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Dispelling Common Headache Myths
Patients may be familiar with several myths and have misconceptions about headaches and migraine, which often arise due to a combination of factors, including limited understanding of the conditions, cultural beliefs, misinformation, and the complex nature of headaches. Being aware of these myths and seeking accurate information help patients to better understand and manage their headaches.
Myth: Migraine Is the Most Common Type of Headache
This is not true. The most common type of headache is tension-type headache, and it's the kind of headache that almost everyone has from time to time. Between 40% and 80% of the US population have had some form of tension-type headache, but only about 13% of the adult population have migraine. Stress can make muscles in the head and neck tense and knotted, and these muscles can be the source of a tension-type headache. Sometimes these headaches are not at all related to muscles or stress. Neck position may also be a factor. Pain from this type of headache is usually felt on both sides of the head and presents more often as steady, dull pressure or pain that’s usually mild to moderate in intensity. The pain can be in the forehead and eyes or further back in the head. Tension-type headaches are not usually associated with nausea, vomiting, or light and sound sensitivity.
When a tension-type headache is really severe, patients could consider this headache a migraine. Clinicians can easily distinguish tension-type headache from migraine, which often presents on one side of the head, with moderate or severe intensity, is throbbing, and is associated with nausea, vomiting, and light and sound sensitivity.
Myth: Only Adults Get Headaches
False. Headaches aren’t experienced just by adults. However, unlike adults, children find it harder to explain their headaches. It is true that adults have more migraines than children; children’s migraines are often hard for doctors to recognize. A 6- to 9-year-old child is 50% less likely than an adult to have migraine, and their attacks are more often bilateral, are shorter, and respond to sleep quickly.
Myth: Migraines Are Just Really Bad Headaches
False. They are bad, but that is only a small part of the story. A migraine attack is different from other headaches; they actually are 1 of the 3 primary headache disorders, along with tension-type headache and cluster headache. A moderate or severe headache is one of the many characteristics of migraine, and some patients do not even have a headache during a migraine attack. Migraine is an inherited disease of the brain and other parts of the nervous system and can feel much worse than a normal headache. During a migraine attack, the brain does not process sensory data, such as lights, sound, or touch, properly. Patients might even experience visual, sensory, or speech problems (ie, auras) and sometime see flashing lights or zigzag lines that blink on and off or blind spots in their vision. Patients with migraine are often nauseated and severely bothered by light, sound, and even smells. Migraine headaches can last between 4 and 72 hours on average, causing disability, tiredness, and inability to think clearly or work productively, which adds to the burden of the disease. So, migraine is not just a headache.
Myth: More Women Than Men Experience Migraine
This is true. Epidemiologic data show a 3-fold higher incidence of migraine in women than men, starting from puberty and throughout life. From about 6 to 12 years, boys have a slightly higher incidence than girls, but then migraine occurrence levels off and becomes a disease primarily of women. The modulation of neuronal and vascular reactivity by hormones (namely estrogens and progesterone) is a crucial aspect of migraine in some women only. These hormones exert influence on a spectrum of neuromediators and neurotransmitters, potentially leading to functional and structural variations in specific brain regions associated with migraine pathogenesis. Beyond their central effects, sex hormones also modulate vascular tone. Therefore, migraine follows a pattern throughout a woman’s life corresponding to the fluctuation of estrogen. Within a year of their first menstrual period, many girls with migraine have their first attack. They are more likely to have a migraine attack just before and at the start of menses, and at other times of the month as well. They feel better when pregnant and worse after they stop breastfeeding, and they start to feel worse prior to menopause. Then they improve a few years after menopause.
While men are less at risk of having migraine, they’re more likely to have cluster headache than women (although this type of headache is rare compared with other headaches like migraine). Only about 0.1% or less of the population of adults in the US experience this type of headache. Cluster headache gets its name from the clustering of attacks occurring 2 to 6 times per day for 4 to 10 weeks and disappearing as quickly as they came. This headache pain is felt exclusively in or behind 1 eye and rarely elsewhere, on the same side of the head. There is also a clustering of other symptoms called autonomic findings, such as tearing and redness of 1 eye, stuffiness and running in 1 nostril, sweating over 1 eyebrow, drooping of 1 eyelid, and a small pupil—all on the same side of the head the pain is radiating from. Most patients have only some of these findings. Cluster headaches tend to occur every year around the same time (circannual). When a patient is in a cycle of cluster headaches, they often occur at the same time each day (circadian). These set times of the year and of the day are caused by the biological clock deep down under the brain in the hypothalamus.
Myth: All Headaches Are Psychological
This is not true. Usually the underlying cause of migraine is genetically-inherited, but each attack may be triggered by an underlying cause (eg, drop in barometric pressure, menses, certain food/drinks, lack of sleep, stress, etc). Even tension-type headaches can be triggered by muscles in the head and neck becoming tense, stressful events, or jaw issues, which in turn send out pain signals that are felt on both sides of the head.
Many years ago (ie, 1950s-1960s), it was thought that the underlying cause of migraine in women was psychological issues; that has been disproven many times. Both men and women have migraine, and they both can have coexisting psychological issues (ie, depression, anxiety, and other psychiatric problems).
Myth: Migraines Aren’t Serious
Most types of migraine in and of themselves are not serious; however, chronic migraine can continue for years and is debilitating and disabling—becoming a serious issue for patients. These patients usually take many medications, are obese, can have big changes in weight and severe insomnia, don’t exercise enough, and develop other illnesses. Migraine can severely impact quality of life; many people living with migraine have reported reduced productivity while at work, lack of promotion, loss of jobs, and a disruption in their family, social, and leisure activities.
Migraine attacks vary from one person to another and can be quite different from one attack to another in the same person. Hemiplegic migraine, a rare and distinct subtype that is sometimes inherited, is characterized by neurologic symptoms (multiple auras, including a significant weakness or paralysis on 1 side of the body). Although these patients seem much sicker and have multiple types of auras and 1-sided weakness with a prolonged headache, most recover without serious consequences.
Myth: Lack of Sleep Causes Migraine
Yes, lack of sleep is a known trigger for migraine in many people, but lack of sleep is not the cause of migraine. Sleep deprivation and irregular sleep patterns can disrupt the delicate balance of neurotransmitters and hormones in the brain, potentially triggering migraine in susceptible individuals. Additionally, inadequate sleep may contribute to increased stress and tension, which are also common triggers for migraine. In fact, many people with migraine do have sleep issues, which can range from trouble falling asleep to early morning awakening without being able to get back to sleep or frequently interrupted sleep each night. Correcting the sleep problem is part of the migraine therapy. Patients should be checked for sleep apnea if they wake with headache in the morning. Medication overuse headache should also be considered.
Establishing a regular sleep routine and ensuring an adequate amount of sleep can be important components of managing migraine symptoms, particularly for those who find a connection between their sleep patterns and the onset of a migraine attack. However, the relationship between sleep and migraine can vary widely among individuals, and other factors may also contribute to migraine triggers.
Myth: Caffeine Causes Migraine
This is a myth; caffeine does not cause migraine but definitely can be a trigger for some people. Coffee and caffeine and migraine have a complex relationship: excessive caffeine consumption or withdrawal can trigger migraine attacks, but caffeine can also help alleviate headaches (including migraine) due to its analgesic properties. Caffeine is a major component of many over-the-counter medicines for migraine. Some people find drinking coffee or a soda or taking a caffeine tablet at the onset of a migraine attack lowers the intensity of a migraine headache. Regular use of caffeine, either as “treatment” or for pleasure, is not advised in patients with migraine. Most doctors limit caffeine to a regular cup of coffee or tea per day, with no caffeine-containing sodas or chocolate in their patients with migraine; caffeine withdrawal is also a frequent migraine trigger. Patients can notice withdrawal headaches when they stop coffee, even if they are only consuming 1 cup per day. Most people drink a lot more.
Myth: Headache Medicine Will Cure Migraine
False. There currently is no “cure” for migraine. There are several medicines available that certainly can help prevent, abort, or control symptoms of migraine. Some of these medications include over-the-counter analgesics; triptans (like sumatriptan or rizatriptan); gepants, which are small molecule CGRP (calcitonin gene-related peptide) antagonists; CGRP antibodies given by injection; antidepressants; antiseizure medicines; and beta-blockers.
Myth: You Cannot Take Any Migraine Medications During Pregnancy
Migraine medications, such as triptans, are relatively safe during pregnancy, particularly after the first trimester. Acetaminophen in low doses is safe as well, but some of the preventive antiseizure medications should be avoided due to the risk of halting the pregnancy or producing a congenital malformation. Noninvasive wearable devices (such as Nerivio), biofeedback training, mindfulness, and relaxation techniques are particularly appealing to pregnant women as they have high efficacy with virtually no lasting side effects.
Although patients who are pregnant might have an increased flurry of migraine headaches in the first trimester of their pregnancy, they will most likely have a decreased number of attacks in the next 2 trimesters of their pregnancy, making them feel really well. The first trimester is a dangerous time for fetuses to be exposed to certain medicines that are foreign to them, as their organs are still being formed. There are medicines that doctors feel are less problematic both for acute care and prevention of migraine during pregnancy; therefore, patients with a history of migraine should always consult with their obstetrician-gynecologist and a neurologist (or other doctor they usually see for their migraine care) before taking any medication if they are planning a pregnancy or are pregnant.
Effective nonpharmaceutical options are available for all patients with migraine, whether pregnant or not. Maintaining a healthy lifestyle, which includes getting 7 to 10 hours of sleep each night, drinking plenty of water each day, getting ample nutrition from healthy foods, and eliminating as many sources of extra stress as possible can help reduce the risk of a migraine, even when exposed to a known trigger.
Medications may also lead to headaches by a phenomenon called medication overuse headache, if the rescue medication is taken too often. Clinicians recommend no more than 2 days per week of any acute care medication and taking a good preventive medication if needed.
Myth: “Migraine Diets” Cure Migraine
This is false. Avoiding known food triggers can reduce the risk of a migraine attack, but a diet regimen is not a cure. Although eating healthy foods and avoiding certain kinds of food that trigger migraine can eliminate triggering the episodes, there are other factors to take into account. For instance, the migraine diet cannot address a lack of sleep, stress, or hormonal changes a person experiences. Only very few patients with migraine can say their medication has cured their migraine, but it could happen.
Myth: Dietary Supplements Can Cure Migraine
This myth is not true. Supplements can help migraine headache or prevent triggering it, but they won’t cure it. Supplements, such as magnesium, vitamin D3, coenzyme Q10, vitamin B2 (riboflavin), feverfew, melatonin, and vitamin B2 are important additions to the migraine treatment armamentarium, but no one specific vitamin/mineral or supplement has been proven to help prevent or relieve migraine for everyone. They help some people immensely and do little for others, just as with any pharmacologic agent.
Myth: It’s Not a Migraine Unless You Experience Aura
This is not true, as most migraines present without aura. Migraine with typical aura affects 30% of patients with migraine.
Myth: Researchers No Longer Investigate Migraine
False; there are several ongoing studies working to address the pathophysiology of migraine and find new treatment options. Recently, neuromodulation devices have entered the market. One such device from Theranica (called Nerivio) now has clearance from the US Food and Drug Administration for acute and preventive migraine treatment from age 12 and up. One phase 4 study by Theranica shows that Nerivio appears to be safe during pregnancy.
Several migraine studies of note include the following:
OnabotulinumtoxinA as a treatment for hemiplegic migraine: This project aims to evaluate the response to onabotulinumtoxinA treatments in patients with hemiplegic migraine evaluated at Mayo Clinic.
Occipital nerve stimulation for migraine: OPTIMISE. This study is evaluating the safety and efficacy of occipital nerve stimulation (ONS) using the Boston Scientific Corporation (BSC) Precision™ System in the management of intractable chronic migraine, when used in conjunction with antimigraine medications.
The Medication Overuse Treatment Strategy trial: This study is comparing the outcomes among patients randomized to 1 of the 2 treatment strategies for treating patients who have chronic migraine with medication overuse.
Metformin is being investigated as a treatment for the prevention of episodic migraine.
Myth: Migraine Cannot Be Diagnosed Without an Imaging Exam
This is false. Migraine is a clinical diagnosis and does not need any imaging to confirm. Imaging is indicated only if the symptoms are not clear or if there are neurologic symptoms or warning signs accompanying the migraine. In such cases, imaging would be warranted to rule out other pathologies. A magnetic resonance imaging scan is performed to rule out other pathology, not to diagnose migraine. A clinician must identify a pattern in the patient’s history according to the diagnostic criteria of the International Headache Society to diagnose migraine, which include that the patient had 5 previous attacks without aura or 2 attacks with aura.
Summary
Headaches, especially migraine, can be unpleasant and disabling and can significantly affect a patient’s quality of life. However, pharmaceutical and nonpharmaceutical interventions that can help are available. Lifestyle changes, including diet, sleep, and stress reduction can ease symptoms and reduce the frequency of migraine attacks. As researchers continue to investigate the pathophysiology of migraine, they are sure to identify better treatments and, perhaps one day—a cure.
Patients may be familiar with several myths and have misconceptions about headaches and migraine, which often arise due to a combination of factors, including limited understanding of the conditions, cultural beliefs, misinformation, and the complex nature of headaches. Being aware of these myths and seeking accurate information help patients to better understand and manage their headaches.
Myth: Migraine Is the Most Common Type of Headache
This is not true. The most common type of headache is tension-type headache, and it's the kind of headache that almost everyone has from time to time. Between 40% and 80% of the US population have had some form of tension-type headache, but only about 13% of the adult population have migraine. Stress can make muscles in the head and neck tense and knotted, and these muscles can be the source of a tension-type headache. Sometimes these headaches are not at all related to muscles or stress. Neck position may also be a factor. Pain from this type of headache is usually felt on both sides of the head and presents more often as steady, dull pressure or pain that’s usually mild to moderate in intensity. The pain can be in the forehead and eyes or further back in the head. Tension-type headaches are not usually associated with nausea, vomiting, or light and sound sensitivity.
When a tension-type headache is really severe, patients could consider this headache a migraine. Clinicians can easily distinguish tension-type headache from migraine, which often presents on one side of the head, with moderate or severe intensity, is throbbing, and is associated with nausea, vomiting, and light and sound sensitivity.
Myth: Only Adults Get Headaches
False. Headaches aren’t experienced just by adults. However, unlike adults, children find it harder to explain their headaches. It is true that adults have more migraines than children; children’s migraines are often hard for doctors to recognize. A 6- to 9-year-old child is 50% less likely than an adult to have migraine, and their attacks are more often bilateral, are shorter, and respond to sleep quickly.
