Migraine ICYMI

The Health Terminology/Ontology Portal (HeTOP), on which the curious can discover information about off-label use, lists 645 medications prescribed for migraine worldwide. Treatments ranging from blood pressure medications to antidepressants, and anticonvulsants to antiepileptics, along with their doses and administrations, are all listed. The number of migraine-indicated medications is 114.  Dominated by triptans and topiramate, the list also includes erenumab, the calcitonin gene-related peptide CGRP agonist. The difference in figures between the predominately off label and migraine-approved lists is a good indicator of the struggle that health care providers have had through the years to help their patients.

 The idea now is to make that list even longer by finding biomarkers that lead to new therapies.

But first, a conversation about the trigeminal ganglia.

The trigeminal ganglia

The trigeminal ganglia sit on either side of the head, in front of the ears. Their primary role is to receive stimuli and convey it to the brain. The humantrigeminal ganglia contain 20,000 to 35,000 neurons and express an array of neuropeptides, including CGRP. Some neuropeptides, like CGRP and pituitary adenylate cyclase–activating peptide 38 (PACAP38) are vasodilators. Others, like substance P, are vasoconstrictors. Edvinsson and Goadsby discussed in 1994 how CGRP was released simultaneously in those with “spontaneous attacks of migraine.”

Over the past 30 years, researchers in our institution  and elsewhere have shown repeatedly that migraine develops in individuals who are exposed to certain signaling molecules, namely nitroglycerin, CGRP, cyclic guanosine monophosphate (cGMP), intracellular cyclic adenosine monophosphate (cAMP), potassium, and PACAP38, among others. Such exposure reinforces the notion that peripheral sensitization of trigeminal sensory neurons brings on headache. The attack could occur due to vasodilation, mast cell degranulation, involvement of the parasympathetic system, or activation of nerve fibers.

Some examples from the literature:

• In our research, results from a small study of patients under spontaneous migraine attack, who underwent a 3-Tesla MRI scan, showed that cortical thickness diminishes in the prefrontal and pericalcarine cortices. The analysis we performed involving individuals with migraine without aura revealed that these patients experience reduced cortical thickness and volume when migraine attacks come on, suggesting that cortical thickness and volume may serve as a potential biomarker.
• A comparison of 20 individuals with chronic migraine and 20 healthy controls by way of 3-Tesla magnetic resonance imaging scans revealed that those with headache appeared to have substantially increased neural connectivity between the hypothalamus and certain brain areas – yet there appeared to be no connectivity irregularities between the hypothalamus and brainstem, which as the authors noted, is the “migraine generator.”

In other words, vasodilation might be  a secondary symptom of migraine but likely isn’t its source.

Other migraine makers

Neurochemicals and nucleotides play a role in migraine formation, too:

• Nitric oxide. Can open blood vessels in the head and brain and has been shown to set migraine in motion. It leads to peak headache intensity 5.5 hours after infusion and causes migraine without aura.

• GRP. Gastrin-releasing peptide receptors cause delayed headache, including what qualifies as an induced migraine attack. Researchers also note that similar pathways trigger migraine with and without aura. 

• Intracellular cGMP and intracellular cAMP. These 2 cyclic nucleotides are found extensively in the trigeminovascular system and have a role in the pathogenesis of migraine.  Studies demonstrate that cGMP levels increase after nitroglycerin administration and cAMP increases after CGRP and PACAP38 exposure.

• Levcromakalim. This potassium channel opener is sensitive to ATP. In a trial published in 2019, researchers showed that modulating potassium channels could cause some headache pain, even in those without migraine. They infused 20 healthy volunteers with levcromakalim; over the next 5-plus hours, the middle meningeal artery of all 20 became and remained dilated. Later research showed that this dilation is linked to substance P. 

Identifying migraine types

Diagnosing migraine is 1 step; determining its type is another.

Consider that a person with a posttraumatic headache can have migraine-like symptoms. To find objective separate characteristics, researchers at Mayo Clinic designed a headache classification model using questionnaires, which were then paired with the patient’s MRI data. The questionnaires delved into headache characteristics, sensory hypersensitivities, cognitive functioning, and mood. The system worked well with primary migraine, with 97% accuracy. But with posttraumatic headache, the system was 65% accurate. What proved to differentiate persistent posttraumatic headache were questions regarding decision making and anxiety. These patients had severe symptoms of anxiety, depression, physical issues, and mild brain injury attributed to blasts.

All of which explains why we and others are actively looking for biomarkers.

The biomarkers

A look at clinicaltrials.gov shows that 15 trials are recruiting patients (including us) in the search for biomarkers. One wants to identify a computational algorithm using AI, based on 9 types of markers in hopes of identifying those predictive elements that will respond to CGRP-targeting monoclonal antibodies (mABs). The factors range from the clinical to epigenetic to structural and functional brain imaging. Another registered study is using ocular coherence tomography, among other technologies, to identify photophobia.

Our interests are in identifying CGRP as a definitive biomarker; finding structural and functional cerebral changes, using MRI, in study subjects before and after they are given erenumab. We also want to create a registry for migraine based on the structural and functional MRI findings.

Another significant reason for finding biomarkers is to identify the alteration that accompany progression from episodic to chronic migraine. Pozo-Rosich et al write that these imaging, neurophysiological, and biochemical changes that occur with this progression could be used “for developing chronic migraine biomarkers that might assist with diagnosis, prognosticating individual patient outcomes, and predicting responses to migraine therapies.” And, ultimately, in practicing precision medicine to improve care of patients.

