should also include your cerebellum exam, so your rapid, alternating movements, finger pass-pointing things to testing your cerebellum. Your ocular exam is very important as well, looking for extraocular motions, saccades, convergence disorders, to divergence disorders. So not just looking at acuity, but looking at the motion of the eyes. Cognitive exam, one commercially available, validated in the dementia population is the MOCA, but you should be doing some sort of cognitive exam. Just looking at some of the screening tools that exist is part of your armamentarium. The sac, which is shown down here in blue, this is the sideline assessment of concussion that sideline musculoskeletal and sports medicine doctors will use. It has a symptom grading scale, as well as a cognitive exam embedded in it. Here's the MOCA version one. This is a quick screen of all the different areas of cognition. There's also screening tools for co-founders of concussion, including the Beck Depression Scale. This is the PHQ-9, so looking at their overall health. The PCL looks at PTSD, the Beck Anxiety Inventory to look at anxiety. Here's your Epstein Sleepiness Scale. So these are all scales that some people are using to try to sort out some of the other symptoms that go along with concussion. That brings me to the point of comorbidities and or symptoms of post-concussion syndrome. There's a high number, one third have depression. Sometimes we don't know whether it's a comorbid condition or it's a symptom of the concussion. Same thing with insomnia. 70% have impaired sleep and 25% of those have clinical diagnosed insomnia. This symptom alone is a very strong predictor that the post-traumatic headache recovery will be prolonged. 25% of people have anxiety. 33% of people with concussion have cognitive issues within the first three months and more than a quarter have it greater than a year. These symptoms co-mingle as well as we sometimes have a hard time of figuring out if they are symptoms of the post-concussion syndrome or they are comorbid meaning another disorder. Other factors that go into our concussion evaluation and our headache management is social, cultural and psychological. Interestingly, some countries have no non-existent rates of post-concussion syndrome. Many studies have shown ethnic disparities and different pain prevalences. Greek studies showed us that 90% had full resolution of pain and other symptoms at four weeks. So there were no chronic disabilities for post-concussion in this study. You also have misattribution. So if you look at all those symptoms of concussion, they're not concussion specific, including headaches. So sometimes patients underestimate having a certain symptom prior to injury and they overestimate it after the concussion. So we're not sure if this is partly something that was just untreated prior to the concussion. Litigation also enters into and the adversity environment can exacerbate the frequency of the symptoms. Also the stress, if they're at workman's comp or they have other pain issues that may increase their central pain control system which can make headache hard to manage. So that's just a quick review of how we get to post-traumatic headache because post-traumatic headache is a secondary headache disorder. And that implies that it only occurs after traumatic brain injury. The definition is loosely been categorized as acute which is a headache less than three months duration. Once the headache goes greater than three months, you go into the chronic post-traumatic headache. In order to be defined as a post-traumatic headache, it must develop within seven days of one of the following, either injury to the head itself or if delayed regaining consciousness. So seven days within regaining consciousness following the head injury or within seven days after you would discontinue medicines that you felt were impairing their ability to determine whether they headache or not. The international classification of headache disorders lumps post-traumatic headache into two different disorders. The post-traumatic headache of mild and then post-traumatic headache of moderate and severe. So mild, you'll see that it has associated with none of the following, which is basically criteria that would make them fall into the moderate or severe. So in order to be most post-traumatic headache of mild, they have to have a mild TBI which can be defined as loss of consciousness. But if you see a number two, you don't have to have a loss of consciousness. It can be also associated with one or the following, confusion, disorientation or impaired consciousness, loss of memory before or after the head injury, two or more symptoms suggestive of TBI which include our nausea, vomiting, visual disturbance, dizziness, vertigo, impaired memory and concentration. And then that not better accounted for any other headache diagnosis. Again, you have the other code which is post-traumatic headache of moderate to severe which is basically that criteria then no longer has that none of the following. So this is your moderate to severe. But the same type of headache is just depending on what kind of head injury. The pathophysiology of post-traumatic headache is largely unknown, large numbers have migraine. So they thought it was similar to the trigeminal vascular system theory. Some of our MRIs density studies have shown us that they're actually different than migraine itself. Schwett et al looked at post-traumatic migraine in compared to migraine and healthier and healthy and he found that the areas of