Myth: Migraines Are Just Really Bad Headaches
False. They are bad, but that is only a small part of the story. A migraine attack is different from other headaches; they actually are 1 of the 3 primary headache disorders, along with tension-type headache and cluster headache. A moderate or severe headache is one of the many characteristics of migraine, and some patients do not even have a headache during a migraine attack. Migraine is an inherited disease of the brain and other parts of the nervous system and can feel much worse than a normal headache. During a migraine attack, the brain does not process sensory data, such as lights, sound, or touch, properly. Patients might even experience visual, sensory, or speech problems (ie, auras) and sometime see flashing lights or zigzag lines that blink on and off or blind spots in their vision. Patients with migraine are often nauseated and severely bothered by light, sound, and even smells. Migraine headaches can last between 4 and 72 hours on average, causing disability, tiredness, and inability to think clearly or work productively, which adds to the burden of the disease. So, migraine is not just a headache.
Myth: More Women Than Men Experience Migraine
This is true. Epidemiologic data show a 3-fold higher incidence of migraine in women than men, starting from puberty and throughout life. From about 6 to 12 years, boys have a slightly higher incidence than girls, but then migraine occurrence levels off and becomes a disease primarily of women. The modulation of neuronal and vascular reactivity by hormones (namely estrogens and progesterone) is a crucial aspect of migraine in some women only. These hormones exert influence on a spectrum of neuromediators and neurotransmitters, potentially leading to functional and structural variations in specific brain regions associated with migraine pathogenesis. Beyond their central effects, sex hormones also modulate vascular tone. Therefore, migraine follows a pattern throughout a woman’s life corresponding to the fluctuation of estrogen. Within a year of their first menstrual period, many girls with migraine have their first attack. They are more likely to have a migraine attack just before and at the start of menses, and at other times of the month as well. They feel better when pregnant and worse after they stop breastfeeding, and they start to feel worse prior to menopause. Then they improve a few years after menopause.
While men are less at risk of having migraine, they’re more likely to have cluster headache than women (although this type of headache is rare compared with other headaches like migraine). Only about 0.1% or less of the population of adults in the US experience this type of headache. Cluster headache gets its name from the clustering of attacks occurring 2 to 6 times per day for 4 to 10 weeks and disappearing as quickly as they came. This headache pain is felt exclusively in or behind 1 eye and rarely elsewhere, on the same side of the head. There is also a clustering of other symptoms called autonomic findings, such as tearing and redness of 1 eye, stuffiness and running in 1 nostril, sweating over 1 eyebrow, drooping of 1 eyelid, and a small pupil—all on the same side of the head the pain is radiating from. Most patients have only some of these findings. Cluster headaches tend to occur every year around the same time (circannual). When a patient is in a cycle of cluster headaches, they often occur at the same time each day (circadian). These set times of the year and of the day are caused by the biological clock deep down under the brain in the hypothalamus.
Myth: All Headaches Are Psychological
This is not true. Usually the underlying cause of migraine is genetically-inherited, but each attack may be triggered by an underlying cause (eg, drop in barometric pressure, menses, certain food/drinks, lack of sleep, stress, etc). Even tension-type headaches can be triggered by muscles in the head and neck becoming tense, stressful events, or jaw issues, which in turn send out pain signals that are felt on both sides of the head.
Many years ago (ie, 1950s-1960s), it was thought that the underlying cause of migraine in women was psychological issues; that has been disproven many times. Both men and women have migraine, and they both can have coexisting psychological issues (ie, depression, anxiety, and other psychiatric problems).
Myth: Migraines Aren’t Serious
Most types of migraine in and of themselves are not serious; however, chronic migraine can continue for years and is debilitating and disabling—becoming a serious issue for patients. These patients usually take many medications, are obese, can have big changes in weight and severe insomnia, don’t exercise enough, and develop other illnesses. Migraine can severely impact quality of life; many people living with migraine have reported reduced productivity while at work, lack of promotion, loss of jobs, and a disruption in their family, social, and leisure activities.
Migraine attacks vary from one person to another and can be quite different from one attack to another in the same person. Hemiplegic migraine, a rare and distinct subtype that is sometimes inherited, is characterized by neurologic symptoms (multiple auras, including a significant weakness or paralysis on 1 side of the body). Although these patients seem much sicker and have multiple types of auras and 1-sided weakness with a prolonged headache, most recover without serious consequences.
Myth: Lack of Sleep Causes Migraine
Yes, lack of sleep is a known trigger for migraine in many people, but lack of sleep is not the cause of migraine. Sleep deprivation and irregular sleep patterns can disrupt the delicate balance of neurotransmitters and hormones in the brain, potentially triggering migraine in susceptible individuals. Additionally, inadequate sleep may contribute to increased stress and tension, which are also common triggers for migraine. In fact, many people with migraine do have sleep issues, which can range from trouble falling asleep to early morning awakening without being able to get back to sleep or frequently interrupted sleep each night. Correcting the sleep problem is part of the migraine therapy. Patients should be checked for sleep apnea if they wake with headache in the morning. Medication overuse headache should also be considered.
Establishing a regular sleep routine and ensuring an adequate amount of sleep can be important components of managing migraine symptoms, particularly for those who find a connection between their sleep patterns and the onset of a migraine attack. However, the relationship between sleep and migraine can vary widely among individuals, and other factors may also contribute to migraine triggers.
Myth: Caffeine Causes Migraine
This is a myth; caffeine does not cause migraine but definitely can be a trigger for some people. Coffee and caffeine and migraine have a complex relationship: excessive caffeine consumption or withdrawal can trigger migraine attacks, but caffeine can also help alleviate headaches (including migraine) due to its analgesic properties. Caffeine is a major component of many over-the-counter medicines for migraine. Some people find drinking coffee or a soda or taking a caffeine tablet at the onset of a migraine attack lowers the intensity of a migraine headache. Regular use of caffeine, either as “treatment” or for pleasure, is not advised in patients with migraine. Most doctors limit caffeine to a regular cup of coffee or tea per day, with no caffeine-containing sodas or chocolate in their patients with migraine; caffeine withdrawal is also a frequent migraine trigger. Patients can notice withdrawal headaches when they stop coffee, even if they are only consuming 1 cup per day. Most people drink a lot more.
Myth: Headache Medicine Will Cure Migraine
False. There currently is no “cure” for migraine. There are several medicines available that certainly can help prevent, abort, or control symptoms of migraine. Some of these medications include over-the-counter analgesics; triptans (like sumatriptan or rizatriptan); gepants, which are small molecule CGRP (calcitonin gene-related peptide) antagonists; CGRP antibodies given by injection; antidepressants; antiseizure medicines; and beta-blockers.
Myth: You Cannot Take Any Migraine Medications During Pregnancy
Migraine medications, such as triptans, are relatively safe during pregnancy, particularly after the first trimester. Acetaminophen in low doses is safe as well, but some of the preventive antiseizure medications should be avoided due to the risk of halting the pregnancy or producing a congenital malformation. Noninvasive wearable devices (such as Nerivio), biofeedback training, mindfulness, and relaxation techniques are particularly appealing to pregnant women as they have high efficacy with virtually no lasting side effects.
Although patients who are pregnant might have an increased flurry of migraine headaches in the first trimester of their pregnancy, they will most likely have a decreased number of attacks in the next 2 trimesters of their pregnancy, making them feel really well. The first trimester is a dangerous time for fetuses to be exposed to certain medicines that are foreign to them, as their organs are still being formed. There are medicines that doctors feel are less problematic both for acute care and prevention of migraine during pregnancy; therefore, patients with a history of migraine should always consult with their obstetrician-gynecologist and a neurologist (or other doctor they usually see for their migraine care) before taking any medication if they are planning a pregnancy or are pregnant.
Effective nonpharmaceutical options are available for all patients with migraine, whether pregnant or not. Maintaining a healthy lifestyle, which includes getting 7 to 10 hours of sleep each night, drinking plenty of water each day, getting ample nutrition from healthy foods, and eliminating as many sources of extra stress as possible can help reduce the risk of a migraine, even when exposed to a known trigger.
Medications may also lead to headaches by a phenomenon called medication overuse headache, if the rescue medication is taken too often. Clinicians recommend no more than 2 days per week of any acute care medication and taking a good preventive medication if needed.
Myth: “Migraine Diets” Cure Migraine
This is false. Avoiding known food triggers can reduce the risk of a migraine attack, but a diet regimen is not a cure. Although eating healthy foods and avoiding certain kinds of food that trigger migraine can eliminate triggering the episodes, there are other factors to take into account. For instance, the migraine diet cannot address a lack of sleep, stress, or hormonal changes a person experiences. Only very few patients with migraine can say their medication has cured their migraine, but it could happen.
Myth: Dietary Supplements Can Cure Migraine
This myth is not true. Supplements can help migraine headache or prevent triggering it, but they won’t cure it. Supplements, such as magnesium, vitamin D3, coenzyme Q10, vitamin B2 (riboflavin), feverfew, melatonin, and vitamin B2 are important additions to the migraine treatment armamentarium, but no one specific vitamin/mineral or supplement has been proven to help prevent or relieve migraine for everyone. They help some people immensely and do little for others, just as with any pharmacologic agent.
Myth: It’s Not a Migraine Unless You Experience Aura
This is not true, as most migraines present without aura. Migraine with typical aura affects 30% of patients with migraine.
Myth: Researchers No Longer Investigate Migraine
False; there are several ongoing studies working to address the pathophysiology of migraine and find new treatment options. Recently, neuromodulation devices have entered the market. One such device from Theranica (called Nerivio) now has clearance from the US Food and Drug Administration for acute and preventive migraine treatment from age 12 and up. One phase 4 study by Theranica shows that Nerivio appears to be safe during pregnancy.
Several migraine studies of note include the following:
OnabotulinumtoxinA as a treatment for hemiplegic migraine: This project aims to evaluate the response to onabotulinumtoxinA treatments in patients with hemiplegic migraine evaluated at Mayo Clinic.
Occipital nerve stimulation for migraine: OPTIMISE. This study is evaluating the safety and efficacy of occipital nerve stimulation (ONS) using the Boston Scientific Corporation (BSC) Precision™ System in the management of intractable chronic migraine, when used in conjunction with antimigraine medications.
The Medication Overuse Treatment Strategy trial: This study is comparing the outcomes among patients randomized to 1 of the 2 treatment strategies for treating patients who have chronic migraine with medication overuse.
Metformin is being investigated as a treatment for the prevention of episodic migraine.
Myth: Migraine Cannot Be Diagnosed Without an Imaging Exam
This is false. Migraine is a clinical diagnosis and does not need any imaging to confirm. Imaging is indicated only if the symptoms are not clear or if there are neurologic symptoms or warning signs accompanying the migraine. In such cases, imaging would be warranted to rule out other pathologies. A magnetic resonance imaging scan is performed to rule out other pathology, not to diagnose migraine. A clinician must identify a pattern in the patient’s history according to the diagnostic criteria of the International Headache Society to diagnose migraine, which include that the patient had 5 previous attacks without aura or 2 attacks with aura.
Summary
Headaches, especially migraine, can be unpleasant and disabling and can significantly affect a patient’s quality of life. However, pharmaceutical and nonpharmaceutical interventions that can help are available. Lifestyle changes, including diet, sleep, and stress reduction can ease symptoms and reduce the frequency of migraine attacks. As researchers continue to investigate the pathophysiology of migraine, they are sure to identify better treatments and, perhaps one day—a cure.
Patients may be familiar with several myths and have misconceptions about headaches and migraine, which often arise due to a combination of factors, including limited understanding of the conditions, cultural beliefs, misinformation, and the complex nature of headaches. Being aware of these myths and seeking accurate information help patients to better understand and manage their headaches.
Myth: Migraine Is the Most Common Type of Headache
This is not true. The most common type of headache is tension-type headache, and it's the kind of headache that almost everyone has from time to time. Between 40% and 80% of the US population have had some form of tension-type headache, but only about 13% of the adult population have migraine. Stress can make muscles in the head and neck tense and knotted, and these muscles can be the source of a tension-type headache. Sometimes these headaches are not at all related to muscles or stress. Neck position may also be a factor. Pain from this type of headache is usually felt on both sides of the head and presents more often as steady, dull pressure or pain that’s usually mild to moderate in intensity. The pain can be in the forehead and eyes or further back in the head. Tension-type headaches are not usually associated with nausea, vomiting, or light and sound sensitivity.
When a tension-type headache is really severe, patients could consider this headache a migraine. Clinicians can easily distinguish tension-type headache from migraine, which often presents on one side of the head, with moderate or severe intensity, is throbbing, and is associated with nausea, vomiting, and light and sound sensitivity.
Myth: Only Adults Get Headaches
False. Headaches aren’t experienced just by adults. However, unlike adults, children find it harder to explain their headaches. It is true that adults have more migraines than children; children’s migraines are often hard for doctors to recognize. A 6- to 9-year-old child is 50% less likely than an adult to have migraine, and their attacks are more often bilateral, are shorter, and respond to sleep quickly.
Myth: Migraines Are Just Really Bad Headaches
False. They are bad, but that is only a small part of the story. A migraine attack is different from other headaches; they actually are 1 of the 3 primary headache disorders, along with tension-type headache and cluster headache. A moderate or severe headache is one of the many characteristics of migraine, and some patients do not even have a headache during a migraine attack. Migraine is an inherited disease of the brain and other parts of the nervous system and can feel much worse than a normal headache. During a migraine attack, the brain does not process sensory data, such as lights, sound, or touch, properly. Patients might even experience visual, sensory, or speech problems (ie, auras) and sometime see flashing lights or zigzag lines that blink on and off or blind spots in their vision. Patients with migraine are often nauseated and severely bothered by light, sound, and even smells. Migraine headaches can last between 4 and 72 hours on average, causing disability, tiredness, and inability to think clearly or work productively, which adds to the burden of the disease. So, migraine is not just a headache.
Myth: More Women Than Men Experience Migraine
This is true. Epidemiologic data show a 3-fold higher incidence of migraine in women than men, starting from puberty and throughout life. From about 6 to 12 years, boys have a slightly higher incidence than girls, but then migraine occurrence levels off and becomes a disease primarily of women. The modulation of neuronal and vascular reactivity by hormones (namely estrogens and progesterone) is a crucial aspect of migraine in some women only. These hormones exert influence on a spectrum of neuromediators and neurotransmitters, potentially leading to functional and structural variations in specific brain regions associated with migraine pathogenesis. Beyond their central effects, sex hormones also modulate vascular tone. Therefore, migraine follows a pattern throughout a woman’s life corresponding to the fluctuation of estrogen. Within a year of their first menstrual period, many girls with migraine have their first attack. They are more likely to have a migraine attack just before and at the start of menses, and at other times of the month as well. They feel better when pregnant and worse after they stop breastfeeding, and they start to feel worse prior to menopause. Then they improve a few years after menopause.
While men are less at risk of having migraine, they’re more likely to have cluster headache than women (although this type of headache is rare compared with other headaches like migraine). Only about 0.1% or less of the population of adults in the US experience this type of headache. Cluster headache gets its name from the clustering of attacks occurring 2 to 6 times per day for 4 to 10 weeks and disappearing as quickly as they came. This headache pain is felt exclusively in or behind 1 eye and rarely elsewhere, on the same side of the head. There is also a clustering of other symptoms called autonomic findings, such as tearing and redness of 1 eye, stuffiness and running in 1 nostril, sweating over 1 eyebrow, drooping of 1 eyelid, and a small pupil—all on the same side of the head the pain is radiating from. Most patients have only some of these findings. Cluster headaches tend to occur every year around the same time (circannual). When a patient is in a cycle of cluster headaches, they often occur at the same time each day (circadian). These set times of the year and of the day are caused by the biological clock deep down under the brain in the hypothalamus.
