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Last updated on January 1st, 2021 at 05:04 am

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FOODS THAT STOP NAUSEA IN ITS TRACKS.

Posted by Dr. Eric P. Baron on  February 13, 2021

FOODS THAT STOP NAUSEA IN ITS TRACKS.

@Neuralgroover

Nausea is an extremely common symptom across a wide spectrum of diseases. It is one of the main symptoms in the ICHD3 diagnostic criteria for migraine. Nausea is one of the 3 “most bothersome migraine symptoms” (along with photophobia (sensitivity to light) and phonophobia (sensitivity to sound)) which most acute/abortive (as-needed) migraine medication clinical research studies assess as a primary data endpoint in trying to resolve, because it is such a disruptive symptom.

 

As the electrical activity of migraine spreads through the brainstem, it activates the nausea centers of the brainstem, and you are well aware of the misery that follows that. So, are there tricks or things that you can do to lessen nausea other than using standard antiemetics (anti-nausea) medications such as Metoclopramide (Reglan), Prochlorperazine (Compazine), Promethazine (Phenergan), and Ondansetron (Zofran)? Are there certain foods or drinks that can help lessen the nausea? I’ll give you the quick answer which is detailed below. Yes there are!!

 

You may be searching terms such as, what helps with nausea, what helps nausea, how to get rid of a stomach ache, home remedy for nausea, home remedy for stomach ache, feeling nauseous, upset stomach remedies, nausea remedies, what to eat when stomach is upset, stomach upset remedy, stomach upset home remedies, how to help nausea, home remedies for stomach upset, how to get rid of stomach ache, home remedies for stomach ache, stomach ache remedies, best foods for nausea, etc., etc.

 

Let’s talk about how to treat nausea symptoms naturally…

 

Occasionally, Virtual Headache Specialist will allow guest bloggers to write an article on a migraine related topic. How to treat nausea including natural treatments for nausea is one of those very relevant migraine associated topics. It is certainly not a symptom associated only with migraine, and has a very wide range of causes. Whatever the cause may be, it is a miserable symptom to have to deal with. So, I hope the following article gives you some additional firepower to add to your migraine treatment war chest in treating the migraine associated symptom of nausea!

 

FOODS THAT STOP NAUSEA IN ITS TRACKS.

Guest author: Kristen Seymour

 

Nausea: It’s one of those universal human experiences we can all commiserate with. In fact, it’s estimated that each year half of the adult population experiences at least one bout of nausea, which may or may not lead to vomiting. That makes sense because there are many reasons people feel nauseous.

 

WHAT TO EAT AND DRINK WHEN YOU FEEL NAUSEOUS

If you feel sick to your stomach, eating or drinking may be the last thing on your mind. And if your symptoms only last for a short time, abstaining could be the right thing to do.

However, if your symptoms persist for more than a couple of hours, not only is it important to stay hydrated (especially if you vomit or experience diarrhea) but there are some foods and drinks that can help quell your nausea, too. That said, if your symptoms persist for more than a day or are especially severe, you should contact your doctor.

 

WATER AND LIGHT OR CLEAR BEVERAGES

Even when you’re healthy, being dehydrated can leave you feeling pretty crummy. When you already feel awful, dehydration exacerbates the effect. And, if you have a fever and/or ­­struggle to keep food or drinks down, you could become dangerously dehydrated without realizing it. Water alone is a great start, but if you lose fluids through vomiting or diarrhea, you may want to incorporate sips of coconut water, clear juices, or sports drinks. Flat ginger ale can also be a good option, but be cautious with carbonation as this could upset your stomach further.

Beverages and foods that are cold may be more appealing (or less likely to turn your stomach) than warm ones because they’re typically less fragrant. Sip small amounts rather than guzzling a whole glass, and consider sucking on small ice chips or a popsicle.

 

GINGER

This ancient herb has historically been used to relieve stomach upset, and the evidence that it works isn’t only anecdotal, it’s been proven in a variety of modern scientific studies, too. Keep in mind that effectiveness is tied to the amount consumed: Most studies use ½ to 1½ grams (or the equivalent) of dried ginger daily. But many common methods of consuming ginger (ginger tea, ginger ale, candied ginger slices, ginger cookies) make it hard to measure how much you’re getting. Taking ginger capsules or using your own fresh or dried ginger for tea is probably the best way to track your intake. If you’re pregnant or breastfeeding, talk to your doctor before using ginger for nausea.

 

BROTH OR SIMPLE SOUPS

When you’re ready to venture beyond clear fluids, broth is a great next step because it provides hydration, electrolytes, and a little more flavor, which may help you ease into real food. Broth is also a versatile base you can add more nutrition to in the form of chicken (diced small), vegetables, noodles, or rice as your body becomes capable of handling heartier fare. Just be sure to keep the spices and seasonings to a minimum at first.

 

BLAND, DRY STARCHY FOODS

Bread, crackers, rice, noodles, and other similarly simple foods are sick-day staples, although interestingly, this is one nausea-fighting food group that lacks scientific research to back up its effectiveness. It’s believed that starchy foods may help absorb some of the stomach acid that contributes to feeling nauseated, and it’s well-documented that we’re more likely to experience nausea on an empty stomach than when we’ve eaten a little something. So if you’re up for it, try nibbling on a soda cracker or a little steamed rice. You can add a small amount of seasoning, such as salt (or ginger) if it sounds appetizing.

 

APPLESAUCE

Not only is applesauce a gentle, healthy source of carbs (which can help you build back your energy), but it can also benefit you if you’re experiencing diarrhea. That’s because it has high dietary pectin, which helps by binding substances in the intestine, adding bulk to loose stools. Applesauce is part of the BRAT diet (bananas, rice, applesauce, and toast), which has long been a go-to grocery list for people with nausea.

 

BANANAS

Many of the foods on this list can soothe your stomach but lack in overall nutritional value. Not so with bananas. This nutrient-dense fruit is not only soft and easy to eat, it also provides you with approximately 105 calories, 27 grams of carbs, and 12 percent of potassium and 22 percent of vitamin B6 needs for the day (for a medium banana). One tip: The riper the banana, the more fragrant, so if smells turn you off, try a greener one.

 

HERBAL TEA

We mentioned that cold drinks are often more appealing than hot, but sometimes sipping on something warm provides much-needed comfort. In that case, try a caffeine-free herbal tea. See if perhaps peppermint, chamomile, or ginger sounds like something you’d like to sip. You may find that lukewarm or iced works better for you than hot.

 

Each person—and each instance of nausea—is different, so if you’re under the weather, don’t force yourself to eat a particular food if the smell turns your stomach. Listen to your body and take it slow; you’ll be back to your regular meals before long.

 

The original article can also be seen here, as originally published on Health Perch – A Digital Health Magazine.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

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HEADACHE CHART AND HEADACHE LOCATIONS FOR DIFFERENT TYPES OF HEADACHES.

@Neuralgroover

 

I can picture it now. You’re sitting there late at night breaking out into a cold sweat, heart racing, convincing yourself a brain tumor is the cause of your headache as you are Googling a variety of terms such as…

 

…temple headache, headache behind eye, headache behind eyes, headache on top of head, headache in the temples, headache back of head, headache in front of head, headache on one side, front of head headache, headache on right side, headache on left side, headache in temple, headache forehead, pain behind eye, headache behind the eyes, headache and nausea, pain behind eyes, headache on left side of head, headache on right side of head, headache in back of head, front head headache, headache temple, headache at the front of head, stomach upset, left side headache, right side headache, headache behind right eye, temples headache, headache behind left eye, nausea and headache, pain in head, sharp pain in head, neck pain and headache, constant headache, head pressure, ice-pick headache, headache front, pressure headache, sex headache, exertion headache, cough headache, right temple headache, left temple headache, throbbing headache, headache meaning location, frontal headache, types of headaches diagram, headache types chart, pounding headache, headache locations chart, headaches in eyes, pain top of head, headache above left eye, headache map, headache above right eye, etc., etc., etc…

 

Ok, I think you get the point. Sound familiar? Now that you’ve earned your honorary Doctor Google degree, let me help provide some direction for you and your headache self-research.

 

And let me tell you a BIG secret…

 

Headaches are not diagnosed based only on their location. They are diagnosed by the “company they keep”. In other words, the characteristics, patterns, and associated symptoms that go with the headache are the more important key pieces of information which narrow down the most likely headache types. Headache location by itself without any other information is actually quite useless. The International Classification of Headache Disorders (ICHD3) classifies every headache type according to the headache and all of the associated features. Each headache type must match a specific set of characteristics and associated symptoms set forth in the criteria, and headache location is only one of many features taken into account.

 

By combining the headache location with associated symptoms, patterns, and characteristics of the headache, it can then be more accurately narrowed down. This in turn makes choosing the correct treatment more accurate and effective. This is absolutely key. The end result is that you are on the more appropriate path to improvement rather than someone throwing “headache” pills randomly at a headache that they haven’t given a specific name to, and the treatment they are using may not be the treatment that your specific type of headache needs (and sometimes it can even make it worse). I see this scenario in my headache clinic every day given the shortage of headache specialists. This is why I created a FREE headache and facial pain symptom checker as discussed further down.

 

Let’s take migraine as just one example. Migraine can vary widely in its location between patients and between attacks within the same patient. Any one of those Googled headache location terms listed at the top could potentially represent migraine. Those locations could also represent many other specific types of headaches as well, and they would require a much different type of treatment or evaluation than migraine would. The headache location doesn’t fully match with migraine until you combine it with the required criteria of associated symptoms that make the migraine diagnosis which may include a combination of symptoms such as nausea, sensitivity to light (photophobia), sensitivity to sound (phonophobia), throbbing or pounding pain, moderate to severe pain intensity, worsening with exercise, one sided predominance, and of course ruling out other more concerning “secondary” causes of the headaches. So clearly, Googling the headache location alone doesn’t help you figure out the cause or type of the headache at all, nor the most effective treatment. The bottom line is that location of pain alone doesn’t narrow down the type of headache or facial pain that you have. The associated symptoms and patterns that go with the headache are the keys to the possible headache types.

 

Thus, I created a FREE headache and facial pain symptom checker. The purpose is to help you with more personalized self-research with a list of possible headache types to discuss with your local doctor in hopes of helping you and your doctor have a better discussion of possible headache types, as well as better treatment considerations. Remember, any type of headache and facial pain requires an office visit and physical examination with your doctor. This symptom checker tool is purely educational to provoke thinking of a variety of headache possibilities. However, bad causes of headache can present as mild and simple headache disorders such as migraine. So, a visit to your doctor to evaluate your headache is a mandatory step that you must do.

 

When you are trying to narrow down the type of headache or facial pain you may have, these are the additional characteristics and symptoms that you need to take into consideration, and are the key questions a headache specialist will ask you in the office. Go through the following list of headache features, think about each one, and write down your responses. If you have different types of headaches, it is important to focus on and think about only one type at a time (even though they are typically different manifestations of the same underlying headache disorder).

 

1) Location of pain. As mentioned above, pain location is only one of many important characteristics of a headache disorder, but without factoring in the associated symptoms, patterns, and characteristics, it is quite useless alone. I have broken down 8 general patterns of headache and facial pain locations to choose from. Go through the following headache location charts and pick the one that is most consistent with your headache or facial pain location. These are screenshots from the first step of the headache and facial pain symptom checker algorithm. There may be some variation to your attacks and the location may vary between different attacks, so pick the one which summarizes the areas involved overall for the particular type of headache you are analyzing.

 

2) Frequency of the headache or facial pain attacks. How often do the attacks of headache of facial pain occur? Once per day and several days per month, 8 different attacks per day, etc.? Is there a pattern to the attacks, such as a seasonal occurrence?

 

3) Duration of the headache or facial pain attacks. When you get an attack of headache or facial pain, how long does each individual attack last until it goes away completely if it is untreated or unsuccessfully treated? 30 minutes, greater than 4 hours, 15 minutes, several days, etc.?

 

4) Description and characterization of the headache or facial pain. How would you describe the pain of the headache or facial pain if you had to put it into words? Throbbing, pounding, pulsating, achy, excruciating, pressure, electrical, shock, burning, sharp, stabbing, ice pick stabbing, etc.?

 

5) Associated neurological symptoms. Is the headache associated with visual disturbances such as lost vision, flashing lights, shapes, zig-zags, colors, wavy lines, kaleidoscope, jagged edges, etc.? Is there numbness or tingling in an area of the body associated with a headache attack such as on one side of the face and body? Is there weakness on one side of the body with the headache? Are there problems speaking or getting words out with a headache attack?

 

6) Additional symptoms. Is your stomach upset or do you feel nauseated or sick to your stomach with a headache attack? Do you vomit? Do you feel sensitive to bright light and/or loud sound when the headache is at its worst (where you would prefer to be in a dark quiet area if you had the chance)? Does an eye turn red or tear excessively during a headache attack? Does your nose run or get congested on one side during a headache attack? Does your eyelid droop on one side or does it get puffy around an eye on one side with a headache attack?

 

When you are done going through and thinking about all of these headache characteristics, patterns, and associated symptoms, take a run through this FREE headache and facial pain symptom checker algorithm questionnaire which I created to help you with more personalized self-research with a list of possible headache types and treatments to discuss with your local doctor.

 

Good luck, and I hope this tool leads you in a better direction of more educational and useful discussions with your doctor regarding possible headache types and more effective treatment considerations!

 

Do me a HUGE favor and if you have found this headache symptom checker tool helpful and it led to a more successful outcome of narrowing down your headache types and treatments when you saw your local doctor, PLEASE let me know and drop me a message here or on Twitter!!

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

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Last updated on February 18th, 2021 at 12:55 am

WAKING UP WITH HEADACHES: 6 TYPES OF WAKE UP HEADACHES.

@Neuralgroover

WAKE UP HEADACHE

Do you frequently wake up with a headache? This is a common feature with several types of headache disorders, but they are all distinct headache types with completely different treatments. Let’s discuss the 6 most common types of wake up headaches and the reasons why you may be waking up with headaches.

 

1) MIGRAINE

Migraine commonly causes wake up headaches for many patients, and is by far THE most common cause of wake up headaches. Sleep stage transitions can be a trigger for migraine attacks in many patients. Migraine is also susceptible to changes in sleep patterns. So for many, sleeping in (such as on the weekends or on vacation) can be a common (and cruel) migraine trigger leading to waking up with headaches. Thus, trying to maintain a similar sleep schedule on the weekends and weekdays can help with this type of trigger.

 

Other causes of wakeup headache commonly occur in patients that are stuck in chronic migraine (15-30 days per month with at least 8 headache days with migraine features), particularly if they are in rebound headache (medication overuse headache) from excess pain or “as-needed” medications. This occurs when a person with migraine is using triptans, OTCs (over-the-counter pain meds), or NSAIDs (non-steroidal anti-inflammatory drugs) more than 10 days per month, opiates or opioids more than 8 days per month, or butalbital medications such as fioricet or fiorinal more than 5 days per month, on average. Rebound headache occurs because as the patient is sleeping, the overused medication is being metabolized and eliminated from the body and the headache (typically migraine) is triggered as a result of withdrawal from the medication and the need to take more. Patients in this cycle will often notice that after they take their overused medication, the headache calms back down again. It starts to worsen again as they are due for another dose and it is wearing off. This pattern is characteristic for rebound headache. Caffeine withdrawal headache can also be a cause of wake up headaches, for similar reasons as described for rebound headache.

 

Treatments for migraine are discussed here. The key for abortive (as-needed) migraine treatment for waking migraines is that is must be something fast acting to have a chance to catch the migraine. The difficulty with waking migraines is that you are already “behind the ball” by the time you wake with the migraine because you’ve missed the early treatment window where most medications such as the triptans would normally be most effective. So for waking migraines, injectable Sumatriptan (Imitrex), nasal Zolmitriptan (Zomig) or Sumatriptan (Imitrex), are typically going to be the most effective triptans. With that said, sometimes patients can get away with a fast-acting oral triptan such as Rizatriptan (Maxalt) as well. Other options for waking migraines would be DHE (Migranal nasal spray or injection), or one of the new gepants (Nurtec ODT, Ubrelvy) since they can still be effective if taken up to 4 hours past the migraine onset, which is really great and expands the migraine onset treatment window. A neuromodulatory device could also be considered.

 

If you are averaging more than 4 migraines per month, a daily preventive treatment is generally recommended. There are many options for this including a daily pill, natural supplements, a once monthly or quarterly CGRP monoclonal antibody (Aimovig, Ajovy, Emgality, Vyepti), Botox, or a neuromodulatory device.

 

 

2) CLUSTER HEADACHE

Cluster headache is another classic cause of wake up headaches. It is a very distinct form of headache that is easy to pick out with its characteristics. Cluster headache is classified as a trigeminal autonomic cephalalgia (TAC). There are 4 types of TAC syndromes, and cluster headache is the most common of them. The other 3 TAC syndromes are hemicrania continua, paroxysmal hemicrania, and SUNCT/SUNA, none of which are waking headache types. There are some overlapping characteristics between all 4 of these TAC headache types, but cluster headache is the only one that often wakes the patient from sleep.

 

Cluster headaches can occur anytime during the day, but classically occur at the same time every night, often waking the patient up from sleep, many times shortly after falling asleep within an hour or two. Men tend to be affected 3 times more than women, but it is seen in both men and women. It is a severely painful headache, and has been termed “suicide headache” at times because of the pain severity.

 

Cluster headache is characterized by attacks of severe unilateral (one-sided) orbital (around the eye), supraorbital (above the eye), and/or temporal pain lasting 15 to 180 minutes if untreated. There is either agitation/restlessness with the headache attack and/or at least 1 autonomic sign or symptom on the side of the headache [lacrimation (runniness/tearing of the eye), conjunctival injection (redness of the eye), facial sweating or flushing (skin turning blushed), nasal congestion, rhinorrhea (runniness of nose), sense of ear fullness, eyelid edema (swelling), or partial Horner’s syndrome (miosis (pupil becomes small)) and/or ptosis (droopiness of the eye)]. Headache attacks typically occur from 1 every other day to 8 per day for more than half the time during a cluster cycle. Chronic cluster headache is defined by attacks that occur for more than 1 year without remission, or with remission periods lasting less than 1 month.

 

Cluster headache attacks occur in “clusters”, or cycles, of frequent headache attacks. These cycles of cluster attacks may last for weeks or months before they go away completely. Remission periods can last months to years. Cluster cycles often occur at a predictable time of year, such as season changes (Fall and Spring are most common).

 

Treatments for cluster headache are discussed here. In general, at the onset of a cluster cycle, a course of high dosed Prednisone is often started over 1-2 weeks to try to break up or shorten the cycle. An abortive option is also mandatory, and the most effective options are oxygen by a face mask, injectable Sumatriptan (Imitrex), nasal Zolmitriptan (Zomig) or Sumatriptan (Imitrex), or DHE (Migranal nasal spray or injection). A preventive daily treatment is also typically started at the onset of a cluster cycle and there are a variety of options for this.

 

 

3) HYPNIC HEADACHE

Hypnic headache has also been called “alarm clock” headache because it often wakes the person up at almost exactly the same time every night. These recurrent attacks occur only during sleep, causing wakening. They typically occur on 10 or more days per month for more than 3 months. The headache lasts 15 minutes and up to 4 hours after waking. This headache usually begins after age 50, but can occur in younger ages too.

 

The pain is typically mild to moderate, but can be severe occasionally. The pain usually occurs on both sides of the head (as opposed to cluster headache which is 1 sided). There is no restlessness during the headache (as opposed to cluster headache). Hypnic headache is NOT associated with autonomic symptoms [lacrimation (runniness/tearing of the eye), conjunctival injection (redness of the eye), facial sweating or flushing (skin turning blushed), nasal congestion, rhinorrhea (runniness of nose), sense of ear fullness, eyelid edema (swelling), or partial Horner’s syndrome (miosis (pupil becomes small)) and/or ptosis (droopiness of the eye)] (as opposed to cluster headache which requires these autonomic symptoms for diagnostic criteria).

 

Treatments for cluster headache are discussed here. The most common treatments are some caffeine before bed (in those who can tolerate it and not cause insomnia), or upon waking. Indomethacin taken before bed is also a common treatment.