Significant barriers still exist in declaring a molecule is a biomarker. For example, a meta-analysis points to the replication challenge observed in neuroimaging research. Additionally, several genetic variants produce small effect sizes, which also might be impacted by environmental factors. This makes it difficult to map genetic biomarkers. Large prospective studies are needed to bring this area of research out of infancy to a place where treatment response can be clinically assessed. Additionally, while research evaluating provocation biomarkers has already contributed to the treatment landscape, large-scale registry studies may help uncover a predictive biomarker of treatment response. Blood biomarker research still needs a standardized protocol. Imaging-based biomarkers show much potential, but standardized imaging protocols and improved characterization and data integration are necessary going forward.

The patients

The discovery of the CGRPs couldn’t have been more timely.

Those of us who have been treating patients with migraine for years have seen the prevalence of this disease slowly rise. In 2018, the age-adjusted prevalence was 15.9% for all adults in the United States; in 2010, it was 13.2%. Worldwide, in 2019, it was 14%. In 2015, it was 11.6%.

In the past few years, journal articles have appeared regarding the connection between obesity, diabetes, hypertension, and migraine severity. Numerous other comorbidities affect our patients – not just the well-known psychiatric disorders – but also the respiratory, digestive, and central nervous system illnesses.

In other words, many of our patients come to us sicker than in years past.

Some cannot take one or more medications designed for acute migraine attacks due to comorbidities, including cardiovascular disease or related risk factors, and gastrointestinal bleeding.

A large survey of 15,133 people with migraine confirmed the findings on these numerous comorbidities; they reported that they have more insomnia, depression, and anxiety. As the authors point out, identifying these comorbidities can help with accurate diagnosis, treatment and its adherence, and prognosis. The authors also noted that as migraine days increase per month, so do the rates of comorbidities.

But the CGRPs are showing how beneficial they can be. One study assessing medication overuse showed how 60% of the enrolled patients no longer fit that description 6 months after receiving erenumab or galcanezumab. Some patients who contend with episodic migraine showed a complete response after receiving eptinezumab and galcanezumab. They also have helped patients with menstrual migraine and refractory migraine.

But they are not complete responses to these medications, which is an excellent reason to continue viewing, recording, and assessing the migraine brain, for all it can tell us.

The Health Terminology/Ontology Portal (HeTOP), on which the curious can discover information about off-label use, lists 645 medications prescribed for migraine worldwide. Treatments ranging from blood pressure medications to antidepressants, and anticonvulsants to antiepileptics, along with their doses and administrations, are all listed. The number of migraine-indicated medications is 114.  Dominated by triptans and topiramate, the list also includes erenumab, the calcitonin gene-related peptide CGRP agonist. The difference in figures between the predominately off label and migraine-approved lists is a good indicator of the struggle that health care providers have had through the years to help their patients.

 The idea now is to make that list even longer by finding biomarkers that lead to new therapies.

But first, a conversation about the trigeminal ganglia.

The trigeminal ganglia

The trigeminal ganglia sit on either side of the head, in front of the ears. Their primary role is to receive stimuli and convey it to the brain. The humantrigeminal ganglia contain 20,000 to 35,000 neurons and express an array of neuropeptides, including CGRP. Some neuropeptides, like CGRP and pituitary adenylate cyclase–activating peptide 38 (PACAP38) are vasodilators. Others, like substance P, are vasoconstrictors. Edvinsson and Goadsby discussed in 1994 how CGRP was released simultaneously in those with “spontaneous attacks of migraine.”

Over the past 30 years, researchers in our institution  and elsewhere have shown repeatedly that migraine develops in individuals who are exposed to certain signaling molecules, namely nitroglycerin, CGRP, cyclic guanosine monophosphate (cGMP), intracellular cyclic adenosine monophosphate (cAMP), potassium, and PACAP38, among others. Such exposure reinforces the notion that peripheral sensitization of trigeminal sensory neurons brings on headache. The attack could occur due to vasodilation, mast cell degranulation, involvement of the parasympathetic system, or activation of nerve fibers.

Some examples from the literature:

• In our research, results from a small study of patients under spontaneous migraine attack, who underwent a 3-Tesla MRI scan, showed that cortical thickness diminishes in the prefrontal and pericalcarine cortices. The analysis we performed involving individuals with migraine without aura revealed that these patients experience reduced cortical thickness and volume when migraine attacks come on, suggesting that cortical thickness and volume may serve as a potential biomarker.
• A comparison of 20 individuals with chronic migraine and 20 healthy controls by way of 3-Tesla magnetic resonance imaging scans revealed that those with headache appeared to have substantially increased neural connectivity between the hypothalamus and certain brain areas – yet there appeared to be no connectivity irregularities between the hypothalamus and brainstem, which as the authors noted, is the “migraine generator.”

In other words, vasodilation might be  a secondary symptom of migraine but likely isn’t its source.

Other migraine makers

Neurochemicals and nucleotides play a role in migraine formation, too:

• Nitric oxide. Can open blood vessels in the head and brain and has been shown to set migraine in motion. It leads to peak headache intensity 5.5 hours after infusion and causes migraine without aura.

• GRP. Gastrin-releasing peptide receptors cause delayed headache, including what qualifies as an induced migraine attack. Researchers also note that similar pathways trigger migraine with and without aura. 