Myth: All Headaches Are Psychological
This is not true. Usually the underlying cause of migraine is genetically-inherited, but each attack may be triggered by an underlying cause (eg, drop in barometric pressure, menses, certain food/drinks, lack of sleep, stress, etc). Even tension-type headaches can be triggered by muscles in the head and neck becoming tense, stressful events, or jaw issues, which in turn send out pain signals that are felt on both sides of the head.
Many years ago (ie, 1950s-1960s), it was thought that the underlying cause of migraine in women was psychological issues; that has been disproven many times. Both men and women have migraine, and they both can have coexisting psychological issues (ie, depression, anxiety, and other psychiatric problems).
Myth: Migraines Aren’t Serious
Most types of migraine in and of themselves are not serious; however, chronic migraine can continue for years and is debilitating and disabling—becoming a serious issue for patients. These patients usually take many medications, are obese, can have big changes in weight and severe insomnia, don’t exercise enough, and develop other illnesses. Migraine can severely impact quality of life; many people living with migraine have reported reduced productivity while at work, lack of promotion, loss of jobs, and a disruption in their family, social, and leisure activities.
Migraine attacks vary from one person to another and can be quite different from one attack to another in the same person. Hemiplegic migraine, a rare and distinct subtype that is sometimes inherited, is characterized by neurologic symptoms (multiple auras, including a significant weakness or paralysis on 1 side of the body). Although these patients seem much sicker and have multiple types of auras and 1-sided weakness with a prolonged headache, most recover without serious consequences.
Myth: Lack of Sleep Causes Migraine
Yes, lack of sleep is a known trigger for migraine in many people, but lack of sleep is not the cause of migraine. Sleep deprivation and irregular sleep patterns can disrupt the delicate balance of neurotransmitters and hormones in the brain, potentially triggering migraine in susceptible individuals. Additionally, inadequate sleep may contribute to increased stress and tension, which are also common triggers for migraine. In fact, many people with migraine do have sleep issues, which can range from trouble falling asleep to early morning awakening without being able to get back to sleep or frequently interrupted sleep each night. Correcting the sleep problem is part of the migraine therapy. Patients should be checked for sleep apnea if they wake with headache in the morning. Medication overuse headache should also be considered.
Establishing a regular sleep routine and ensuring an adequate amount of sleep can be important components of managing migraine symptoms, particularly for those who find a connection between their sleep patterns and the onset of a migraine attack. However, the relationship between sleep and migraine can vary widely among individuals, and other factors may also contribute to migraine triggers.
Myth: Caffeine Causes Migraine
This is a myth; caffeine does not cause migraine but definitely can be a trigger for some people. Coffee and caffeine and migraine have a complex relationship: excessive caffeine consumption or withdrawal can trigger migraine attacks, but caffeine can also help alleviate headaches (including migraine) due to its analgesic properties. Caffeine is a major component of many over-the-counter medicines for migraine. Some people find drinking coffee or a soda or taking a caffeine tablet at the onset of a migraine attack lowers the intensity of a migraine headache. Regular use of caffeine, either as “treatment” or for pleasure, is not advised in patients with migraine. Most doctors limit caffeine to a regular cup of coffee or tea per day, with no caffeine-containing sodas or chocolate in their patients with migraine; caffeine withdrawal is also a frequent migraine trigger. Patients can notice withdrawal headaches when they stop coffee, even if they are only consuming 1 cup per day. Most people drink a lot more.
Myth: Headache Medicine Will Cure Migraine
False. There currently is no “cure” for migraine. There are several medicines available that certainly can help prevent, abort, or control symptoms of migraine. Some of these medications include over-the-counter analgesics; triptans (like sumatriptan or rizatriptan); gepants, which are small molecule CGRP (calcitonin gene-related peptide) antagonists; CGRP antibodies given by injection; antidepressants; antiseizure medicines; and beta-blockers.
Myth: You Cannot Take Any Migraine Medications During Pregnancy
Migraine medications, such as triptans, are relatively safe during pregnancy, particularly after the first trimester. Acetaminophen in low doses is safe as well, but some of the preventive antiseizure medications should be avoided due to the risk of halting the pregnancy or producing a congenital malformation. Noninvasive wearable devices (such as Nerivio), biofeedback training, mindfulness, and relaxation techniques are particularly appealing to pregnant women as they have high efficacy with virtually no lasting side effects.
Although patients who are pregnant might have an increased flurry of migraine headaches in the first trimester of their pregnancy, they will most likely have a decreased number of attacks in the next 2 trimesters of their pregnancy, making them feel really well. The first trimester is a dangerous time for fetuses to be exposed to certain medicines that are foreign to them, as their organs are still being formed. There are medicines that doctors feel are less problematic both for acute care and prevention of migraine during pregnancy; therefore, patients with a history of migraine should always consult with their obstetrician-gynecologist and a neurologist (or other doctor they usually see for their migraine care) before taking any medication if they are planning a pregnancy or are pregnant.
Effective nonpharmaceutical options are available for all patients with migraine, whether pregnant or not. Maintaining a healthy lifestyle, which includes getting 7 to 10 hours of sleep each night, drinking plenty of water each day, getting ample nutrition from healthy foods, and eliminating as many sources of extra stress as possible can help reduce the risk of a migraine, even when exposed to a known trigger.
Medications may also lead to headaches by a phenomenon called medication overuse headache, if the rescue medication is taken too often. Clinicians recommend no more than 2 days per week of any acute care medication and taking a good preventive medication if needed.
Myth: “Migraine Diets” Cure Migraine
This is false. Avoiding known food triggers can reduce the risk of a migraine attack, but a diet regimen is not a cure. Although eating healthy foods and avoiding certain kinds of food that trigger migraine can eliminate triggering the episodes, there are other factors to take into account. For instance, the migraine diet cannot address a lack of sleep, stress, or hormonal changes a person experiences. Only very few patients with migraine can say their medication has cured their migraine, but it could happen.
Myth: Dietary Supplements Can Cure Migraine
This myth is not true. Supplements can help migraine headache or prevent triggering it, but they won’t cure it. Supplements, such as magnesium, vitamin D3, coenzyme Q10, vitamin B2 (riboflavin), feverfew, melatonin, and vitamin B2 are important additions to the migraine treatment armamentarium, but no one specific vitamin/mineral or supplement has been proven to help prevent or relieve migraine for everyone. They help some people immensely and do little for others, just as with any pharmacologic agent.
Myth: It’s Not a Migraine Unless You Experience Aura
This is not true, as most migraines present without aura. Migraine with typical aura affects 30% of patients with migraine.
Myth: Researchers No Longer Investigate Migraine
False; there are several ongoing studies working to address the pathophysiology of migraine and find new treatment options. Recently, neuromodulation devices have entered the market. One such device from Theranica (called Nerivio) now has clearance from the US Food and Drug Administration for acute and preventive migraine treatment from age 12 and up. One phase 4 study by Theranica shows that Nerivio appears to be safe during pregnancy.
Several migraine studies of note include the following:
OnabotulinumtoxinA as a treatment for hemiplegic migraine: This project aims to evaluate the response to onabotulinumtoxinA treatments in patients with hemiplegic migraine evaluated at Mayo Clinic.
Occipital nerve stimulation for migraine: OPTIMISE. This study is evaluating the safety and efficacy of occipital nerve stimulation (ONS) using the Boston Scientific Corporation (BSC) Precision™ System in the management of intractable chronic migraine, when used in conjunction with antimigraine medications.
The Medication Overuse Treatment Strategy trial: This study is comparing the outcomes among patients randomized to 1 of the 2 treatment strategies for treating patients who have chronic migraine with medication overuse.
Metformin is being investigated as a treatment for the prevention of episodic migraine.
Myth: Migraine Cannot Be Diagnosed Without an Imaging Exam
This is false. Migraine is a clinical diagnosis and does not need any imaging to confirm. Imaging is indicated only if the symptoms are not clear or if there are neurologic symptoms or warning signs accompanying the migraine. In such cases, imaging would be warranted to rule out other pathologies. A magnetic resonance imaging scan is performed to rule out other pathology, not to diagnose migraine. A clinician must identify a pattern in the patient’s history according to the diagnostic criteria of the International Headache Society to diagnose migraine, which include that the patient had 5 previous attacks without aura or 2 attacks with aura.
Summary
Headaches, especially migraine, can be unpleasant and disabling and can significantly affect a patient’s quality of life. However, pharmaceutical and nonpharmaceutical interventions that can help are available. Lifestyle changes, including diet, sleep, and stress reduction can ease symptoms and reduce the frequency of migraine attacks. As researchers continue to investigate the pathophysiology of migraine, they are sure to identify better treatments and, perhaps one day—a cure.
Retinal Perfusion Is Reduced During Migraine Attacks
Together, these changes could one day represent migraine biomarkers, authors say. The study was published online in Headache.
“We’re always looking for a biological marker for migraine,” said Alan M. Rapoport, MD, a clinical professor of neurology in the David Geffen School of Medicine at the University of California Los Angeles and past president of the International Headache Society. Researchers have identified many parameters that make people more likely to experience migraine, he said, but there remains no smoking gun. “We do not yet have a diagnostic test.”
Investigators have long been examining ocular vascular supply, added Dr. Rapoport, who was not involved with the study, because the eyes, visual system of the brain, and migraine are closely related. “But no one has ever figured out that one could use anything related to the eye as a definitive diagnostic test. This study was interesting because researchers used a very advanced technique to see if there are changes in the vascular supply to the eyeball during migraine.”
During Attacks
Study investigators prospectively enrolled 37 patients diagnosed with migraine with aura (MA), 30 with migraine without aura (MO), and 20 healthy controls. All subjects underwent macular OCTA for interictal analysis. A total of 20 patients with migraine (12 with MA and 8 with MO) underwent repeat scans during migraine attacks, and 5 control patients had repeat scans.
Compared with interictal measurements, significant parafoveal reductions in vessel flux index, an indicator of retinal perfusion, occurred in both the MA and MO groups during migraine attacks: –7% (95% CI, –10% to –4%; P = .006) and –7% (95% CI, –10% to –3%; P = .016), respectively, versus controls (2%, 95% CI, –3% to 7%).
The fact that migraine attacks resulted in reduced blood supply to the retinal region responsible for central vision is intriguing, said Dr. Rapoport, because sufficient reductions in blood supply there could result in blurred vision or other visual difficulties that might be mistaken for a true aura. “Many patients describe blurred vision related to their migraine headaches which do not usually qualify for an aura diagnosis,” he said.
Diagnostic criteria for MA, which afflicts around one third of people with migraine, include visual aberrations lasting at least 5 minutes and no more than 60 minutes. Visual aberrations average about 20-25 minutes, said Dr. Rapoport. “And we don’t usually accept blurred vision.” For most people who experience ictal blurred vision, he added, the phenomenon only lasts a short time and is not considered an aura.
More typical visual manifestations of MA include zigzag lines in an overall crescent shape that may blink, have bright edges, grow and shrink in size, and/or move across the visual field; patients also may have blind spots or distortions (e.g. far away vision, smaller or larger vision, or kaleidoscopic fractured vision). Nevertheless, said Dr. Rapoport, the study may shed light on why some people experiencing a migraine attack may suffer a brief bout of blurred vision and mistakenly report experiencing an aura.
Between Attacks
Comparing the two migraine groups interictally showed statistically significant differences in macular structure and function. Compared with the MO cohort, the MA cohort had higher circularity (mean [SD] 0.686 [0.088] vs. 0.629 [0.120] MO, P = .004), as well as a 13% (SD ± 10%, P = .003) lower foveal vessel flux index. “Not only is perfusion lower in both types of migraine during the attack,” said Dr. Rapoport, “but between attacks, people with MA had a lower blood supply to the retina than those who had MO.”
Unilateral Migraine
In a subset of patients (14 with MA and 12 with MO) whose headaches occurred unilaterally, investigators found retinal vascular parameters consistent with greater perfusion in the ipsilateral eye versus the contralateral eye. The significance of these findings remains unclear, Dr. Rapoport said, because circulatory findings revealed by CAT or MRI scans of patients with unilateral headaches are often normal or involve complex changes or mild edema on the side of the headache. The visual cortex on either side receives input from both eyes, he added.
Study Limitations
Authors acknowledged several study shortcomings. Most notably, COVID-19 restrictions resulted in a small sample size, and several patients (excluded from analysis) failed to return for repeat scans during migraine attacks. The study included patients with migraine attacks of varying frequency, and a handful of patients used acute rescue medications before undergoing ictal scans.
“If a future study corrected all these shortcomings,” Dr. Rapoport said, “the results might be more impressive and even more significant.” Based on these results alone, he said, it would be premature to pronounce OCTA-derived measurements of retinal perfusion and related parameters as future migraine biomarkers.
“But it’s a good start. If this hasn’t been done before, in quite this way, this is a very interesting study which, when repeated, should lead to even more significant findings.”
For now, the paper should remind practicing neurologists to dig deeper when patients complain of visual problems during migraine attacks. “It might be blurred vision for just 3 minutes,” he said. “Some patients may be calling it an aura, or the doctor may be thinking it is an aura because they’re not digging for further information in the history. We may now have a window into decreased retinal perfusion during a migraine attack and why some patients have blurred vision.”
The study was funded by the Amgen and the Baldwin Foundation. Dr. Rapoport is editor-in-chief of Neurology Reviews but reports no relevant relationships with the funders of this research.
Together, these changes could one day represent migraine biomarkers, authors say. The study was published online in Headache.
“We’re always looking for a biological marker for migraine,” said Alan M. Rapoport, MD, a clinical professor of neurology in the David Geffen School of Medicine at the University of California Los Angeles and past president of the International Headache Society. Researchers have identified many parameters that make people more likely to experience migraine, he said, but there remains no smoking gun. “We do not yet have a diagnostic test.”
Investigators have long been examining ocular vascular supply, added Dr. Rapoport, who was not involved with the study, because the eyes, visual system of the brain, and migraine are closely related. “But no one has ever figured out that one could use anything related to the eye as a definitive diagnostic test. This study was interesting because researchers used a very advanced technique to see if there are changes in the vascular supply to the eyeball during migraine.”
During Attacks
Study investigators prospectively enrolled 37 patients diagnosed with migraine with aura (MA), 30 with migraine without aura (MO), and 20 healthy controls. All subjects underwent macular OCTA for interictal analysis. A total of 20 patients with migraine (12 with MA and 8 with MO) underwent repeat scans during migraine attacks, and 5 control patients had repeat scans.