 

 

4) OCCIPITAL NEURALGIA

Occipital neuralgia is a miserable nagging soreness, pain, and headache in the back of the head. I tell patients to think of occipital neuralgia as “sciatica of the head”. It is sometimes associated with cervicogenic headache (headache originating from the cervical spine with associated prominent neck pain), but more commonly occurs by itself. It is typically felt in the suboccipital region (where the base of the skull meets the top of the neck) and radiates variably into the back and top of the head and behind the ears. It can less commonly even radiate to the frontal areas (by the trigeminocervical circuitry in the upper cervical spinal cord and brainstem). It can be one sided or both sides. The pain is often described as an intense stabbing, sharp, shooting, shocking, or burning pain. It often occurs in attacks of pain which may last seconds to minutes, but can also be a continuous unrelenting pain. Sometimes it may not be as intense and may be a lower-level pain such as pressure, aching, soreness or throbbiness. Some patients may have a sensation of numbness or tingling in the back of the head. Associated neck pain is typically in the mix too. The back of the head in the area where the skull meets the neck often feels very sore or tender along the ridge of the skull bone. The pain and tenderness often increase by pushing on the back of the head and along the skull base, or lying on the back of the head. Thus, for some patients, when they lie on the back of the head during sleep, it puts pressure on the occipital nerves and they continue to get more irritated and painful until they may wake the person up from sleep due to the pain.

 

Treatment for occipital neuralgia is discussed in much greater deal here and here. In general, first line options are neck physical therapy to this area, as well as an anti-neuritic pain medication such a tricyclic antidepressant (TCA) of Amitriptyline (Elavil) or Nortriptyline (Pamelor), an anticonvulsant such as Gabapentin (Neurontin), or an SSRI such as Duloxetine (Cymbalta) or Venlafaxine XR (Effexor XR).

 

 

5) SLEEP APNEA HEADACHE:

Sleep apnea is a common cause of a headache present upon waking in the morning. However, in comparison to the headache types listed above, this headache does not “wake you up”, but rather, you “wake up with it”. It generally fades away as the morning goes on and most often has tension type headache characteristics. So if you snore, often feel unrefreshed when you wake up in the morning, and this is associated with a headache, wake with a sore throat or dry mouth, a conversation with your doctor about possible obstructive sleep apnea evaluation should be pursued. If your bed partner witnesses times where you seem to stop breathing during sleep, then this is very likely. Sleep apnea is associated with elevated high blood pressure and increased risk of stroke and heart attack, so it is important to not let it go untreated. During the deep stages of sleep, your brain is replenishing its neurotransmitters. So, if you are not getting into those deep stages because the sleep apnea is disrupting progression through normal sleep stages, fatigue, memory and cognitive complaints are common.

 

Treatment varies depending on the severity of the sleep apnea. This is determined by an overnight sleep study called a polysomnogram. These have historically been done in a controlled setting such as a hotel room, but they are now commonly done remotely in your own bed from home too.

 

 

6) HEADACHE ATTRIBUTED TO INTRACRANIAL NEOPLASM (BRAIN TUMOR)

Lastly, brain tumor is always in the differential (and at the very top of everyone’s mind when they come in the office), depending on age, prior headache history, and other clinical symptoms. These headaches are typically associated with some other neurological complaints or findings on neurological exam such as vision deficit, imbalance, speech dysfunction, memory or cognitive impairment, or one-sided numbness or weakness. However, this isn’t an absolute, and headaches can certainly present by just themselves as well. With all of that said, this is an uncommon reason for wake up headache or headache in general, surprisingly. Thus, why I have listed it last. However, it is still a reason that you should always be evaluated by your doctor for not only wake up headaches, but for any headache, especially if you don’t have a prior history of headaches, it is a different type of headache from your prior headaches, or you have any associated neurological symptoms.

 

These are certainly not the only causes of nocturnal headaches, but they are typically the top 6 that are evaluated for first. Disorders such as nocturnal bruxism (teeth grinding and jaw clenching) and TMJ dysfunction, or headache attributed to temporomandibular disorder can also be a contributor to headaches. However, these types of disorders don’t typically cause the patient to wake up with the pain. In addition, the pain is primarily in the temples, in the areas in front of the ear, into the face, and in the master muscles in the jaw. The headaches related to this are more often a tension type headache in description and not severe, and an ache and soreness in the jaw muscles and around the TMJ regions. A dentist should be able to easily diagnose if there is significant nocturnal bruxism happening by evaluating the teeth. Bed partners are also good historians on observations of teeth grinding during sleep.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

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RIMEGEPANT (NURTEC ODT) VS. ATOGEPANT FOR MIGRAINE PREVENTION. THE GEPANTS AREN’T JUST FOR ABORTIVE TREATMENT ANYMORE!

@Neuralgroover

BACKGROUND

The gepants were the first to emerge as new migraine abortive options, and the first new migraine specific abortive class since the triptans came to market in 1992. The first to become available was Ubrogepant (Ubrelvy) from Allergan in January 2020. Then Rimegepant (Nurtec ODT (orally dissolvable tablet)) became available by Biohaven shortly after in February 2020. The gepants have been game changers in the migraine abortive arena. However, they are now bringing their benefits to the migraine preventive realm, following a mind-blowing trifecta collision of the worlds of gepants, abortive and preventive therapy with Rimegepant (Nurtec ODT) and Atogepant!

 

I can hear you now. Rimegepant (Nurtec ODT) for migraine prevention? Atogepant for migraine prevention? Yes, you heard correctly. Are these available yet? We’ll discuss this and these new options a bit further down.

 

HOW DO THE GEPANTS WORK?

To review, during a migraine attack, the trigeminal nerves release a variety of inflammatory proteins. One of the main proteins is called CGRP (calcitonin gene related peptide). CGRP causes inflammation around the brain and cerebral arteries (“sterile inflammation”) in the dural membrane surrounding the brain, intensified pain signals, enhanced transmission of pain signals through the trigeminal nerves into the brainstem and into the brain, and dilation of the cerebral arteries through the dural membrane, which in turn leads to further increasing pain signals via the trigeminal nerve endings covering the cerebral arteries. The result is intense migraine pain (as you are unfortunately very familiar with). So, if we can block these steps of migraine pain, the attack should be aborted quickly, and not as severe. That’s the thinking here, and that’s where the CGRP medications (gepants and CGRP monoclonal antibodies) come into play.

 

The gepants work as CGRP receptor antagonists, which means they directly target and block (antagonist) the CGRP receptor. This results in the medication “blocking” the CGRP inflammatory protein from sticking to the CGRP receptor to activate it, and thus prevents it from “turning on” these pathways of migraine pain. So, you get reversal of cerebral vasodilation, which decreases the firing off of the trigeminal nerves, and cessation of electrical pain signals. Notably, the gepants do this in a way that does not cause vasconstriction, in contrast to the triptans. Thus, they are felt to be safe in those with cardiovascular or cerebrovascular disease (as opposed to the triptans). By blocking the CGRP receptor, you also get reversal of the neurogenic inflammation going on through the brain and around the arteries, and you block the electrical transmission of migraine pain from traveling from the trigeminal nerves into the brainstem, and ultimately into the brain.

 

GEPANTS FOR MIGRAINE PREVENTION

Rimegepant (Nurtec ODT) and Ubrogepant (Ubrelvy) were created and FDA approved for the abortive (as needed) treatment of migraine in 2020. The goal of migraine abortive treatment is to stop individual migraine attacks at onset so the migraine does not reach full severity, ends quickly, and your function is restored and maintained. We want you to avoid having to go lay down and miss that family/social event, work meeting, or whatever else you had planned, and instead end up spending the whole day in a dark quiet bedroom. As opposed to conventional migraine abortives such as triptans, NSAIDs, and other analgesics, the gepants have the unique characteristic that they do not cause rebound headache (medication overuse headache), which is why they have also been evaluated as daily preventive medications as we’ll discuss below.

 

Abortive treatments are in contrast to migraine preventive treatments which are a continuous treatment (not just taken as needed). Preventive treatments include a daily pill, a monthly/quarterly treatment such as CGRP mAbs (Aimovig, Ajovy, Emgality, Vyepti), or neuromodulation devices. The goal of migraine preventive treatment is to lessen the frequency and/or severity of migraine attacks and are discussed in more detail here. If you have migraine, you want to have both a good abortive and preventive treatment plan to lessen migraine’s nasty habit of interfering and disrupting life and function.

 

Notably, for many decades, we have never had migraine specific preventive treatment. What I mean is that the treatments we have always used have been adopted from and limited to medications including antiseizure, antidepressant/anxiety, and blood pressure medications. Although many patients certainly do well with these preventive options, none of these medicines have been scientifically engineered and created specifically to target migraine pathophysiology for migraine prevention. That was until 2018 with the first once monthly self-injection CGRP monoclonal antibody (mAb) Erenumab (Aimovig) came to market, and was followed by 3 more CGRP mAbs; Fremanazumab (Ajovy), Galcanezumab (Emgality), and Eptinizumab (Vyepti).

 

The CGRP mAbs were a major step forward for migraine prevention. However, up to this point, we still have not had an oral pill that has been engineered and created purely and only for migraine prevention (not “adopted” from a different medicine class). That was until now. These new gepant medications will be the first in history to assume this new role.

 

As mentioned earlier, the worlds of the gepants, abortive and preventive treatments are all colliding. There are 2 gepants which have been submitted to the FDA for their pending approval as migraine preventives, and both seem very effective!! As of now, neither has officially received FDA approval for migraine prevention yet. Stay tuned to this blog for developments in FDA approval, further data and information.

 

These gepants are Rimegepant (Nurtec ODT, but unknown if the preventive name will be different) from Biohaven and Atogepant (brand name currently unknown) from Allergan/Abbvie. Notably, Rimegepant would be FDA approved as both an abortive and preventive medicine simultaneously, which would be a first ever. Yes, I know your mind has just been blown. Let’s discuss them and the currently available data, which can be found on each company’s website.

 

RIMEGEPANT

Rimegepant 75 mg every other day was studied in the preventive treatment of both episodic (4-14 days per month) and chronic migraine (15-30 days per month) during a 12-week double-blind randomized placebo-controlled treatment which included 747 patients. Patients were allowed to take 1 preventive migraine medication, (excluding CGRP receptor antagonists and CGRP monoclonal antibodies), as long as they were on a stable dose for at least 3 months and did not change it during the study. Patients were instructed to take 1 tablet every other day for preventive purposes during the study. They were allowed to use rescue medications including triptans, nonsteroidal anti-inflammatory drugs (NSAIDs), and other typical analgesics. Rimegepant was not permitted as a rescue medication during the 12-week double-blind treatment phase.

 

A 52-week open-label extension phase was also conducted in which patients dosed rimegepant 75 mg every other day and were allowed to take up to one dose of rimegepant 75 mg as needed on non-scheduled dosing days to treat migraine attacks. The data from this will be forthcoming.

 

The primary endpoint of this study measured the change from baseline in mean number of migraine days per month in weeks 9-12. Secondary endpoints included achievement of at least a 50% reduction in the mean number of moderate to severe migraine days per month during weeks 9-12, change in the mean number of migraine days per month across the full treatment phase (Weeks 1-12), mean number of rescue medication days per month during weeks 9-12, and change in the mean number of migraine days per month in the first 4 weeks (Weeks 1-4). The study met its primary endpoint, demonstrating a statistically significant reduction from baseline in monthly migraine days in patients treated with rimegepant compared with placebo. Patients receiving rimegepant 75 mg every other day (N=348) experienced a statistically significant reduction of 4.3 monthly migraine days for Rimegepant compared to a 3.5 day reduction in the placebo group (N=347).

 

Rimegepant was more effective than placebo regarding the percent of participants with at least a 50% reduction in the mean number of moderate to severe migraine days per month during weeks 9-12. Rimegepant was also superior to placebo for the mean change in mean number of total migraine days per month over the 3-month treatment period. The rimegepant and placebo treatment groups were not statistically different with respect to the mean days of rescue medication per month during weeks 9-12.

 

The safety and tolerability of rimegepant across the 12-week double-blind treatment phase was similar to that of placebo. Adverse events (AEs) occurring in greater than 2% of participants in the rimegepant treated group were nasopharyngitis, nausea, urinary tract infection, and upper respiratory tract infection. Nearly all AEs were mild or moderate in intensity. No treatment-related serious AEs were reported in the rimegepant group. Discontinuations due to an AE were low in both groups (rimegepant 2% and placebo 1%). Four (1%) participants who were treated with rimegepant and 2 (1%) participants who were treated with placebo experienced transaminase (ALT or AST) elevations greater than 3x upper limit of normal (ULN). One participant in the rimegepant group had asymptomatic elevation of transaminases with ALT greater than 10x ULN; alkaline phosphatase and bilirubin levels remained within normal limits. One participant in the rimegepant group had bilirubin levels greater than 2x ULN and was diagnosed with Gilbert’s syndrome after genomic testing.

 

ATOGEPANT

Atogepant 10 mg, 30 mg and 60 mg doses once daily were studied in the preventive treatment of episodic migraine (4-14 days per month) during a 12-week double-blind randomized placebo-controlled treatment which included 910 patients. Atogepant met the primary endpoint of statistically significant reduction from baseline in mean monthly migraine days, compared to placebo, for all doses evaluated across the 12-week treatment period. Patients treated in the 10 mg/30 mg/60 mg atogepant arms experienced a decrease of 3.69/3.86/4.2 days per month, respectively, all compared to patients in the placebo arm, who experienced a decrease of 2.48 days.

 

Atogepant also showed statistically significant improvements in six secondary endpoints in the 30 mg and 60 mg once-daily treatment arms. A key secondary endpoint measured the proportion of patients that achieved at least a 50% reduction in mean monthly migraine days across the 12-week treatment period. Results showed that 55.6%/58.7%/60.8% of patients in the 10 mg/30 mg/60 mg atogepant arms, respectively, achieved at least a 50% reduction, compared to 29.0% of patients in the placebo arm. Additional secondary endpoints measured across the 12-week treatment period included change from baseline in mean monthly headache days, mean monthly acute-medication use days, and mean monthly performance of daily activities and physical impairment domain scores. The 30 mg and 60 mg doses resulted in statistically significant improvements in all secondary endpoints, while treatment with the 10 mg dose resulted in statistically significant improvements in four out of the six secondary endpoints.

 

No significant safety risks were observed. Serious adverse events occurred in 0.9% of patients treated in the atogepant 10 mg arm compared to 0.9% of patients in the placebo arm (so basically, no difference). No patients in the atogepant 30 mg or 60 mg treatment arms experienced a serious adverse event. The most common adverse events reported with a frequency ≥ 5% in at least one atogepant treatment arm, and greater than placebo, were constipation (6.9-7.7% across all doses vs. 0.5% for placebo), nausea (4.4-6.1% across all doses vs. 1.8% for placebo), and upper respiratory tract infection (3.9-5.7% across all doses vs. 4.5% for placebo). The majority of cases of constipation, nausea and upper respiratory tract infection were mild or moderate in severity and did not lead to discontinuation. There were no hepatic safety issues identified in the trial.

 

Stay tuned! As more information, data, and official FDA approval is granted for each medication, this blog will continue to be updated…

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

 

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Last updated on February 6th, 2021 at 02:28 am

WHAT A PAIN IN THE BACK OF THE HEAD! OCCIPITAL NEURALGIA, TREATMENTS, AND TECHNIQUE FOR OCCIPITAL NERVE BLOCK.

@Neuralgroover

 

HEADACHE IN THE BACK OF THE HEAD – OCCIPITAL NEURALGIA SYMPTOMS

Occipital neuralgia is a miserable nagging soreness, pain, and headache in the back of the head, often described as a base of skull headache. I tell patients to think of occipital neuralgia as “sciatica of the head”. This back of head pain is typically felt in the suboccipital region (where the base of the skull meets the top of the neck) and occipital region (back of head) and radiates variably into the back and top of the head (by the greater occipital nerve) and there is often pain behind the ear on the effected side as well (by the lesser occipital nerve). This headache in the base of the skull can less commonly even radiate to the frontal areas (by the trigeminocervical circuitry in the upper cervical spinal cord and brainstem). It can be one sided or both sides. The pain is often described as an intense stabbing, sharp, shooting, shocking, or burning pain. It often occurs in attacks of pain which may last seconds to minutes, but can also be a continuous unrelenting pain. Sometimes it may not be as intense and may be a lower-level pain such as pressure, aching, soreness or throbbiness. The back of the head often feels very sore or tender. The pain and tenderness often increases by pushing on the back of the head and along the skull base, or lying on the back of the head. Some patients may have a sensation of numbness or tingling in the back of the head. These headaches and neck pain are commonly intermingled. There may or may not be associated cervicogenic headache (headache coming from the neck) associated with occipital neuralgia.

 

Although patients often have isolated occipital neuralgia, I see many patients with occipital neuralgia who also have associated migraine and chronic migraine. This always creates an even more miserable feedback loop between frequent exacerbations of both the occipital neuralgia and migraine. The reason is because these two headache types influence and feed into each other. For example, 70% of patients with straightforward episodic migraine will get neck pain and tightness at the beginning of a migraine attack. So, if someone is stuck in a smoldering cycle of chronic migraine (15-30 days per month), neck pain and occipital neuralgia are commonly associated. The flip side is if someone has structural abnormalities in the cervical spine (herniated disc, injury, whiplash, etc.), it can also be a contributor to frequent or daily headaches (especially if they have a history of migraine).

 

OCCIPITAL NEURALGIA CAUSES

What are the causes of occipital neuralgia? The cause of occipital neuralgia is most commonly idiopathic, meaning there isn’t a specific cause. If you have had surgery or an injury to the back of the head, this can cause scarring of the tissues in the back of the head and base of the skull where the occipital nerves travel. This scarring can pull, twist, and tangle up the occipital nerves over time which causes persistent occipital pain in the back of the head. Sometimes the cause can be from a lot of arthritis in the upper cervical spine, tight muscles through the upper neck and skull base, or following a viral illness which can cause them to become inflamed.

 

TREATMENT FOR OCCIPITAL NEURALGIA

What is the best occipital neuralgia treatment? Neck physical therapy should always be considered as a first line treatment. The physical therapist can instruct you on the best exercises for occipital neuralgia. The goal is to stretch out and loosen the muscles below the skull base and neck. The occipital nerves pierce directly through these muscles as they travel to the back of the scalp. So imagine what is happening to those nerves if these muscles are in a state of constant tightness and spasm. The muscles will continually squeeze and irritate the nerves traveling through them, which keeps them irritated and keeps the pain going.

 

Along with the neck physical therapy, I typically suggest a daily preventive medication until the patient is consistently doing much better for several months. A more detailed list of commonly used medications for occipital neuralgia can be read here. In general, typical first line options are the anticonvulsants with Gabapentin (Neurontin) being a first line medication, or the antidepressant/anxiety class of medications, with the most effective ones being Amitriptyline (Elavil), Nortriptyline (Pamelor), Duloxetine (Cymbalta) and Venlafaxine XR (Effexor XR).

 

If there is associated chronic migraine or frequent migraine, a migraine preventive medication or treatment should be chosen, optimally one that can be helpful for both disorders. Preventive migraine treatments include daily pills, CGRP monoclonal antibodies (mAbs), neuromodulation devices, and Botox injections. Botox injections in particular are a great consideration for the combination of chronic migraine and occipital neuralgia because it can be very effective for both. I always give additional dosing over the occipital nerves in this scenario.

 

If there is a migraine component (as there often is), it’s always important to make sure to have a good abortive option for migraine exacerbations. NSAIDs (non-steroidal anti-inflammatory drugs) can be helpful for both migraine and the occipital neuralgia component. Diclofenac potassium tends to be one that I prefer, but some people do better with one or another, so it can be a trial-and-error process. If NSAIDs are not effective for aborting the migraine, then a more migraine specific option should be used such as a triptan, one of the new gepant options such as Nurtec ODT (Rimegepant) or Ubrelvy (Ubrogepant), or the new ditan medication Reyvow (Lasmiditan). A neuromodulation device could also be considered.

