Posts Tagged "migraine"


Last updated on April 10th, 2021 at 05:34 am

MIGRAINE HEADACHES EXPLAINED.

@Neuralgroover

Migraines are a very intense type of headache that are often accompanied by other symptoms, including nausea, vomiting, sensitivity to light and sound, as well as neurological symptoms such as visual disturbances, numbness or tingling, speech disturbances (slurred speech, difficulty getting words out), weakness, vertigo, cognitive dysfunction or “cognitive fog”, among other things. Migraines tend to be more prevalent in women than in men, with a 3:1 ratio. A common risk factor for migraines often involves family history, but not for everyone.  People who suffer from migraines report intense feelings of pain, including a pulsating/throbbing sensation. This often occurs on 1 side of the head, but can also involve both sides. Exercise and activity during a migraine will often make it worse. Migraine is usually associated with nausea, and/or sensitivity to light (photophobia) and sound (phonophobia)  Migraines often come in different phases, which are called prodrome, aura, the headache phase, and postodome, but not everyone gets all 4 phases:

  • The prodromal phase of a migraine often marks the beginning of a migraine attack and can happen over a period of a few hours ranging to a few days. Some of the symptoms include irritability and depression; food cravings; yawning and tiredness; and fatigue or muscle stiffness. Some patients report their prodrome as just a difficult to describe feeling that they recognize as an early warning sign of an impending migraine. Not every migraine attack includes the prodromal phase.
  • The aura phase of a migraine doesn’t necessarily always happen in every migraine attack, and only about 25% of patients with migraine get aura. Historically, those that get aura are called “classical migraine”, whereas “common migraine” refers to the more common variety of migraine which isn’t associated with aura. A large number of people who have migraines report that during the aura phase, they experience loss of sight, numbness, and other symptoms. Visual aura (loss of vision, jagged lines, flashing, colors, shapes, wavy lines, kaleidoscope, shimmering, expanding blind spot, etc.) are the most common aura. This is followed by numbness and tingling on 1 side (especially face and arm), and then dysphasia (trouble speaking; slurred speech, getting words out). There are also less common types of aura such as hemiplegic migraine aura (1-sided weakness), and brainstem aura (previously called “basilar migraine”; slurred speech, vertigo, tinnitus, double vision, hearing impairment, decreased level of consciousness, ataxia/imbalance). The aura phase should last between 5-60 minutes per ICHD3 criteria. Hemiplegic migraine can be associated with 1-sided weakness which can last up to 3 days. If the other types of aura last longer than 60 minutes, it is called prolonged or atypical aura, and usually warrants a brain CT or MRI, although it is not too uncommon to see. .
  • The headache phase of a migraine is often the longest and most intense period of a migraine. Symptoms include intensive throbbing, nausea, giddiness, irritability, stiffness, and soreness. According to ICHD3 criteria, an untreated or unsuccessfully treated migraine attack should last 4-72 hours. A headache lasting longer than 72 hours (3 days) is called status migrainosus. It is not uncommon for a refractory migraine to last days and sometimes weeks for some patients.
  • The postdrome phase is the drawing down of a migraine attack. It can last for up to 48 hours and some of the lingering symptoms remain from the other phases of a migraine attack. Patients often report feeling wiped out, fatigued, and sore as if they were “hit by a bus”.

 

According to the American Migraine Foundation, more than 36 million people suffer from migraines (although now estimated to be closer to 39 million), but only one out of three people actually talk to their doctors about their pain.

Statistics About Migraines and Their Prevalence

According to several different sources, migraines are one of the most common types of illness in the world. More specifically, it is ranked as the 3rd most prevalent illness in the world. It is estimated that migraine affects about 39 million Americans, and 1 billion worldwide. For example, 1 in 4 households in the United States have an individual that suffers from migraine attacks. Migraines impact 18-20% of women (1 in 5) and 6% of men (1 in 16) in the United States and they are also fairly common in children.