• Intracellular cGMP and intracellular cAMP. These 2 cyclic nucleotides are found extensively in the trigeminovascular system and have a role in the pathogenesis of migraine.  Studies demonstrate that cGMP levels increase after nitroglycerin administration and cAMP increases after CGRP and PACAP38 exposure.

• Levcromakalim. This potassium channel opener is sensitive to ATP. In a trial published in 2019, researchers showed that modulating potassium channels could cause some headache pain, even in those without migraine. They infused 20 healthy volunteers with levcromakalim; over the next 5-plus hours, the middle meningeal artery of all 20 became and remained dilated. Later research showed that this dilation is linked to substance P. 

Identifying migraine types

Diagnosing migraine is 1 step; determining its type is another.

Consider that a person with a posttraumatic headache can have migraine-like symptoms. To find objective separate characteristics, researchers at Mayo Clinic designed a headache classification model using questionnaires, which were then paired with the patient’s MRI data. The questionnaires delved into headache characteristics, sensory hypersensitivities, cognitive functioning, and mood. The system worked well with primary migraine, with 97% accuracy. But with posttraumatic headache, the system was 65% accurate. What proved to differentiate persistent posttraumatic headache were questions regarding decision making and anxiety. These patients had severe symptoms of anxiety, depression, physical issues, and mild brain injury attributed to blasts.

All of which explains why we and others are actively looking for biomarkers.

The biomarkers

A look at clinicaltrials.gov shows that 15 trials are recruiting patients (including us) in the search for biomarkers. One wants to identify a computational algorithm using AI, based on 9 types of markers in hopes of identifying those predictive elements that will respond to CGRP-targeting monoclonal antibodies (mABs). The factors range from the clinical to epigenetic to structural and functional brain imaging. Another registered study is using ocular coherence tomography, among other technologies, to identify photophobia.

Our interests are in identifying CGRP as a definitive biomarker; finding structural and functional cerebral changes, using MRI, in study subjects before and after they are given erenumab. We also want to create a registry for migraine based on the structural and functional MRI findings.

Another significant reason for finding biomarkers is to identify the alteration that accompany progression from episodic to chronic migraine. Pozo-Rosich et al write that these imaging, neurophysiological, and biochemical changes that occur with this progression could be used “for developing chronic migraine biomarkers that might assist with diagnosis, prognosticating individual patient outcomes, and predicting responses to migraine therapies.” And, ultimately, in practicing precision medicine to improve care of patients.

Significant barriers still exist in declaring a molecule is a biomarker. For example, a meta-analysis points to the replication challenge observed in neuroimaging research. Additionally, several genetic variants produce small effect sizes, which also might be impacted by environmental factors. This makes it difficult to map genetic biomarkers. Large prospective studies are needed to bring this area of research out of infancy to a place where treatment response can be clinically assessed. Additionally, while research evaluating provocation biomarkers has already contributed to the treatment landscape, large-scale registry studies may help uncover a predictive biomarker of treatment response. Blood biomarker research still needs a standardized protocol. Imaging-based biomarkers show much potential, but standardized imaging protocols and improved characterization and data integration are necessary going forward.

The patients

The discovery of the CGRPs couldn’t have been more timely.

Those of us who have been treating patients with migraine for years have seen the prevalence of this disease slowly rise. In 2018, the age-adjusted prevalence was 15.9% for all adults in the United States; in 2010, it was 13.2%. Worldwide, in 2019, it was 14%. In 2015, it was 11.6%.

In the past few years, journal articles have appeared regarding the connection between obesity, diabetes, hypertension, and migraine severity. Numerous other comorbidities affect our patients – not just the well-known psychiatric disorders – but also the respiratory, digestive, and central nervous system illnesses.

In other words, many of our patients come to us sicker than in years past.

Some cannot take one or more medications designed for acute migraine attacks due to comorbidities, including cardiovascular disease or related risk factors, and gastrointestinal bleeding.

A large survey of 15,133 people with migraine confirmed the findings on these numerous comorbidities; they reported that they have more insomnia, depression, and anxiety. As the authors point out, identifying these comorbidities can help with accurate diagnosis, treatment and its adherence, and prognosis. The authors also noted that as migraine days increase per month, so do the rates of comorbidities.

But the CGRPs are showing how beneficial they can be. One study assessing medication overuse showed how 60% of the enrolled patients no longer fit that description 6 months after receiving erenumab or galcanezumab. Some patients who contend with episodic migraine showed a complete response after receiving eptinezumab and galcanezumab. They also have helped patients with menstrual migraine and refractory migraine.

But they are not complete responses to these medications, which is an excellent reason to continue viewing, recording, and assessing the migraine brain, for all it can tell us.

The Health Terminology/Ontology Portal (HeTOP), on which the curious can discover information about off-label use, lists 645 medications prescribed for migraine worldwide. Treatments ranging from blood pressure medications to antidepressants, and anticonvulsants to antiepileptics, along with their doses and administrations, are all listed. The number of migraine-indicated medications is 114.  Dominated by triptans and topiramate, the list also includes erenumab, the calcitonin gene-related peptide CGRP agonist. The difference in figures between the predominately off label and migraine-approved lists is a good indicator of the struggle that health care providers have had through the years to help their patients.

 The idea now is to make that list even longer by finding biomarkers that lead to new therapies.

But first, a conversation about the trigeminal ganglia.