 

Other treatment options include occipital nerve blocks, occipital nerve stimulators, and occipital nerve decompression to detangle the occipital nerves through the scalp tissue. Most centers have moved away from occipital nerve stimulators since insurance rarely covers them and there are common problems with lead migration (leads move out of place) or lead infection. If there is a strong cervicogenic component along with the occipital neuralgia, pain management procedures such as cervical facet blocks can also be helpful. However, if the patient has only occipital neuralgia and not much of a neck pain component, cervical facet blocks and other procedures targeting the cervical spine are typically not helpful.

 

OCCIPITAL NERVE BLOCKS

Occipital nerve blocks should also be considered and offered. They are easy to perform in the office, can provide quick dramatic relief, and only take a minute or so to do. These can act as both an abortive option to cool down an ongoing flare of both migraine and occipital neuralgia. It can also help to prevent the pain returning for a period of time, or making it much more tolerable. However, they are typically more of a temporary benefit (days to weeks to months). However, I have quite a few patients that can get 3 months of relief until they wear off. I have occasionally seen patients break the cycle of occipital neuralgia for much longer, or even indefinitely, but this should not be the expectation. Unfortunately, it is hard to predict how much benefit one may have, or how long it may last. Pain relief typically occurs rapidly, often within minutes of the procedure, but full benefit should be seen by 2-3 days. There may or may not be some associated temporary numbness in the back of the scalp for part of the day as well. If they are done with steroids, they should not be repeated at intervals any less than 3 months. If they are done without steroids, there is no limitation on how frequent they can be done.

 

For these injections, I prefer to have the patient sitting up on the exam table with their legs hanging over 1 side. Some physicians have them sit backwards on a chair, resting their arms and head on the back of the chair. I stand on the opposite side of the exam table behind them. These are done with an anesthetic (numbing) medication such as Bupivacaine, Lidocaine, or Ropivacaine. Some physicians combine these injections with a steroid, most commonly Triamcinolone (Kenalog) or Betamethasone (Celestone). The existing evidence suggests steroids do not add much value to occipital nerve blocks, unless they are done for cluster headache. However, anecdotally many physicians still feel patients tend to do better with steroids, which makes sense given the inflammatory component of occipital neuralgia and potent anti-inflammatory effect of steroids. I prefer to use a small ½ inch 30-gauge needle (same as for Botox) to minimize the temporary pain of injection, although it takes a bit more force to inject the medicine through the needle.

 

I prefer to do 3 injections per side of occipital neuralgia (or both sides if both are affected) to ensure the occipital nerve is treated at all major points. These spots are illustrated on the photograph below. Some physicians do only 1 or 2, so this varies between physicians. The 1st injection site is located by feeling the occipital protuberance, or inion, (bump in the middle along the skull base), and going 2 fingerbreadths down and 1 over. This is the region where the greater occipital nerve pierces through the musculature. The 2nd injection site is located just lateral to the occipital protuberance, about 1/3rd of the way over between the occipital protuberance and the mastoid process behind the ear. Feel for a small groove in this area. This is the occipital groove, or notch, where the occipital nerve travels. The patient typically has the most tenderness over this spot as well, so it is typically quite easy to find. The occipital nerve travels along side the occipital artery, so it’s important to withdraw the syringe in this location, as well as all locations, prior to injection to ensure there is no blood retraction into the syringe. The 3rd site is located just behind the ear, posterior to the mastoid bone in another palpable groove. This also happens to be where the lesser occipital nerve travels.

 

Side effects of occipital nerve blocks are typically minimal and well tolerated. There are no limitations to activity afterwards and they will not make you drowsy. Some temporary tenderness in the sites is possible. Dizziness and nausea are infrequent brief side effects. Some patients can develop slight divots in the area of injection if steroids are used. If steroids are used, some patients can also feel more energized for a couple days, and sometimes some flushing.

 

Here is an example of how I do a typical bilateral (both sides) occipital nerve block procedure (following discussion of risks, benefits, alternatives, informed consent, etc.). If only one side is done, dosing can be split in two.

 

PROCEDURE

A combination of Triamcinolone (Kenalog) 40 mg (1 cc) OR Betamethasone (Celestone) 6 mg (1 cc) and 9 cc of 0.25% Bupivacaine was prepared in a single syringe and the injection sites were sterilized with alcohol swabs.

For both sides, the greater occipital nerve was injected 3 cm caudal and 1.5 cm lateral to the inion where the main trunk of the occipital nerve penetrates the semispinalis muscle. The needle was placed perpendicular and the needle advanced 1 cm. After aspiration to ensure no obstruction or presence of blood, the area was injected with 2 cc. The needle was then repositioned at the greater occipital nerve at the level of the occipital groove. After aspiration to ensure no obstruction or presence of blood, the area was injected with 2 cc.

For both sides, the needle was repositioned at the posterior border of the sternocleidomastoid at the level of the angle of the jaw, where the lesser occipital nerve is located. After aspiration to ensure no obstruction or presence of blood, the area was injected with 1 cc.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

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Last updated on January 15th, 2021 at 05:21 pm

SYNCOPE EPISODE, SYNCOPE DEFINITION, AND AN EASY TOOL TO QUICKLY RECALL ALL CAUSES OF SYNCOPE.

@Neuralgroover

If you have ever had a syncope episode (passing out, or fainting), you know how scary it can be. It is scary not only from the event itself, but sorting out the causes of syncope can be both scary and frustrating. Syncope is not an uncommon association with migraine attacks. This is most often due to a vasovagal response related to the severe pain of the migraine or dehydration from vomiting. However, many migraineurs can also have some degree of dysautonomia during an attack. Dysautonomia is a dysfunction of the autonomic nervous system, which controls blood pressure, arterial dilation or constriction, heart rate, heart rhythm, sweating, and gastric motility. This is illustrated with migraine associated symptoms such as gastroparesis, dizziness, POTS, and complaints of cold hands and feet during an attack for some.

 

So what is syncope? Let’s first discuss the syncope definition, which is also frequently termed syncope and collapse. Syncope is a temporary loss of consciousness typically due to a brief lack of blood flow to the brain. The most common reasons are from a drop in blood pressure upon standing (orthostatic hypotension), from a vasovagal response (a form of neurocardiogenic syncope), or from the heart not pumping enough blood to the brain from an arrythmia (heart temporarily beating too fast or too low), or a weak heart muscle (such as in congestive heart failure). Near syncope is the term for “almost” having a syncope episode. This is where you feel like you “almost pass out”, and perhaps briefly get dizzy, lightheaded, woozy, and unsteady.

 

Syncope is rarely ever of a true neurologic cause. However, for some reason, this is still one of the most common reasons for neurology consults in the hospital setting. Therefore, I created a simple mnemonic tool that will help you consistently remember every possible cause of syncope to check off your differential diagnosis list of possibilities. I always teach this tool to the residents and medical students who are rotating on the inpatient neurology hospital service because syncope is such a common reason for neurological consultation. However, it can be helpful across all medical specialties since syncope is such a common event across all specialties. It can also be used by patients suffering from syncope to help them gain a better understanding of syncope and syncope causes.

 

The mnemonic tool is CONSNOC. It’s a palindrome spelled the same forwards and backwards. It’s a nonsensical word, but remembering it will quickly bring to memory every possible differential diagnosis of syncope to run through in your mind. Let’s go through each letter:

 

Cardiac: Think the SA (sinoatrial) node, and then think Structural and Arrhythmia causes. Structural can be outflow obstruction or low ejection fraction in CHF (congestive heart failure). Arrhythmia can be from the heart beating too fast (tachycardia) or too slow (bradycardia).

 

Orthostatic: This is from low blood pressure which occurs when someone stands up from a lying or sitting position. It is often seen with dehydration or blood pressure medication doses that are too high. Orthostatic intolerance is another term for this. Since this is typically such a common cause of syncope, near syncope, and dizziness, I have listed a number of treatment suggestions to help with treatment at the bottom of this page.

 

Neurocardiogenic: This is your classic vasovagal response where there is a sudden decrease in heart rate followed by an abrupt drop in blood pressure leading to syncope and collapse (passing out, or fainting). The physiologic mechanism for neurocardiogenic syncope can be triggered by several things. Vasovagal syncope classically occurs with a sudden scare (sees blood, intense pain, fright, etc.). Variants of the vasovagal response also include micturition or defecation syncope (think about the old lady who passed out after standing up from using the toilet, triggered by a large parasympathetic discharge), carotid hypersensitivity (think about the old guy shaving and becomes bradycardic by inadvertent carotid massage from pressing on the neck during shaving), and cough syncope or syncope with coughing.

 

Seizure: This is a common reason for inpatient neurological consult even though syncopal episodes are almost never from a seizure. Look for additional symptoms such as tongue biting, incontinence, and witnesses to the event for description (preceded by staring off, posturing, tonic-clonic activity, etc.). Keep in mind, you can still have convulsions during syncope called convulsive syncope (syncope with convulsions), which are not true seizures but just a manifestation of sudden drop in blood pressure and lack of blood flow to the brain. Incontinence can also occur with syncope, so it does not confirm a seizure cause. The diagnosis of seizure is best made by the company it keeps (associated symptoms with the syncopal event).

 

Neuropathic: This correlates to dysautonomia, also known as autonomic neuropathy. This is neuropathy involving the small nerve fibers that control heart rate, heart rhythm, blood pressure, gastrointestinal motility, sweating, and other things. The result is often a disconnect between blood pressure and heart rate where they are not working in synchronicity together, leading to symptoms such as syncope. There are a wide variety of these disorders, but the top categories to keep in mind are from chronic/toxic autonomic neuropathy such as from diabetes, autoimmune dysautonomia (such as acetylcholine receptor (AchR) autoantibody, paraneoplastic), post-viral dysautonomia, neurodegenerative dysautonomia (such as Shy-Drager Syndrome in Parkinson’s Disease), and POTS (Postural Orthostatic Tachycardia Syndrome). These disorders are often easily diagnosed by a tilt table test, or even a good set of orthostatic vitals.

 

Other: Think additional possibilities such as mechanical (the patient simply tripped or lost their footing), glucose (hyperglycemia, hypoglycemia)

 

Cerebrovascular: Think posterior circulation and vertebrobasilar ischemia. This is the other most common reason for inpatient neurology consultation in terms of TIA (transient ischemic attack) or stroke, but again, syncope is rarely the result of this. If this is the cause, it is typically associated with other neurological symptoms, particularly of the posterior circulation. So, assess for associated brainstem symptoms such as double vision, hemiparesis or hemisensory loss, slurred speech, vertigo, dysphagia, etc. Similar to seizures, the diagnosis of posterior circulation TIA or stroke is best made by the company it keeps (associated symptoms with the syncopal event).

 

As mentioned above, since orthostatic intolerance (orthostasis) is such a common symptom and disorder, here are some suggestions to consider to help treat it.

Guidelines for the Treatment of Orthostatic Intolerance (OI):

 

  1.  Make all postural changes from lying to sitting or sitting to standing, slowly.

 

  1.  Drink to 2.0 -2.5 L of fluids per day. If you have a history of congestive heart failure (CHF), you should discuss fluid intake with your cardiologist to avoid a CHF exacerbation.

 

  1.  Increase sodium (salt) in the diet to 3 – 5 g per day. If not helpful and blood pressure is stable, may try 5-7 g per day. If you have a history of high blood pressure, you should discuss these adjustments with your cardiologist or primary care physician.

 

  1.  Avoid large meals which can cause low blood pressure during digestion. It is better to eat smaller meals more often than three large meals.

 

  1.  Avoid alcohol.  Alcohol and cause blood to pool in the legs which may worsen low blood pressure reactions when standing.  This can aggravate OI.

 

  1.  Perform lower extremity exercises to improve strength of the leg muscles.  This will help prevent blood from a pooling in the legs when standing and walking.

 

  1.  Raise the head of the bed by 6 to 10 inches.  The entire bed must be at an angle.  Raising only the head portion of the bed at waist level or using pillows will not be effective.  Raising the head of the bed will reduce urine formation overnight and there will be more volume in the circulation in the morning.

 

  1.  During bad days, drink 500 cc of water quickly.  This will result in an increased blood pressure within 5 minutes of drinking the water.  The effect will last up to one hour and may improve orthostatic intolerance.

 

  1.  Use custom fitted elastic support stockings.  These will reduce a tendency for blood to pool in the legs when standing and may improve orthostatic intolerance.

 

  1.  Use physical counter maneuvers such as leg crossing, squatting, or raising and resting the leg on a chair.  These maneuvers increase blood pressure and can improve orthostatic intolerance.

 

  1. Avoid temperature extremes, particularly excessive heat.

 

  1. For activity planning involving higher levels of physical activity, try to plan for:

-Before rather than after a meal

-Afternoon rather than morning

-Avoid excess heavy lifting

-Avoid during excessively hot weather

 

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

 

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Last updated on February 4th, 2021 at 11:19 pm

BOTOX (OnabotulinumtoxinA) FOR CHRONIC MIGRAINE; EFFECTIVE PATTERN, TECHNIQUE, AND EVERYTHING YOU NEED TO KNOW. NOT ALL BOTOX TREATMENTS ARE CREATED EQUAL.

@Neuralgroover

Background

Let’s talk about Botox for migraines. Botox (Onabotulinum Toxin A) has been a game changer for the treatment of chronic migraine. I’ve frequently seen it give people their life back (as they often tell me), restored their ability to function normally in all aspects of life, and pulled them from the dark rut of chronic migraine that people get stuck in as described here. It can assist in stopping medication overuse headache (rebound headache), which often accompanies and drives chronic migraine. Once Botox is working, patients can often wean off daily pills being used for migraine prevention. Botox is a neurotoxin made by the Clostridium botulinum bacteria. When ingested, it is the same toxin that causes botulism, a severe form of food poisoning. Yes, this concept freaks many patients out. However, the amount used for chronic migraine is a much lower potency and dose, and when used correctly, can be an amazingly helpful medication.

 

Botox is produced by Allergan (now an AbbVie company), and was FDA approved for the treatment of chronic migraine in October 2010 following this study. Since that time, it has technically remained the only FDA-approved treatment specifically indicated for the treatment of chronic migraine prevention. With that said, the array of standard preventive migraine treatments as well as the CGRP monoclonal antibodies are also commonly used for all spectrum of migraine from episodic migraine (14 or less headache days per month) to chronic migraine (15 or more headache days per month). Most insurances will generally require a failure of at least 2 categories of standard preventive medications before they will approve Botox coverage. With that said, 98% of commercial insurance plans cover Botox, and it’s actually fairly easy to get it approved through Medicare and Medicaid. In addition, Allergan provides a Botox Savings Program which will cover $1500 of any out of pocket costs per treatment and $4000 per year. So for most patients, Botox treatments can be covered 100% between this savings program and insurance coverage.

 

It is my hope that this blog can provide the education and guidance in optimizing Botox procedure precision and technique for medical providers to give the best results, as well as a great educational overview on Botox for patients so they have a better idea of how Botox works, the best pattern to get (which can be shared with their doctors), and what to expect in terms of how long it takes to work, suggested duration of use, side effects, and safety in pregnancy and breastfeeding.

 

How does Botox work for chronic migraine?

The primary and most important mechanism of how Botox works for chronic migraine is by disrupting the electrical communication signals of pain between nerves and ultimately stopping these signals from reaching the pain circuitry of the brain. Thus, it prevents the activation of pain and migraine networks in the brain. Botox does this by entering the nerve endings and cleaving a specific protein called SNAP25. The inactivation of this protein leads to the inhibition (stopping) of neurotransmitter and neuropeptide release from the nerve endings and the prevention of the electrical pain signals from firing off. It also causes temporary (3 months) paralysis of the muscle being innervated by those nerve endings. Thus, it also causes the muscles to chemically relax (by chemically paralyzing them). For example, this muscle relaxation is why Botox works for facial wrinkles. It causes the thin muscular layers to relax to where they can’t contract (and wrinkle the skin), and wrinkles go away. Interestingly, one of the early clues that led to Botox being studied for migraine treatment was that women who were getting Botox were also noticing that they would have much less migraine headaches. This eventually led to further trials looking at Botox treatment to prevent migraine.

 

How long does it take for Botox to work, how long should Botox be used for chronic migraine, and how effective is Botox?

Botox typically starts to kick in within 1-2 weeks, but many times patients say they feel it working within a day or so after they have been getting it for a while. Botox lasts about 3 months. Patients commonly notice some gradually increasing migraines 1-2 weeks or so before getting to the 3-month wear-off window. I have quite a few patients that can actually get a good 4 months out of a treatment, but that is not common. If patients consistently start to come in for their 3-month Botox appointment and migraines are not starting to increase significantly as it is wearing off, I will often try to extend the next treatment to 4 months. If they are still doing well at that time, I suggest that we try stopping it to see if the migraines have entered and sustained into a more infrequent episodic pattern. It can always be restarted if needed in the future. It should be avoided from repeating much earlier than 3 months because early dosing before the prior dose has worn off can lead to cumulative medication and subsequent side effects. This can also increase the risk of antibody formation against Botox which can make it less effective over time.

 

It is recommended to give the Botox a minimum of 2 rounds 3 months apart to get a good sense of how much benefit one can likely expect. The reason for this is that in the trials after the 2nd round, there was continued upwards improvement. With that said, I typically expect (and usually see) good improvement with the 1st round. Some doctors advocate for giving a full year (4 rounds separated by 3-month intervals) to see the full effect. However, I typically tell patients if they have gotten absolutely no benefit after the 2nd round that we should move on to another treatment option. On average, Botox decreased chronic migraine days by 8-9 days per month, as opposed to placebo which was 6-7 days per month.

 

What are the Botox side effects?

A great thing about Botox is that it is so well tolerated with much lower side effect risks compared to many of the medications used for migraine prevention. I’ve done thousands of Botox treatments and have never seen someone have a bad reaction or an allergic response. In general, I tell patients there may be some tenderness in the injection sites temporarily. It is a very tiny needle injected just under the skin in a specific standardized dosing pattern and takes only a few minutes. Infrequently, patients can have a temporary flu-like muscle achiness for a day or so after the Botox. If the Botox spreads into some of the muscles in the forehead, I always mention that there is a risk of eye lid droopiness (ptosis), although I have not seen this occur. A more extensive list of potential side effect risks (which are extremely rare and I’ve not seen), can be read on the Botox for chronic migraine Allergan website. Caution is also advised if Botox is mixed with bupivacaine or other “caine” medications as this can be a fairly common allergy of some patients to these medications.

 

Can I get Botox with the Covid-19 vaccine?

The short answer is that we need to gather more data on this, so check back periodically for updates. However, this hasn’t been a reported issue thus far. Patients receiving Botox were not excluded from the Covid-19 vaccine trials. There is no evidence at this time that Botox can not be used along with receiving Covid-19 vaccination, nor does it need to be delayed or timed any differently in relation to receiving Covid-19 vaccination. Most physicians feel that there should theoretically be no interaction or contraindication to receiving both because they are entirely different proteins with different mechanisms of action. The Covid-19 vaccine stimulates the immune system to form antibodies against the virus, should you encounter it.  However, Botox does not have any significant influence on the immune system (it does not cause immunosuppression, etc). Rarely, the immune system of some patients can form neutralizing antibodies against Botox, and this can weaken Botox’s effectiveness in decreasing migraine frequency and severity. However, this issue really has nothing to do with the mechanism and how the Covid-19 vaccine works. So, it is not felt that the Covid-19 vaccine will lessen the effectiveness of Botox, nor will Botox lessen the effectiveness of the Covid-19 vaccine. The topic of Covid-19 headache, Covid-19 vaccination, and the use of Botox or CGRP monoclonal antibodies (Aimovig, Ajovy, Emgality, Vyepti) is discussed further here.

Notably, there have been just a few isolated reports of dermal fillers used in dermatology causing some facial swelling in association with Covid-19 vaccination. These reports were with the Moderna Covid vaccine and resolved with steroids and/or antihistamines.

 

Is Botox safe in breastfeeding and pregnancy?