Migraines are also a common cause for an emergency room visit. In fact, there are more than 1.2 million emergency room visits each year in the United States for someone who is suffering from an acute migraine attack. Patients with migraine have a greater than 1.5 fold increase in office visits, and a greater than 2 fold increase in ER visits and hospital admissions. Migraines can also diminish the quality of life for the people who suffer from them. More than 4 million adults suffer from chronic migraine pain, which is an individual who is experiencing more than 15 days of migraine pain each month. Approximately 3% of patients will transform from episodic migraine to chronic migraine each year. Overall, it is estimated that 3-5% of patients in the United States have chronic migraine. Also, 20% of people who suffer from chronic migraines are disabled. Disability due to migraine peaks between the ages of 15-49 years old, which are peak employment years. Thus, migraine now accounts for the 2nd leading cause of years lived with disability following low back pain! Migraine also accounts for 50% of all neurologic disability. All of this puts a very high price tag on migraine, with an estimated 36 billion dollars spent in migraine costs in the United States each year.

 

Migraines in Children

Migraines are commonly undiagnosed in children. They are more commonplace in adolescent children, but 10% of school-age children suffer from migraines. Half of all migraine sufferers have their first migraine attack before they turn twelve and if a child has one parent who suffers from migraines, they have a 50% chance of developing migraines during their lifetime. Also, boys under the age of twelve tend to have migraines more often than girls, but that trend reverses in adolescence, typically with onset of menarche (which also highlights the hormonal influence on migraine).

 

What Causes Migraines?

There are a number of reasons that people suffer from migraines, but the true cause of them is not fully understood. Genetics and environmental factors play a role. In fact, around ⅔ of migraine cases run in families. Migraines also tend to happen in people who are prone to stress, bipolar disorder, and depression. There are also some common triggers for migraines, including:

  • Drinks, such as alcohol and caffeinated beverages.
  • Work stress or stress at home.
  • Bright lights or strong smells.
  • Drastic changes in one’s sleep cycle.
  • Bouts of overexertion.
  • Changes in the weather or other barometric pressure changes
  • Certain foods and food additives such as MSG, nitrates, aspartame, and other substances such as artificial sweeteners.

 

Migraine Theories:

1) Vascular theory; “vascular headache” (outdated):

a) Lack of blood flow (ischemia) caused by vasoconstriction (narrowing) of the intracranial arteries (arteries inside the brain) caused migraine aura.

b) The vasoconstriction was then followed by rebound vasodilation (dilation) of the arteries. This dilation activated pain receptors on the arteries, and this was the cause of the pulsating headache.

c) This theory has since been disproven and outdated. Studies have also shown that the physical pulsations of the arteries did not correlate to the pulsating sensations of the headache pain.

2) Neurovascular theory (current):

a) Migraine is a neurogenic process with secondary changes in cerebral perfusion (related to neuronal dysfunction and hypometabolism during an attack). In other words, migraine is an electrical neurological event in the brain, not an event triggered by blood flow changes. This electrical event influences changes in brain metabolism such as hypometabolism and hypermetabolism. When the neurons are in a hypometabolism state, they have less oxygen and glucose requirement since they are not as active, and thus there is a lack of blood flow (not due to vasoconstriction of the brain arteries). This can be followed by hypermetabolism in which there is an increase in oxygen and glucose requirements and thus, increase in blood flow (so not necessarily simply rebound vasodilation).

 

b) Migraine aura is a good illustration of this phenomenon. Migraine aura is caused by an electrical wave spreading across the cortex of the brain moving at about 3 mm per minute (not by vasoconstriction as per the older vascular theory). At the front of this spreading electrical wave it causes hypermetabolism and an increase in blood flow. This hypermetabolism causes the “positive” migraine aura features (colors, flashing lights, kaleidoscope, shapes, zig-zags, tingling sensory changes, etc.). Following this electrical wave there is “neuronal depression” and hypometabolism, associated with a decrease in blood flow. This hypometabolism causes the “negative” migraine aura features (loss of vision, black spots, numbness, etc.). Depending on where this wave spreads, you may get different aura symptoms; visual aura as it spreads across the occipital (visual) cortex, sensory/numbness/tingling as it spreads across the parietal (sensory) cortex, dysphasia (trouble speaking, slurred speech) as it spreads across the frontotemporal (speech) cortex, one sided weakness in hemiplegic migraine as it spreads across the frontal (motor) cortex, brainstem symptoms such as vertigo, tinnitus, double vision, hearing loss, imbalance, decreased level of consciousness, slurred speech (previously called basilar migraine, now called migraine with brainstem aura) as it spreads across the brainstem.