Compared with interictal measurements, significant parafoveal reductions in vessel flux index, an indicator of retinal perfusion, occurred in both the MA and MO groups during migraine attacks: –7% (95% CI, –10% to –4%; P = .006) and –7% (95% CI, –10% to –3%; P = .016), respectively, versus controls (2%, 95% CI, –3% to 7%).
The fact that migraine attacks resulted in reduced blood supply to the retinal region responsible for central vision is intriguing, said Dr. Rapoport, because sufficient reductions in blood supply there could result in blurred vision or other visual difficulties that might be mistaken for a true aura. “Many patients describe blurred vision related to their migraine headaches which do not usually qualify for an aura diagnosis,” he said.
Diagnostic criteria for MA, which afflicts around one third of people with migraine, include visual aberrations lasting at least 5 minutes and no more than 60 minutes. Visual aberrations average about 20-25 minutes, said Dr. Rapoport. “And we don’t usually accept blurred vision.” For most people who experience ictal blurred vision, he added, the phenomenon only lasts a short time and is not considered an aura.
More typical visual manifestations of MA include zigzag lines in an overall crescent shape that may blink, have bright edges, grow and shrink in size, and/or move across the visual field; patients also may have blind spots or distortions (e.g. far away vision, smaller or larger vision, or kaleidoscopic fractured vision). Nevertheless, said Dr. Rapoport, the study may shed light on why some people experiencing a migraine attack may suffer a brief bout of blurred vision and mistakenly report experiencing an aura.
Between Attacks
Comparing the two migraine groups interictally showed statistically significant differences in macular structure and function. Compared with the MO cohort, the MA cohort had higher circularity (mean [SD] 0.686 [0.088] vs. 0.629 [0.120] MO, P = .004), as well as a 13% (SD ± 10%, P = .003) lower foveal vessel flux index. “Not only is perfusion lower in both types of migraine during the attack,” said Dr. Rapoport, “but between attacks, people with MA had a lower blood supply to the retina than those who had MO.”
Unilateral Migraine
In a subset of patients (14 with MA and 12 with MO) whose headaches occurred unilaterally, investigators found retinal vascular parameters consistent with greater perfusion in the ipsilateral eye versus the contralateral eye. The significance of these findings remains unclear, Dr. Rapoport said, because circulatory findings revealed by CAT or MRI scans of patients with unilateral headaches are often normal or involve complex changes or mild edema on the side of the headache. The visual cortex on either side receives input from both eyes, he added.
Study Limitations
Authors acknowledged several study shortcomings. Most notably, COVID-19 restrictions resulted in a small sample size, and several patients (excluded from analysis) failed to return for repeat scans during migraine attacks. The study included patients with migraine attacks of varying frequency, and a handful of patients used acute rescue medications before undergoing ictal scans.
“If a future study corrected all these shortcomings,” Dr. Rapoport said, “the results might be more impressive and even more significant.” Based on these results alone, he said, it would be premature to pronounce OCTA-derived measurements of retinal perfusion and related parameters as future migraine biomarkers.
“But it’s a good start. If this hasn’t been done before, in quite this way, this is a very interesting study which, when repeated, should lead to even more significant findings.”
For now, the paper should remind practicing neurologists to dig deeper when patients complain of visual problems during migraine attacks. “It might be blurred vision for just 3 minutes,” he said. “Some patients may be calling it an aura, or the doctor may be thinking it is an aura because they’re not digging for further information in the history. We may now have a window into decreased retinal perfusion during a migraine attack and why some patients have blurred vision.”
The study was funded by the Amgen and the Baldwin Foundation. Dr. Rapoport is editor-in-chief of Neurology Reviews but reports no relevant relationships with the funders of this research.
Together, these changes could one day represent migraine biomarkers, authors say. The study was published online in Headache.
“We’re always looking for a biological marker for migraine,” said Alan M. Rapoport, MD, a clinical professor of neurology in the David Geffen School of Medicine at the University of California Los Angeles and past president of the International Headache Society. Researchers have identified many parameters that make people more likely to experience migraine, he said, but there remains no smoking gun. “We do not yet have a diagnostic test.”
Investigators have long been examining ocular vascular supply, added Dr. Rapoport, who was not involved with the study, because the eyes, visual system of the brain, and migraine are closely related. “But no one has ever figured out that one could use anything related to the eye as a definitive diagnostic test. This study was interesting because researchers used a very advanced technique to see if there are changes in the vascular supply to the eyeball during migraine.”
During Attacks
Study investigators prospectively enrolled 37 patients diagnosed with migraine with aura (MA), 30 with migraine without aura (MO), and 20 healthy controls. All subjects underwent macular OCTA for interictal analysis. A total of 20 patients with migraine (12 with MA and 8 with MO) underwent repeat scans during migraine attacks, and 5 control patients had repeat scans.
Compared with interictal measurements, significant parafoveal reductions in vessel flux index, an indicator of retinal perfusion, occurred in both the MA and MO groups during migraine attacks: –7% (95% CI, –10% to –4%; P = .006) and –7% (95% CI, –10% to –3%; P = .016), respectively, versus controls (2%, 95% CI, –3% to 7%).
The fact that migraine attacks resulted in reduced blood supply to the retinal region responsible for central vision is intriguing, said Dr. Rapoport, because sufficient reductions in blood supply there could result in blurred vision or other visual difficulties that might be mistaken for a true aura. “Many patients describe blurred vision related to their migraine headaches which do not usually qualify for an aura diagnosis,” he said.
Diagnostic criteria for MA, which afflicts around one third of people with migraine, include visual aberrations lasting at least 5 minutes and no more than 60 minutes. Visual aberrations average about 20-25 minutes, said Dr. Rapoport. “And we don’t usually accept blurred vision.” For most people who experience ictal blurred vision, he added, the phenomenon only lasts a short time and is not considered an aura.
More typical visual manifestations of MA include zigzag lines in an overall crescent shape that may blink, have bright edges, grow and shrink in size, and/or move across the visual field; patients also may have blind spots or distortions (e.g. far away vision, smaller or larger vision, or kaleidoscopic fractured vision). Nevertheless, said Dr. Rapoport, the study may shed light on why some people experiencing a migraine attack may suffer a brief bout of blurred vision and mistakenly report experiencing an aura.
Between Attacks
Comparing the two migraine groups interictally showed statistically significant differences in macular structure and function. Compared with the MO cohort, the MA cohort had higher circularity (mean [SD] 0.686 [0.088] vs. 0.629 [0.120] MO, P = .004), as well as a 13% (SD ± 10%, P = .003) lower foveal vessel flux index. “Not only is perfusion lower in both types of migraine during the attack,” said Dr. Rapoport, “but between attacks, people with MA had a lower blood supply to the retina than those who had MO.”
Unilateral Migraine
In a subset of patients (14 with MA and 12 with MO) whose headaches occurred unilaterally, investigators found retinal vascular parameters consistent with greater perfusion in the ipsilateral eye versus the contralateral eye. The significance of these findings remains unclear, Dr. Rapoport said, because circulatory findings revealed by CAT or MRI scans of patients with unilateral headaches are often normal or involve complex changes or mild edema on the side of the headache. The visual cortex on either side receives input from both eyes, he added.
Study Limitations
Authors acknowledged several study shortcomings. Most notably, COVID-19 restrictions resulted in a small sample size, and several patients (excluded from analysis) failed to return for repeat scans during migraine attacks. The study included patients with migraine attacks of varying frequency, and a handful of patients used acute rescue medications before undergoing ictal scans.
“If a future study corrected all these shortcomings,” Dr. Rapoport said, “the results might be more impressive and even more significant.” Based on these results alone, he said, it would be premature to pronounce OCTA-derived measurements of retinal perfusion and related parameters as future migraine biomarkers.
“But it’s a good start. If this hasn’t been done before, in quite this way, this is a very interesting study which, when repeated, should lead to even more significant findings.”
For now, the paper should remind practicing neurologists to dig deeper when patients complain of visual problems during migraine attacks. “It might be blurred vision for just 3 minutes,” he said. “Some patients may be calling it an aura, or the doctor may be thinking it is an aura because they’re not digging for further information in the history. We may now have a window into decreased retinal perfusion during a migraine attack and why some patients have blurred vision.”
The study was funded by the Amgen and the Baldwin Foundation. Dr. Rapoport is editor-in-chief of Neurology Reviews but reports no relevant relationships with the funders of this research.
FROM HEADACHE
Building a Toolkit for the Treatment of Acute Migraine
Selecting a treatment plan to deal with acute migraine attacks can be like putting together a toolkit of possible therapies, individualized for each patient, one expert said.
The toolkit should comprise reliable treatments that patients know are going to work and that act quickly, allowing them to get back to functioning normally in their daily lives, said Jessica Ailani, MD, during a talk at the 17th European Headache Congress held recently in Barcelona, Spain.
“Everyone with migraine needs acute treatment,” Dr. Ailani, who is a clinical professor of neurology at MedStar Georgetown University Hospital and director of the Georgetown Headache Center, Washington, DC, noted. “Sometimes we can reduce acute treatment with preventative agents, but some disability will remain, so we have to focus on good acute treatment, and this becomes more complex if a person has a lot of comorbidities, which is common in older patients.”
In selecting suitable treatments for migraine, consideration has to be given to the patient profile, any other conditions they have, speed of onset of the migraine attack, length of the attack, associated symptoms, and side effects of the medications, she said.
A Complex Case
As an example, Dr. Ailani described the process she used to treat one of her patients who had frequent severe migraines and other issues causing difficult decisions when selecting medications — a woman in her late 60s with several other comorbidities.
“This is the kind of case I see on a daily basis and which keeps me up at night,” she said. “Many times in clinical practice, we see complex cases like this, and through the course of a year, we may try every treatment option we have in a patient like this.”
On the first presentation, the patient had a chronic migraine with severe headaches every day. She had a history of previous cervical discectomy with fusion surgery; uncontrolled hypertension, for which she was taking an angiotensin blocker; high cholesterol, for which she was taking a statin; and diabetes with an A1c of 8. She did not smoke or drink alcohol, exercised moderately, and her body mass index was in a good range.
“Before a patient ever sees a doctor for their migraine, they will have already tried a lot of different things. Most people are already using NSAIDs and acetaminophen, the most commonly used treatments for acute migraine,” Dr. Ailani explains.
Her patient was taking a triptan and the barbiturate, butalbital. Dr. Ailani notes that the triptan is very effective, but in the United States, they are not available over the counter, and the patient is only allowed nine doses per month on her insurance, so she was supplementing with butalbital.
Over the course of a year, Dr. Ailani got her off the butalbital and started her on onabotulinum toxin A for migraine prevention, which reduced her headache days to about 15 per month (8 severe). She then added the anti-calcitonin gene-related peptide (CGRP) monoclonal antibody, galcanezumab, as another preventative, which further reduced the headache days down to 8-10 days per month (all migraine).
The attacks are rapid onset and can last multiple days. They come with photophobia and phonophobia and cause her to be bedridden, she noted.
“I was still worried about this frequency of headache and the fact she was using a triptan for acute treatment when she had uncontrolled hypertension and other cardiovascular risk factors, Dr. Ailani commented.
She explained that triptans are generally not used in individuals aged over 65 years because of a lack of data in this age group. They are also contraindicated in patients with cardiovascular (CV) disease, and caution is advised in patients with CV risk factors. Noting that migraine is an independent risk factor for stroke in healthy individuals, and this patient already had three other major risk factors for stroke, Dr. Ailani said she did not think a triptan was the best option.
When triptans do not work, Dr. Ailani said she thinks about dihydroergotamine, which she describes as “a great drug for long-lasting migraine” as it tends to have a sustained response. But it also has vasoconstrictive effects and can increase blood pressure, so it was not suitable for this patient.
CV risk is also an issue with nonsteroidal anti-inflammatory drugs (NSAIDs), one of the staple treatments for acute migraine.
“NSAIDs are available over the counter, inexpensive, quite effective, and have minimal immediate side effects,” Dr. Ailani said. But long-term adverse events include CV events, particularly in those who already have CV risk factors, and it is now thought that NSAIDs actually carry more CV risk than triptans.
She noted that out of all the NSAIDs, celecoxib carries the lowest CV risk, and in the United States, it is available as a liquid formulation. There is also a study of ketorolac nasal spray showing it to be as effective as sumatriptan nasal spray for acute migraine.
As her patient was still going to the emergency room (ER) quite frequently at this point, Dr. Ailani prescribed ketorolac nasal spray as an emergency rescue medication, which did help to reduce ER visits but did not solve the acute treatment problem.
The next option she tried was the CGRP antagonists or “gepants” because of their good tolerability.
Because her patient had long attacks, Dr. Ailani said her first choice gepant was rimegepant as it has a long half-life.
She noted that in patients who have frequent migraine attacks (> 6 migraine days per month), using rimegepant as needed has been shown to lead to migraine frequency declining over time. “This shows that if we treat acute attacks properly, we can minimize the risk of chronic migraine.”
She pointed out that if a patient has prodrome that is easy to identify or has short attacks, ubrogepant may be a good option, having shown effectiveness in preventing or reducing the onset of the headache in the recently reported PRODROME trial when given the day before migraine starts.
Then there is also zavegepant, which is available as a nasal spray, so it is a good option for patients with nausea and vomiting. Dr. Ailani suggested that zavegepant as a third-generation gepant may be worth trying in patients who have tried the other gepants, as it is a different type of molecule.
For this patient, neither rimegepant nor ubrogepant worked. “We tried treating in the prodrome, when the pain was starting, adding to other treatments, but she is not a ‘gepant’ responder. We have yet to try zavegepant,” she said.
The next consideration was lasmiditan. “This patient is a triptan responder and lasmiditan is a 5HT1 agonist, so it makes sense to try this. Also, it doesn’t have a vasoconstrictor effect as it doesn’t work on the blood vessels, so it is safe for patients with high blood pressure,” Dr. Ailani noted.
She pointed out, however, that lasmiditan has become a rescue medication in her practice because of side effect issues such as dizziness and sleepiness.
But Dr. Ailani said she has learned how to use the medication to minimize the side effects, by increasing the dose slowly and advising patients to take it later in the day.
“We start with 50 mg for a few doses then increase to 100 mg. This seems to build tolerability.”
Her patient has found good relief from lasmiditan 100 mg, but she can’t take it during the day as it makes her sleepy.
As a last resort, Dr. Ailani went back to metoclopramide, which she described as “a tried and tested old-time drug.”
While this does not make the patient sleepy, it has other adverse effects limiting the frequency of its use, she noted. “I ask her to try to limit it to twice a week, and this has been pretty effective. She can function when she uses it.”
Dr. Ailani also points out that neuromodulation should be in everyone’s tool kit. “So, we added an external combined occipital and trigeminal (eCOT device) neurostimulation device.”
The patient’s tool kit now looks like this:
- Neuromodulation device and meditation at first sign of an attack.
- Add metoclopramide 10 mg and acetaminophen 1000 mg.
- If the attack lasts into the second day, add lasmiditan 100 mg in the evening of the second day (limit 8 days a month).
- If the patient has a sudden onset severe migraine with nausea and vomiting that might make her go to the ER, add in ketorolac nasal spray (not > 5 days per month).