Historically, Botox has generally been avoided and saved as a last resort option in these scenarios, and often still is. The longstanding concern for using Botox during breastfeeding is based in theoretical concern that the Botox could seep into the breastmilk and effect the baby, although this really hasn’t been reported. It has been shown that Botox is not detectable in the blood after intramuscular use, so excretion into breast milk is considered unlikely. In fact, there was a reported case of a lactating woman who had foodborne botulism. However, when the breastmilk and infant were analyzed, neither showed any botulinum toxin at all, and the infant was safely breastfed. With this in mind, the doses of Botox used medically are much lower than those that cause botulism. Therefore, the amounts ingested by an infant, if any, are suspected to be small and not cause any adverse effects in breastfed infants. Regardless, for extra precaution, it is suggested to breastfeed before the Botox treatment, store some milk, and then wait a few hours after the treatment before breastfeeding again.

 

Similar to breastfeeding, there are no published studies on Botox use during pregnancy. So, it is still often avoided if possible and saved as a last resort option. However, since Botox is not detectable in the blood after intramuscular use it is not expected to affect fertility or pregnancy outcomes, and an Allergan safety database report has remained consistent with this conclusion. Botox is designated as a US Food and Drug Administration (FDA) pregnancy category C medicine, meaning that there are no well controlled studies in pregnant women, so it should only be used during pregnancy if the benefits outweigh the potential risks. The good thing is that the majority of women naturally get significant migraine improvement during pregnancy (especially 2nd and 3rd trimester) and it is not uncommon to hear migraines go away during pregnancy. So many times preventive therapy may not even be necessary.

 

What is the best way to do Botox for chronic migraine?

If you are going to get Botox, you need to make sure you are getting the optimal dose, pattern, and technique. A headache specialist will have the most refined technique and experience doing Botox injections, and should be sought out to ensure you are getting the best technique if one is available near you. If you cannot find a headache specialist near you, make sure whomever you get the Botox injections from does them very frequently with good reviews. Other doctors that may do Botox injections as alternatives if a headache specialist is not available include some neurologists, pain management doctors, and primary care doctors, as well as some physician assistants (PA) and nurse practitioners (NP). With knowledge of the precise pattern and technique as outlined below, and enough practice, anyone should be able to do Botox procedures proficiently in the office. It is an easy procedure and can provide dramatic improvement in chronic migraine pain and disability.

 

The pattern that should be used and modeled after is the PREEMPT protocol (Phase III REsearch Evaluating Migraine Prophylaxis Therapy), based off the trial that led to FDA approval for Botox in the prevention of chronic migraine. The pattern of injections described and illustrated below are of the PREEMPT protocol. However, sometimes I will tweak some of the injection sites depending on the patient’s pain pattern. For example, if their chronic migraine is 100% one sided, I may give additional on that side in the temporalis muscle and occipital regions, taken from the opposite side where they have no or minimal pain. If they have prominent occipital neuralgia, then I will give additional dosing over the occipital nerves. The PREEMPT protocol used 155-195 units of Botox. Botox vials come in 200 units (either two 100 unit vials or one 200 unit vial). For almost all patients, I use the full 200 units and spread the additional 5 between the trapezius muscles, or use it somewhere else where the pain is most common such as over an occipital nerve in the back of the head. I may use slightly less in patients that have no pain at all in many areas of the head or shoulders and have a very localized pain (such as just in one side of the forehead), are elderly, or young in late teens or early twenties and have not had it before. Regardless, many of the spots the patient may receive it in, they may not have much pain. However, there should still be some degree of symmetry for muscle weakness balance and to still hit potential areas of chronic migraine input that aren’t recognized as overly painful areas by the patient. I also prefer to gently and briefly rub in the Botox spots right after injection. This helps to distract the brain from the immediate injection pain, flattens the area so it doesn’t leave the Botox as a small lump, and helps to slightly spread the area of coverage for the Botox to work (hitting as many of those nerve fibers and neuromuscular junctions as possible with each injection.

 

The depth of injection isn’t supposed to be deep. So if the needle is hitting the bone, it is too deep and will be less effective. The target of the injections is just below the skin and into the top of the muscle. This is where the neuromuscular junction occurs (where the nerves that innervate and control the muscles enter the muscle). This is the main target of the Botox. I like to be strategic where the Botox goes. If your doctor or health care provider is just rapid firing it in (which is always more painful), hitting the bone, you have Botox running down your face, it is more painful than when you get it done with other providers, or you get eye-lid droopiness (ptosis), you should think about moving on to someone with a more refined technique. I see patients all the time that have been getting Botox with me and then they have to get a round sometimes with a different provider for some reason. They invariably say it doesn’t work as well, is significantly more painful, and afterwards they refuse to get Botox with anyone else besides me following that experience. There is validity in that. I’ve spoken to one of the main doctors/scientists involved with developing the original Botox pattern, technique, and dosing for chronic migraine and he agreed that technique and spreading the Botox around strategically and precisely will certainly lead to a better result as opposed to just quickly and less carefully “throwing the injections in”. In fact, they were originally thinking of adding more spots to further spread the Botox around to hit more nerve endings, but they settled on the current pattern to make it easier and less complex to do.

 

The Botox trials were done by mixing Botox in 0.9% normal saline (basically, sterile water). However, I will sometimes mix the Botox instead with a numbing medicine such as bupivacaine or ropivacaine. The Botox typically takes about 1-2 weeks to start kicking in. So the addition of a numbing medicine can provide some temporary relief as the Botox is slowly kicking in. Many times chronic migraine patients are significantly tender throughout their head to the point the hair can “hurt” and feel sore. This is called allodynia, or central sensitization, and is a common finding in chronic migraine. The additional numbing medicine can also provide some temporary relief throughout some of these sore areas. In most patients, they have tenderness over their occipital nerves in the back of the head (occipital neuralgia), and this can also provide some additional temporary relief over these nerves. Many chronic migraine patients also have tenderness throughout their shoulders, and many have associated fibromyalgia. This can also be helpful with some temporary relief through these muscles, and in a way is like getting trigger point injections at the same time.

 

So, let’s go over the treatment pattern that I have seen to be most useful. First, you will need to get the supplies together, of course. For doctors and health care providers who are here to learn how to do Botox or fine-tune their skills, a detailed video of what you need and how to draw up the Botox can be seen here. I won’t go through the detailed steps here in mixing and drawing the Botox up, but in short, you will need:

-Botox 200 units (100 unit vials x 2 are typically used, but single 200 unit vials available too)

-1 cc syringes x 4

-3 cc syringe x 1 (to draw up diluent and mix in Botox vial)

-30 gauge ½ inch needles x 4 (to place on end of 1 cc syringes prior to injections)

-18-22 gauge needle x 1 (to place on end of 3 cc syringe to draw up diluent and mix in Botox vial)

-0.9% normal saline vial x 1 (alternatively can consider 0.25% bupivacaine or similar)

-Alcohol pads

-Gauze pads

 

The Botox procedure: Face and frontal regions of head (frontalis and corrugator muscles)

For these injections, I prefer to have the patient lying supine on their back and I stand at the head of the exam table behind them. That way they don’t see the needle coming towards their face and all spots are easily accessed from the top and sides of the patient. These spots are pretty standard in all patients. The things to keep in mind are not doing the Botox too low in the forehead. This can cause ptosis, eyelid droop, and asymmetric eyebrow pointing (think Joker in Batman). I typically inject somewhere just below the hair line and in the very top edge portion of the frontalis muscles or just above it. The 1stfrontalis muscle injection is identified as drawing an imaginary line from mid-pupil up to the top of the frontalis muscle and injecting there. The 2nd is in a horizontal line about a half inch medial to the first injection on each side. The procerus is injected at approximately the middle of the brow right between the eyebrows. The corrugators are injected just lateral to each side of this central injection, about a half inch to each side. All injection sites are 5 units.

 

The Botox procedure: Side of head (temporalis muscles)

For these injections, I prefer to have the patient lying supine on their back and I stand at the head of the exam table behind them. That way they don’t see the needle coming towards their face and all spots are easily accessed from the sides of the patient. The way that I teach our headache fellows and other staff to do the temporalis muscles are to have the patient clench their jaw and feel for the temporalis muscle to contract. This is felt at the anterior point of the muscle just behind the hair line in the temple region. This is the 1st injection. From here, imagine a triangle with this 1st injection as the 1stpoint in the triangle. Then draw an imaginary triangle from here extending further back on the side of the head with the next 2 injection points above and below (see illustration) this 1st point. Then from here, imagine a square connected to the triangle. The next 2 injection points are horizontal and further back from the prior 2 injections points. All injection sites are 5 units.

 

The Botox procedure: Back of head (cervical paraspinal and occipitalis muscles)

For these injections, I prefer to have the patient sitting up on the exam table with their legs hanging over 1 side. I stand on the opposite side of the exam table behind them. The cervical paraspinal muscles are injected 1st on each side. The 1st cervical injection site is located by feeling the occipital protuberance (bump in the middle along the skull base), and going 2 fingerbreadths down and 1 over. This happens to be where the greater occipital nerve pierces through the musculature, and is also the first site of where occipital nerve blocks are done. The 2nd cervical injection site is located just superior and lateral to the 1st injection site.

 

Next come the 4 occipitalis muscle injections. These are done along the skull base and are evenly spaced out. The 1st site is just lateral to the occipital protuberance. The 2nd site is lateral to the 1st over the occipital groove (this is a palpable groove). This is where the occipital nerve travels, and is also the 2nd site where I normally do an occipital nerve block. The 3rd site is lateral to the 2nd site. The 4th site is lateral to the 3rd site and is located just posterior to the mastoid bone in another palpable groove. This also happens to be where the lesser occipital nerve travels, and is typically the 3rdspot I usually do for an occipital nerve block.

 

If the patient has prominent occipital neuralgia on one or both sides, instead of the standard 5 units over the occipital groove region (where the occipital nerves travel), I will inject 10 units at once and take that extra dose away from the shoulder or temporalis muscle regions (depending on where they typically have the least amount of pain and may not need it as much). Otherwise, all injection sites are normally 5 units. Notice that the PREEMPT protocol does not include Botox injections further down through the neck. The reason is because this can often increase headaches and can cause head drop to the point where some patients may need to wear a soft collar for 3 months. Therefore, this area should be avoided.

 

The Botox procedure: Shoulders (trapezius muscles)

For these injections, I prefer to have the patient sitting up on the exam table with their legs hanging over 1 side. I stand on the opposite side of the exam table behind them. Patients with chronic migraine most often have a lot of neck and shoulder pain. 70% of patients that get a migraine will get pain and tightness in these regions. So, if they are stuck in a smoldering cycle of chronic migraine and high frequency headaches, it would make sense that they would have a lot pain and tightness in these areas. Many patients also have concurrent fibromyalgia, so these injections can also be helpful, similar to trigger point injections. The 1st 3 injections are along the top ridge of the trapezius muscle. If you feel the superior medial corner of the scapula, there is invariably a tender point and knot here. This is the 4th injection site. The 5th site is in the middle of the trapezius muscle bulk. This is the end of the PREEMPT protocol dosing. However, the last 5 units that is left over I typically split between sides by giving 2.5 units somewhere in the trapezius region on each side where there may be a tender or trigger point, or I’ll just give it all on one side if they have more spasm or pain on one side compared to the other.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

 

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Last updated on January 14th, 2021 at 10:47 pm

STOP LETTING YOUR CHRONIC MIGRAINE AND CHRONIC PAIN DEFINE YOU AND YOUR BRAIN PLASTICITY.

@Neuralgroover

Background

I see the worst of the worst headache, migraine, chronic migraine, facial pain, fibromyalgia, and chronic pain from many states and countries. I see patients who have been debilitated by pain, patients whose pain has destroyed their family, marriage, work life, social life, and the ability to function normally. They are void of hope and have lost all self-esteem and confidence, replaced by depression and seclusion. They hide in the shadows of life. They come into the office with dark sunglasses, hoods up, appear detached, soft-spoken with little to say, and have fully committed themselves to the mindset that they will never get better. And they won’t because they don’t allow their brain to develop the plasticity to escape out of that mindset and behavior. We’ll talk about this concept and brain plasticity more later. I have seen patients who slide into this mindset commit suicide because they see no way out. These patients are rampant and come from all walks of life; professionals such as attorneys to blue collar workers to the jobless. It is an equal opportunity nightmare of chronic pain syndromes. These patients evolve from a once normal life and function to one of minimal to no ability to function normally in life, career, or relationships. I have seen plenty of people pull out of this described rut of a chronic pain lifestyle. It’s possible, but it takes work. Most importantly, it takes the step of convincing yourself that it is possible and will be done, and then readjusting your behaviors, mindset, and thought process accordingly. Give yourself no other option than improvement and realize that there is always hope for improvement. The placebo response in clinical trials involving pain patients (and similar in other subgroups) averages around 30%! That means on average, 30% of pain patients will develop significant improvement despite taking a placebo (fake) treatment. This happens because they convince themselves that they are using the new treatment, and thus they convince their mind that they are improving, and they do! Your mind is the most powerful weapon in your battle against your chronic pain, so learn to use it to your advantage.

 

Let me be clear that chronic pain is real, it is valid, it can be debilitating, it shouldn’t be ignored or overlooked, it can validly negatively impact all aspects of life which can be out of the control of the patient. I profoundly empathize with these patients. However, there is a lot that is in control of the patient which they often do not realize, and that is my purpose for this blog article. Specifically, they do not realize that they are creating a self-fulfilling prophecy of never improving in pain or function, directly related to their behavior and mindset. No, this discussion doesn’t apply to everyone and all cases, but I would say it does apply to the majority of patients.

 

Many of these patients create websites, blogs, and social media accounts dedicated and centered around their chronic pain experiences. Their chronic pain becomes their persona, and who they are. It redefines them. This can certainly be helpful to others to learn about similar pain experiences and to feel that they are not alone, and I think it is fantastic that other patients can have these outlets and sources to share their experiences. However, it can also become a dominating way of life which dissolves away any thought, hope or attempt at improving their pain and overall function. These patients get to a point where living any other way besides centered around their chronic pain would seem abnormal to them. They focus their life, their daily activities, their restrictions, their abilities, and their relationships around their chronic pain. It defines them and dictates their life. They are chained and restrained from this focus. This behavior begins to feed into itself and they continue down a path where there becomes no chance at improvement because they don’t allow their mindset or focus to see that as a valid option, and thus do not initiate behavioral changes to try to influence positive changes.

 

This phenomenon is also reflected in patients who have chronic daily headache, chronic pain, chronic neck pain and whiplash syndrome related to a motor vehicle accident, work related injury, or some other event where they were injured. If there is litigation (lawsuit) involved, it is well known as a clinical predictor that they will rarely improve, because of potential secondary gain (financial, disability, etc.) from their pain, which their subconscious maintains focus on. There have been studies supporting this correlation as well. This phenomenon is not seen in other countries which are not as litigious and ready to sue over anything. We used to have a large unique chronic pain rehabilitation program which was very effective and helpful to many patients. A large focus of this program was on behavioral changes to influence improvements in overall pain and functional abilities. However, patients were excluded from entry if they were involved in any ongoing lawsuit related to their pain, because these patients invariably never got better until the lawsuit was settled and done, and it would be much more beneficial and cost effective to them after legal issues were resolved. We would then admit them following the conclusion of their legal battles if they continued to have chronic pain issues. I have seen many patients reverse their course from that dark reclusive patient scenario described above with the right mindset and approach.

 

How does pain behavior influence brain plasticity and your chances of improvement?

Anatomically and physiologically, this reclusive and socially isolated behavior and mindset of telling yourself that it is impossible for pain to improve or that one cannot function and live a normal life with chronic pain becomes a self-fulfilling prophecy. DON’T LET THAT HAPPEN!! This is solidly based in scientific and biological evidence. Behavior influences cellular, molecular, and physiological changes in the body and brain. Studies have shown that behavior (such as pain limiting behavior, social avoidance, etc.) causes structural and circuitry changes in the brain, which can be lifelong. Social behavior can also cause changes in the brain, although this can be more reversible. These structural changes in the brain and the circuitry of the brain, influenced by behavioral changes (behavioral neuroscience) and mindset, are called brain plasticity. Essentially, plasticity refers to the nervous system’s ability to constantly modify its organization, structure, function, and circuitry connections in response to experiences, behavior, and an endless list of other influencing factors such as pain, stress, diet, emotion, medications, and many other things. Brain circuits related to chronic pain overlap with circuits involving anxiety, depression and some mood disorders. Mood disorders such as depression can affect the plasticity of chronic pain, and likewise chronic pain can influence plasticity of depression and other mood disorder circuitry.

 

Treatment and conclusions of chronic pain

Treatment is difficult, requires patience, and involves treatment trial and errors (if one treatment doesn’t work, another is tried). The single most important treatment involves you, your behavior in how you respond to your pain, your mindset, and attitude which all in turn influence your brain plasticity positively, and chances of improvement. Do not let your pain define who you are and what you are able to do. Expectations are important in that you should realize that (typically) there is no quick fix or “cure” (but if you stumble across one, which can happen, great!). Learning to live, deal, and function with the chronic pain is vital. If you realize this and make it a primary goal, it can in turn lead to improvements over time by modulating your brain plasticity and electrical circuitry. Most preventive treatments can take 2-3 months to see effects, and there is no way to expedite that. Hang in there and be patient.

 

Chronic migraine, fibromyalgia, and some other chronic pain syndromes often cluster together. The way to look at these types of chronic pain syndromes is that the neurological system is “hyperactive”, “overactive” or “hypersensitive”. So, the goal is to try to “turn down the volume” of this “hypersensitive” neurological system with medications or other types of treatments.  Never conclude that there is no possibility of improving. Remain active physically, socially, emotionally, and maintain active relationships. Treating depression or mood disorders is very important, and a good psychiatrist can make a big difference with this. Chronic migraine and chronic daily headache should have appropriate treatments which may include preventive treatments, CGRP mAb once monthly treatments, supplements and natural therapies, neuromodulation devices, eliminating rebound (medication overuse headache), and using appropriate abortive (as needed) therapy such as triptans, gepants and ditans. Most importantly, remain hopeful. There is always hope and there are constantly new types of treatments becoming available. You can do this!!!

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

 

 

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Last updated on February 4th, 2021 at 11:11 pm

CORONAVIRUS (COVID-19) HEADACHE AND TREATMENT, AND WHY YOUR MIGRAINES ARE WORSE WITHOUT EVEN BEING INFECTED.
@Neuralgroover

Background

Covid-19 headache, coronavirus headache, Covid headache and Covid19 headache are all terms for the same headaches which have been on the rise thanks to Coronavirus (Covid-19). This has been happening in patients who have gotten infected with Covid-19. We’ll be discussing that in much greater detail further down, as well as how to treat Covid-19 headache. Headache from the Covid-19 vaccine is also being reported for high proportion of patients, and this is also discussed further down.

Interestingly though, migraines and headache have been worsening in patients who have not been infected at all as well. So how is Covid-19 worsening headaches in patients who haven’t been infected? This phenomenon on worsening headaches related to Covid-19 in patients who haven’t been infected is predominantly occurring in patients with migraine. Let me tell you the reasons why.

 

Why are my migraines worse since Covid-19 and how are they treated?

We look at migraine as an electrical neurological event. It is no longer considered a “vascular headache”, which older terminology suggested. People with migraine have a hypersensitive, or hyperactive, neurological system. So when they encounter triggers, their migraine circuitry switch turns on easier, compared to someone without a migraine history. Basically, they have a lower threshold to trigger a migraine compared to someone without migraine.

Stress is a major, major migraine trigger, and one of the top triggers. Did I mention it is a MAJOR migraine trigger? Ok, you get the point. In addition to stress, there are a wide spectrum of triggers ranging from weather changes, hormones, foods, food additives, too little sleep, excess sleep, and a whole array of others. However, let’s talk about Covid-19 stress.