The trigeminal ganglia

The trigeminal ganglia sit on either side of the head, in front of the ears. Their primary role is to receive stimuli and convey it to the brain. The humantrigeminal ganglia contain 20,000 to 35,000 neurons and express an array of neuropeptides, including CGRP. Some neuropeptides, like CGRP and pituitary adenylate cyclase–activating peptide 38 (PACAP38) are vasodilators. Others, like substance P, are vasoconstrictors. Edvinsson and Goadsby discussed in 1994 how CGRP was released simultaneously in those with “spontaneous attacks of migraine.”

Over the past 30 years, researchers in our institution  and elsewhere have shown repeatedly that migraine develops in individuals who are exposed to certain signaling molecules, namely nitroglycerin, CGRP, cyclic guanosine monophosphate (cGMP), intracellular cyclic adenosine monophosphate (cAMP), potassium, and PACAP38, among others. Such exposure reinforces the notion that peripheral sensitization of trigeminal sensory neurons brings on headache. The attack could occur due to vasodilation, mast cell degranulation, involvement of the parasympathetic system, or activation of nerve fibers.

Some examples from the literature:

• In our research, results from a small study of patients under spontaneous migraine attack, who underwent a 3-Tesla MRI scan, showed that cortical thickness diminishes in the prefrontal and pericalcarine cortices. The analysis we performed involving individuals with migraine without aura revealed that these patients experience reduced cortical thickness and volume when migraine attacks come on, suggesting that cortical thickness and volume may serve as a potential biomarker.
• A comparison of 20 individuals with chronic migraine and 20 healthy controls by way of 3-Tesla magnetic resonance imaging scans revealed that those with headache appeared to have substantially increased neural connectivity between the hypothalamus and certain brain areas – yet there appeared to be no connectivity irregularities between the hypothalamus and brainstem, which as the authors noted, is the “migraine generator.”

In other words, vasodilation might be  a secondary symptom of migraine but likely isn’t its source.

Other migraine makers

Neurochemicals and nucleotides play a role in migraine formation, too:

• Nitric oxide. Can open blood vessels in the head and brain and has been shown to set migraine in motion. It leads to peak headache intensity 5.5 hours after infusion and causes migraine without aura.

• GRP. Gastrin-releasing peptide receptors cause delayed headache, including what qualifies as an induced migraine attack. Researchers also note that similar pathways trigger migraine with and without aura. 

• Intracellular cGMP and intracellular cAMP. These 2 cyclic nucleotides are found extensively in the trigeminovascular system and have a role in the pathogenesis of migraine.  Studies demonstrate that cGMP levels increase after nitroglycerin administration and cAMP increases after CGRP and PACAP38 exposure.

• Levcromakalim. This potassium channel opener is sensitive to ATP. In a trial published in 2019, researchers showed that modulating potassium channels could cause some headache pain, even in those without migraine. They infused 20 healthy volunteers with levcromakalim; over the next 5-plus hours, the middle meningeal artery of all 20 became and remained dilated. Later research showed that this dilation is linked to substance P. 

Identifying migraine types

Diagnosing migraine is 1 step; determining its type is another.

Consider that a person with a posttraumatic headache can have migraine-like symptoms. To find objective separate characteristics, researchers at Mayo Clinic designed a headache classification model using questionnaires, which were then paired with the patient’s MRI data. The questionnaires delved into headache characteristics, sensory hypersensitivities, cognitive functioning, and mood. The system worked well with primary migraine, with 97% accuracy. But with posttraumatic headache, the system was 65% accurate. What proved to differentiate persistent posttraumatic headache were questions regarding decision making and anxiety. These patients had severe symptoms of anxiety, depression, physical issues, and mild brain injury attributed to blasts.

All of which explains why we and others are actively looking for biomarkers.

The biomarkers

A look at clinicaltrials.gov shows that 15 trials are recruiting patients (including us) in the search for biomarkers. One wants to identify a computational algorithm using AI, based on 9 types of markers in hopes of identifying those predictive elements that will respond to CGRP-targeting monoclonal antibodies (mABs). The factors range from the clinical to epigenetic to structural and functional brain imaging. Another registered study is using ocular coherence tomography, among other technologies, to identify photophobia.

Our interests are in identifying CGRP as a definitive biomarker; finding structural and functional cerebral changes, using MRI, in study subjects before and after they are given erenumab. We also want to create a registry for migraine based on the structural and functional MRI findings.

Another significant reason for finding biomarkers is to identify the alteration that accompany progression from episodic to chronic migraine. Pozo-Rosich et al write that these imaging, neurophysiological, and biochemical changes that occur with this progression could be used “for developing chronic migraine biomarkers that might assist with diagnosis, prognosticating individual patient outcomes, and predicting responses to migraine therapies.” And, ultimately, in practicing precision medicine to improve care of patients.

Significant barriers still exist in declaring a molecule is a biomarker. For example, a meta-analysis points to the replication challenge observed in neuroimaging research. Additionally, several genetic variants produce small effect sizes, which also might be impacted by environmental factors. This makes it difficult to map genetic biomarkers. Large prospective studies are needed to bring this area of research out of infancy to a place where treatment response can be clinically assessed. Additionally, while research evaluating provocation biomarkers has already contributed to the treatment landscape, large-scale registry studies may help uncover a predictive biomarker of treatment response. Blood biomarker research still needs a standardized protocol. Imaging-based biomarkers show much potential, but standardized imaging protocols and improved characterization and data integration are necessary going forward.