Dr. Ailani noted that other patients will need different toolkits, and in most cases, it is recommended to think about “situational prevention” for times when migraine attacks are predictable, which may include air travel, high-stress times (holidays, etc.), occasions when alcohol will be consumed, and at times of certain weather triggers.
Dr. Ailani disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Selecting a treatment plan to deal with acute migraine attacks can be like putting together a toolkit of possible therapies, individualized for each patient, one expert said.
The toolkit should comprise reliable treatments that patients know are going to work and that act quickly, allowing them to get back to functioning normally in their daily lives, said Jessica Ailani, MD, during a talk at the 17th European Headache Congress held recently in Barcelona, Spain.
“Everyone with migraine needs acute treatment,” Dr. Ailani, who is a clinical professor of neurology at MedStar Georgetown University Hospital and director of the Georgetown Headache Center, Washington, DC, noted. “Sometimes we can reduce acute treatment with preventative agents, but some disability will remain, so we have to focus on good acute treatment, and this becomes more complex if a person has a lot of comorbidities, which is common in older patients.”
In selecting suitable treatments for migraine, consideration has to be given to the patient profile, any other conditions they have, speed of onset of the migraine attack, length of the attack, associated symptoms, and side effects of the medications, she said.
A Complex Case
As an example, Dr. Ailani described the process she used to treat one of her patients who had frequent severe migraines and other issues causing difficult decisions when selecting medications — a woman in her late 60s with several other comorbidities.
“This is the kind of case I see on a daily basis and which keeps me up at night,” she said. “Many times in clinical practice, we see complex cases like this, and through the course of a year, we may try every treatment option we have in a patient like this.”
On the first presentation, the patient had a chronic migraine with severe headaches every day. She had a history of previous cervical discectomy with fusion surgery; uncontrolled hypertension, for which she was taking an angiotensin blocker; high cholesterol, for which she was taking a statin; and diabetes with an A1c of 8. She did not smoke or drink alcohol, exercised moderately, and her body mass index was in a good range.
“Before a patient ever sees a doctor for their migraine, they will have already tried a lot of different things. Most people are already using NSAIDs and acetaminophen, the most commonly used treatments for acute migraine,” Dr. Ailani explains.
Her patient was taking a triptan and the barbiturate, butalbital. Dr. Ailani notes that the triptan is very effective, but in the United States, they are not available over the counter, and the patient is only allowed nine doses per month on her insurance, so she was supplementing with butalbital.
Over the course of a year, Dr. Ailani got her off the butalbital and started her on onabotulinum toxin A for migraine prevention, which reduced her headache days to about 15 per month (8 severe). She then added the anti-calcitonin gene-related peptide (CGRP) monoclonal antibody, galcanezumab, as another preventative, which further reduced the headache days down to 8-10 days per month (all migraine).
The attacks are rapid onset and can last multiple days. They come with photophobia and phonophobia and cause her to be bedridden, she noted.
“I was still worried about this frequency of headache and the fact she was using a triptan for acute treatment when she had uncontrolled hypertension and other cardiovascular risk factors, Dr. Ailani commented.
She explained that triptans are generally not used in individuals aged over 65 years because of a lack of data in this age group. They are also contraindicated in patients with cardiovascular (CV) disease, and caution is advised in patients with CV risk factors. Noting that migraine is an independent risk factor for stroke in healthy individuals, and this patient already had three other major risk factors for stroke, Dr. Ailani said she did not think a triptan was the best option.
When triptans do not work, Dr. Ailani said she thinks about dihydroergotamine, which she describes as “a great drug for long-lasting migraine” as it tends to have a sustained response. But it also has vasoconstrictive effects and can increase blood pressure, so it was not suitable for this patient.
CV risk is also an issue with nonsteroidal anti-inflammatory drugs (NSAIDs), one of the staple treatments for acute migraine.
“NSAIDs are available over the counter, inexpensive, quite effective, and have minimal immediate side effects,” Dr. Ailani said. But long-term adverse events include CV events, particularly in those who already have CV risk factors, and it is now thought that NSAIDs actually carry more CV risk than triptans.
She noted that out of all the NSAIDs, celecoxib carries the lowest CV risk, and in the United States, it is available as a liquid formulation. There is also a study of ketorolac nasal spray showing it to be as effective as sumatriptan nasal spray for acute migraine.
As her patient was still going to the emergency room (ER) quite frequently at this point, Dr. Ailani prescribed ketorolac nasal spray as an emergency rescue medication, which did help to reduce ER visits but did not solve the acute treatment problem.
The next option she tried was the CGRP antagonists or “gepants” because of their good tolerability.
Because her patient had long attacks, Dr. Ailani said her first choice gepant was rimegepant as it has a long half-life.
She noted that in patients who have frequent migraine attacks (> 6 migraine days per month), using rimegepant as needed has been shown to lead to migraine frequency declining over time. “This shows that if we treat acute attacks properly, we can minimize the risk of chronic migraine.”
She pointed out that if a patient has prodrome that is easy to identify or has short attacks, ubrogepant may be a good option, having shown effectiveness in preventing or reducing the onset of the headache in the recently reported PRODROME trial when given the day before migraine starts.
Then there is also zavegepant, which is available as a nasal spray, so it is a good option for patients with nausea and vomiting. Dr. Ailani suggested that zavegepant as a third-generation gepant may be worth trying in patients who have tried the other gepants, as it is a different type of molecule.
For this patient, neither rimegepant nor ubrogepant worked. “We tried treating in the prodrome, when the pain was starting, adding to other treatments, but she is not a ‘gepant’ responder. We have yet to try zavegepant,” she said.
The next consideration was lasmiditan. “This patient is a triptan responder and lasmiditan is a 5HT1 agonist, so it makes sense to try this. Also, it doesn’t have a vasoconstrictor effect as it doesn’t work on the blood vessels, so it is safe for patients with high blood pressure,” Dr. Ailani noted.
She pointed out, however, that lasmiditan has become a rescue medication in her practice because of side effect issues such as dizziness and sleepiness.
But Dr. Ailani said she has learned how to use the medication to minimize the side effects, by increasing the dose slowly and advising patients to take it later in the day.
“We start with 50 mg for a few doses then increase to 100 mg. This seems to build tolerability.”
Her patient has found good relief from lasmiditan 100 mg, but she can’t take it during the day as it makes her sleepy.
As a last resort, Dr. Ailani went back to metoclopramide, which she described as “a tried and tested old-time drug.”
While this does not make the patient sleepy, it has other adverse effects limiting the frequency of its use, she noted. “I ask her to try to limit it to twice a week, and this has been pretty effective. She can function when she uses it.”
Dr. Ailani also points out that neuromodulation should be in everyone’s tool kit. “So, we added an external combined occipital and trigeminal (eCOT device) neurostimulation device.”
The patient’s tool kit now looks like this:
- Neuromodulation device and meditation at first sign of an attack.
- Add metoclopramide 10 mg and acetaminophen 1000 mg.
- If the attack lasts into the second day, add lasmiditan 100 mg in the evening of the second day (limit 8 days a month).
- If the patient has a sudden onset severe migraine with nausea and vomiting that might make her go to the ER, add in ketorolac nasal spray (not > 5 days per month).
Dr. Ailani noted that other patients will need different toolkits, and in most cases, it is recommended to think about “situational prevention” for times when migraine attacks are predictable, which may include air travel, high-stress times (holidays, etc.), occasions when alcohol will be consumed, and at times of certain weather triggers.
Dr. Ailani disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Selecting a treatment plan to deal with acute migraine attacks can be like putting together a toolkit of possible therapies, individualized for each patient, one expert said.
The toolkit should comprise reliable treatments that patients know are going to work and that act quickly, allowing them to get back to functioning normally in their daily lives, said Jessica Ailani, MD, during a talk at the 17th European Headache Congress held recently in Barcelona, Spain.
“Everyone with migraine needs acute treatment,” Dr. Ailani, who is a clinical professor of neurology at MedStar Georgetown University Hospital and director of the Georgetown Headache Center, Washington, DC, noted. “Sometimes we can reduce acute treatment with preventative agents, but some disability will remain, so we have to focus on good acute treatment, and this becomes more complex if a person has a lot of comorbidities, which is common in older patients.”
In selecting suitable treatments for migraine, consideration has to be given to the patient profile, any other conditions they have, speed of onset of the migraine attack, length of the attack, associated symptoms, and side effects of the medications, she said.
A Complex Case
As an example, Dr. Ailani described the process she used to treat one of her patients who had frequent severe migraines and other issues causing difficult decisions when selecting medications — a woman in her late 60s with several other comorbidities.
“This is the kind of case I see on a daily basis and which keeps me up at night,” she said. “Many times in clinical practice, we see complex cases like this, and through the course of a year, we may try every treatment option we have in a patient like this.”
On the first presentation, the patient had a chronic migraine with severe headaches every day. She had a history of previous cervical discectomy with fusion surgery; uncontrolled hypertension, for which she was taking an angiotensin blocker; high cholesterol, for which she was taking a statin; and diabetes with an A1c of 8. She did not smoke or drink alcohol, exercised moderately, and her body mass index was in a good range.
“Before a patient ever sees a doctor for their migraine, they will have already tried a lot of different things. Most people are already using NSAIDs and acetaminophen, the most commonly used treatments for acute migraine,” Dr. Ailani explains.
Her patient was taking a triptan and the barbiturate, butalbital. Dr. Ailani notes that the triptan is very effective, but in the United States, they are not available over the counter, and the patient is only allowed nine doses per month on her insurance, so she was supplementing with butalbital.
Over the course of a year, Dr. Ailani got her off the butalbital and started her on onabotulinum toxin A for migraine prevention, which reduced her headache days to about 15 per month (8 severe). She then added the anti-calcitonin gene-related peptide (CGRP) monoclonal antibody, galcanezumab, as another preventative, which further reduced the headache days down to 8-10 days per month (all migraine).
The attacks are rapid onset and can last multiple days. They come with photophobia and phonophobia and cause her to be bedridden, she noted.
“I was still worried about this frequency of headache and the fact she was using a triptan for acute treatment when she had uncontrolled hypertension and other cardiovascular risk factors, Dr. Ailani commented.
She explained that triptans are generally not used in individuals aged over 65 years because of a lack of data in this age group. They are also contraindicated in patients with cardiovascular (CV) disease, and caution is advised in patients with CV risk factors. Noting that migraine is an independent risk factor for stroke in healthy individuals, and this patient already had three other major risk factors for stroke, Dr. Ailani said she did not think a triptan was the best option.
When triptans do not work, Dr. Ailani said she thinks about dihydroergotamine, which she describes as “a great drug for long-lasting migraine” as it tends to have a sustained response. But it also has vasoconstrictive effects and can increase blood pressure, so it was not suitable for this patient.
CV risk is also an issue with nonsteroidal anti-inflammatory drugs (NSAIDs), one of the staple treatments for acute migraine.
“NSAIDs are available over the counter, inexpensive, quite effective, and have minimal immediate side effects,” Dr. Ailani said. But long-term adverse events include CV events, particularly in those who already have CV risk factors, and it is now thought that NSAIDs actually carry more CV risk than triptans.
She noted that out of all the NSAIDs, celecoxib carries the lowest CV risk, and in the United States, it is available as a liquid formulation. There is also a study of ketorolac nasal spray showing it to be as effective as sumatriptan nasal spray for acute migraine.
As her patient was still going to the emergency room (ER) quite frequently at this point, Dr. Ailani prescribed ketorolac nasal spray as an emergency rescue medication, which did help to reduce ER visits but did not solve the acute treatment problem.
The next option she tried was the CGRP antagonists or “gepants” because of their good tolerability.
Because her patient had long attacks, Dr. Ailani said her first choice gepant was rimegepant as it has a long half-life.
She noted that in patients who have frequent migraine attacks (> 6 migraine days per month), using rimegepant as needed has been shown to lead to migraine frequency declining over time. “This shows that if we treat acute attacks properly, we can minimize the risk of chronic migraine.”
She pointed out that if a patient has prodrome that is easy to identify or has short attacks, ubrogepant may be a good option, having shown effectiveness in preventing or reducing the onset of the headache in the recently reported PRODROME trial when given the day before migraine starts.
Then there is also zavegepant, which is available as a nasal spray, so it is a good option for patients with nausea and vomiting. Dr. Ailani suggested that zavegepant as a third-generation gepant may be worth trying in patients who have tried the other gepants, as it is a different type of molecule.
For this patient, neither rimegepant nor ubrogepant worked. “We tried treating in the prodrome, when the pain was starting, adding to other treatments, but she is not a ‘gepant’ responder. We have yet to try zavegepant,” she said.
The next consideration was lasmiditan. “This patient is a triptan responder and lasmiditan is a 5HT1 agonist, so it makes sense to try this. Also, it doesn’t have a vasoconstrictor effect as it doesn’t work on the blood vessels, so it is safe for patients with high blood pressure,” Dr. Ailani noted.
She pointed out, however, that lasmiditan has become a rescue medication in her practice because of side effect issues such as dizziness and sleepiness.
But Dr. Ailani said she has learned how to use the medication to minimize the side effects, by increasing the dose slowly and advising patients to take it later in the day.
“We start with 50 mg for a few doses then increase to 100 mg. This seems to build tolerability.”
Her patient has found good relief from lasmiditan 100 mg, but she can’t take it during the day as it makes her sleepy.
As a last resort, Dr. Ailani went back to metoclopramide, which she described as “a tried and tested old-time drug.”
While this does not make the patient sleepy, it has other adverse effects limiting the frequency of its use, she noted. “I ask her to try to limit it to twice a week, and this has been pretty effective. She can function when she uses it.”
Dr. Ailani also points out that neuromodulation should be in everyone’s tool kit. “So, we added an external combined occipital and trigeminal (eCOT device) neurostimulation device.”
The patient’s tool kit now looks like this:
- Neuromodulation device and meditation at first sign of an attack.
- Add metoclopramide 10 mg and acetaminophen 1000 mg.
- If the attack lasts into the second day, add lasmiditan 100 mg in the evening of the second day (limit 8 days a month).
- If the patient has a sudden onset severe migraine with nausea and vomiting that might make her go to the ER, add in ketorolac nasal spray (not > 5 days per month).
Dr. Ailani noted that other patients will need different toolkits, and in most cases, it is recommended to think about “situational prevention” for times when migraine attacks are predictable, which may include air travel, high-stress times (holidays, etc.), occasions when alcohol will be consumed, and at times of certain weather triggers.