 

c) The electrical event of migraine not only causes the changes in metabolism as described above, but the trigeminal nerves are also activated. Think of migraine as an electrical switch that gets turned on in the brainstem. It then turns on and activates the trigeminal nerves. The trigeminal nerves innervate all of the arteries in the brain and through the meninges surrounding the brain. When activated, the trigeminal nerves release a variety of inflammatory proteins (such as CGRP) and neuropeptides. The result of this is 3-fold:

1st, these inflammatory peptides cause neurogenic inflammation around the brain. Think of it like a sterile (non-infectious) meningitis. So, when you’re having a migraine, exercise and activity, moving around, bouncing in a car, etc. often worsen the pain.

2nd, it causes cerebral vasodilation in the brain and meninges. The dilation itself does not cause the pain, but rather it triggers the trigeminal nerves which innervate the arteries, and this sends signals back to the brain that something is going on, which in turn causes more release of inflammatory proteins and causes the migraine to worsen. This is the basis of why it is called the neurovascular theory of migraine.

3rd, it enhances and exaggerates the transmission of pain from the trigeminal nerves, into the brainstem, and into the cortex of the brain where the pain is recognized.

 

At baseline, a patient with migraine who is not having a headache always has a state of neuronal hyperexcitability in the cerebral cortex, especially in the occipital cortex (which is why the majority of aura symptoms tend to be visual aura). So, they have a much lower threshold to a migraine being activated and triggered as compared to someone without migraine. In other words, the neurological system in a patient with migraine can be thought of as always being in a hyperactive, hypersensitive, overdrive state with the “volume turned way up” compared to a person without migraine. Thus, I tell my patients the goal of preventive treatment is to “turn the volume down” and increase the threshold of migraine being triggered so easily.

 

What Are Some Common Treatments for Migraines?

There are two categories of treatment for any type of headache, including migraines. Migraines can be treated through abortive or preventive means. Abortive treatment for any type of headache includes medications such as aspirin, which treats the headache while it’s happening. Preventative treatments are intended to keep a headache or migraine from happening so frequently. Here are some of the different types of treatments for migraines.

 

Abortive Treatment for Migraines

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.  Over-the-counter pain relievers for migraines, such as aspirin or ibuprofen, are fairly commonplace. Some more aggressive abortive treatments include prescription medications like triptans (such as Maxalt) that block pain pathways within the brain. Some people may also receive anti-nausea drugs and opioid prescriptions to deal with more intense migraine symptoms. The migraine specific abortive/acute (as needed) treatments include triptansgepants (Ubrelvy, Nurtec), ditans (Reyvow) or neuromodulatory devices.

Preventative Treatments for Migraines

Medications that lower blood pressure, antidepressants, anti-seizure drugs, CGRP monoclonal antibodies, and even botox are some of the common preventative treatments for migraines. The classification of the preventive medicine typically has nothing to do with its purpose when it is used for migraine. For example, there are specific anti-blood pressure medicines that are good for migraine prevention. However, they do not work for migraine because of blood pressure changes, but rather they affect the electrical pathways of migraine. The same scenario goes for the antidepressant/anti-anxiety and anti-seizure categories. The medicines selected within each of these preventive categories are very specific and based on clinical trials and evidence. In other words, not all medicines within a specific medication class (such as all antidepressants) have evidence for migraine prevention, but rather very specific ones within that class. Medications that are designed to lower blood pressure can sometimes prevent migraines with aura and without aura. Certain types of antidepressants can help prevent migraines, but have some undesirable side effects in some individuals. Anti-seizure drugs, such as Topamax, can reduce the frequency of migraines in some individuals. The preventive migraine treatments should be used until the migraine and headache frequency is significantly improved consistently for several months. As mentioned above, this can be done with a variety of medications which may also include the CGRP monoclonal antibody (mAb) treatments (Aimovig, Ajovy, Emgality, Vyepti), Botox, natural supplements, herbals and vitamins, or neuromodulatory devices.

Alternative Treatments for Migraines

Some other types of treatment for migraines include acupuncture, cognitive behavioral therapy, supplements, essential oils, yoga, meditation, and other techniques designed to enhance relaxation. For some individuals, exercise can decrease the frequency of migraines. In fact, some studies have shown that a routine exercise program can be just as effective as some of the prescription preventive medications used for 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. There are also nutraceuticals and supplements which have good evidence for migraine prevention.