The patients

The discovery of the CGRPs couldn’t have been more timely.

Those of us who have been treating patients with migraine for years have seen the prevalence of this disease slowly rise. In 2018, the age-adjusted prevalence was 15.9% for all adults in the United States; in 2010, it was 13.2%. Worldwide, in 2019, it was 14%. In 2015, it was 11.6%.

In the past few years, journal articles have appeared regarding the connection between obesity, diabetes, hypertension, and migraine severity. Numerous other comorbidities affect our patients – not just the well-known psychiatric disorders – but also the respiratory, digestive, and central nervous system illnesses.

In other words, many of our patients come to us sicker than in years past.

Some cannot take one or more medications designed for acute migraine attacks due to comorbidities, including cardiovascular disease or related risk factors, and gastrointestinal bleeding.

A large survey of 15,133 people with migraine confirmed the findings on these numerous comorbidities; they reported that they have more insomnia, depression, and anxiety. As the authors point out, identifying these comorbidities can help with accurate diagnosis, treatment and its adherence, and prognosis. The authors also noted that as migraine days increase per month, so do the rates of comorbidities.

But the CGRPs are showing how beneficial they can be. One study assessing medication overuse showed how 60% of the enrolled patients no longer fit that description 6 months after receiving erenumab or galcanezumab. Some patients who contend with episodic migraine showed a complete response after receiving eptinezumab and galcanezumab. They also have helped patients with menstrual migraine and refractory migraine.

But they are not complete responses to these medications, which is an excellent reason to continue viewing, recording, and assessing the migraine brain, for all it can tell us.

Key clinical point: Erenumab is effective and well tolerated in patients with chronic migraine who did not respond to previous migraine treatments.

Major finding: Overall, 71.4% of patients treated with erenumab achieved ≥30% reduction in monthly migraine days from baseline to 9-12 weeks and 34.0% of patients at all assessment periods through 52 weeks. Constipation was the most common adverse event and 13.7% of patients discontinued treatment because of a lack of tolerability.

Study details: The data come from a 52-week, prospective, observational study including 300 patients with chronic migraine who received ≥1 dose of erenumab, of which 273 and 119 patients completed 12 and 52 weeks of treatment, respectively.

Disclosures: This study was funded by and conducted in collaboration with Novartis Pharma AG, Basel, Switzerland. Some authors reported being consultants, speakers, or scientific advisors for or receiving personal fees from various sources, including Novartis. Two authors declared being employees of and holding stocks in Novartis.

Source: Cullum CK et al. Real-world long-term efficacy and safety of erenumab in adults with chronic migraine: A 52-week, single-center, prospective, observational study. J Headache Pain. 2022;23(1):61 Jun 2). Doi:10.1186/s10194-022-01433-9

Key clinical point: Erenumab is effective and well tolerated in patients with chronic migraine who did not respond to previous migraine treatments.

Major finding: Overall, 71.4% of patients treated with erenumab achieved ≥30% reduction in monthly migraine days from baseline to 9-12 weeks and 34.0% of patients at all assessment periods through 52 weeks. Constipation was the most common adverse event and 13.7% of patients discontinued treatment because of a lack of tolerability.

Study details: The data come from a 52-week, prospective, observational study including 300 patients with chronic migraine who received ≥1 dose of erenumab, of which 273 and 119 patients completed 12 and 52 weeks of treatment, respectively.

Disclosures: This study was funded by and conducted in collaboration with Novartis Pharma AG, Basel, Switzerland. Some authors reported being consultants, speakers, or scientific advisors for or receiving personal fees from various sources, including Novartis. Two authors declared being employees of and holding stocks in Novartis.

Source: Cullum CK et al. Real-world long-term efficacy and safety of erenumab in adults with chronic migraine: A 52-week, single-center, prospective, observational study. J Headache Pain. 2022;23(1):61 Jun 2). Doi:10.1186/s10194-022-01433-9

Key clinical point: Erenumab is effective and well tolerated in patients with chronic migraine who did not respond to previous migraine treatments.

Major finding: Overall, 71.4% of patients treated with erenumab achieved ≥30% reduction in monthly migraine days from baseline to 9-12 weeks and 34.0% of patients at all assessment periods through 52 weeks. Constipation was the most common adverse event and 13.7% of patients discontinued treatment because of a lack of tolerability.

Study details: The data come from a 52-week, prospective, observational study including 300 patients with chronic migraine who received ≥1 dose of erenumab, of which 273 and 119 patients completed 12 and 52 weeks of treatment, respectively.

Disclosures: This study was funded by and conducted in collaboration with Novartis Pharma AG, Basel, Switzerland. Some authors reported being consultants, speakers, or scientific advisors for or receiving personal fees from various sources, including Novartis. Two authors declared being employees of and holding stocks in Novartis.

Source: Cullum CK et al. Real-world long-term efficacy and safety of erenumab in adults with chronic migraine: A 52-week, single-center, prospective, observational study. J Headache Pain. 2022;23(1):61 Jun 2). Doi:10.1186/s10194-022-01433-9

Key clinical point: Severe migraine without aura increased the long-term risk for atrial fibrillation (AF) by 16%-21% in both men and women. The risk for future AF was highest in women with severe migraine with aura but not significant in male counterparts.