Dr. Ailani disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
FROM THE EUROPEAN HEADACHE CONGRESS
Commentary: Examining CGRP Antagonists for Migraine Relief, January 2024
The recent 3-month double-blind study by Schwedt and colleagues included 580 participants and compared the effects of galcanezumab (Emgality) with those of rimegepant (Nurtec ODT). These medications are administered by different methods when used for migraine prevention; galcanezumab is given subcutaneously (SC) every month, whereas rimegepant is taken by mouth every other day. To blind the study, participants were randomly assigned to receive either 120 mg galcanezumab SC per month (after a 240 mg loading dose) and a placebo oral disintegrating tablet every other day or every-other-day 75 mg rimegepant as oral disintegrating tablets and a monthly SC placebo. According to the study authors, 62% of the patients receiving galcanezumab vs 61% of those receiving rimegepant achieved ≥ 50% reduction in monthly migraine headache days after 3 months, with no statistically significant difference between the groups. Comparisons between CGRP receptor antagonists are scarce. The studies tend to be of a short duration and to include small sample sizes — and most are retrospective. To date, physicians who treat patients with these drugs do not have information about the distinguishing characteristics between these treatments that could be used to guide drug selection for subtypes of migraine or different patient populations. As further research emerges, we may see distinctions between these therapies, or we might continue to see that their effects are similar in terms of benefits, duration of action, and patient characteristics.
Many patients who are prescribed these new medications have already been treated with a variety of other previously available migraine therapies, with varying degrees of improvement. Physicians who prescribe treatments for migraine patients often move on to new therapeutic options when patients only experience partial relief, but recent research suggests that even these incomplete responses could be beneficial for patients.
Researchers at the Headache Centre — Neurology Clinic at the Spedali Civili di Brescia in Brescia, Italy, conducted a retrospective study to examine whether previous treatment with onabotulinumtoxinA affected patent response to anti-CGRP mAb (Ceccardi et al). These treatments have differing mechanisms. OnabotulinumtoxinA is an exotoxin produced by Clostridium botulinum that blocks the acetylcholine release from nerve endings temporarily disabling postsynaptic action. Anti-CGRP mAb work by inhibiting the inflammatory receptor, thereby inhibiting the pain sensation.2
Several studies have examined the effects of combining onabotulinumtoxinA (Botox) with anti-CGRP mAb, with varying results. For example, researchers of a study designed to compare the two treatments concluded, "In patients with chronic migraine who have only had a partial response to Botox, adjunctive preventative therapy with a CGRP-mAb drug is safe and effective."2 A review examining several small studies that evaluated the response of dual therapy included a few studies that found no significant differences between an anti-CGRP mAb monotherapy and dual therapy with onabotulinumtoxinA, as well as some studies that noted improvement with dual therapy over either therapy alone. The review authors concluded that a real-life application is not yet determined and that "Further sufficiently powered, placebo-controlled studies are warranted to shed light on potential additive or synergistic effects of combining onabotulinumtoxin A with a CGRP antagonist."3
The Brescia study was designed to examine the effect of previous onabotulinumtoxinA treatment on subsequent anti-CGRP mAb response. The researchers enrolled 128 patients, of whom 51 (39.9%) had previously been treated with onabotulinumtoxinA, with the last dose 3 months before preventive treatment with an anti-CGRP mAb was started. The study was conducted between November 2018 and May 2023. The outcomes noted included monthly headache days, monthly migraine days, mean analgesic consumption, and clinical disability according to the Migraine Disability Assessment test (MIDAS). Participants received 3 months of treatment with an anti-CGRP mAb.
In addition to comparing patients who had previously received onabotulinumtoxinA with those who did not, the researchers also "aimed to evaluate whether the clinical response to anti-CGRP mAb was affected by the number of previous Onabotulinumtoxin-A administrations.
The documented baseline prior to treatment with an anti-CGRP mAb was as follows: mean monthly headache days 23.7 (SD 5.7), monthly migraine days 13.9 (SD 8.0); mean MIDAS score 108.9 (SD 76.1); and mean analgesic consumption 24.8 (SD 18.8). After 3 months of treatment with an anti-CGRP mAb, both groups experienced significant improvement in all these parameters. Furthermore, after 3 months of treatment with an anti-CGRP mAb, the patients who received at least three onabotulinumtoxinA administrations prior to the study experienced lower MMD compared with those who had received fewer cycles.
For physicians and patients, this outcome provides validation that patients can potentially gain long-term benefits from migraine treatment, even if such interventions do not provide sufficient migraine relief. The conclusion cannot be generalized to other migraine treatment sequences, and the authors did not suggest deliberately postponing any treatment or using any treatment as "priming" for another treatment. Yet physicians may be able to give patients some reassurance that an incomplete response in migraine therapy is not futile.
Migraine treatment can be very effective, but sometimes it is not clear whether patients should take their medication before or during a migraine episode, or whether the signal to take medication should be based on specific symptoms. Many patients wait to take their migraine treatment until they are sure that they will have a migraine, especially if they frequently have prodromal symptoms that do not consistently lead to a migraine. Additionally, some of the new CGRP receptor antagonists are expensive, and many payers only approve a limited amount per month. Patients might not want to waste their CGRP receptor antagonist supply in case they run out before their next refill authorization.
AbbVie, the makers of ubrogepant (Ubrelvy), a CGRP receptor antagonist approved for acute treatment of migraine, conducted a phase 3, multicenter, randomized, double-blind, placebo-controlled, crossover trial of ubrogepant at 75 research centers and headache clinics in the US (Dodick et al). According to the manufacturer, the aim of the trial was to evaluate the efficacy, safety, and tolerability of 100 mg ubrogepant for the acute treatment of migraine when administered during the prodrome of a migraine attack. The study included 518 participants age 18-75 years who had at least a 1-year history of migraine and had had two to eight migraine attacks per month that included symptoms of a moderate to severe headache in each of the 3 months before the study. Because this was a crossover trial, the participants were randomly assigned to either receive placebo for treatment of the first qualifying prodrome event and 100 mg ubrogepant for treatment of the second qualifying prodrome event or to receive 100 mg ubrogepant to treat the first qualifying prodrome event and placebo to treat the second qualifying prodrome event.
According to AbbVie's news release following publication of the study, "Absence of moderate or severe intensity headache within 24 hours was achieved following 46% of qualifying prodrome events when treated with UBRELVY vs 29% of placebo-treated events" and "absence of moderate or severe intensity headache within 48 hours was achieved following 41% of qualifying prodrome events when treated with UBRELVY vs 25% of placebo-treated events" (both P < .0001).4 Safety and tolerability of treatment during the prodromal period were also established.
In clinical practice, these results hold promise because patients can gain some assurance in knowing that taking their migraine treatment during their early prodromal symptoms is safe and could potentially improve the outcome of the event, preventing migraine symptoms for 48 hours. Even for patients who do not have an ample supply of ubrogepant or another CGRP antagonist, taking a treatment that is approved by their doctor at the onset of prodromal symptoms can provide relief compared with waiting until symptoms worsen.
Additional References
1. Waliszewska-Prosół M, Vuralli D, Martelletti P. What to do with non-responders to CGRP(r) monoclonal antibodies: Switch to another or move to gepants? J Headache Pain. 2023;24:163. doi: 10.1186/s10194-023-01698-8
2. Pallapothu MR, Quintana Mariñez MG, Chakkera M, et al. Long-term management of migraine with OnabotulinumtoxinA (Botox) vs calcitonin gene-related peptide antibodies (Anti-CGRP). Cureus. 2023;15:e46696. doi: 10.7759/cureus.46696
3. Pellesi L. Combining onabotulinumtoxin A with a CGRP antagonist for chronic migraine prophylaxis: Where do we stand? Front Pain Res (Lausanne). 2023;4:1292994. doi: 10.3389/fpain.2023.1292994
4. AbbVie. Results published in The Lancet show UBRELVY® (ubrogepant) reduces the headache phase of a migraine attack when dosed during the prodrome of migraine. November 16, 2023. Source
The recent 3-month double-blind study by Schwedt and colleagues included 580 participants and compared the effects of galcanezumab (Emgality) with those of rimegepant (Nurtec ODT). These medications are administered by different methods when used for migraine prevention; galcanezumab is given subcutaneously (SC) every month, whereas rimegepant is taken by mouth every other day. To blind the study, participants were randomly assigned to receive either 120 mg galcanezumab SC per month (after a 240 mg loading dose) and a placebo oral disintegrating tablet every other day or every-other-day 75 mg rimegepant as oral disintegrating tablets and a monthly SC placebo. According to the study authors, 62% of the patients receiving galcanezumab vs 61% of those receiving rimegepant achieved ≥ 50% reduction in monthly migraine headache days after 3 months, with no statistically significant difference between the groups. Comparisons between CGRP receptor antagonists are scarce. The studies tend to be of a short duration and to include small sample sizes — and most are retrospective. To date, physicians who treat patients with these drugs do not have information about the distinguishing characteristics between these treatments that could be used to guide drug selection for subtypes of migraine or different patient populations. As further research emerges, we may see distinctions between these therapies, or we might continue to see that their effects are similar in terms of benefits, duration of action, and patient characteristics.
Many patients who are prescribed these new medications have already been treated with a variety of other previously available migraine therapies, with varying degrees of improvement. Physicians who prescribe treatments for migraine patients often move on to new therapeutic options when patients only experience partial relief, but recent research suggests that even these incomplete responses could be beneficial for patients.
Researchers at the Headache Centre — Neurology Clinic at the Spedali Civili di Brescia in Brescia, Italy, conducted a retrospective study to examine whether previous treatment with onabotulinumtoxinA affected patent response to anti-CGRP mAb (Ceccardi et al). These treatments have differing mechanisms. OnabotulinumtoxinA is an exotoxin produced by Clostridium botulinum that blocks the acetylcholine release from nerve endings temporarily disabling postsynaptic action. Anti-CGRP mAb work by inhibiting the inflammatory receptor, thereby inhibiting the pain sensation.2
Several studies have examined the effects of combining onabotulinumtoxinA (Botox) with anti-CGRP mAb, with varying results. For example, researchers of a study designed to compare the two treatments concluded, "In patients with chronic migraine who have only had a partial response to Botox, adjunctive preventative therapy with a CGRP-mAb drug is safe and effective."2 A review examining several small studies that evaluated the response of dual therapy included a few studies that found no significant differences between an anti-CGRP mAb monotherapy and dual therapy with onabotulinumtoxinA, as well as some studies that noted improvement with dual therapy over either therapy alone. The review authors concluded that a real-life application is not yet determined and that "Further sufficiently powered, placebo-controlled studies are warranted to shed light on potential additive or synergistic effects of combining onabotulinumtoxin A with a CGRP antagonist."3
The Brescia study was designed to examine the effect of previous onabotulinumtoxinA treatment on subsequent anti-CGRP mAb response. The researchers enrolled 128 patients, of whom 51 (39.9%) had previously been treated with onabotulinumtoxinA, with the last dose 3 months before preventive treatment with an anti-CGRP mAb was started. The study was conducted between November 2018 and May 2023. The outcomes noted included monthly headache days, monthly migraine days, mean analgesic consumption, and clinical disability according to the Migraine Disability Assessment test (MIDAS). Participants received 3 months of treatment with an anti-CGRP mAb.
In addition to comparing patients who had previously received onabotulinumtoxinA with those who did not, the researchers also "aimed to evaluate whether the clinical response to anti-CGRP mAb was affected by the number of previous Onabotulinumtoxin-A administrations.
The documented baseline prior to treatment with an anti-CGRP mAb was as follows: mean monthly headache days 23.7 (SD 5.7), monthly migraine days 13.9 (SD 8.0); mean MIDAS score 108.9 (SD 76.1); and mean analgesic consumption 24.8 (SD 18.8). After 3 months of treatment with an anti-CGRP mAb, both groups experienced significant improvement in all these parameters. Furthermore, after 3 months of treatment with an anti-CGRP mAb, the patients who received at least three onabotulinumtoxinA administrations prior to the study experienced lower MMD compared with those who had received fewer cycles.
For physicians and patients, this outcome provides validation that patients can potentially gain long-term benefits from migraine treatment, even if such interventions do not provide sufficient migraine relief. The conclusion cannot be generalized to other migraine treatment sequences, and the authors did not suggest deliberately postponing any treatment or using any treatment as "priming" for another treatment. Yet physicians may be able to give patients some reassurance that an incomplete response in migraine therapy is not futile.
Migraine treatment can be very effective, but sometimes it is not clear whether patients should take their medication before or during a migraine episode, or whether the signal to take medication should be based on specific symptoms. Many patients wait to take their migraine treatment until they are sure that they will have a migraine, especially if they frequently have prodromal symptoms that do not consistently lead to a migraine. Additionally, some of the new CGRP receptor antagonists are expensive, and many payers only approve a limited amount per month. Patients might not want to waste their CGRP receptor antagonist supply in case they run out before their next refill authorization.
AbbVie, the makers of ubrogepant (Ubrelvy), a CGRP receptor antagonist approved for acute treatment of migraine, conducted a phase 3, multicenter, randomized, double-blind, placebo-controlled, crossover trial of ubrogepant at 75 research centers and headache clinics in the US (Dodick et al). According to the manufacturer, the aim of the trial was to evaluate the efficacy, safety, and tolerability of 100 mg ubrogepant for the acute treatment of migraine when administered during the prodrome of a migraine attack. The study included 518 participants age 18-75 years who had at least a 1-year history of migraine and had had two to eight migraine attacks per month that included symptoms of a moderate to severe headache in each of the 3 months before the study. Because this was a crossover trial, the participants were randomly assigned to either receive placebo for treatment of the first qualifying prodrome event and 100 mg ubrogepant for treatment of the second qualifying prodrome event or to receive 100 mg ubrogepant to treat the first qualifying prodrome event and placebo to treat the second qualifying prodrome event.
According to AbbVie's news release following publication of the study, "Absence of moderate or severe intensity headache within 24 hours was achieved following 46% of qualifying prodrome events when treated with UBRELVY vs 29% of placebo-treated events" and "absence of moderate or severe intensity headache within 48 hours was achieved following 41% of qualifying prodrome events when treated with UBRELVY vs 25% of placebo-treated events" (both P < .0001).4 Safety and tolerability of treatment during the prodromal period were also established.
In clinical practice, these results hold promise because patients can gain some assurance in knowing that taking their migraine treatment during their early prodromal symptoms is safe and could potentially improve the outcome of the event, preventing migraine symptoms for 48 hours. Even for patients who do not have an ample supply of ubrogepant or another CGRP antagonist, taking a treatment that is approved by their doctor at the onset of prodromal symptoms can provide relief compared with waiting until symptoms worsen.