pain processing were the areas that were really affected and they were a little different than migraine. Chong also found a similar finding with MRI studies. So again, it's largely unknown and as you'll see different post-traumatic headache has different presentations which is why it's hard to determine one pathophysiology. The prevalence is anywhere from 30 to 90% in the literature. Primary types are migraine and tension and depending on which study as to which one is higher but they make up 60 to 85% of all post-traumatic headaches. So largely they're migraine and tension. There doesn't seem to be a clear relationship with severity of TBI in post-traumatic. So it doesn't look like all the milds are getting it and severers aren't, there's no correlation. Some trends have been found though that they seem to score higher on the MMPI scales especially the hypochondriasis, depression, hysteria and schizophrenia scales. And it has been found post-traumatic headache has been found to be the highest psychopathology of all pain disorders. And when looking at PTSD that seems to increase the frequency and severity of post-traumatic headache. So the first thing in managing post-traumatic headache is really trying to define what it most closely looks like. And these are four broad categories that may define your headache type. So looking at, is it migraine? Is it tension? Is it cervicogenic? Or is it neuropathic? So we're gonna briefly review those four categories. Again, once you define that category, you have, it may not, there's no treatment specifically for post-traumatic headache. So we're gonna define the category and then treat it most like that category but that's not necessarily gonna respond. So when looking at migraine, it's a headache that lasts anywhere from four to 72 hours. So this is the classification of what migraine looks like. It's usually unilateral, has a pulsing quality and it's moderate or severe pain. And then it would be aggravated by routine physical activity. So climbing up the stairs, walking around in your house will make the headache pain feel worse. One of the following are usually, must be associated with the headache. Light sensitivity or sound sensitivity or phonophobia and photophobia and nausea or vomiting. This is poorly understood as to how migraine pathophysiology but the trigeminal cervical complex is thought to be part of it as well as CGRP. So this is where the central sensitization and CGRP are highly regarded as part of migraine and that's where we target our medications and our therapeutics. The treatment is, first line is identify the triggers and try to modify them. And in concussion, a lot of light sensitivity is a trigger. So we look at different tinting and sunglasses which may even include nighttime glasses or computer glasses, blue light filters, those kinds of things to reduce the trigger for the migraine looking at their sleep pattern because that may have been disrupted with the concussion as well and is triggering their migraine. Trying to get them to return to activity as we have learned from the Buffalo treadmill trial that returned activity has improved concussion symptoms. And then different modalities, relaxation, training, cognitive behavioral therapy and biofeedback as well as acupuncture have worked and some of the nerve stimulators along the trigeminal nerve can be tried that lack FDA approval. Just to look at some of the behavioral therapies, cognitive behavioral therapy, interesting when Khaldar did the study, he did wait-listed versus what people write into cognitive behavioral therapy and those that were on the wait list. So waited for the cognitive behavioral therapy had a small size effect that they did better. So he concluded that it may be effective early and with less severe symptoms because as he hypothesized, those in cognitive behavioral therapy were attending to the symptoms and actually had more somatic symptoms. Biofeedback is also another modality and acupuncture as you can see, these are the acupuncture points. So these all have some evidence for some reduction in migraine. Medications, migraine and medications for migraine probably have the most evidence of all the headache patterns. You have different types of medicines. You have your abortives and your prophylactics. So your abortives, when it's mild to moderate, you can try aspirin and incense, but when they become severe, that's when you start using your triptans, some of the newer classes, the CGRPs, as well as your ergots. Your first-line prophylactic and post-traumatic headache tend to be your TCAs, your AEDs and your beta blockers. Of note, the four medications that have FDA approval for migraine include Depakote and Tipiramate, which are your AEDs and propranolol and metoprolol. Although we tend to use TCAs a lot because we have sleep co-commitment and sleep disorders, and TCAs tend to do better for that. And you go with your brain injury, go slow and try to use as few medications as possible. Your second-line prophylactics are your SSRI and SNRIs, as well as your botulinum toxin. And there's no medication that has post-traumatic headache approval. So looking at the ones just for medication review first, the ones that are FDA approved in their mechanism. So you have Tipiramate and Depakote, which are your AEDs. And there's multiple ways they're hypothesized to work for migraine, including the blockage of the voltage-dependent sodium channels and the L-type calcium channels, the inhibited glutamate-mediated excitatory neurotransmitters. They facilitate