 

Finding Help For Migraines

Migraines remain a poorly understood medical condition, but there are treatments available. Only 4% of people suffering from migraines work with a headache specialist or a pain specialist. It is estimated that preventative treatment could benefit around 25% of people who suffer from severe migraines.

If you suspect that your headaches are migraines, you should see your doctor. Furthermore, any type of headache warrants at least one visit with your doctor to make sure there are no concerns by medical history or examination for any other worrisome causes of your headaches. They may refer you to a neurologist or other type of headache specialist. Oftentimes, a wide variety of tests may be given, including CT scans and MRIs, to see what is contributing to the cause of the migraine. The good news is that migraines can be successfully managed for the majority of patients, and that many people live with them thanks to the treatments that they receive.

 

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 April 7th, 2021 at 08:07 pm

ONE-SIDED HEADACHE WITH CONGESTED RUNNY NOSE, OR RED, TEARING AND SWOLLEN EYE. 5 REASONS WHY – 2021.

@Neuralgroover

BACKGROUND

Do you have a one-sided headache, left-sided headache, right-sided headache, or one-sided head pain with some variation of one-sided symptoms such as runny nose, nasal congestion or stuffiness, red eye, tearing eye, droopiness of the eyelid, puffiness or swelling around the eye, facial sweating or flushing, or clogged ear feeling? These symptoms are called autonomic symptoms, and they are a central part of several distinct headache syndromes. The headaches that occur with this combination of features are distinct types of headaches, all requiring different treatments. Therefore, it is important in differentiating them to ensure proper treatment and less misery!

 

TRIGEMINAL AUTONOMIC CEPHALALGIAS (TACs)

There is a class of headaches called the trigeminal autonomic cephalalgias (TACs), and all are terribly painful. There are 4 types of headaches within the TAC family, and include cluster headache, hemicrania continua, paroxysmal hemicrania, and SUNCT / SUNA (Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing / Short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms). All of the TAC syndromes warrant preferably a brain MRI and MRA to exclude other causes such as pituitary lesions, aneurysms, or other abnormalities.

 

The TACs all share 2 common and core features. 1st, they are characterized by a severe headache that is strictly one-sided and focused around the eye, behind the eye, below the eye, in the temple or forehead areas. 2nd, they must include at least 1 autonomic symptom on the same 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)].

 

So how do you differentiate these headache types when they all have similar features? Differentiation between them is based purely on their headache attack duration and pattern. So, it is actually quite easy to differentiate them as contrasted below.

 

CLUSTER HEADACHE

Cluster headache is the most common TAC syndrome and is discussed and detailed further here. It 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 as described above. 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. Within a cluster cycle, patients may get multiple attacks during the day or overnight. They often classically wake the patient up in the middle of sleep, usually around the same time every night or morning. The patient often gets up and paces around the house in agitated misery. They certainly can occur during the day as well. 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). 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” because of the pain severity.

 

Treatment of cluster headache is detailed further here.

 

HEMICRANIA CONTINUA

Hemicrania continua a continuous daily one-sided headache (side-locked, does not alternate sides) of at least 3 months duration with moderate to severe exacerbations. There should be either agitation or restlessness and/or at least 1 autonomic sign or symptom on the side of the headache as described above. Although not included in the criteria, sometimes patients describe a sensation such as something irritating in the eye on the side of the headache, such as sand, grit, or a hair, but nothing is found. Hemicrania continua is discussed and detailed further here.

 

To make the full diagnosis of hemicrania continua, the patient must respond completely to a therapeutic trial of indomethacin (a specific anti-inflammatory (NSAID) medication), used in a very specific way (“Indomethacin trial”). For this reason, this headache is 1 of 2 types of “Indomethacin-sensitive” headaches because Indomethacin is typically the only thing that works (paroxysmal hemicrania is the other Indomethacin-sensitive headache). The diagnosis of hemicrania continua is confirmed by the headache completely stopping after reaching a specific dose of Indomethacin.

 

Besides indomethacin, other treatments of hemicrania continua are detailed further here.