Additional References
1. Waliszewska-Prosół M, Vuralli D, Martelletti P. What to do with non-responders to CGRP(r) monoclonal antibodies: Switch to another or move to gepants? J Headache Pain. 2023;24:163. doi: 10.1186/s10194-023-01698-8
2. Pallapothu MR, Quintana Mariñez MG, Chakkera M, et al. Long-term management of migraine with OnabotulinumtoxinA (Botox) vs calcitonin gene-related peptide antibodies (Anti-CGRP). Cureus. 2023;15:e46696. doi: 10.7759/cureus.46696
3. Pellesi L. Combining onabotulinumtoxin A with a CGRP antagonist for chronic migraine prophylaxis: Where do we stand? Front Pain Res (Lausanne). 2023;4:1292994. doi: 10.3389/fpain.2023.1292994
4. AbbVie. Results published in The Lancet show UBRELVY® (ubrogepant) reduces the headache phase of a migraine attack when dosed during the prodrome of migraine. November 16, 2023. Source
The recent 3-month double-blind study by Schwedt and colleagues included 580 participants and compared the effects of galcanezumab (Emgality) with those of rimegepant (Nurtec ODT). These medications are administered by different methods when used for migraine prevention; galcanezumab is given subcutaneously (SC) every month, whereas rimegepant is taken by mouth every other day. To blind the study, participants were randomly assigned to receive either 120 mg galcanezumab SC per month (after a 240 mg loading dose) and a placebo oral disintegrating tablet every other day or every-other-day 75 mg rimegepant as oral disintegrating tablets and a monthly SC placebo. According to the study authors, 62% of the patients receiving galcanezumab vs 61% of those receiving rimegepant achieved ≥ 50% reduction in monthly migraine headache days after 3 months, with no statistically significant difference between the groups. Comparisons between CGRP receptor antagonists are scarce. The studies tend to be of a short duration and to include small sample sizes — and most are retrospective. To date, physicians who treat patients with these drugs do not have information about the distinguishing characteristics between these treatments that could be used to guide drug selection for subtypes of migraine or different patient populations. As further research emerges, we may see distinctions between these therapies, or we might continue to see that their effects are similar in terms of benefits, duration of action, and patient characteristics.
Many patients who are prescribed these new medications have already been treated with a variety of other previously available migraine therapies, with varying degrees of improvement. Physicians who prescribe treatments for migraine patients often move on to new therapeutic options when patients only experience partial relief, but recent research suggests that even these incomplete responses could be beneficial for patients.
Researchers at the Headache Centre — Neurology Clinic at the Spedali Civili di Brescia in Brescia, Italy, conducted a retrospective study to examine whether previous treatment with onabotulinumtoxinA affected patent response to anti-CGRP mAb (Ceccardi et al). These treatments have differing mechanisms. OnabotulinumtoxinA is an exotoxin produced by Clostridium botulinum that blocks the acetylcholine release from nerve endings temporarily disabling postsynaptic action. Anti-CGRP mAb work by inhibiting the inflammatory receptor, thereby inhibiting the pain sensation.2
Several studies have examined the effects of combining onabotulinumtoxinA (Botox) with anti-CGRP mAb, with varying results. For example, researchers of a study designed to compare the two treatments concluded, "In patients with chronic migraine who have only had a partial response to Botox, adjunctive preventative therapy with a CGRP-mAb drug is safe and effective."2 A review examining several small studies that evaluated the response of dual therapy included a few studies that found no significant differences between an anti-CGRP mAb monotherapy and dual therapy with onabotulinumtoxinA, as well as some studies that noted improvement with dual therapy over either therapy alone. The review authors concluded that a real-life application is not yet determined and that "Further sufficiently powered, placebo-controlled studies are warranted to shed light on potential additive or synergistic effects of combining onabotulinumtoxin A with a CGRP antagonist."3
The Brescia study was designed to examine the effect of previous onabotulinumtoxinA treatment on subsequent anti-CGRP mAb response. The researchers enrolled 128 patients, of whom 51 (39.9%) had previously been treated with onabotulinumtoxinA, with the last dose 3 months before preventive treatment with an anti-CGRP mAb was started. The study was conducted between November 2018 and May 2023. The outcomes noted included monthly headache days, monthly migraine days, mean analgesic consumption, and clinical disability according to the Migraine Disability Assessment test (MIDAS). Participants received 3 months of treatment with an anti-CGRP mAb.
In addition to comparing patients who had previously received onabotulinumtoxinA with those who did not, the researchers also "aimed to evaluate whether the clinical response to anti-CGRP mAb was affected by the number of previous Onabotulinumtoxin-A administrations.
The documented baseline prior to treatment with an anti-CGRP mAb was as follows: mean monthly headache days 23.7 (SD 5.7), monthly migraine days 13.9 (SD 8.0); mean MIDAS score 108.9 (SD 76.1); and mean analgesic consumption 24.8 (SD 18.8). After 3 months of treatment with an anti-CGRP mAb, both groups experienced significant improvement in all these parameters. Furthermore, after 3 months of treatment with an anti-CGRP mAb, the patients who received at least three onabotulinumtoxinA administrations prior to the study experienced lower MMD compared with those who had received fewer cycles.
For physicians and patients, this outcome provides validation that patients can potentially gain long-term benefits from migraine treatment, even if such interventions do not provide sufficient migraine relief. The conclusion cannot be generalized to other migraine treatment sequences, and the authors did not suggest deliberately postponing any treatment or using any treatment as "priming" for another treatment. Yet physicians may be able to give patients some reassurance that an incomplete response in migraine therapy is not futile.
Migraine treatment can be very effective, but sometimes it is not clear whether patients should take their medication before or during a migraine episode, or whether the signal to take medication should be based on specific symptoms. Many patients wait to take their migraine treatment until they are sure that they will have a migraine, especially if they frequently have prodromal symptoms that do not consistently lead to a migraine. Additionally, some of the new CGRP receptor antagonists are expensive, and many payers only approve a limited amount per month. Patients might not want to waste their CGRP receptor antagonist supply in case they run out before their next refill authorization.
AbbVie, the makers of ubrogepant (Ubrelvy), a CGRP receptor antagonist approved for acute treatment of migraine, conducted a phase 3, multicenter, randomized, double-blind, placebo-controlled, crossover trial of ubrogepant at 75 research centers and headache clinics in the US (Dodick et al). According to the manufacturer, the aim of the trial was to evaluate the efficacy, safety, and tolerability of 100 mg ubrogepant for the acute treatment of migraine when administered during the prodrome of a migraine attack. The study included 518 participants age 18-75 years who had at least a 1-year history of migraine and had had two to eight migraine attacks per month that included symptoms of a moderate to severe headache in each of the 3 months before the study. Because this was a crossover trial, the participants were randomly assigned to either receive placebo for treatment of the first qualifying prodrome event and 100 mg ubrogepant for treatment of the second qualifying prodrome event or to receive 100 mg ubrogepant to treat the first qualifying prodrome event and placebo to treat the second qualifying prodrome event.
According to AbbVie's news release following publication of the study, "Absence of moderate or severe intensity headache within 24 hours was achieved following 46% of qualifying prodrome events when treated with UBRELVY vs 29% of placebo-treated events" and "absence of moderate or severe intensity headache within 48 hours was achieved following 41% of qualifying prodrome events when treated with UBRELVY vs 25% of placebo-treated events" (both P < .0001).4 Safety and tolerability of treatment during the prodromal period were also established.
In clinical practice, these results hold promise because patients can gain some assurance in knowing that taking their migraine treatment during their early prodromal symptoms is safe and could potentially improve the outcome of the event, preventing migraine symptoms for 48 hours. Even for patients who do not have an ample supply of ubrogepant or another CGRP antagonist, taking a treatment that is approved by their doctor at the onset of prodromal symptoms can provide relief compared with waiting until symptoms worsen.
Additional References
1. Waliszewska-Prosół M, Vuralli D, Martelletti P. What to do with non-responders to CGRP(r) monoclonal antibodies: Switch to another or move to gepants? J Headache Pain. 2023;24:163. doi: 10.1186/s10194-023-01698-8
2. Pallapothu MR, Quintana Mariñez MG, Chakkera M, et al. Long-term management of migraine with OnabotulinumtoxinA (Botox) vs calcitonin gene-related peptide antibodies (Anti-CGRP). Cureus. 2023;15:e46696. doi: 10.7759/cureus.46696
3. Pellesi L. Combining onabotulinumtoxin A with a CGRP antagonist for chronic migraine prophylaxis: Where do we stand? Front Pain Res (Lausanne). 2023;4:1292994. doi: 10.3389/fpain.2023.1292994
4. AbbVie. Results published in The Lancet show UBRELVY® (ubrogepant) reduces the headache phase of a migraine attack when dosed during the prodrome of migraine. November 16, 2023. Source
Fremanezumab benefits migraine patients with inadequate response to prior preventive medications
Key clinical point: Fremanezumab demonstrated improved efficacy, tolerability, and safety outcomes in patients with chronic or episodic migraine who reported prior inadequate response to 2-4 classes of preventive migraine medications.
Major finding: At 12 weeks, the number needed to treat to achieve ≥50% reduction in monthly average number of migraine days was 3.9 with both quarterly and monthly fremanezumab dosing. The numbers needed to harm for one patient to discontinue treatment due to adverse events were 1000 and 144 for quarterly and monthly fremanezumab dosing, respectively.
Study details: This post hoc analysis of the FOCUS trial included 838 patients with chronic (n = 509) or episodic (n = 329) migraine who had prior inadequate response to 2-4 migraine preventive medication classes and were randomly assigned to receive quarterly or monthly fremanezumab or placebo.
Disclosures: This study was funded by Teva Pharmaceuticals. Three authors declared being employees of Teva Pharmaceuticals, and other authors declared having ties with various sources including Teva Pharmaceuticals.
Source: Ashina M et al. Numbers needed to treat or harm and likelihood of being helped versus harmed for fremanezumab in patients who had prior inadequate response to two to four classes of migraine preventive medications: A post hoc analysis. Headache. 2023;63(10):1351-1358 (Nov 13). doi: 10.1111/head.14651
Key clinical point: Fremanezumab demonstrated improved efficacy, tolerability, and safety outcomes in patients with chronic or episodic migraine who reported prior inadequate response to 2-4 classes of preventive migraine medications.
Major finding: At 12 weeks, the number needed to treat to achieve ≥50% reduction in monthly average number of migraine days was 3.9 with both quarterly and monthly fremanezumab dosing. The numbers needed to harm for one patient to discontinue treatment due to adverse events were 1000 and 144 for quarterly and monthly fremanezumab dosing, respectively.
Study details: This post hoc analysis of the FOCUS trial included 838 patients with chronic (n = 509) or episodic (n = 329) migraine who had prior inadequate response to 2-4 migraine preventive medication classes and were randomly assigned to receive quarterly or monthly fremanezumab or placebo.
Disclosures: This study was funded by Teva Pharmaceuticals. Three authors declared being employees of Teva Pharmaceuticals, and other authors declared having ties with various sources including Teva Pharmaceuticals.
Source: Ashina M et al. Numbers needed to treat or harm and likelihood of being helped versus harmed for fremanezumab in patients who had prior inadequate response to two to four classes of migraine preventive medications: A post hoc analysis. Headache. 2023;63(10):1351-1358 (Nov 13). doi: 10.1111/head.14651
Key clinical point: Fremanezumab demonstrated improved efficacy, tolerability, and safety outcomes in patients with chronic or episodic migraine who reported prior inadequate response to 2-4 classes of preventive migraine medications.
Major finding: At 12 weeks, the number needed to treat to achieve ≥50% reduction in monthly average number of migraine days was 3.9 with both quarterly and monthly fremanezumab dosing. The numbers needed to harm for one patient to discontinue treatment due to adverse events were 1000 and 144 for quarterly and monthly fremanezumab dosing, respectively.
Study details: This post hoc analysis of the FOCUS trial included 838 patients with chronic (n = 509) or episodic (n = 329) migraine who had prior inadequate response to 2-4 migraine preventive medication classes and were randomly assigned to receive quarterly or monthly fremanezumab or placebo.
Disclosures: This study was funded by Teva Pharmaceuticals. Three authors declared being employees of Teva Pharmaceuticals, and other authors declared having ties with various sources including Teva Pharmaceuticals.
Source: Ashina M et al. Numbers needed to treat or harm and likelihood of being helped versus harmed for fremanezumab in patients who had prior inadequate response to two to four classes of migraine preventive medications: A post hoc analysis. Headache. 2023;63(10):1351-1358 (Nov 13). doi: 10.1111/head.14651
Galcanezumab and rimegepant offer effective options for prevention of episodic migraine
Key clinical point: Both galcanezumab and rimegepant were effective as a preventive treatment for episodic migraine, with galcanezumab not being superior to rimegepant.
Major finding: Overall, 62% vs 61% of the patients receiving galcanezumab vs rimegepant achieved ≥ 50% reduction in monthly migraine headache days after 3 months, respectively, with no statistically significant difference between the groups (P = .70). Treatment-emergent adverse events were similar between study interventions and were mostly mild or moderate in severity.
Study details: Findings are from the CHALLENGE-MIG study including 580 patients with episodic migraine with or without aura who were randomly assigned to receive galcanezumab (n = 287) or rimegepant (n = 293) for 3 months.
Disclosures: This study was funded by Eli Lilly and Company, Indianapolis, IN, USA. Eight authors declared being employees of Eli Lilly and Company. Some other authors declared ties with various sources, including Eli Lilly and Company.
Source: Schwedt TJ et al. Comparing the efficacy and safety of galcanezumab versus rimegepant for prevention of episodic migraine: Results from a randomized, controlled clinical trial. Neurol Ther. 2023 (Nov 10). doi: 10.1007/s40120-023-00562-w
Key clinical point: Both galcanezumab and rimegepant were effective as a preventive treatment for episodic migraine, with galcanezumab not being superior to rimegepant.
Major finding: Overall, 62% vs 61% of the patients receiving galcanezumab vs rimegepant achieved ≥ 50% reduction in monthly migraine headache days after 3 months, respectively, with no statistically significant difference between the groups (P = .70). Treatment-emergent adverse events were similar between study interventions and were mostly mild or moderate in severity.
Study details: Findings are from the CHALLENGE-MIG study including 580 patients with episodic migraine with or without aura who were randomly assigned to receive galcanezumab (n = 287) or rimegepant (n = 293) for 3 months.
Disclosures: This study was funded by Eli Lilly and Company, Indianapolis, IN, USA. Eight authors declared being employees of Eli Lilly and Company. Some other authors declared ties with various sources, including Eli Lilly and Company.
Source: Schwedt TJ et al. Comparing the efficacy and safety of galcanezumab versus rimegepant for prevention of episodic migraine: Results from a randomized, controlled clinical trial. Neurol Ther. 2023 (Nov 10). doi: 10.1007/s40120-023-00562-w
Key clinical point: Both galcanezumab and rimegepant were effective as a preventive treatment for episodic migraine, with galcanezumab not being superior to rimegepant.
Major finding: Overall, 62% vs 61% of the patients receiving galcanezumab vs rimegepant achieved ≥ 50% reduction in monthly migraine headache days after 3 months, respectively, with no statistically significant difference between the groups (P = .70). Treatment-emergent adverse events were similar between study interventions and were mostly mild or moderate in severity.
Study details: Findings are from the CHALLENGE-MIG study including 580 patients with episodic migraine with or without aura who were randomly assigned to receive galcanezumab (n = 287) or rimegepant (n = 293) for 3 months.
Disclosures: This study was funded by Eli Lilly and Company, Indianapolis, IN, USA. Eight authors declared being employees of Eli Lilly and Company. Some other authors declared ties with various sources, including Eli Lilly and Company.