Unless you’ve been living in isolation in a doom’s day bunker deep in the remote countryside, the Covid-19 pandemic has been very stressful on everyone. So not surprisingly, migraine has also been much worse in general for patients with migraine given these increased stress levels. Everyone’s world has been turned upside down with Covid-19. Our routines and life as we’ve known it were abruptly changed. Parents suddenly became teachers at home, despite no knowledge or ability of knowing how to teach. Screen time skyrocketed (which is often a migraine trigger) from virtual teaching, virtual school, Zoom meetings, and a whole spectrum of other nightmarish virtual work meetings. The frequent crashing of these virtual platforms for many people is also very stress inducing, and likely led to some broken computer screens followed by unanticipated repair costs, and ok, you get the point here. People became socially isolated, which worsened mood for many people, and this often correlates with migraines worsening as well. Spouses and family members found themselves in quarantines and spending way more time together than they were used to or liked to, and that can also be stress inducing for many couples. Kids were home constantly, needing entertainment for their perpetual “I’m bored” complaints, basically just never letting parents get a break, and there were many reports of children actually turning into demons at home. Ok, maybe not, but I think you get the picture. The bottom line is that there have been many changes in our normal routines which were often very intrusive, disruptive, and stress inducing.

In addition to stress, quarantining and working from home have introduced many other variables into day to day life which are common migraine triggers such as changes in eating habits, changes in sleep patterns, types of foods and snacks eaten (which means consumption of more migraine triggering food additives, sugars, etc.), and for some, weight gain (by the way, obesity is associated with a 5x increased risk of chronic migraine (15-30 days of headache with 8 or more days being migrainous).

Treatment of the increased migraine frequency during Covid-19 (or any other time of increase) consists of typical management strategies. Conservative measures including mindfulness techniques such as yoga and medication, diet, hydration, proper sleep and exercise certainly play a role. You’ll want to ensure you have a consistently effective well tolerated abortive/acute (as needed) migraine specific treatment such as the new gepant (Nurtec and Ubrelvy) or ditan (Reyvow) optionstriptans, neuromodulatory device, or other abortive option. If frequency remains high, then preventive treatment should be considered for a few months until migraines improve. Having 4 or more migraines per month is a general guideline of when a preventive treatment is often considered. Preventive treatments include natural therapies, supplements and nutraceuticals, daily medications, CGRP monoclonal antibody therapy (Aimovig, Ajovy, Emgality, Vyepti), Botox, and neuromodulatory devices.

 

What is Coronavirus (Covid-19) Headache?

First of all, the International Classification of Headache Disorders 3rd Edition (ICHD-3) accounts for Headache attributed to systemic viral infection, which is common with many nonspecific infections including viral infections such as the common cold or other upper respiratory viral infections. So headache is certainly not specific only to Coronavirus, but it is common with many common viral infections. These types of nonspecific headaches are diagnosed with the following criteria:

 

  1. Headache of any duration fulfilling criterion C
  2. Both of the following:
    1. systemic viral infection has been diagnosed
    2. no evidence of meningitic or encephalitic involvement
  3. Evidence of causation demonstrated by at least two of the following:
    1. headache has developed in temporal relation to onset of the systemic viral infection
    2. headache has significantly worsened in parallel with worsening of the systemic viral infection
    3. headache has significantly improved or resolved in parallel with improvement in or resolution of the systemic viral infection
    4. headache has either or both of the following characteristics: a) diffuse pain, b) moderate or severe intensity

4. Not better accounted for by another ICHD-3 diagnosis

 

Coronavirus (Covid-19) headache refers to headaches that have been triggered in direct relation to becoming infected with Covid-19, which is also associated with a variety of other symptoms and a positive Covid-19 test. First of all, if you already have migraine, you will generally be much more likely to have an increase in headaches since your internal electrical wiring already predisposes you to having headaches easier when the body is under any stress (emotional, physical, infection, stress, etc.), as discussed above. So if you get infected with Covid-19, you may have an increase in your baseline migraines for this reason, similar to what often happens with other types of infections (including the common cold). However, headache is a common (and often early) Covid-19 symptom in patients who do not have a migraine or headache either, similar to headaches which can be caused by many other types of infections as well.

The Covid-19 associated headache is often daily and commonly has migraine characteristics (throbbing, pounding, nausea, sensitivity to light and sound), or it can have tension type headache character (dull achy pressure throughout head), or a combination of both. One small study reported that Covid-19 associated headaches also had some unusual features, including new rapid onset unrelenting pain (including a thunderclap headache presentation), higher intensity, and association with anosmia/ageusia (loss of smell/taste), diarrhea, reduced appetite, and weight loss.

Coronavirus headache may also present with a story which fits well with New Daily Persistent Headache (NDPH). This is a headache that begins as a daily headache and persists as daily for more than 3 months, without any other known cause. Classically, patients with NDPH often will come into the office and tell you the specific date the headache began and that it has never gone away since. It may fluctuate in the severity levels, but it never fully goes away. It often has an overlapping mixture of migraine characteristics (throbbing, pounding, nausea, sensitivity to light and sound), and tension type headache characteristics (dull achy pressure throughout head). NDPH most often occurs without a clear reason. However, notably one of the most common associations if there is one is a nonspecific viral infection such as a cold or upper respiratory infection that precedes the headache. Covid-19 is simply another type of virus which can be associated with this form of headache.

Covid headache may also be associated with a variety of Covid-19 neurological symptoms. Patients with COVID-19 headache (or without headache) include loss of taste and/or smell, dizziness, muscle weakness, sensory disturbances such as tingling or numbness in the hands and feet, confusion, delirium, persistent neurocognitive symptoms (memory, concentration, attention, etc.), stroke (seen in many young patients as well as older), and seizures.

 

HEADACHES FROM COVID-19 VACCINE

Now that the Covid-19 vaccine is available, Covid-19 vaccine side effects are reported in some patients, including headaches. The Covid-19 vaccine headaches have ranged from mild and a temporary side effect to more severe and extended. So further observation will be useful. Some early data has reported that headaches occur in 35.4% of patients receiving the first Moderna Covid-19 vaccine injection, and 62.8% of patients after receiving the second injection. For the Pfizer Covid-19 vaccine, 41% of patients reported headaches after the first injection, and 51.7% of patients got a headache after the second injection. The Covid-19 vaccine side effects of headaches are typically associated with other common transient side effects of some vaccinations (fevers, chills, body aches, fatigue, exhaustion, soreness at injection site), which are just a sign of your body mounting an immune response in preparation for potential Covid-19 exposure and infection. Regardless, Covid-19 vaccination headache, if present, is milder and of shorter duration than Covid headache from the direct infection itself.

 

CAN I STILL GET BOTOX WITH THE COVID-19 VACCINE?

CAN I STILL USE MY CGRP MONOCLONAL ANTIBODY TREATMENT (AIMOVIG, AJOVY, EMGALITY, VYEPTI) WITH THE COVID-19 VACCINE?

The short answer is that we need to gather more data on this, so check back periodically for updates. However, this hasn’t been a reported issue thus far. Patients receiving Botox or CGRP monoclonal antibodies (Aimovig, Ajovy, Emgality, Vyepti) were not excluded from the Covid-19 vaccine trials. There is no evidence at this time that these treatments can not be used along with receiving Covid-19 vaccination, nor do they need to be delayed or timed any differently in relation to receiving Covid-19 vaccination. Most physicians feel that there should theoretically be no interaction or contraindication to receiving either of these treatments in relation to Covid-19 vaccination because they are entirely different proteins with different mechanisms of action. The Covid-19 vaccine stimulates the immune system to form antibodies against the virus, should you encounter it. However, neither Botox nor the CGRP mAbs have any significant influence on the immune system (they do not cause immunosuppression, etc.). Rarely, the immune system of some patients can form neutralizing antibodies against Botox and the CGRP mAbs, and this can weaken the effectiveness of these treatments in their ability to decrease migraine frequency and severity. However, this rarity really has nothing to do with the mechanism and how the Covid-19 vaccine works. So, it is not felt that the Covid-19 vaccine will lessen the effectiveness of these treatments, nor will these treatments lessen the effectiveness of the Covid-19 vaccine.

Notably, there have been just a few isolated reports of dermal fillers used in dermatology causing some facial swelling in association with Covid-19 vaccination, but not with Botox. These reports were with the Moderna Covid vaccine and resolved with steroids and/or antihistamines.

How is Coronavirus (Covid-19) Headache treated?

Treatment of Covid-19 itself should follow current guidelines as directed by your regular doctor as well as the CDC (Centers for Disease Control) and WHO (World Health Organization) guidelines. For many patients, treatment of Covid-19 headache and the infection itself revolves around symptomatic treatment such as rest, hydration, over the counter common cold and virus type medications (analgesics, decongestants, etc.), and vitamins such as vitamin C, zinc, and vitamin D. Symptomatic treatment basically means you are treating the symptoms rather than the virus itself, as is the case with the majority of viral infections (such as common cold viruses) besides treatable ones such as herpes simplex virus (HSV) and varicella zoster virus (VZV).

However, treatment may also include intravenous medications such as steroids (typically dexamethasone), Remdesivir, and supplemental oxygen, especially for more serious infections. Intravenous antibiotics may also be necessary if the Covid-19 infection progresses to pneumonia, in which bacterial infections begin within the inflamed and injured lung tissue from the Covid-19 infection. There have also been conflicting reports of Covid-19 treatment success with Hydroxychloroquine and Ivermectin, but these are not currently listed in the standard treatment guidelines. Any Covid-19 infection should be evaluated and managed by your doctor to ensure you are optimizing your treatment strategy to prevent progression to pneumonia or other Covid-19 complications. Your treatment may vary depending on the infection severity, your medical history and risk factors for more severe disease, guidelines, and your doctor’s treatment preferences and experience. So, you should see your doctor or local emergency department if you have any symptoms or concern for Covid-19 infection because early treatment is crucial.

If the headaches have migraine features, they can be treated as migraine, tension-type headache, or NDPH with acute/abortive options as detailed above, and preventive daily treatment options, also as detailed above, if the frequency of headaches remains high and is not improving.

Covid-19 vaccination is also recommended in order to prevent infection, as well as prevention of Covid headache and Covid neurologic symptoms.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

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Last updated on January 14th, 2021 at 10:49 pm

WHEN TO SEE A HEADACHE SPECIALIST AND HOW TO PREPARE TO GET THE MOST FROM THE APPOINTMENT.

@Neuralgroover

 

Background

I see patients in our headache center from all over the United States and from many other countries. Many patients travel hundreds of miles by car or airplane for these visits, due to the shortage of available headache specialists (about 570 in the US). Many patients are lucky enough to be relatively close to a headache specialist. Whichever scenario you fall into, you want to get the most out of your appointment with a headache specialist in order to get on a better path to less headache or facial pain burden.

 

When to see a headache specialist

So first of all, when should you see a headache specialist? First off, any type of headache, head pain, or facial pain, is reason enough to see a headache specialist. Basically, headache specialists specialize in any type of pain or discomfort involving anywhere in the head or face. They also commonly see patients that may have other neurological symptoms which may not necessarily be associated with headaches, but their doctor wants to rule out a migraine “equivalent” disorder. Some patients can have neurologic symptoms without headache (visual, sensory, speech, vertigo, weakness, nausea/vomiting, abdominal pain), which may actually reflect a painless migraine disorder, such as migraine aura without headache. I have compiled a list below of a few of my thoughts of when your headache or facial pain treatment journey signals that it is time to see a headache specialist.

 

Reasons to see a headache specialist:

-You have a headache, head pain, or facial pain.

-Your doctor tells you, “your headache is all in your head”.

-Your doctor tells you, “there’s nothing else I can do for you”.

-Your doctor says, “I don’t treat much headache, but…”.

-You continue to have frequent headaches despite trying several preventive medications.

-You just don’t feel like you are making any progress despite a couple office visits with your doctor or their NP or PA (or you never even get to see the doctor).

-You don’t feel like your doctor is listening to you or taking your symptoms seriously.

-The doctor spends only a few minutes in the visit, so you feel rushed and unable to discuss all of your concerns.

-Your doctor is googling your symptoms in the office.

-Your doctor recommends that you take opiates/opioids for migraine treatment.

-Your doctor says it is ok to use NSAIDs, OTCs or triptans more than 10 days per month or butalbital/fioricet/fiorinal more than 5 days per month on average for migraine treatment.

-Your doctor says your headache is “because you are depressed”.

-Your doctor does not give you a more specific classification or name for your diagnosis.

 

What information should you gather before the visit?

Unfortunately, we all know how strapped for time most physicians are during office visits due to a variety of factors such as low insurance reimbursement and the need to increase patient volume to compensate for this and break even. So to get the most out of your office visit, making it efficient and helpful, it is important to compile certain information in preparation. Typing out this information and bringing it to your office visit is a great idea. It is also a great idea to keep this as a running file that you can continue adding to in your personal files. This helps to eliminate time wasted in the office that could easily be organized and thought through prior to the visit, allowing more time for the important parts of the office visit; optimizing the diagnosis and treatment plans. Some of this information you may not have available, and that is certainly ok. You may be able to retrieve some of it from records, memory, and your local pharmacist.

Never assume that your local doctor’s office has faxed all of your records ahead of the visit. If that happens, great. However, many times patients are told that the records will be sent, but when we see the patient, we have no records that were sent. So, it is always best to bring all of your records yourself. Furthermore, it is good to have copies of all of your medical records, testing, etc. for your personal files anyway.

 

The following list are items that I have found to be the most useful for patients to have gathered and thought of prior to the visit, allowing the most efficient and useful office visit:

A) Acute/abortive headache or pain treatments (used “as needed”). This information is also needed in order to pursue insurance approvals for various types of treatments such as the newer gepants (Ubrelvy, Nurtec) or ditans (Reyvow).

-All that have been tried (which triptans, NSAIDs, neuromodulation devices, etc.)

-Doses used

-Responses (effectiveness, side effects) of each treatment

 

B) Preventive headache or pain treatments (used daily to lessen headache frequency/severity). This information is also needed in order to pursue insurance approvals for various treatments such as Botox or the CGRP mAb antagonists (Aimovig, Ajovy, Emgality, Vyepti).

-All that have been tried

-Maximum doses used

-Duration that each treatment was used

-Responses (effectiveness, side effects) of each treatment

 

C) Testing

-All CD and radiology reports for all brain MRIs, CTs, and other relevant testing for your headache or pain. Most CDs do not include the radiology report, and you need to request that separately. It is a good idea to have copies of all of these things for your personal files regardless. Bring them all to the office visit for the doctor to review.

-All bloodwork done in the past 5 years. Labs particularly important for headache evaluations include TSH, CBC, CMP, Vitamin D, Vitamin B12, ESR, CRP, ANA, to name a few, but this may vary and include more or less, depending on the specific clinical scenario.

 

D) Think about the clinical features of your headache or facial pain as listed below. These will be important questions that your headache specialist will ask. So, it is good to answer these questions in your head prior to the visit, so you can provide more accurate and thought out answers. This helps to prevent being put on the spot by questions you never really thought about which may result in forgetting some important details. For a free headache and facial pain self-diagnosis tool which incorporates all of these important questions that a headache specialist asks, look here.

-Location of the headache or facial pain

-Frequency of the headache or facial pain attacks

-Duration of the headache or facial pain attacks

-Description and characterization of the headache or facial pain attacks

-Neurological symptoms associated with the headache or facial pain (visual disturbances, numbness, tingling, weakness, speech disturbances, vertigo, etc.)

-Other associated symptoms with the headache or facial pain (nausea, sensitivity to light or sound, one sided autonomic features (runny eye, red eye, runny or congested nose, droopy or puffiness around eye))

 

Conclusions:

If you are able to gather all or much of the above listed information prior to your headache specialist appointment, you’ll be well on your way to a much more efficient and beneficial office visit. As a result, you and your doctor will be able spend more time in the office discussing the most important things rather than spending it trying to look up records or digging through your memory for various details. As a result, your doctor will have more time to better formulate a list of the most likely diagnoses, and best treatment approaches for minimizing the disruption of your headache or facial pain on your life. Good luck!!

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

 

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Last updated on January 24th, 2021 at 03:04 am

AIMOVIG vs AJOVY vs EMGALITY vs VYEPTI. BATTLE OF THE CGRP MONOCLONAL ANTIBODY ANTAGONISTS; WHAT ARE THE DIFFERENCES AND WHICH IS BEST FOR YOU?
@Neuralgroover

Background

Aimovig vs. Ajovy, Aimovig vs. Emgality, Aimovig vs Vyepti, Ajovy vs. Emgality, Emgality vs. Vyepti, Ajovy vs. Vyepti. So many questions. so many answers. Let’s discuss them all. So it finally happened! The 1st migraine specific preventive medications FINALLY became available with the CGRP (calcitonin gene related peptide) monoclonal antibody (CGRP mAb) antagonists which first came to market in 2018. Prior to 2018, all of the migraine preventive medication options had been “adopted” from other specialties. For example, the 3 main categories of preventive medicines prior to 2018 were select evidence-based options within the anticonvulsant (antiseizure), antidepressant/antianxiety, and antihypertensive (blood pressure) medicine categories. These conventional migraine preventive treatments are certainly still used, can be very effective, and are discussed in much greater detail here. Migraine preventive therapies also include nutraceuticals and natural treatments, and neuromodulatory devices. This blog article will discuss and compare the 4 new options of CGRP mAb medications; Aimovig (Erenumab), Ajovy (Fremanezumab), Emgality (Galcanezumab), and Vyepti (Eptinezumab).

CGRP plays a strong role in neurogenic inflammation in the nervous system and is involved in the transmission of pain. It is also a potent vasodilator (dilates blood vessels), and increases overexcitability of neurons, both factors of which increase the intensity of migraine pain. CGRP has been studied since the early 1980s when it was discovered. It was found throughout the trigeminovascular system and trigeminal cranial nerves which transmit pain, so a role in migraine was suspected. The trigeminal nerves and their associated electrical circuitry throughout the brain, brainstem, and arteries in the brain is called the trigeminovascular system. This system is the basis and “on switch” for migraine. In the early 1990s it was shown that CGRP was released by the trigeminal nerves and levels increased during an acute migraine attack. In 2004, a CGRP antagonist (blocks the binding of CGRP to its receptor) was shown to abort an acute migraine attack, and decrease CGRP levels. Subsequent studies including preventive migraine studies done since 2014 with a CGRP antibody to block the effects of CGRP eventually led to 3 FDA approved CGRP mAbs in 2018, and a 4th CGRP mAb FDA approved in 2020.

 

How are the CGRP mAbs made and what is the science behind them?

The CGRP mAbs are considered biologic drugs because they are made by the cells of living organisms. This is in contrast to conventional medications made by chemical synthesis. The 4 CGRP mAbs are all classified as “humanized” monoclonal antibodies. Humanized CGRP mAbs are made in a laboratory by combining part of a human antibody with a small part of a non-human (such as hamster or yeast) monoclonal antibody by a process called recombinant DNA technology. The non-human part of the antibody binds to the target antigen (in this case, either the CGRP ligand (protein) or CGRP receptor), and the human part makes it less likely to be seen as a “foreign antigen” destroyed by our immune system. To explain further, these humanized CGRP mAbs are produced and cloned repeatedly in non-human immune system living cells (hamster ovarian cells or yeast cells), ensuring that they are all of identical genetic material (monoclonal), and their protein structure is modified to increase their similarity to antibody structures produced naturally in humans.

As a review, antibodies are proteins made by living organism cells which bind unique parts of other proteins that are recognized as a “foreign” to that biologic system. For example, when your body is exposed to a virus or bacteria by infection or immunization, your body makes specific antibodies against that microbe to destroy it. If your body encounters that microbe in the future, it remembers it (immune response), and your antibodies attach to it to neutralize and destroy it.

 

How do the CGRP mAbs work for migraine?

The CGRP mAbs target either the CGRP receptor and block it (antagonist) to prevent the CGRP ligand (protein) from binding, or they target the CGRP ligand itself and prevent it from binding (sticking) to the CGRP receptor. Clinically, some patients tend to respond better to the CGRP receptor blockade, whereas others tend to do better with binding the CGRP ligand itself. There is not really any data on this in terms of who may respond to which type of CGRP mAb target, but I’m sure it will be studied further eventually. In general, the CGRP mAbs tend to all be quite effective. However, the point is if one type of CGRP mAb doesn’t work, it doesn’t mean the others won’t work either. I have seen many patients who did not respond to one type of CGRP mAb, but responded dramatically well to another. So, if you do not respond to one type of CGRP mAb target (such as the CGRP receptor), it may be worth trying another type of CGRP mAb target (such as the CGRP ligand). The bottom-line is don’t lose hope if one type doesn’t work well for you!