 

PAROXYSMAL HEMICRANIA

Paroxysmal hemicrania is characterized by attacks of severe unilateral (one-sided) orbital (around the eye), supraorbital (above the eye), and/or temporal pain lasting 2 to 30 minutes. There must be at least 1 autonomic sign or symptom on the side of the headache as described above. The attacks have a frequency of more than 5 per day for more than 50% of the time when the disorder is active.  Chronic paroxysmal hemicrania continua is defined by attacks occurring for more than 1 year without remission, or with remission periods lasting less than 1 month. Paroxysmal hemicrania is discussed and detailed further here.

 

To make the full diagnosis of paroxysmal hemicrania, the patient must respond completely to a therapeutic trial of indomethacin (a specific anti-inflammatory (NSAID) medication), used in a very specific way (“Indomethacin trial”). For this reason, this headache is 1 of 2 types of “Indomethacin-sensitive” headaches because Indomethacin is typically the only thing that works (hemicrania continua is the other “Indomethacin-sensitive” headache). The diagnosis of paroxysmal hemicrania is confirmed by the headache completely stopping after reaching a specific dose of Indomethacin.

 

Besides indomethacin, other treatments of paroxysmal hemicrania are detailed further here.

 

SUNCT / SUNA

SUNCT/SUNA are two variations of a rare type of headache called short-lasting unilateral neuralgiform headache attacks, and they are discussed and detailed further here. Short-lasting unilateral neuralgiform headache attacks (which include SUNCT and SUNA) are characterized by moderate to severe unilateral (one-sided) orbital (around the eye), supraorbital (above the eye), and/or temporal pain. The duration of the pain lasts for 1–600 seconds (1 second to 10 minutes, although most often about 5 seconds to 4 minutes), and may occur as single stabs, series of stabs, or in a sawtooth pattern. There must be at least 1 autonomic sign or symptom on the side of the headache as described above. Attacks must have a frequency of at least one per day for more than half of the time when the disorder is active. However, the attacks generally occur in a very high daily frequency when active, sometimes even up to 200 attacks per day or 5-6 attacks per hour.

 

SUNCT and SUNA both share the above criteria. The difference between the two is that SUNCT requires both conjunctival injection (redness of the eye) and lacrimation (runniness/tearing of the eye), whereas SUNA requires only 1 or neither of these 2 features.

 

Treatment of SUNCT / SUNA is detailed further here.

 

MIGRAINE

Migraine is not a TAC syndrome, but it can sometimes have overlapping characteristics with the TACs in terms of its one-sided nature and associated autonomic features in some patients. For this reason, I have included it in this discussion. Migraine is discussed and detailed further here. The autonomic symptoms seen in migraine are not required by criteria for diagnosis, in contrast to the TAC syndromes which do require these symptoms for diagnosis. In some patients with migraine, their headache attacks can have some of the autonomic features described above. For many patients, migraine also activates the sinus pathways, so sinus symptoms of sinus/facial pressure, congestion and drainage are common. This is often misdiagnosed as “sinus headache”. However, if there is any throbbiness, pulsating, or pounding, it is almost guaranteed to actually be of a migraine origin rather than of a sinus origin.

 

Migraine headache attacks last 4 to 72 hours if untreated or unsuccessfully treated. There must be 2 of the following 4 features present: a unilateral (one-sided) headache, pounding/throbbing/pulsating quality, moderate-to-severe pain intensity, and worsening by routine physical activity. There must also be 1 of the following 2 features present: nausea and/or vomiting, or both photophobia (sensitivity to light) and phonophobia (sensitivity to sound).

 

Treatment of migraine headache is detailed further here.

 

 

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 April 10th, 2021 at 05:26 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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Last updated on April 10th, 2021 at 05:00 am

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 April 9th, 2021 at 12:50 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 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. There is no current evidence for an interaction between the Covid-19 vaccine and CGRP mAbs, the same as any other vaccine. This has also been stated by the American Migraine Foundation. Patients receiving 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. The CGRP mAbs do not 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 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 or the CGRP mAbs. These reports were with the Moderna Covid vaccine and resolved with steroids and/or antihistamines. The topic of Covid-19 headache, Covid-19 vaccination, and the use of Botox is discussed further here.

 

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 lityhave 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

 

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