GABA-A and they reduce CGRP. Your beta blockers, metoprolol and propanolol, are FDA approved for migraine. They are felt to work by inhibiting nitric oxide synthesis, as well as interacting with the serotonergic system, inhibiting the thalamic relay systems, and blocking that central sensitization. Other medications that are used for prophylaxis but don't have FDA indication include your calcium channel blockers, which are thought to block the voltage-gated sodium channel and reducing your cortical excitability. Flanrazazine is actually the most effective and most studied, but it is not approved in the FDA. It is approved in other countries. We tend to use for rapamil here in the US. The SSRIs, they are thought to block your serotonin reuptake. Fluoxetine is one of the more commonly used for migraine. Your TCAs, which block your serotonin norepinephrine and facilitate your endogenous pain control mechanism. We typically amitriptyline, the dose for migraine is anywhere from 25 to 75, but we tend to start at 10 milligrams. And then you have your renin-angiotensin system modulators, your lysinopril, your common example, and that's modulating our thought to modulate ratio reactivity and the sympathetic tone as well as thought to modulate the endogenous opioid system. The newer agents are your CGRP-related peptide agents. You have two classes. You have the monoclonal antibodies, which came on the market first, and they target either CGRP or CGRP receptors. These are subcutaneous medications, and those are amivig, ajv, imgality, and virsepi. They're all new to the market. Well, some are 2018, but they're all newer to the market. And then you have your receptive antagonists, which have Gopansis small molecule drugs, and they're oral, and they actually block the receptor. So these are really new to the market. So this is an emerging field in medications that are being used for migraine. Your abortive medications are your classic ones, your triptans, and that blocks that 5-HT1 receptor. It has a bunch of side effects, pretty much that numbness, tingling, tightness feeling, and that flushing that you feel when you take them. They're contraindicated in anyone with a history of high blood pressure or coronary artery disease. The majority of them are oral. Rizitriptan and zolimitriptan, zomig and maxalt, have that melt under your tongue sublingual type, and sumitriptan have the nasal spray and subcutaneous injection. So these are helpful when you have the patient that has so much nausea that they couldn't take an oral medication. Our older migraine abortive medications are your ergots. They're believed to be non-specific serotonergic agonist invasive constrictor. Your DHE comes in injection or a nasal spray and migranol, and your ergotamine comes as a sublingual tab, and it comes as an oral form with caffeine, and that's cafrogat. Onobotulinum toxin, Yeri did a study of chronic post-traumatic headache and had good results, although it is not FDA approved for this indication. He has 64% improvement. As far as migraine, it is FDA approved for chronic daily migraine only, so more than 14 migraines a month. Under the PREEMP study, it's dosed between 155 and 195 units every three months. This is the paradigm here of the muscles that you inject. 155 is these muscles, and then you increase the temporalis, the excipitalis, the cervical paraspinal, and the temporalis to go up to the 195 dose. The mechanism of action is believed to block peripheral and central sensitization. It was thought that it would relax the head and neck muscles as to how it was working, although the data for chronic tension headache has not panned out, which you would think that if it was doing the relaxation that you would have better results for tension headache, so it is uncertain if that is part of the reason it works. The PREEMP study and the FDA approval came with you had to fail two oral prophylactic agents, so that is why this is a second-line medication. Also, other intervention is the sphenopalantine ganglion block, which is used to be pivoting intranasally to go right to the ganglions and block migraine. The second major category of post-traumatic headache is tension headache. This is much harder to treat. It is defined as generally episodic and bilateral. It is that classic band-like tightening across the forehead. It can last anywhere from minutes to days and should not worsen with activity, which is one of its key features. It is also not associated with nausea and vomiting, but they may have light or sound sensitivity. This is definitely the least understood of all the headache patterns, which is probably part of the reason why it is so hard to treat. The treatment is many. The mainstay of treatment of tension and all tension as well as tension is environmental control and sleep hygiene, so looking at their posture, looking at their computer use, looking at their sleep, those kind of things to try to reduce triggers for their tension headache. Also, progressive return to activity is highly advocated, looking at their caffeine intake and trying to modify it. Other non-medicine managements include physical therapy, stress management, acupuncture, relaxation training, CBT, biofeedback, massage, and trigger points all have some evidence of efficacy for the treatment of tension headache. Looking at some of our physical modalities for tension headache, headache PT, spinal mobilization, and cervical spinal manipulation all have some central tenets that there's myofascial release or massage, but it's not the only thing, so