Major finding: Men (adjusted hazard ratio [aHR] 1.21; 95% CI 1.12-1.31) and women (aHR 1.16; 95% CI 1.09-1.22) with severe migraine without aura had a modest but significantly higher risk for AF. The risk was most prominent in women with severe migraine with aura (aHR 1.48; 95% CI 1.18-1.85), but was not significant in men.

Study details: Findings are from a large-scale population-based study including 4,020,488 participants without AF, of which 4986 and 105,029 had migraine with and without aura, respectively.

Disclosures: This study was supported by a Korea Medical Device Development Fund grant funded by the Korea Government. E-K Choi and GYH Lip reported receiving research grants or speaking fees or serving as consultants or speakers for various sources.

Source: Rhee T-M et al. Type and severity of migraine determines risk of atrial fibrillation in women.Front Cardiovasc Med. 2022;9:910225(May 31). Doi:10.3389/fcvm.2022.910225

Key clinical point: Severe migraine without aura increased the long-term risk for atrial fibrillation (AF) by 16%-21% in both men and women. The risk for future AF was highest in women with severe migraine with aura but not significant in male counterparts.

Major finding: Men (adjusted hazard ratio [aHR] 1.21; 95% CI 1.12-1.31) and women (aHR 1.16; 95% CI 1.09-1.22) with severe migraine without aura had a modest but significantly higher risk for AF. The risk was most prominent in women with severe migraine with aura (aHR 1.48; 95% CI 1.18-1.85), but was not significant in men.

Study details: Findings are from a large-scale population-based study including 4,020,488 participants without AF, of which 4986 and 105,029 had migraine with and without aura, respectively.

Disclosures: This study was supported by a Korea Medical Device Development Fund grant funded by the Korea Government. E-K Choi and GYH Lip reported receiving research grants or speaking fees or serving as consultants or speakers for various sources.

Source: Rhee T-M et al. Type and severity of migraine determines risk of atrial fibrillation in women.Front Cardiovasc Med. 2022;9:910225(May 31). Doi:10.3389/fcvm.2022.910225

Key clinical point: Severe migraine without aura increased the long-term risk for atrial fibrillation (AF) by 16%-21% in both men and women. The risk for future AF was highest in women with severe migraine with aura but not significant in male counterparts.

Major finding: Men (adjusted hazard ratio [aHR] 1.21; 95% CI 1.12-1.31) and women (aHR 1.16; 95% CI 1.09-1.22) with severe migraine without aura had a modest but significantly higher risk for AF. The risk was most prominent in women with severe migraine with aura (aHR 1.48; 95% CI 1.18-1.85), but was not significant in men.

Study details: Findings are from a large-scale population-based study including 4,020,488 participants without AF, of which 4986 and 105,029 had migraine with and without aura, respectively.

Disclosures: This study was supported by a Korea Medical Device Development Fund grant funded by the Korea Government. E-K Choi and GYH Lip reported receiving research grants or speaking fees or serving as consultants or speakers for various sources.

Source: Rhee T-M et al. Type and severity of migraine determines risk of atrial fibrillation in women.Front Cardiovasc Med. 2022;9:910225(May 31). Doi:10.3389/fcvm.2022.910225

Key clinical point: A higher proportion of patients with migraine treated with atogepant vs. placebo showed a significant reduction in the monthly migraine days (MMD) during the 12 weeks of treatment.

Major finding: At 12 weeks, ≥50% reduction in the mean MMD was achieved by a significantly higher proportion of patients receiving 10 mg (55.6%), 30 mg (58.7%), or 60 mg (60.8%) atogepantcompared with placebo (29.0%; all P < .001), with findings being similar for ≥25%, ≥75%, and 100% reduction in mean MMD. The incidence of treatment-emergent adverse events was similar among the treatment groups.

Study details: This was a secondary analysis of the ADVANCE trial including 873 patients with a ≥1-year history of migraine with or without aura who were randomly assigned to receive atogepant (10, 30, or 60 mg; n=659) or placebo (n=214).

Disclosures: This study was sponsored by Allergan. Some authors declared receiving speaking fees, consulting fees, personal fees, research grants, or royalties or owing stocks or stock options in various sources, including Allergan/AbbVie.

Source: Lipton RB et al.Rates of response to atogepant for migraine prophylaxis among adults:

A secondary analysis of a randomized clinical trial.JAMA Netw Open. 2022;5(6):e2215499 Jun 8). Doi: 10.1001/jamanetworkopen.2022.15499

Key clinical point: A higher proportion of patients with migraine treated with atogepant vs. placebo showed a significant reduction in the monthly migraine days (MMD) during the 12 weeks of treatment.

Major finding: At 12 weeks, ≥50% reduction in the mean MMD was achieved by a significantly higher proportion of patients receiving 10 mg (55.6%), 30 mg (58.7%), or 60 mg (60.8%) atogepantcompared with placebo (29.0%; all P < .001), with findings being similar for ≥25%, ≥75%, and 100% reduction in mean MMD. The incidence of treatment-emergent adverse events was similar among the treatment groups.

Study details: This was a secondary analysis of the ADVANCE trial including 873 patients with a ≥1-year history of migraine with or without aura who were randomly assigned to receive atogepant (10, 30, or 60 mg; n=659) or placebo (n=214).

Disclosures: This study was sponsored by Allergan. Some authors declared receiving speaking fees, consulting fees, personal fees, research grants, or royalties or owing stocks or stock options in various sources, including Allergan/AbbVie.