The CGRP mAbs are administered by injection or infusion because oral absorption is poor and degradation in the gastrointestinal system would inactivate the antibodies before they would even be able to enter the circulatory system. They are systemically absorbed by transport through the lymphatic system and into the blood. Metabolism occurs in the reticuloendothelial system, not the liver or kidneys.

 

How effective are the CGRP mAbs?

All 4 of the CGRP mAbs have shown excellent tolerability, safety, and superior effectiveness in migraine prevention when compared to placebo. Compared to oral preventive therapies which have been the mainstay for decades (discussed here), the CGRP mAbs work much faster and do not require a slow dose titration, as is done with most oral preventives. They are sometimes seen to be effective in just a few days, often within a month, and the data suggests that the longer a patient is on a CGRP mAb, the more effective it is. I typically recommend a minimum of at least 3 months, and if receiving some benefit at that point, at least 6 months is suggested.

The majority of CGRP mAb studies had at least 50% (half) of patients who were 50% responders (migraine days cut in half), which is great! In general, the CGRP mAbs provide an overall average net reduction of around 2 migraine days per month for episodic migraine and 4-6 days for chronic migraine. With that said, this number can be much higher depending on the patient and migraine characteristics being studied, such as baseline migraine frequency.

There are a group of patients that we see called “super responders” because they improve dramatically to having greater than 75% decrease in migraine days, and sometimes even no migraines. In the CGRP mAb studies, about 1/3rd of patients were “super responders”, with many them obtaining 100% reduction in migraine days. Although this is wonderful to see when it happens, it should not be the expectation or goal (nor should this be the goal with any preventive migraine treatment).

 

What are the CGRP mAb side effects and are they safe in pregnancy and breastfeeding?

Side effects are minimal, and very similar to placebo in most of the studies, which is great compared to the frequent side effects seen with most of the oral preventive pills we often use. The most common side effects are listed in the table below, but mild injection site reactions tend to be the most common reported side effect among the 3 subcutaneous self-injection CGRP mAbs. Cumulative data show no immunological (they do not suppress or alter the immune system because they do not have a target within the immune system), cardiovascular, or neurological safety concerns of significance. CGRP is suspected to play a possible role in regulating uteroplacental blood flow, myometrial and uterine relaxation, and in maintaining normal gestational blood pressure. Since the mAbs have a long half-life and can last in the system for 5 months, it is recommended to stop it about 6 months prior to pregnancy planning. The CGRP mAbs are also not recommended to use during breast-feeding since we do not have enough safety data at this time.

 

Can I use a CGRP mAb with Botox injections or with the gepants (Nurtec, Ubrelvy)?

Insurance companies often present various hurdles to using preferred treatment options (the bane of my existence). One common issue for patients with chronic migraine who are receiving Botox injections is that most insurance companies will now make the patient choose between Botox or the CGRP mAb. There is of course no good scientific basis for this, other than the company doesn’t want to pay for both. In fact, there is evidence that using Botox with the CGRP mAbs works better together than with either individually. An abstract presented at the American Headache Society Annual Scientific meeting in June 2020 showed that in patients with chronic migraine and a baseline frequency of 25.7 days per month, the frequency dropped to 14.8 days with Botox, and 9.1 days with Botox plus a CGRP mAb.

A similar insurance battle often ensues when trying to use the large molecule preventive CGRP mAbs with the small molecule abortive gepant medications (Nurtec, Ubrelvy), which also work by a CGRP mechanism. Insurance companies will often not allow these to be used together, but again, no good scientific basis. Actually, there is some limited evidence showing that these medications can work synergistically together, which would make sense when taking their mechanisms of action into account. Specifically, there was a publication of data from only a 2-patient cohort showing that the use of these acute and preventive CGRP migraine therapies together can be successful and safe. These two patients had been using rimegepant (Nurtec) in a long-term safety study and had added erenumab (Aimovig). The combination of both successfully aborted 100% of their acute migraine attacks. Certainly we need need larger studies to confirm the suspicion that they likely work together synergistically.

The bottom line is that the CGRP mAbs as a class are all very effective for the majority of patients. Ultimately, the one prescribed will often depend on insurance formulary preferences, but there are no “bad options” among them!

 

Clinical comparisons of the CGRP mAbs

There are currently 4 CGRP mAbs available, and each is detailed and compared below in order of FDA approval and becoming available for use. There are some characteristics for each one which can be used to fine tune selection based on specific patient clinical perspectives.

 

Aimovig (Erenumab)

Aimovig was the first of the CGRP mAbs to come on the scene. It is made by Amgen and was FDA approved for migraine prevention 5/17/18. The antibody is produced by recombinant DNA technology in Chinese hamster ovary cells. It is the only one thus far which targets the CGRP receptor rather that the CGRP ligand (protein) itself. Therefore, it binds to the receptor, blocking the ability of the CGRP ligand to bind to the receptor and activate the migraine. It is dosed by either a 70 mg or 140 mg once monthly subcutaneous autoinjector. Since Aimovig came out first, we have longer term data available for it. At close to 5 years on the 140 mg dose, 77% of patients had a 50% reduction in monthly migraine days, 56% of patients had a 75% reduction in monthly migraine days, and 33% of patients had a 100% reduction in monthly migraine days. The dose can be administered to the abdomen, arm, buttocks, or thigh areas.

In post-marketing observations, there have been some reports of hypersensitivity reactions (rash, allergic reactions, itching) in which most were not serious and occurred within hours of administration, and up to 1 week after. Constipation was noted in the studies to occur in a very small percentage (1% for 70 mg, 3% for 140 mg). In post-marketing observations, there have been further reports of constipation with serious complications as well. Constipation occurs after the first dose in the majority of patients who will have this side effect (keep in mind the vast majority do not). Regardless, if you already have problems with constipation, I typically suggest trying one of the other CGRP mAbs (although it doesn’t mean it still can’t be tried). Post-marketing observations have also shown some worsening of pre-existing hypertension or development of hypertension. This observation was most frequently reported within 7 days of administration. Most of these patients already had pre-existing hypertension, or risk factors for developing it.

There is an Aimovig coupon available on the company’s website in which most commercial insurance plans can get the medication for $5 per month, with the first 3 doses free.

 

Ajovy (Fremanezumab)

Ajovy was the 2nd of the CGRP mAbs to come along. It is made by Teva and was FDA approved for migraine prevention 9/14/18. It is produced by recombinant DNA technology in Chinese hamster ovary cells. It targets the CGRP ligand, rather than the CGRP receptor. It binds to the CGRP ligand, interfering with its ability to bind to the CGRP receptor and activate the migraine. It is dosed by either a 225 mg once monthly or 675 mg once quarterly autoinjector or syringe. The dose can be administered to the abdomen, arm, buttocks, or thigh areas. There have been some reports of hypersensitivity reactions (rash, allergic reactions, itching) as well, typically mild to moderate and occurred hours to 1 month after administration. Ajovy has the least potential for constipation, so if that is an ongoing significant issue for a patient, then I typically suggest trying Ajovy first. Ajovy also has the longest half-life, so if the patient tends to wear off early towards the end of the month, it may help to extend relief closer to the next monthly injection.

Of note, in the Ajovy chronic migraine studies, all patients receiving medication were given a loading dose of 675 mg for dose 1 followed by the standard 225 mg each subsequent month. However, this is not how it is normally dosed clinically for patients doing monthly treatments of 225 mg (no loading dose). Therefore, this initial loading dose could have potentially influenced some of the subsequent data.

There is an Ajovy coupon available on the company’s website in which most commercial insurance plans can get the medication for $5 per month.

 

Emgality (Galcanezumab)

Emgality was the 3rd of the CGRP mAbs to come along. It is made by Eli Lilly and was FDA approved for migraine prevention 9/26/18. Notably, it is the only one which also has FDA approval for prevention of episodic cluster headache, which was received on 6/4/19. It is produced by recombinant DNA technology in Chinese hamster ovary cells. It targets the CGRP ligand, rather than the CGRP receptor. Thus, it binds to the CGRP ligand, interfering with its ability to bind to the CGRP receptor and activate the migraine. It is dosed by a 240 mg subcutaneous autoinjector for the 1st month only, followed by a 120 mg once monthly injection thereafter. The higher initial loading dose allows for obtaining a rapid steady state concentration level in the blood compared to Aimovig and Ajovy. The dose can be administered to the abdomen, arm, buttocks, or thigh areas. There have been some reports of hypersensitivity reactions (rash, allergic reactions, itching) as well.

There is an Emgality coupon available on the company’s website in which most commercial insurance plans can get the medication for $0 per month for up to 12 months.

 

Vyepti (Eptinezumab)

Vyepti was the 4th and most recent of the CGRP mAbs to become available. It is made by Lundbeck and was FDA approved for migraine prevention 2/21/20. The antibody is produced in Pichia pastoris yeast cells by recombinant DNA technology. It targets the CGRP ligand, rather than the CGRP receptor. It binds very strongly to the CGRP ligand, interfering with its ability to bind to the CGRP receptor and activate the migraine. It comes in 100 mg and 300 mg doses and is dosed once quarterly (every 3 months) by a quick 30-minute infusion. The 100 mg dose is the recommended starting dose which can be titrated as needed to the higher dose later.

This is the only intravenous (IV) option available. Since it is administered IV, it is 100% bioavailable compared to the bioavailability of the other subcutaneous injections of 50-82%. It also reaches Cmax (maximum concentration) in about 30 minutes compared to 5-7 days of the other subcutaneous injections. Therefore, not surprisingly Vyepti showed treatment benefit in the first 7 days, often as early as 1 day post treatment, and showed continued effect through week 4, which is great since many patients on the once monthly self-injection CGRP mAbs often report a wearing off effect as they are approaching their next due injection.

This is certainly a good first line consideration, but also a good option for patients who do not like the thought of giving themselves a once monthly shot, have injection site reactions, or have failed the other CGRP mAbs options. Studies have shown some impressive highlights compared to other mAbs. In both the chronic and episodic migraine studies, almost 31% of patients had 75% or more reduction in migraine days in the 1st month alone. In the chronic migraine studies, about 27% of patients had a 75% or more reduction in migraine days over the first 3 months with 100 mg. After the 2nd dose (months 4-6), this increased to over 39% of patients! In the episodic migraine studies, over 22% of patients had a 75% or more reduction in migraine days over the first 3 months with 100 mg. After the 2nd dose (months 4-6), this increased to over 33.5% of patients.

There is a Vyepti coupon available on the company’s website in which most commercial insurance plans can get the medication for $5 per infusion every 3 months.

 

Data comparisons of the CGRP mAbs

The comprehensive table which follows compares all available data between the 4 CGRP mAbs, as I have compiled from a combination of published studies, scientific posters, and supplemental data provided from medical science liaisons from each company. I have highlighted some of the data throughout the table when it is a unique aspect or superior response in that category. All 4 CGRP mAbs have variable highlights that makes them stand out from the others in various categories, but overall they are all very effective options as a medication class. It is important to realize that the data compiled in the table should not be considered as a direct head to head comparison between the medications, and not all data points were looked at for each drug. For each CGRP mAb, there were variations and differences in many trial aspects such as the study designs, how responder rates were calculated, statistical analysis used, trial endpoints, some responses were based on open label portions of trials (in which patients typically report a higher response rate when they know they are receiving the drug and not placebo), varying definitions such as “headache of at least moderate severity”, what defined a “headache” or “migraine day”, preventive medications being used simultaneously, and baseline migraine frequencies included in the studies. The extent of reduction in migraine days can be influenced by the patient’s baseline migraine frequency in both the episodic and chronic migraine studies (high frequency vs lower frequency). For example, some studies included patients with a much higher baseline migraine frequency, and thus the extent of their migraine day reduction may not be as great as a group studied with a lower baseline frequency to start with.

 

  Aimovig (Erenumab) Ajovy (Fremanezumab) Emgality (Galcanezumab) Vyepti (Eptinezumab)
Dosing 70 mg or 140 mg once monthly by subcutaneous autoinjector 225 mg once monthly or 675 mg once quarterly by autoinjector or syringe 240 mg subcutaneous autoinjector for 1st month followed by 120 mg monthly 100 mg or 300 mg quarterly by 30-minute intravenous (IV) infusion
Target CGRP receptor CGRP ligand CGRP ligand CGRP ligand
Half-life 28 days 31 days 27 days 27 days
Median Peak Serum Concentration 6 days 5-7 days 5 days 30 minutes (after infusion)
Steady State 3 months 168 days (6 months) After the 240 mg loading dose After 1st dose
Bioavailability 82% 54-57% N/A 100%
Episodic migraine: Reduction in mean monthly migraine days in month 1 70 mg: -2.32 days

140 mg: -2.72 days Placebo: -0.9 days

675 mg quarterly: -3.3 days

225 mg monthly: -3.5 days

Placebo: -1.7 days

N/A N/A
Episodic migraine: Reduction in mean monthly migraine days in months 1-3 N/A 675 mg quarterly: -3.7 days

225 mg monthly: -3.4 days

Placebo: -2.2 days

 

*Months 1-3 in long term extension study (open label):

675 mg quarterly: -4.7 days

225 mg monthly: -4.8 days

120 mg monthly: -4.1 days

Placebo: -2.1 days

100 mg: -3.9 days

300 mg: -4.3 days

Placebo: -3.2 days

Episodic migraine: Reduction in mean monthly migraine days in months 4-6 70 mg: -3.2 +/- 0.2 days

140 mg: -3.7 +/- 0.2 days

Placebo: -1.8 +/- 0.2 days

N/A 120 mg monthly: -5 days

Placebo: -3 days

100 mg: -4.5 days

300 mg: -4.8 days

Placebo: -3.8 days

Episodic migraine: Reduction in mean monthly migraine days in months 1-6 N/A 675 mg quarterly: -5 days

225 mg monthly: -4.9 days

 

*months 1-3 placebo, months 4-6 open label

120 mg: -4.3-4.7 days

Placebo: -2.3-2.8 days

N/A
Episodic migraine: Reduction in mean monthly migraine days in months 1-12 70 mg: -4.22 +/- 0.22 days

140 mg: -4.64 +/- 0.19 days

Placebo: -1.8 days

675 mg quarterly: -5.2 days

225 mg monthly: -5.1 days

 

*months 1-3 placebo, months 4-12 open label

120 mg: -5.13 days

 

*12 month safety study with no placebo

100 mg: -4.6 days

300 mg: -5.2 days

Placebo: -4 days

 

*Reported as months 7-12

Episodic migraine:

50% or more reduction in migraine days in month 1

70 mg: 32.7%

140 mg: 35.5% Placebo: 15.5%

675 mg quarterly: 44%

225 mg monthly: 47% Placebo: 25%

 

120 mg: 50.8%

Placebo: 23.7%

100 mg: 59.3%

300 mg: 56.3%

Placebo: 40.5%

Episodic migraine:

50% or more reduction in migraine days in months 1-3

70 mg: 41.3%

140 mg: 48.1% Placebo: 26.3%

675 mg quarterly: 44.4%

225 mg monthly: 47.7% Placebo: 27.9%

 

*At month 3 alone (not averaged over months 1-3):

675 mg quarterly: 49%

225 mg monthly: 51% Placebo: 37%

 

*At month 3 in long term extension study (open label):

675 mg quarterly: 59%

225 mg monthly: 61%

120 mg: 55%

Placebo: 32%

 

*At month 2 alone:

120 mg: 54.1%

Placebo: 34.5%

 

*At month 3 alone:

120 mg: 57.7%

Placebo: 37.9%

 

 

100 mg: 49.8%

300 mg: 56.3%

Placebo: 37.4%

Episodic migraine:

50% or more reduction in migraine days in months 4-6

70 mg: 43%

140 mg: 50%

Placebo: 26.6%

N/A 120 mg: 67%

Placebo: 43%

 

*At month 4 alone:

120 mg: 65.2%

Placebo: 41.9%

 

*At month 5 alone:

120 mg: 68.6%

Placebo: 43.7%

 

*At month 6 alone:

120 mg: 66%

Placebo: 44.8%

100 mg: 62%

300 mg: 65.3%

Placebo: 51.4%

Episodic migraine:

50% or more reduction in migraine days in months 1-6

N/A 675 mg quarterly: 65%

225 mg monthly: 60%

 

*months 1-3 placebo, months 4-6 open label, data is at month 6

120 mg: 59.3-62.3% days

Placebo: 36-38.6%

N/A
Episodic migraine:

50% or more reduction in migraine days in months 1-12

70 mg: 61%

140 mg: 64.9% Placebo: N/A

675 mg quarterly: 66%

225 mg monthly: 68%

 

*months 1-3 placebo, months 4-12 open label, data is at month 12

N/A 100 mg: 64.7%

300 mg: 69.4%

Placebo: 55.9%

 

*Reported as months 7-12

Episodic migraine:

75% or more reduction in migraine days in month 1

N/A 675 mg quarterly: 20%

225 mg monthly: 22% Placebo: 10%

 

120 mg: 25.7%

Placebo: 6.5%

 

100 mg: 30.8%

300 mg: 31.5%

Placebo: 20.3%

Episodic migraine:

75% or more reduction in migraine days in months 1-3

N/A 675 mg quarterly: 18.4%

225 mg monthly: 18.5% Placebo: 9.7%

 

*At month 3 alone (not averaged over months 1-3):

675 mg quarterly: 30%

225 mg monthly: 29% Placebo: 10%

120 mg: 30%

Placebo: 14%

 

*At month 2 alone:

120 mg: 31.2%

Placebo: 11%

 

*At month 3 alone:

120 mg: 34.2%

Placebo: 12.8%

100 mg: 22.2%

300 mg: 29.7%

Placebo: 16.2%

Episodic migraine:

75% or more reduction in migraine days in months 4-6

70 mg: 20.8%

140 mg: 22%

Placebo: 7.9%

N/A 120 mg: 42%

Placebo: 24%

 

*At month 4 alone:

120 mg: 41.6%

Placebo: 15.2%

 

*At month 5 alone:

120 mg: 41.4%

Placebo: 15.5%

 

*At month 6 alone:

120 mg: 43.9%

Placebo: 15.8%

100 mg: 33.5%

300 mg: 40.1%

Placebo: 24.8%

Episodic migraine:

75% or more reduction in migraine days in months 1-6

N/A 675 mg quarterly: 39%

225 mg monthly: 37%

 

*months 1-3 placebo, months 4-6 open label, data is at month 6

120 mg: 33.5-38.8%

Placebo: 17.8%-19.3%

 

N/A
Episodic migraine:

75% or more reduction in migraine days in months 1-12

70 mg: 38.5%

140 mg: 40.8% Placebo: N/A

675 mg quarterly: 42%

225 mg monthly: 45%

 

*months 1-3 placebo, months 4-12 open label, data is at month 12

N/A 100 mg: 41.2%

300 mg: 47.7%

Placebo: 32%

 

*Reported as months 7-12

Episodic migraine:

100% reduction in migraine days in month 1

N/A 675 mg quarterly: 5%

225 mg monthly: 8% Placebo: 2%

 

120 mg: 8.8%

Placebo: 2.2%

 

100 mg: 8.6%

300 mg: 14.9%

Placebo: 5.9%

Episodic migraine:

100% reduction in migraine days in months 1-3

N/A 675 mg quarterly: 0.7%

225 mg monthly: 2.4% Placebo: 0%

 

120 mg: 11%

Placebo: 4%

 

*At month 2 alone:

120 mg: 11.8%

Placebo: 3.7%

 

*At month 3 alone:

120 mg: 12.2%

Placebo: 7.3%

100 mg: 11.4%

300 mg: 16.8%

Placebo: 9.1%

Episodic migraine:

100% reduction in migraine days in months 4-6

70 mg: 3.2%

140 mg: 5%

Placebo: 2.8%

N/A 120 mg: 17%

Placebo: 9%

 

*At month 4 alone:

120 mg: 16.3%

Placebo: 8.5%

 

*At month 5 alone:

120 mg: 17.6%

Placebo: 8.7%

 

*At month 6 alone:

120 mg: 16.5%

Placebo: 9.5%

100 mg: 19.8%

300 mg: 24.5%

Placebo: 14.3%

Episodic migraine:

100% reduction in migraine days in months 1-6

N/A 675 mg quarterly: 18%

225 mg monthly: 20%

 

*months 1-3 placebo, months 4-6 open label, data is at month 6

120 mg: 11.5-15.6%

Placebo: 5.7-6.2%

 

N/A
Episodic migraine:

100% reduction in migraine days in months 1-12

70 mg: 19.8%

140 mg: 21.2% Placebo: N/A

675 mg quarterly: 17%

225 mg monthly: 21%

 

*months 1-3 placebo, months 4-12 open label, data is at month 12

N/A 100 mg: 26.8%

300 mg: 30.6%

Placebo: 20.5%

 

*Reported as months 7-12

Chronic migraine: Reduction in mean monthly migraine days in month 1 70 mg: -5 +/- 0.42 days

140 mg: -5.1 +/- 0.42 days

Placebo: -2.7 +/- 0.34 days

675 mg quarterly: -4.8 days

225 mg monthly: -4.7 days

Placebo: -2.7 days

120 mg: -4.06

Placebo: -1.78

 

N/A
Chronic migraine: Reduction in mean monthly migraine days in months 1-3 70 mg: -6.6 +/- 0.4 days

140 mg: -6.6 +/- 0.4 days

Placebo: -4.2 +/- 0.4 days

675 mg quarterly: -5 days

225 mg monthly: -4.9 days

Placebo: -3.2 days

 

*Months 1-3 in long term extension study (open label):

675 mg quarterly: -6 days

225 mg monthly: -6.7 days

120 mg: -4.8 days

Placebo -2.7 days

 

*At month 2 alone:

120 mg: -5.01

Placebo: -3.04

 

*At month 3 alone:

120 mg: -5.41

Placebo: -3.39

100 mg: -7.7 days

300 mg: -8.2 days

Placebo: -5.6 days

Chronic migraine: Reduction in mean monthly migraine days in months 4-6 N/A N/A N/A 100 mg: -8.2 days

300 mg: -8.8 days

Placebo: -6.2 days

Chronic migraine: Reduction in mean monthly migraine days in months 1-6 N/A 675 mg quarterly: -6.5 days

225 mg monthly: -7.6 days

 

*months 1-3 placebo, months 4-6 open label

N/A N/A
Chronic migraine: Reduction in mean monthly migraine days in months 1-12 70 mg: -8.5 days

140 mg: -10.5 days

Combined 70 mg and 140 mg: -9.3 days

Placebo: N/A

675 mg quarterly: -7.2 days

225 mg monthly: -8 days

 

*months 1-3 placebo, months 4-12 open label

120 mg: -7.21

 

*12 month safety study with no placebo

N/A
Chronic migraine:

50% or more reduction in migraine days in month 1

70 mg: 23.9%

140 mg: 28.3% Placebo: 11.4%

675 mg quarterly: 33%

225 mg monthly: 36%

Placebo: 19%

120 mg: 26.4%

Placebo 11%

 

100 mg: 54.5%

300 mg: 60.6%

Placebo: 36.1%

Chronic migraine:

50% or more reduction in migraine days in months 1-3

70 mg: 40%

140 mg: 41%

Placebo: 23%

675 mg quarterly: 30.7%

225 mg monthly: 33.3%

Placebo: 19.9%

 

*At month 3 alone (not averaged over months 1-3):

675 mg quarterly: 37%

225 mg monthly: 39% Placebo: 25%

 

*At month 3 in long term extension study (open label):

675 mg quarterly: 42%

225 mg monthly: 48%

120 mg: 27.6%

Placebo 15.4%

 

*At month 2 alone:

120 mg: 30.7%

Placebo: 17.7%

 

*At month 3 alone:

120 mg: 35.2%

Placebo: 24.7%

 

100 mg: 57.6%

300 mg: 61.4%

Placebo: 39.3%

Chronic migraine:

50% or more reduction in migraine days in months 4-6

N/A N/A N/A

 

 

100 mg: 61%

300 mg: 64%

Placebo: 44%

Chronic migraine:

50% or more reduction in migraine days in months 1-6

N/A 675 mg quarterly: 44%

225 mg monthly: 54%

 

*months 1-3 placebo, months 4-6 open label, data is at month 6

N/A, however:

 

*At month 6 in open label extension trial:

120 mg: 44.5%

N/A
Chronic migraine:

50% or more reduction in migraine days in months 1-12

70 mg: 53.3%

140 mg: 67.3%

Combined 70 mg and 140 mg: 59%

Placebo: N/A

675 mg quarterly: 53%

225 mg monthly: 57%

 

*months 1-3 placebo, months 4-12 open label, data is at month 12

N/A, however:

 

*At month 9 in open label extension trial:

120 mg: 53.9%

 

*At month 12 in open label extension trial:

120 mg: 56.9%

N/A
Chronic migraine:

75% or more reduction in migraine days in month 1

N/A Month 1 in long term extension study (open label):

675 mg quarterly: 21%

225 mg monthly: 21%

N/A 100 mg: 30.9%

300 mg: 36.9%

Placebo: 15.6%

Chronic migraine:

75% or more reduction in migraine days in months 1-3

70 mg: 17%

140 mg: 20.9% Placebo: 7.8%

675 mg quarterly: 9.6%

225 mg monthly: 12.3%

Placebo: 5.4%

 

*At month 3 in long term extension study (open label):

675 mg quarterly: 20%

225 mg monthly: 24%

120 mg: 7%

Placebo 4.5%

 

100 mg: 26.7%

300 mg: 33.1%

Placebo: 15%

Chronic migraine:

75% or more reduction in migraine days in months 4-6

N/A N/A N/A 100 mg: 39.3%

300 mg: 43.1%

Placebo: 23.8%

Chronic migraine:

75% or more reduction in migraine days in months 1-6

N/A 675 mg quarterly: 28%

225 mg monthly: 24%

 

*months 1-3 placebo, months 4-6 open label, data is at month 6

N/A, however:

 

*At month 6 in open label extension trial:

120 mg: 21.7%

N/A
Chronic migraine:

75% or more reduction in migraine days in months 1-12

70 mg: 27.1%

140 mg: 41.8%

Combined 70 mg and 140 mg: 33.2%

Placebo: N/A

675 mg quarterly: 28%

225 mg monthly: 31%

 

*months 1-3 placebo, months 4-12 open label, data is at month 12

N/A, however:

 

*At month 9 in open label extension trial:

120 mg: 27.9%

 

*At month 12 in open label extension trial:

120 mg: 31.1%

N/A
Chronic migraine:

100% reduction in migraine days in month 1

N/A Month 1 in long term extension study (open label):

675 mg quarterly: 6%

225 mg monthly: 5%

N/A 100 mg: 7.9%

300 mg: 13.4%

Placebo: 2.7%

Chronic migraine:

100% reduction in migraine days in months 1-3

70 mg: 4.3%

140 mg: 2.7%

Placebo: 0.4%

675 mg quarterly: 5.3%

225 mg monthly: 4.5%

Placebo: 4%

 

*At month 3 in long term extension study (open label):

675 mg quarterly: 5%

225 mg monthly: 6%

120 mg: 0.7%

Placebo 0.5%

 

100 mg: 10.8%

300 mg: 15.1%

Placebo: 5.1%

Chronic migraine:

100% reduction in migraine days in months 4-6

N/A N/A N/A 100 mg: 17.8%

300 mg: 20.8%

Placebo: 9.3%

Chronic migraine:

100% reduction in migraine days in months 1-6

N/A 675 mg quarterly: 8%

225 mg monthly: 8%

 

*months 1-3 placebo, months 4-6 open label, data is at month 6

N/A N/A
Chronic migraine:

100% reduction in migraine days in months 1-12

70 mg: 6.1%

140 mg: 12.7%

Combined 70 mg and 140 mg: 8.9%

Placebo: N/A

675 mg quarterly: 9%

225 mg monthly: 10%

 

*months 1-3 placebo, months 4-12 open label, data is at month 12

N/A N/A
Side effects:

Nasopharyngitis

70 mg: 3-9.9%

140 mg: 2-11%

Placebo 6-10%

675 mg quarterly: 5-8%

225 mg monthly: <1-8%

Placebo: 4-9%

120 mg: 7.4%

Placebo: 6.5%

100 mg: 6%

300 mg: 8%

Placebo: 6%

Side effects:

Hypersensitivity reactions

70 mg: <1%

140 mg: <1%

Placebo : <1%

675 mg quarterly: <1%

225 mg monthly: <1%

Placebo: <1%

120 mg: 1%

Placebo: 1%

100 mg: 1%

300 mg: 2%

Placebo: 0%

Side effects:

Constipation

70 mg: 1%

140 mg: 3%

Placebo 1%

675 mg quarterly: <1%

225 mg monthly: <1%

Placebo: <1%

120 mg: 1%

Placebo: <1%

100 mg: <1%

300 mg: <1%

Placebo: <1%

Side effects:

Cramps, muscle spasms

70 mg: <1%

140 mg: 2%

Placebo <1%

675 mg quarterly: <1%

225 mg monthly: <1%

Placebo: <1%

120 mg: <1%

Placebo: <1%

100 mg: <1%

300 mg: <1%

Placebo: <1%

Side effects:

Injection site reactions

70 mg: 6%

140 mg: 5%

Placebo 3%

675 mg quarterly: 18-19%

225 mg monthly: 23%

Placebo: 4%

120 mg: 18%

Placebo: 13%

N/A

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

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Last updated on February 5th, 2021 at 01:01 am

BEST HEADACHE AND MIGRAINE PREVENTION MEDS AND TREATMENTS, WHEN YOU SHOULD START ONE, AND WHEN YOU SHOULD STOP IT.

@Neuralgroover

BACKGROUND

Migraine is a very disruptive disorder to have to deal with. It interferes with patients’ family, work, and social lives. When the burden of migraine becomes excessive on one or more of these life aspects, preventive migraine therapy should be used. In general, if someone is averaging more than 4 migraines per month, preventive treatment should be offered and discussed, although this number is not an absolute. For example, if someone has 1 migraine per month, but it wipes them out for 1 week and they are missing work, there are certainly variations on when preventive medications should be considered, such as this scenario. If the decision to use a preventive migraine medication has been made, there are several important factors to keep in mind in order to optimize treatment success, as discussed below.

So this blog will focus on migraine preventive meds and treatments, which are a continuous treatment such as a daily pill or a monthly/quarterly treatment such as CGRP mAbs, all of which are detailed below. The goal of migraine preventive treatment is to lessen the frequency and/or severity of migraine attacks. This is in contrast to migraine abortive/acute (as needed) options such as triptans, gepants and ditans. The goal of migraine abortive treatments is to stop individual migraine attacks at onset so the migraine does not reach full severity, ends quickly, and your function is restored and maintained rather than having to go lay down and miss the whole day in bed.  If you have migraine, you want to have both a good abortive and preventive treatment plan to lessen migraine’s nasty habit of interfering and disrupting life and function.

 

TIME

Any preventive medication needs an adequate “therapeutic trial”. In short, you need to be patient and give it enough time to work, as well as get to the correct dose. I see patients all the time that tell me their doctor put them on a medication (usually at too low of a dose), and they stopped it after 3 weeks because it “wasn’t doing anything”. Well, it’s not going to do anything that soon, and that is too early to expect any significant improvement. In general, any preventive medication needs 4-6 weeks to begin working, and 2-3 months until full effect is seen (assuming a good dose has been reached). A good rule of thumb is evaluation of response a minimum of 8 weeks after reaching a target therapeutic dose. If there is a partial response at that time, it’s possible that cumulative benefit can continue to occur over 6-12 months. So the decision on whether to continue really depends on how much benefit has been received, and how well the the patient is tolerating the medication. Unfortunately, there is no way to expedite this process. That doesn’t mean the treatment can’t work sooner. However, that is the standard duration of treatment for a medication to have had a fair trial. Finding a migraine preventive is often a trial and error process. If a treatment is not starting to help by at least 8 weeks at a good dose, changing to a different therapy is suggested. However, once an effective treatment is found, the wait is well worth the decline of migraine frequency and severity!

 

DOSE

In addition to an adequate trial duration, an adequate trial dose is also necessary. For example, a common first line medication used for migraine prevention is Topiramate (which is also FDA approved for migraine prevention). I often see patients who come in on 25 mg or 50 mg and have been on that dose for a year or more without much benefit. I discuss with them that the goal dose is at least 100 mg total daily dose, so the dose is too low. For example, in the migraine preventive trials, once patients reached 100 mg and had been at that dose specifically for at least 4 weeks, that is when improvement of statistical significance began. So, I typically start 25 mg at bedtime for 1 week. Then each week increase by 25 mg at bedtime until 100 mg is reached, and then I give a 100 mg pill to begin. I tell them if there is no improvement starting after at least 4 weeks from reaching the 100 mg dose specifically, let me know. I usually dose it all at bedtime which can help limit side effect potential (since you’ll be sleeping). However, it is generally meant to be taken as a twice daily medicine (such as 50 mg twice daily), and most patients tolerate that fine too.

 

With that said, patients can certainly respond to low doses of medications. However, if improvement has been minimal after a month of a lower dose, it is always a good idea to begin titration up to a better dose. The American Headache Society and American Academy of Neurology published guidelines of migraine preventive medications which includes common goal dose targets for some of these preventive medications here.

 

TREATMENT SELECTION

There are many preventive treatments used, although most of them are considered “off-label” for migraine prevention. This means they are not actually FDA approved for migraine prevention, but there is enough evidence based on research trials or clinical experience to warrant them as a valid option to try. As far as true FDA approved oral (pills by mouth) preventive medications, there are 4 available that have this distinction; Topiramate, Divalproex, Propranolol, and Timolol. There are also a number of natural migraine treatments with supplements which have evidence for migraine prevention, and those are detailed and discussed here.

 

So, let’s discuss migraine prevention medicine.  The categories of oral preventive migraine medications all sound bizarre. They consist of anti-seizure (anti-convulsant), anti-depressant/anti-anxiety, and anti-hypertension (blood pressure) medications. It is important for patients to know that the medicine is being used specifically for migraine. I often see patients who say they didn’t start the medicine their doctor prescribed because they got home, Googled it, and they tell me, “I’m not depressed”. I explain the reasoning for the medication and that it is not for depression, but for migraine prevention since there are overlapping electrical pathways between many of these types of disorders. Furthermore, there are select medications within each of these categories that have evidence from trials and clinical experience for migraine prevention, as listed here and here. For patients that have chronic migraine (15 or more headache days per month with 8 or more days having migrainous features), Botox is another highly effective option to consider.

 

It is also important to know that the medications in each of these medication classes are not a “one size fits all” for every medicine within that category. For example, there is no good evidence for migraine prevention in the SSRI (selective serotonin reuptake inhibitors) anti-depressant/anti-anxiety medication category (Fluoxetine, Sertraline, Escitalopram, Citalopram, etc.). However, there is evidence for benefit in some of the SNRIs (serotonin and norepinephrine reuptake inhibitors) such as Venlafaxine XR, Duloxetine, as well as some of the TCAs (tricyclic antidepressants), primarily Amitriptyline and Nortriptyline. Similarly, there are select medications within the anti-seizure/anti-convulsant category which have the best evidence (Topiramate, Divalproex), as well as the anti-hypertension category (Propranolol, Metoprolol, Atenolol, Nadolol, Verapamil).

 

There are now 4 monoclonal antibody CGRP receptor antagonists which have this FDA approval for migraine prevention also. Three of them are once monthly auto/self-injections (Aimovig, Ajovy, Emgality), and one is a once quarterly (every 3 months) 30 minute IV (intravenous) infusion (Vyepti). In general, these are an option for those with 4 or more migraines per month on average.  The great thing about these treatment options as opposed to standard pill options is that they do not require a gradual dose escalation, they tend to have a much more rapid onset of improvement, and they have very low side effect risk. These medications are all discussed in much greater detail and comparison here.

 

Neuromodulatory devices that are FDA cleared for migraine prevention are also available and include sTMS (SAVI, SpringTMS, sTMS mini),  eTNS (CEFALY), and nVNS (GAMMACORE), all of which are discussed in much greater detail here. There are also nutraceuticals and supplements which have good evidence for migraine prevention. Yoga, relaxation and wellness therapies are also helpful in migraine prevention.

 

An exciting development is that there are 2 migraine preventive medications in the new gepant classification which are currently in clinical trials, and showing good evidence of effectiveness. They are both oral pills and include Atogepant and Rimegepant (currently FDA approved for abortive migraine treatment under the name Nurtec ODT 75 mg). So these will open up another new class of preventive migraine medications engineered purely for migraine treatment! Notably, Biohaven submitted a request to the FDA in October 2020 to approve Rimegepant as a preventive migraine treatment, in addition to its current migraine abortive FDA approved indication. This decision is pending. This move followed clinical trials showing that patients taking 75 mg of Rimegepant every other day experienced a 4.3 day reduction from baseline in monthly migraine days.

 

When choosing a preventive treatment, I like to fine-tune the treatment to “hit as many birds with one stone”. In other words, pick something that will not only help with migraine prevention, but may also help with other medical conditions at the same time. Doing this can allow you to help minimize the number of medications used overall, by using something with benefit for several disorders in addition to the migraine. For example, if someone has depression or anxiety, targeting their migraine preventive medication with an anti-depressant/anti-anxiety category would make sense. If the patient has other chronic musculoskeletal pain issues, fibromyalgia, occipital neuralgia, etc., the SNRIs and the TCAs are good considerations. If the patient has insomnia, Amitriptyline or Nortriptyline are great options. If they have seizures, an anti-seizure medication such as Topiramate or Divalproex would make sense. If they are overweight, Topiramate also causes weight loss. Divalproex is another anti-seizure medicine which is also FDA approved for migraine prevention. However, this should be avoided when possible in young women of child-bearing age given the high risk of congenital birth defects while taking it (and most pregnancies are unplanned).

 

Here are some treatment considerations to take into account for migraine preventive therapy in addition to the following medical conditions the patient may also have:

-Obese/Overweight: Topiramate (Topamax), Topiramate ER/XR (extended release, Trokendi or Qudexy XR), Zonisamide  (Zonegran): All can cause weight loss, which can be helpful in overweight patients. However, use with caution if patient is extremely thin to limit further weight loss. If they improve with Topamax, but have Topamax side effects (numbness and tingling, word-finding difficulty, speech disturbances, memory and cognitive disturbances, mood changes), changing to Topiramate ER/XR (extended release) or Zonisamide tend to have similar benefit with less side effects. Women who are on oral contraceptive pills are often warned prematurely by their pharmacist that Topiramate will effect their oral contraceptive. This is partly true. Topiramate at a daily dose of 200 mg or less does not interact with oral contraceptives according to this study, but it can at higher doses which could potentially decrease effectiveness. However, the goal dose for effective migraine prevention is typically 100 mg per day, well below that 200 mg dose that could impact effectiveness of the oral contraceptive. I would avoid Amitriptyline, Nortriptyline since there is a risk of weight gain for some.

-Underweight/Excessively thin: Side effects of Nortriptyline and Amitriptyline can occasionally be weight gain (but not necessarily), but this may be beneficial in some patients.

-Depression and/or anxiety: Venlafaxine ER, Duloxetine, Amitriptyline, Nortriptyline, Desvenlafaxine

-Mood disorder such as bipolar or psychosis: Divalproex, Topiramate, Carbamazepine

-Anxiety without depression: Venlafaxine ER, Amitriptyline, Duloxetine, Nortriptyline, Desvenlafaxine, Propranolol

-Insomnia: Amitriptyline, Nortriptyline

-Fatigue/Low energy: Venlafaxine ER, Duloxetine (these can be energizing for many, so are best taken in morning)

-Hypertension: Propranolol, Metoprolol, Nadolol, Atenolol, Lisinopril, Candesartan, Verapamil

-Palpitations: Propranolol, Metoprolol, Nadolol, Atenolol

-Chronic musculoskeletal pains, fibromyalgia, neuropathy/nerve pains: Amitriptyline, Duloxetine, Nortriptyline, Gabapentin

-Pregnancy: This one is tricky since the goal during pregnancy is to minimize the use of as many medications as possible. Mindfulness treatments such as yoga and meditation are always good recommendations. With that said, the first line option we typically begin with is magnesium supplementation of 400-800 mg daily. If a prescription medication is needed, cyproheptadine 4 mg at bedtime has been a long time medicine used in this scenario, and it can be titrated to 4 mg three times daily if needed. The good thing with pregnancy is that migraines improve in about 2/3rd of women (especially 2nd and 3rd trimester), and it is not uncommon to hear that migraines resolved during pregnancy. So many times a preventive treatment may not even be needed. For menstrually related migraine outside of pregnancy, further discussions and treatment considerations can be read here.