Source: Schwedt TJ et al. Comparing the efficacy and safety of galcanezumab versus rimegepant for prevention of episodic migraine: Results from a randomized, controlled clinical trial. Neurol Ther. 2023 (Nov 10). doi: 10.1007/s40120-023-00562-w
Galcanezumab and rimegepant offer effective options for prevention of episodic migraine
Key clinical point: Both galcanezumab and rimegepant were effective as a preventive treatment for episodic migraine, with galcanezumab not being superior to rimegepant.
Major finding: Overall, 62% vs 61% of the patients receiving galcanezumab vs rimegepant achieved ≥ 50% reduction in monthly migraine headache days after 3 months, respectively, with no statistically significant difference between the groups (P = .70). Treatment-emergent adverse events were similar between study interventions and were mostly mild or moderate in severity.
Study details: Findings are from the CHALLENGE-MIG study including 580 patients with episodic migraine with or without aura who were randomly assigned to receive galcanezumab (n = 287) or rimegepant (n = 293) for 3 months.
Disclosures: This study was funded by Eli Lilly and Company, Indianapolis, IN, USA. Eight authors declared being employees of Eli Lilly and Company. Some other authors declared ties with various sources, including Eli Lilly and Company.
Source: Schwedt TJ et al. Comparing the efficacy and safety of galcanezumab versus rimegepant for prevention of episodic migraine: Results from a randomized, controlled clinical trial. Neurol Ther. 2023 (Nov 10). doi: 10.1007/s40120-023-00562-w
Key clinical point: Both galcanezumab and rimegepant were effective as a preventive treatment for episodic migraine, with galcanezumab not being superior to rimegepant.
Major finding: Overall, 62% vs 61% of the patients receiving galcanezumab vs rimegepant achieved ≥ 50% reduction in monthly migraine headache days after 3 months, respectively, with no statistically significant difference between the groups (P = .70). Treatment-emergent adverse events were similar between study interventions and were mostly mild or moderate in severity.
Study details: Findings are from the CHALLENGE-MIG study including 580 patients with episodic migraine with or without aura who were randomly assigned to receive galcanezumab (n = 287) or rimegepant (n = 293) for 3 months.
Disclosures: This study was funded by Eli Lilly and Company, Indianapolis, IN, USA. Eight authors declared being employees of Eli Lilly and Company. Some other authors declared ties with various sources, including Eli Lilly and Company.
Source: Schwedt TJ et al. Comparing the efficacy and safety of galcanezumab versus rimegepant for prevention of episodic migraine: Results from a randomized, controlled clinical trial. Neurol Ther. 2023 (Nov 10). doi: 10.1007/s40120-023-00562-w
Key clinical point: Both galcanezumab and rimegepant were effective as a preventive treatment for episodic migraine, with galcanezumab not being superior to rimegepant.
Major finding: Overall, 62% vs 61% of the patients receiving galcanezumab vs rimegepant achieved ≥ 50% reduction in monthly migraine headache days after 3 months, respectively, with no statistically significant difference between the groups (P = .70). Treatment-emergent adverse events were similar between study interventions and were mostly mild or moderate in severity.
Study details: Findings are from the CHALLENGE-MIG study including 580 patients with episodic migraine with or without aura who were randomly assigned to receive galcanezumab (n = 287) or rimegepant (n = 293) for 3 months.
Disclosures: This study was funded by Eli Lilly and Company, Indianapolis, IN, USA. Eight authors declared being employees of Eli Lilly and Company. Some other authors declared ties with various sources, including Eli Lilly and Company.
Source: Schwedt TJ et al. Comparing the efficacy and safety of galcanezumab versus rimegepant for prevention of episodic migraine: Results from a randomized, controlled clinical trial. Neurol Ther. 2023 (Nov 10). doi: 10.1007/s40120-023-00562-w
Comparative efficacy of anti-CGRP mAb in chronic and high-frequency episodic migraine
Key clinical point: The anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) fremanezumab, erenumab, and galcanezumab demonstrated similar efficacy during the first year of therapy in patients with chronic and high-frequency episodic migraine, and galcanezumab demonstrated a higher response rate than the other two mAb during the 1-month suspension period in patients with chronic migraine.
Major finding: The three anti-CGRP mAb significantly reduced overall migraine frequency and intensity and symptomatic medication intake per month with similar efficacy across all follow-ups up to 12 months. Patients with chronic migraine receiving galcanezumab vs fremanezumab or erenumab showed higher response rates during the 1-month suspension period (57% vs 39% or 17%, respectively; P = .009).
Study details: This retrospective longitudinal single-center study included 160 patients with chronic and high-frequency episodic migraine who were treated with an anti-CGRP mAb (fremanezumab, erenumab, or galcanezumab) for 12 months.
Disclosures: This study did not receive any funding. The authors declared no conflicts of interests.
Source: Tereshko Y et al. Comparative study of the efficacy of anti-CGRP mAbs on migraineurs: Analysis of the first year of therapy, 1-month suspension period, and reprisal. J Clin Med. 2023;12(23):7329 (Nov 26). doi: 10.3390/jcm12237329
Key clinical point: The anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) fremanezumab, erenumab, and galcanezumab demonstrated similar efficacy during the first year of therapy in patients with chronic and high-frequency episodic migraine, and galcanezumab demonstrated a higher response rate than the other two mAb during the 1-month suspension period in patients with chronic migraine.
Major finding: The three anti-CGRP mAb significantly reduced overall migraine frequency and intensity and symptomatic medication intake per month with similar efficacy across all follow-ups up to 12 months. Patients with chronic migraine receiving galcanezumab vs fremanezumab or erenumab showed higher response rates during the 1-month suspension period (57% vs 39% or 17%, respectively; P = .009).
Study details: This retrospective longitudinal single-center study included 160 patients with chronic and high-frequency episodic migraine who were treated with an anti-CGRP mAb (fremanezumab, erenumab, or galcanezumab) for 12 months.
Disclosures: This study did not receive any funding. The authors declared no conflicts of interests.
Source: Tereshko Y et al. Comparative study of the efficacy of anti-CGRP mAbs on migraineurs: Analysis of the first year of therapy, 1-month suspension period, and reprisal. J Clin Med. 2023;12(23):7329 (Nov 26). doi: 10.3390/jcm12237329
Key clinical point: The anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) fremanezumab, erenumab, and galcanezumab demonstrated similar efficacy during the first year of therapy in patients with chronic and high-frequency episodic migraine, and galcanezumab demonstrated a higher response rate than the other two mAb during the 1-month suspension period in patients with chronic migraine.
Major finding: The three anti-CGRP mAb significantly reduced overall migraine frequency and intensity and symptomatic medication intake per month with similar efficacy across all follow-ups up to 12 months. Patients with chronic migraine receiving galcanezumab vs fremanezumab or erenumab showed higher response rates during the 1-month suspension period (57% vs 39% or 17%, respectively; P = .009).
Study details: This retrospective longitudinal single-center study included 160 patients with chronic and high-frequency episodic migraine who were treated with an anti-CGRP mAb (fremanezumab, erenumab, or galcanezumab) for 12 months.
Disclosures: This study did not receive any funding. The authors declared no conflicts of interests.
Source: Tereshko Y et al. Comparative study of the efficacy of anti-CGRP mAbs on migraineurs: Analysis of the first year of therapy, 1-month suspension period, and reprisal. J Clin Med. 2023;12(23):7329 (Nov 26). doi: 10.3390/jcm12237329
Prior onabotulinumtoxin-A improves subsequent anti-CGRP mAb response in chronic migraine
Key clinical point: Prior treatment with onabotulinumtoxin-A may improve subsequent clinical response to preventive treatment with anti-calcitonin gene-related peptide (anti-CGRP) monoclonal antibodies (mAb) in patients with chronic migraine.
Major finding: At 3 months of treatment with anti-CGRP mAb, patients who received vs did not receive prior onabotulinumtoxin-A had fewer mean monthly migraine days (3.3 days vs 5.2 days; P = .017), lower pain intensity (Numerical Rating Scale scores: 5.9 vs 6.6; P = .013), and a lower mean Migraine Disability Assessment score (23.2 vs 37.4; P = .013).
Study details: The data come from a retrospective observational study including 128 patients with chronic migraine who received treatment with anti-CGRP mAb, of whom 39.9% received prior treatment with onabotulinumtoxin-A.
Disclosures: This study did not receive any external funding. Three authors declared receiving speaker honoraria from or serving as consultants or scientific advisory board members for various sources.
Source: Ceccardi G et al. Onabotulinumtoxin-A: Previous prophylactic treatment might improve subsequent anti-CGRP monoclonal antibodies response in patients with chronic migraine. Toxins. 2023;15(12):677 (Nov 30). doi: 10.3390/toxins15120677
Key clinical point: Prior treatment with onabotulinumtoxin-A may improve subsequent clinical response to preventive treatment with anti-calcitonin gene-related peptide (anti-CGRP) monoclonal antibodies (mAb) in patients with chronic migraine.
Major finding: At 3 months of treatment with anti-CGRP mAb, patients who received vs did not receive prior onabotulinumtoxin-A had fewer mean monthly migraine days (3.3 days vs 5.2 days; P = .017), lower pain intensity (Numerical Rating Scale scores: 5.9 vs 6.6; P = .013), and a lower mean Migraine Disability Assessment score (23.2 vs 37.4; P = .013).
Study details: The data come from a retrospective observational study including 128 patients with chronic migraine who received treatment with anti-CGRP mAb, of whom 39.9% received prior treatment with onabotulinumtoxin-A.
Disclosures: This study did not receive any external funding. Three authors declared receiving speaker honoraria from or serving as consultants or scientific advisory board members for various sources.
Source: Ceccardi G et al. Onabotulinumtoxin-A: Previous prophylactic treatment might improve subsequent anti-CGRP monoclonal antibodies response in patients with chronic migraine. Toxins. 2023;15(12):677 (Nov 30). doi: 10.3390/toxins15120677
Key clinical point: Prior treatment with onabotulinumtoxin-A may improve subsequent clinical response to preventive treatment with anti-calcitonin gene-related peptide (anti-CGRP) monoclonal antibodies (mAb) in patients with chronic migraine.
Major finding: At 3 months of treatment with anti-CGRP mAb, patients who received vs did not receive prior onabotulinumtoxin-A had fewer mean monthly migraine days (3.3 days vs 5.2 days; P = .017), lower pain intensity (Numerical Rating Scale scores: 5.9 vs 6.6; P = .013), and a lower mean Migraine Disability Assessment score (23.2 vs 37.4; P = .013).
Study details: The data come from a retrospective observational study including 128 patients with chronic migraine who received treatment with anti-CGRP mAb, of whom 39.9% received prior treatment with onabotulinumtoxin-A.
Disclosures: This study did not receive any external funding. Three authors declared receiving speaker honoraria from or serving as consultants or scientific advisory board members for various sources.
Source: Ceccardi G et al. Onabotulinumtoxin-A: Previous prophylactic treatment might improve subsequent anti-CGRP monoclonal antibodies response in patients with chronic migraine. Toxins. 2023;15(12):677 (Nov 30). doi: 10.3390/toxins15120677
Galcanezumab effective for migraine prevention in women with menstrually related migraine
Key clinical point: Galcanezumab effectively reduced the effect of menstrually related migraine (MRM) and led to improved functioning in women with episodic migraine.
Major finding: Across months 4 through 6, galcanezumab vs placebo led to greater mean reduction in the monthly migraine headache days (MHD; least squares mean change from baseline [Δ] −5.1 vs −3.2), monthly perimenstrual MHD (Δ −0.75 vs −0.49), non-perimenstrual MHD (Δ −4.6 vs −2.8), and greater improvement in Role Function-Restrictive domain scores of the Migraine-Specific Quality of Life Questionnaire (Δ 30.9 vs 22.3 points; all P < .001).
Study details: This post hoc analysis of the EVOLVE-1 and EVOLVE-2 trials included 1133 women with episodic migraine who received either 120 mg galcanezumab per month or placebo, of whom 40.8% met the criteria for MRM.
Disclosures: This study was sponsored by Eli Lilly and Company. Four authors declared being current or former employees and stockowners of Eli Lilly and Company. Two authors declared receiving consulting honoraria from various sources including Eli Lilly.
Source: MacGregor EA et al. Effect of galcanezumab in women with episodic migraine meeting criteria for menstrually related migraine: A post hoc analysis of EVOLVE-1 and EVOLVE-2. Headache. 2023 (Nov 28). doi: 10.1111/head.14652
Key clinical point: Galcanezumab effectively reduced the effect of menstrually related migraine (MRM) and led to improved functioning in women with episodic migraine.
Major finding: Across months 4 through 6, galcanezumab vs placebo led to greater mean reduction in the monthly migraine headache days (MHD; least squares mean change from baseline [Δ] −5.1 vs −3.2), monthly perimenstrual MHD (Δ −0.75 vs −0.49), non-perimenstrual MHD (Δ −4.6 vs −2.8), and greater improvement in Role Function-Restrictive domain scores of the Migraine-Specific Quality of Life Questionnaire (Δ 30.9 vs 22.3 points; all P < .001).
Study details: This post hoc analysis of the EVOLVE-1 and EVOLVE-2 trials included 1133 women with episodic migraine who received either 120 mg galcanezumab per month or placebo, of whom 40.8% met the criteria for MRM.
Disclosures: This study was sponsored by Eli Lilly and Company. Four authors declared being current or former employees and stockowners of Eli Lilly and Company. Two authors declared receiving consulting honoraria from various sources including Eli Lilly.
Source: MacGregor EA et al. Effect of galcanezumab in women with episodic migraine meeting criteria for menstrually related migraine: A post hoc analysis of EVOLVE-1 and EVOLVE-2. Headache. 2023 (Nov 28). doi: 10.1111/head.14652
Key clinical point: Galcanezumab effectively reduced the effect of menstrually related migraine (MRM) and led to improved functioning in women with episodic migraine.
Major finding: Across months 4 through 6, galcanezumab vs placebo led to greater mean reduction in the monthly migraine headache days (MHD; least squares mean change from baseline [Δ] −5.1 vs −3.2), monthly perimenstrual MHD (Δ −0.75 vs −0.49), non-perimenstrual MHD (Δ −4.6 vs −2.8), and greater improvement in Role Function-Restrictive domain scores of the Migraine-Specific Quality of Life Questionnaire (Δ 30.9 vs 22.3 points; all P < .001).
Study details: This post hoc analysis of the EVOLVE-1 and EVOLVE-2 trials included 1133 women with episodic migraine who received either 120 mg galcanezumab per month or placebo, of whom 40.8% met the criteria for MRM.
Disclosures: This study was sponsored by Eli Lilly and Company. Four authors declared being current or former employees and stockowners of Eli Lilly and Company. Two authors declared receiving consulting honoraria from various sources including Eli Lilly.
Source: MacGregor EA et al. Effect of galcanezumab in women with episodic migraine meeting criteria for menstrually related migraine: A post hoc analysis of EVOLVE-1 and EVOLVE-2. Headache. 2023 (Nov 28). doi: 10.1111/head.14652