Source: Lipton RB et al.Rates of response to atogepant for migraine prophylaxis among adults:

A secondary analysis of a randomized clinical trial.JAMA Netw Open. 2022;5(6):e2215499 Jun 8). Doi: 10.1001/jamanetworkopen.2022.15499

Key clinical point: A higher proportion of patients with migraine treated with atogepant vs. placebo showed a significant reduction in the monthly migraine days (MMD) during the 12 weeks of treatment.

Major finding: At 12 weeks, ≥50% reduction in the mean MMD was achieved by a significantly higher proportion of patients receiving 10 mg (55.6%), 30 mg (58.7%), or 60 mg (60.8%) atogepantcompared with placebo (29.0%; all P < .001), with findings being similar for ≥25%, ≥75%, and 100% reduction in mean MMD. The incidence of treatment-emergent adverse events was similar among the treatment groups.

Study details: This was a secondary analysis of the ADVANCE trial including 873 patients with a ≥1-year history of migraine with or without aura who were randomly assigned to receive atogepant (10, 30, or 60 mg; n=659) or placebo (n=214).

Disclosures: This study was sponsored by Allergan. Some authors declared receiving speaking fees, consulting fees, personal fees, research grants, or royalties or owing stocks or stock options in various sources, including Allergan/AbbVie.

Source: Lipton RB et al.Rates of response to atogepant for migraine prophylaxis among adults:

A secondary analysis of a randomized clinical trial.JAMA Netw Open. 2022;5(6):e2215499 Jun 8). Doi: 10.1001/jamanetworkopen.2022.15499

Key clinical point: Migraine was significantly associated with fetal-type posterior cerebral artery (PCA) status in patients with ischemic stroke.

Major finding: Fetal-type PCA status was independently associated with migraine (adjusted odds ratio [aOR] 2.06; P = .005). The other factors independently associated with migraine were hypertension (aOR 1.97; P = .011), female gender (aOR 2.03; P = .017) and National Institutes of Health Stroke Scale score at admission (aOR 1.08; P = .018).

Study details: This cross-sectional study included 750 patients aged ≥18 yearswith ischemic stroke, of which 11.3% had migraine history.

Disclosures: This study received no specific funding. The authors declared no conflicts of interest.

Source: Zhang Y et al. The association between migraine and fetal-type posterior cerebral artery in patients with ischemic stroke. Cerebrovasc Dis. 2022 (May 13). Doi:10.1159/000524616

Key clinical point: Migraine was significantly associated with fetal-type posterior cerebral artery (PCA) status in patients with ischemic stroke.

Major finding: Fetal-type PCA status was independently associated with migraine (adjusted odds ratio [aOR] 2.06; P = .005). The other factors independently associated with migraine were hypertension (aOR 1.97; P = .011), female gender (aOR 2.03; P = .017) and National Institutes of Health Stroke Scale score at admission (aOR 1.08; P = .018).

Study details: This cross-sectional study included 750 patients aged ≥18 yearswith ischemic stroke, of which 11.3% had migraine history.

Disclosures: This study received no specific funding. The authors declared no conflicts of interest.

Source: Zhang Y et al. The association between migraine and fetal-type posterior cerebral artery in patients with ischemic stroke. Cerebrovasc Dis. 2022 (May 13). Doi:10.1159/000524616

Key clinical point: Migraine was significantly associated with fetal-type posterior cerebral artery (PCA) status in patients with ischemic stroke.

Major finding: Fetal-type PCA status was independently associated with migraine (adjusted odds ratio [aOR] 2.06; P = .005). The other factors independently associated with migraine were hypertension (aOR 1.97; P = .011), female gender (aOR 2.03; P = .017) and National Institutes of Health Stroke Scale score at admission (aOR 1.08; P = .018).

Study details: This cross-sectional study included 750 patients aged ≥18 yearswith ischemic stroke, of which 11.3% had migraine history.

Disclosures: This study received no specific funding. The authors declared no conflicts of interest.

Source: Zhang Y et al. The association between migraine and fetal-type posterior cerebral artery in patients with ischemic stroke. Cerebrovasc Dis. 2022 (May 13). Doi:10.1159/000524616

Key clinical point: Erenumab is effective and welltolerated in patients with chronic migraine who did not respond to previous migraine treatments.

Major finding: Overall,71.4% of patients treated with erenumabachieved ≥30% reduction in monthly migraine days from baseline to 9-12 weeks and 34.0% of patients at all assessment periods through 52weeks. Constipation was the most common adverse event and 13.7% of patients discontinued treatment because of a lack of tolerability.

Study details: The data come from a 52-week, prospective, observational study including 300 patients with chronic migraine who received ≥1 dose of erenumab, of which 273 and 119 patients completed 12 and 52 weeks of treatment, respectively.

Disclosures: This study was funded by and conducted in collaboration with Novartis Pharma AG, Basel, Switzerland. Some authors reported being consultants, speakers, or scientific advisorsfor or receiving personal fees from various sources, including Novartis. Two authors declared being employees of and holding stocks in Novartis.

Source: Cullum CK et al.Real-world long-term efficacy and safety of erenumab in adults with chronic migraine: A 52-week, single-center, prospective, observational study. J Headache Pain. 2022;23(1):61 Jun 2). Doi:10.1186/s10194-022-01433-9

Key clinical point: Erenumab is effective and welltolerated in patients with chronic migraine who did not respond to previous migraine treatments.