-Epilepsy: Topiramate, Topiramate ER/XR (extended release), Divalproex, Carbamazepine, and Zonisamide are the anticonvulsant medications we see most useful for migraine prevention. In fact, Topiramate and Divalproex are also FDA approved for migraine prevention. If patients improve with Topiramate but have side effects, changing to Topiramate ER/XR (extended release) or Zonisamide tend to have similar benefit with less side effects. Women who are on oral contraceptive pills are often warned prematurely by their pharmacist that Topiramate will effect their oral contraceptive. This is partly true. Topiramate at a daily dose of 200 mg or less does not interact with oral contraceptives according to this study, but it can at higher doses which could potentially decrease effectiveness. However, the goal dose for effective migraine prevention is typically 100 mg per day, well below that 200 mg dose that could impact effectiveness of the oral contraceptive.

-Non-oral route needed or preferred: Once monthly self/auto injections of monoclonal antibody CGRP receptor antagonists (Aimovig, Ajovy, Emgality) or once quarterly 30 minute IV infusion (Yvepti), which are all detailed here. Botox is another non-pill option for those averaging 15 or more headache days per month with at least 8 of those days having any migrainous features (throbbing, nausea, sensitivity to light (photophobia) or sound (phonophobia)) for 3 or more consecutive months (chronic migraine). Neuromodulatory devices that are FDA cleared for migraine prevention are also available and include sTMS (SAVI, SpringTMS, sTMS mini),  eTNS (CEFALY), and nVNS (GAMMACORE), all of which are discussed in much greater detail here.

-Averaging 15 or more headache days per month with at least 8 of those days having any migrainous features (throbbing, nausea, sensitivity to light (photophobia) or sound (phonophobia)) for 3 or more consecutive months (chronic migraine): Botox (Onabotulinumtoxin-A) injections every 3 months according to the PREEMPT chronic migraine treatment protocol. This is the only truly FDA approved medication for prevention of chronic migraine as of 2010. Any of the above listed medications are also options to consider, and most insurances will require failure of at least 2 classes of preventative oral medications before Botox is approved anyway, but this varies by insurance.

 

EXPECTATIONS

Expectations in migraine management are important. If your expectation is that your migraines will stop completely when you use preventive medications, you will be sorely disappointed. Of course it can certainly happen, but that is rare and should never be the expectation or goal. The goal of preventive therapy is a decrease in migraine frequency and/or severity of attacks (optimally both) to some extent to make them more tolerable and less intrusive into life. A general goal is 50% improvement in frequency and/or severity. Some patients can get much more than that, while others get much less (which would signal trials of a different medication class). With that said, success with migraine preventive benefit can also be considered in significant decreases is migraine attack duration or severity, reduction in migraine associated disability, improving the patient’s functioning in various areas of life, improvements in quality of life, and improvement in acute treatment responses. In general, studies estimate that about 45% of patients on conventional preventive therapy (such as oral medications) receive 50% reduction in monthly migraine days. Thus, 55% will receive less improvement than this. The CGRP mAbs tend to have a higher rate of improvement then conventional treatments as detailed here.

 

WHEN TO STOP

There is no absolute answer of when to stop preventive therapy. It depends on how well one is doing, how long they have been doing well, and how much they want to get rid of treatments. Some people want off as soon as they can, others prefer to stay on for years since they are doing very well with few migraines, and don’t want to “rock the boat”. In general, the goal is to continue preventive therapy until the patient is doing significantly better for at least 3 months, but preferably closer to 6 months or so. I always make sure to tell patients that preventive medicines or treatments are not necessarily meant to be a life-long commitment. Rather, we use these treatments to “reboot” and “reset” the brain’s electrical system to have less frequent and/or severe migraines, and then try to sneak away off the medications once they are consistently doing better.

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

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Last updated on January 28th, 2021 at 01:57 pm

CEFALY vs. NERIVIO vs. GAMMACORE vs. SPRING TMS. NEUROMODULATORY DEVICES FOR MIGRAINE AND CLUSTER HEADACHE: WHAT ARE THE DIFFERENCES AND WHICH IS BEST?

@Neuralgroover

 

 

Cefaly vs. Nerivio, Nerivio vs. GammaCore, Cefaly vs. GammaCore, Nerivio vs. SpringTMS, Cefaly vs. SpringTMS, GammaCore vs. SpringTMS. These are common questions that patients have about migraine neuromodulation devices. Many patients do not respond to conventional migraine abortive medications, they do not tolerate them, do not like taking medications, or they cannot take them due to medical contraindications. These standard migraine abortive options are discussed here. Luckily, there have been several neuromodulatory devices for the treatment of migraine which have entered the market over the last few years. These non-invasive neuromodulation devices open up new migraine treatment options for those in these sensitive and difficult patient populations, including pregnancy as well. These also avoid the complications of medication overuse headache (rebound headache) that is often an issue with using too much abortive migraine medication, as discussed in greater detail here.

But do they really work? Is one better than the other? Do they hurt? Are they used for abortive or preventive treatment? Are they expensive? Does insurance cover them? How do they compare, and is one best for you? This blog will address all of these questions.

These devices include Single-Pulse Transcranial Magnetic Stimulation (sTMS) (SAVI, SpringTMS, sTMS mini), external trigeminal nerve stimulation (eTNS) (Cefaly), noninvasive Vagus Nerve Stimulation (nVNS) (GammaCore), and the most recent, wireless remote electrical neuromodulation (REN) (Nerivio). We’ll discuss these devices in the order in which they became available and FDA cleared. The table further down is a summary of comparison data between devices gathered from published studies and directly from the companies as well. It’s important to keep in mind that the data in this table are not from head to head studies between devices. Each of these devices had separate study designs (which were quite varied), and the results of those studies is what is reflected here, certainly not a direct comparison between devices. All devices require a prescription from your doctor. Pricing and intermittent promotional specials can be found on each device’s website and some of these are discussed below. Sometimes the long-term costs equal out or can even be less than the cumulative cost of many medications and treatments used abortively and preventively.

 

SINGLE-PULSE TRANSCRANIAL MAGNETIC STIMULATION (sTMS)

The first device which was FDA cleared was the Single-Pulse Transcranial Magnetic Stimulation (sTMS), made by the company eNeura. It was initially FDA cleared for the acute treatment of episodic migraine with aura in adults in December 2013. It then received FDA clearance for both acute and preventive treatment of migraine in adults in 2017. This clearance was then expanded to the acute and preventive treatment of migraine in children 12 years of age and older in February 2019. Prior models included the Spring TMS and sTMS mini. The newest model, SAVI, is currently the only FDA cleared device for both the acute and preventive treatment of migraine in adults and children 12 years of age or older. Since the device is used acutely and preventively, the FDA approved it for a maximum of 17 pulses per day.

The user holds the device against the back of the head, and presses a button to release a very short magnetic pulse at the onset of aura or a migraine attack with or without aura. The magnetic pulse delivers a fluctuating magnetic field which induces a mild electric current through the skull and onto the surface of the occipital cortex (visual cortex) of the back part of the brain. This modifies the electrical excitability and hyperactivity of the cortical neurons to block or prevent the onset of a migraine from evolving to a full-blown migraine. The device stops cortical spreading depression, which is suspected to be the basis of migraine aura in the occipital cortex. It is also suspected to interfere with thalamocortical pain pathways that are normally activated during a migraine. The company offers a 90-day money back guarantee, and it is typically rented in 3-month increments.

The most common side effects were mild and brief light-headedness/dizziness, tingling over the back of the head where treatment is performed, brief tinnitus (ringing in ears), nausea, and muscle spasm. You should not use this device if you have a cardiac pacemaker, vagus stimulator (VNS) or other implanted neurostimulator, implanted cardioverter defibrillator (ICD) or any implanted medical device that stimulates the body or uses any signal from the body. It is also suggested that patients with implants affected by a magnetic field should not use this device. Examples of such implants include aneurysm clips or coils, cochlear implants, cerebral spinal fluid shunts, bullets or pellets lodged in the head or upper body, metal plates, screws, staples or sutures in skull, neck, shoulders, arms or hands, and facial tattoos with metallic ink. Dental implants, fillings or other dental appliances are okay to use the device.

Acute migraine treatment consists of 3 sequential pulses (early) at the onset of a migraine (aura or pain). Then wait 15 minutes. If needed, treat with an additional 3 pulses. Then wait another 15 minutes. If needed, treat with an additional 3 pulses. Studies reported that 39% of patients were pain free at 2 hours.

Prevention treatment consists of 4 pulses twice daily. This is performed by giving 2 consecutive pulses, waiting 15 minutes, and then repeating 2 consecutive pulses. Studies reported that 46% of patients had a greater than 50% reduction in monthly headache days and averaged approximately 3 less migraine days per month.

Unfortunately, eNeura filed for Chapter 7 bankruptcy on 8/7/20, so it is unclear what exactly the future holds for these sTMS devices.

 

CEFALY

Cefaly was the next neuromodulation migraine treatment device that became available, and is an external trigeminal nerve stimulation (eTNS) device (similar to a TENS unit mechanism). It is made by Cefaly Technology. It works by neurostimulation of the trigeminal nerve branches in the forehead. It was FDA cleared for the prophylactic (preventive) treatment of migraine in adults in March 2014, and acute treatment of episodic migraines in adults in November 2017. The Cefaly Dual device is the most recent model, and has settings for both acute and preventive migraine treatment. The company offers a 60-day money-back guarantee. As of 10/13/20, the Cefaly Dual neuromodulation device became the first FDA-approved trigeminal nerve stimulator for migraine treatment available without a prescription and can now be purchased over-the-counter. The Cefaly Dual kit includes the Cefaly device, 1 electrode (good for 20 uses), power adapter, charging cable, and storage case. It normally retails for $499. Three packs of electrodes are $25, or by a cost-saving subscription service.

Cefaly treatment is often described as a mild buzzing and pressure sensation. It should be avoided in patients with implanted metallic or electronic devices in the head, or who have a cardiac pacemaker or implanted or wearable defibrillator.

Acute migraine treatment consists of a 1-hour session. It may be repeated for a second 60-minute session if the migraine pain is not relieved within two hours, or if another migraine attack occurs. Studies reported that at 1 hour, 32% were pain free and 79% had significant pain relief. At 2 hours, 17% were pain free and 65% significant pain relief.

Migraine prevention consists of a nightly 20-minute session. Studies reported a 29.7% decrease in migraine attacks, and 38.1% of patients received at least 50% decrease in migraine attacks.

 

VAGUS NERVE STIMULATOR (GAMMACORE)

Noninvasive Vagal Nerve Stimulation (nVNS) is made possible by a hand-held device called GammaCore, from the company ElectroCore. The most recent model is called GammaCore Sapphire. It was initially FDA cleared for the acute treatment of episodic cluster headache in adults in April 2017, followed by the acute treatment of migraine in January 2018, cluster headache prevention in November 2018, and migraine prevention in March 2020. It was the first and remains the only therapy which is FDA-cleared for the prevention of cluster headache This device is placed over the vagus nerve on the side of the neck, just below the angle of the jaw where the pulse of the carotid is felt in the neck. It is suspected that the device works by suppressing cortical spreading depression (a central process in migraine and aura formation), and blocking and modulating the thalamocortical, trigeminovascular and trigeminocervical pain pathways that are normally activated during a migraine.

Acute migraine treatment consists of 2 two-minute stimulations. If the pain remains 20 minutes after the start of the initial treatment, 2 more two-minute stimulations are given. Two more two-minute stimulations may be applied if the pain remains 2 hours after the start of the initial treatment. Studies showed significant pain relief in as soon as 30 minutes, and reported that at 1 hour, 21% were pain free and 35.8% had significant pain relief. At 2 hours, 30.4% were pain free and 40.8% significant pain relief. GammaCore reduced pain intensity over 3x greater than sham (fake device) at 60 minutes and over 6x greater at 120 minutes, and reduced the need for other rescue medications.

Preventive migraine treatment is done by giving 3 treatments daily (morning, mid-day, and night) consisting of two consecutive 2-minute stimulations. Studies showed a 29% reduction in migraine days per month when used preventively, although this number was even higher in those with aura at a 35.8% decrease. Overall, 33.6% of patients received at least a 50% decrease in migraine frequency.

Acute cluster headache treatment is done by giving 3 two-minute stimulations. After completing the 3rd stimulation, the user waits 3 minutes. If pain remains, 3 more two-minute stimulations can be applied. You may treat up to 4 attacks (8 treatments) for a total of 24 stimulations per day. Significantly more episodic cluster attacks treated with GammaCore were pain-free at 15 minutes vs those treated with sham   (47.5% vs 6.2%). Combined study data showed that significantly more (over 2-4x greater response) episodic cluster headache patients responded (no pain or mild pain) to GammaCore at 15 minutes for 50% or more of all treated attacks vs those receiving sham (34.2-64.3% vs 14.9-15.4%). At 15 minutes, there were also significant reductions in pain duration and intensity with GammaCore compared to sham.

Preventative cluster treatment is done by giving 2 treatments (morning and night) consisting of 3 two-minute stimulations. Weekly attack frequency decreased by 40% from baseline when GammaCore was added to standard of care therapy. There was a 57% decrease in the frequency of acute medication use when GammaCore was added.

GammaCore treatment is often described as a deep vibration. GammaCore should not be used with an active implantable medical device, such as a pacemaker, hearing aid implant, or any implanted electronic device. It should be avoided in patients who have a metallic device such as a stent, bone plate, or bone screw implanted at or near their neck, are using another device at the same time (e.g., TENS Unit, muscle stimulator) or any portable electronic device (e.g., mobile phone).

 

NERIVIO

The Nerivio device is made by the company Theranica. It is a wireless remote electrical neuromodulation (REN) device wearable for the acute treatment of migraine applied to the upper-arm. It was FDA-cleared for the acute treatment of episodic migraine in adults in May 2019. In October 2020, FDA clearance was extended to acute treatment of migraine in chronic migraine patients as well. In January 2021, Nerivio received FDA clearance for acute migraine treatment for episodic or chronic migraine in patients 12 years and older.

Each device provides 12 treatments. When the device is used up, it is recycled and a new refill device is sent. It is the most economical option on the market. Costs can often be similar to monthly triptan prescription costs. The device works through an app downloaded on your smartphone which controls the strength and treatments. The device itself is an arm band that easily straps around the upper arm, and was recognized in TIME Magazine’s annual list of the 100 Best Inventions in 2019. In October 2020, Nerivio became the first neuromodulation device to receive a pharmacy/medical benefit.  is available for $10 on the initial prescription for anyone with any form of medical or pharmaceutical insurance, including government insured patients such as Medicare and Medicaid! Commercially insured patients may have their Co-pay reduced to $0 on future refills, while government insured patients will pay $99 for refills. No patient ever pays more than $99 for a refill, and most will hopefully pay $0 on refills.

It delivers electronic pulses into the skin to generate a proprietary “Conditioned Pain Modulation” response which helps to abort the effects of a migraine in patients with or without aura. Nerivio stimulates specific sensory nerves of the upper arm which normally sense pain. The stimulation from the device is not strong enough to actually trigger pain for the user, but the signal still travels to the brainstem, as it normally would. From here, it interferes and blocks the ongoing activated electrical circuitry of the migraine, and helps to abort it. Many think this is basically a TENS unit, but it is not. It has a proprietary stimulation signal which targets specific pain transmitting nerve fibers that disrupts the electrical activity of a migraine centrally from a remote location peripherally (on the arm).

The device is applied within 60 minutes (preferably at onset) of a migraine headache or migraine aura and stimulation is performed for 45 minutes. It is described as a vibrating sensation. Studies showed that 66.7% of patients had significant pain relief at 2 hours, and 37.4% of patients achieved complete pain relief at 2 hours. Furthermore, 89.7% of patients studied avoided having to take other abortive medications when treating with Nerivio. In the study leading to Nerivio treatment extension to adolescents 12 years and older in January 2021, 71% of patients had pain relief by 2 hours after Nerivio treatment, while 35% received complete pain relief. Pain relief and pain freedom were sustained for 24 hours in 90% of cases.

Side effects may include a temporary sensation of warmth, local tingling, numbness in the arm, pain in the arm, or redness of the skin, although 96.4% of patients studied did not report any device related adverse events. It is recommended to avoid in congestive heart failure, severe cardiac or cerebrovascular disease and uncontrolled epilepsy. It should not be used with certain medical devices such as a pacemaker or hearing aid implant. Using Nerivio with other implantable medical devices could potentially cause electric shock, electrical interference, or other injury. So it should not be used near any metallic implants.

 

  sTMS Cefaly GammaCore Nerivio
Acute Migraine Yes Yes Yes Yes
Preventive Migraine Yes Yes Yes No
Acute Cluster No No Yes No
Preventive Cluster No No Yes No
1-hour migraine pain free N/A 32% (13% sham) 21% (sham 10%) N/A
1-hour migraine pain relief N/A 79% (39% sham) 35.8% (sham 24.4%) N/A
2-hour migraine pain free 39% (sham 22%) 17% (sham 7%) 30.4% (sham 19.7%) 37.4% (18.4% sham)
2-hour migraine pain relief N/A 65% (sham 52%) 40.8% (sham 27.6%) 66.7% (38.8% sham)
Migraine preventive relief 46% had > 50% decrease in monthly HA days (20% “statistically derived” placebo) and averaged 3 less migraine days/month 29.7% decrease (sham 4.9%)

38.1% received at least 50% decrease in migraines (sham 12.12%)

29% decrease (sham 18%)

35.8% decrease in patients with aura

33.6% received at least 50% decrease in migraines (sham 23.4%)

N/A

 

IF YOU HAVE HEADACHE, MIGRAINE, OR FACIAL PAIN AND ARE LOOKING FOR ANSWERS ON ANYTHING RELATED TO IT, A HEADACHE SPECIALIST IS HERE TO HELP, FOR FREE!

FIRST, LET’S DECIDE WHERE TO START:

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR THE LATEST INFORMATION, HOT TOPICS, AND TREATMENT TIPS, VISIT OUR FREE BLOG OF HOT TOPICS AND HEADACHE TIPS HERE. THIS IS WHERE I WRITE AND CONDENSE A BROAD VARIETY OF COMMON AND COMPLEX  MIGRAINE AND HEADACHE RELATED TOPICS INTO THE IMPORTANT FACTS AND HIGHLIGHTS YOU NEED TO KNOW, ALONG WITH PROVIDING FIRST HAND CLINICAL EXPERIENCE FROM THE PERSPECTIVE OF A HEADACHE SPECIALIST.

 

IF YOU DON’T HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR POSSIBLE TYPES OF HEADACHES OR FACIAL PAINS BASED ON YOUR SYMPTOMS, USE THE FREE HEADACHE AND FACIAL PAIN SYMPTOM CHECKER TOOL DEVELOPED BY A HEADACHE SPECIALIST NEUROLOGIST HERE!

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING FOR FURTHER EDUCATION AND SELF-RESEARCH ON YOUR DIAGNOSIS, VISIT OUR FREE EDUCATION CENTER HERE.

 

IF YOU HAVE AN EXISTING HEADACHE, MIGRAINE, OR FACIAL PAIN DIAGNOSIS AND ARE LOOKING TO ASK QUESTIONS TO A HEADACHE SPECIALIST OR OTHER HEADACHE, MIGRAINE, AND FACIAL PAIN WEBSITE MEMBERS, VISIT OUR FREE DISCUSSION FORUMS HERE.

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Last updated on January 20th, 2021 at 01:26 am

VISUAL SNOW, PERSISTENT MIGRAINE AURA, MIGRAINOUS STROKE, AND WHAT YOU SHOULD KNOW.

@Neuralgroover

INTRODUCTION</