the massage literature showed that it was not as effective as when you add other modalities, so adding the headache PT to give you the therapeutic exercise and other modalities. The traction and stretching exercises showed in the spinal mobilization decreased headache duration, intensity, and frequency. When looking at OMT, this was preferred at the low velocity rather than the high velocity, especially in concussion because you look at the high velocity cervical spinal manipulation, and you think of the rotational forces of concussion, they mirror each other, and it may actually exacerbate the symptoms. There's little literature to support high velocity chiropractic treatment in concussion at this time, although the studies are ongoing. Medications that are used, basically your NSAIDs and acetaminophen are your main things for tension, and there is no preventative medicine known for tension headache. Cervicogenic is another broad category of post-traumatic headache. If you think of the mechanisms of action, it's often a motor vehicle or a pedestric where the neck may be concomitantly injured, so this is often overlooked and missed when you're struggling to manage one of your headache patients. If you're not getting good results, you should go back and do your neck exam again. So you're looking at the cervical spine itself as well as the soft tissues. You should find some kind of restriction of range of motion or pain worse movement, and if you think of the pathophysiology of cervicogenic, it has a lot of overlap with the trigeminal afferent, so where it's housed, where the cervical chain C1 through 3, and where the overlap is, excuse me, interacts with your trigeminal system, giving you a headache pattern. Your treatment is similar to other headache patterns, starting with physical therapy, really to reduce that cervical component. Acupuncture to also look at the muscle, muscular component as well as the pain component. Myofascial release is important. Trigger point injections, again, both looking at the myofascial muscle type component, and nerve blocks, so the underlying nerves that are irritated, trigeminal nerve and occipital nerve can be blocked as part of your treatment paradigm. Medications, there's, again, just like a few, your NSAIDs, muscle relaxants for a short period of time can be used given the muscle component from the neck. Other meds that are tried are your anti-epileptics, your TCAs, and your SNRIs, again, going at that nerve type pain as part of the pathway. When looking at cervical spine interventions, again, you've got to look at your biomechanics of how it's happening, so any of these can be affected, your facets, your ligaments, your dorsal glandulons, your cervical muscles, and your peripheral nerves, so all can target as part of your treatment plan. One of the big part of the treatment plan for cervicogenic is the peripheral nerve blocks. This is showing you a occipital nerve. You look at the overlap in C2, C3, C4, C5, C6, C7, C8, C9, C10, C11, C12, C13, C14, C15, C16, C17, C18, C19, C19, C20, C21, C22, C4, which is generally the nerve roots that are injured with a whiplash or other neck cervicogenic headache. It also converges into your trigeminal nerve spinal tract, so doing the injection, either you do Pivocaine or Lidocaine, when looking at the literature, it's kind of all over the place as to what it does and how much, but in general, half a milligram to two milligrams per site is recommended. The mechanism action, it's thought to be acting on those unmyelinated C-fibers and your thinly myelinated A-delta fibers, and those are what are mediated in the pain. When looking at adding steroids, the literature has not shown efficacy if it's not a cluster headache, so for cervicogenic, really just needing to do Pivocaine or Lidocaine, as this shows, this is right over the greater occipital nerve, which kind of classically radiates the eye. If it's radiating more along the side of the face, then you might want to also block the lesser occipital nerve. Generally can last six weeks or even longer. Trigger points, also the same type of nerve intervention that goes along with cervicogenic, there's classic patterns of headache that go with different muscles, so suboccipitalis, semispinalis, here's the sternocleidomastoid radiation, the temporalis radiation, so when you are doing your NAC exam, you're going to put inflection, extension, rotation, and you're going to find these spots that they're going to complain about. This is the theory as to why it works. The theory of trigger points isn't fully known, but it's thought that there is abnormality in the end-plane potentials, which is making that muscle just continue to be in contraction, and that the trigger point relaxing it will actually reduce that sustained muscle contraction and thereby reducing pain. Again, there's not a whole lot of studies. There's no study in post-traumatic headache that's showing it's efficacious. There is efficacy being seen in studies when it's with cervogenic in addition to nerve blocks. You can use up to 15 milliliters total of lidocaine or bupivacaine at a time, dispersed throughout the muscle, so it depends on how many trigger points. You really want to use your physical exam, and if you find a trigger point that is classically reproducing their pain pattern, then trigger points is definitely something you want to consider as part of your treatment. Neuralgia is another kind of overlap that you can get, especially because nerves are injured by the trauma itself of the injury or a surgery for a microcrania. They have a scar. Sometimes they get a neuroma from the surgical scar as well, so that classic nerve pain from those reasons is the same as all nerve pain. You want to use your oral agents, your AEDs. Cobramazepine is the classic medication for trigeminal neuralgia, but gabapentin, TCAs, SNRs are also used. Topical, so the anesthetic creams, capsaicin, or you're compounded with your gabapentin, those kind of creams. Nerve blocks along the distribution of whatever nerve. This is trigeminal distribution. Occipital, if that's a nerve block and the nerve that's irritated, or there is some evidence for botulinum toxin for trigeminal neuralgia. Overall treatment plan always starts with the environmental modification, so really looking for triggers and trying to reduce those because as you saw through all of this, none of these treatments have really great evidence that they cure. They kind of just keep the headache at bay. The more triggers that you can modify and the more you can get the headache down, the easier they're going to be to treat. It's also very important, especially in concussion, to look for comorbidities and treat those because if those are driving forces, they will help you figure out medications that may be second line in these classic headache definitions, but they become your first go-to because of these comorbid. Because in brain injury, again, we want to try to limit the amount of medications we're prescribing, so if depression is a big part of your clinical presentation with your post-traumatic headache, picking one of those medications that's known to do headache, but also depression may be your first choice. Cognition can also drive the headache. If they're overwhelmed and they're not processing, that may be leading to their headache, so looking at the different agents that have some literature to show improvement, the imantadine or ritalin methylphenidate agents, also managing your sleep, so there's lots of different evidence of medications used in sleep in brain injury and trying to use one of those medications may be more beneficial for you than one of your headache medications because the more you get your comorbidities under control, you may have improvement of a headache without using a headache medication, and the classic topiramy has so many cognitive side effects that we really want to rule out other reasons for the headache before committing them to medications that may actually make their other symptoms worse. Considering the different behavioral therapies and physical therapies prior to oral medicines can benefit your patient. Also, if they have a classic nerve distribution, a simple nerve block may be better than some of the medications. Acupuncture should be considered, and it is of note, as I've said many times, there's not a specific FDA-approved medication for post-traumatic headaches. We're really just trying to define the type of headache it is, and we've rolled out all of their treatment plans, and now we're going to go down the pathway of the headache that it most looks like. Unfortunately, with concussion, it's generally more than one headache pattern, and like I said, probably the biggest headache pattern that's overlooked is the cervicogenic, so looking at the neck as part of your pattern. So that is the basics to, and these are all my many references, so that's the basics to treatment of post-traumatic headache, and I open it up to questions. Thank you very much. Other than caffeine, any other dietary recommendations for individuals with post-traumatic headache? So when you look at the migraine literature, there's a long list of dietary modifications. When you look at the nutraceuticals, magnesium, riboflavin have also been implicated in migraine. I don't think it's necessarily bad to try magnesium or vitamin B. Often, if they have a classic migraine, I'll give them the quote-unquote list of migraine medications or migraine diet to decrease their chocolate or mint and MSG. I do have all my patients start out by doing a headache diary so that we can get a sense that potentially a food is triggering, but I subscribe more to the headache diary than telling them to go on a specific headache diet. Okay, that's really helpful. I'm not seeing any other questions at this time. If any come in here in the next couple of minutes, we will pass them along, but do you have, let's see if we have that, we have your contact information. Yes, we have your email address here. So if we do get further questions, people can reach out to you directly. Is that okay? Absolutely. Okay. Again, thank you so much for joining us. We appreciate it. This was a fantastic lecture and I think will be eminently useful for all of us. Oops. So again, thank you for everybody who joined us. Thank you to Dr. Heath. There's her email address right there, kelly.heath.pennmedicine.upenn.edu. And then you can track us down on Twitter as well, AAP and then me, Sterling Herring. Again, this series, the lectures are updated, the schedule is updated every day. So physiatry.org slash webinars. You can also see past lectures there. They do not require a paid membership. If you have any questions or problems with that, reach out to me and let me know. We can walk you through that. Again, thank you for joining us. We appreciate everybody today and we look forward to having you tomorrow. Thank you. Thank you.

post-traumatic headache

Dr. Kelly Heath

headaches

migraine

tension headache

cervicogenic headache

neuropathic pain

individualized treatment plans