Major finding: Overall,71.4% of patients treated with erenumabachieved ≥30% reduction in monthly migraine days from baseline to 9-12 weeks and 34.0% of patients at all assessment periods through 52weeks. Constipation was the most common adverse event and 13.7% of patients discontinued treatment because of a lack of tolerability.

Study details: The data come from a 52-week, prospective, observational study including 300 patients with chronic migraine who received ≥1 dose of erenumab, of which 273 and 119 patients completed 12 and 52 weeks of treatment, respectively.

Disclosures: This study was funded by and conducted in collaboration with Novartis Pharma AG, Basel, Switzerland. Some authors reported being consultants, speakers, or scientific advisorsfor or receiving personal fees from various sources, including Novartis. Two authors declared being employees of and holding stocks in Novartis.

Source: Cullum CK et al.Real-world long-term efficacy and safety of erenumab in adults with chronic migraine: A 52-week, single-center, prospective, observational study. J Headache Pain. 2022;23(1):61 Jun 2). Doi:10.1186/s10194-022-01433-9

Key clinical point: Erenumab is effective and welltolerated in patients with chronic migraine who did not respond to previous migraine treatments.

Major finding: Overall,71.4% of patients treated with erenumabachieved ≥30% reduction in monthly migraine days from baseline to 9-12 weeks and 34.0% of patients at all assessment periods through 52weeks. Constipation was the most common adverse event and 13.7% of patients discontinued treatment because of a lack of tolerability.

Study details: The data come from a 52-week, prospective, observational study including 300 patients with chronic migraine who received ≥1 dose of erenumab, of which 273 and 119 patients completed 12 and 52 weeks of treatment, respectively.

Disclosures: This study was funded by and conducted in collaboration with Novartis Pharma AG, Basel, Switzerland. Some authors reported being consultants, speakers, or scientific advisorsfor or receiving personal fees from various sources, including Novartis. Two authors declared being employees of and holding stocks in Novartis.

Source: Cullum CK et al.Real-world long-term efficacy and safety of erenumab in adults with chronic migraine: A 52-week, single-center, prospective, observational study. J Headache Pain. 2022;23(1):61 Jun 2). Doi:10.1186/s10194-022-01433-9

Key clinical point: Intravenous (IV) ketorolac plus metoclopramide failed to improve pain intensity in children presenting to the emergency department (ED) for the acute treatment of migraine compared with metoclopramide monotherapy.

Major finding: The mean change in pain intensity as assessed by a 100 mm Visual Analog Scale at 120 minutes was −44 mm (95% CI 32-57 mm) in the monotherapy group and −36 mm (95% CI 23-49 mm) in the ketorolac group, corresponding to a mean difference of 8 mm between the groups (P = .355),with no significant between-group difference in headache recurrence and adverse events.

Study details: Findings arefrom a double-blind, randomized placebo-controlled trialincluding 53children aged 6-17 years presenting to the ED for the acute treatment of migraine. They were randomly assigned to receive IV ketorolac plus metoclopramide (n=26) or IV metoclopramide plus placebo (n=27).

Disclosures: This study was funded by the Canadian Institutes of Health Research through a Drug Safety and Effectiveness Network grant. The authors declared no conflicts of interest.

Source: Richer LP et al.A randomized trial of ketorolac and metoclopramide for migraine in the emergency department.Headache. 2022; 62: 681-689(Jun 7). Doi:10.1111/head.14307

Key clinical point: Intravenous (IV) ketorolac plus metoclopramide failed to improve pain intensity in children presenting to the emergency department (ED) for the acute treatment of migraine compared with metoclopramide monotherapy.

Major finding: The mean change in pain intensity as assessed by a 100 mm Visual Analog Scale at 120 minutes was −44 mm (95% CI 32-57 mm) in the monotherapy group and −36 mm (95% CI 23-49 mm) in the ketorolac group, corresponding to a mean difference of 8 mm between the groups (P = .355),with no significant between-group difference in headache recurrence and adverse events.

Study details: Findings arefrom a double-blind, randomized placebo-controlled trialincluding 53children aged 6-17 years presenting to the ED for the acute treatment of migraine. They were randomly assigned to receive IV ketorolac plus metoclopramide (n=26) or IV metoclopramide plus placebo (n=27).

Disclosures: This study was funded by the Canadian Institutes of Health Research through a Drug Safety and Effectiveness Network grant. The authors declared no conflicts of interest.

Source: Richer LP et al.A randomized trial of ketorolac and metoclopramide for migraine in the emergency department.Headache. 2022; 62: 681-689(Jun 7). Doi:10.1111/head.14307

Key clinical point: Intravenous (IV) ketorolac plus metoclopramide failed to improve pain intensity in children presenting to the emergency department (ED) for the acute treatment of migraine compared with metoclopramide monotherapy.

Major finding: The mean change in pain intensity as assessed by a 100 mm Visual Analog Scale at 120 minutes was −44 mm (95% CI 32-57 mm) in the monotherapy group and −36 mm (95% CI 23-49 mm) in the ketorolac group, corresponding to a mean difference of 8 mm between the groups (P = .355),with no significant between-group difference in headache recurrence and adverse events.

Study details: Findings arefrom a double-blind, randomized placebo-controlled trialincluding 53children aged 6-17 years presenting to the ED for the acute treatment of migraine. They were randomly assigned to receive IV ketorolac plus metoclopramide (n=26) or IV metoclopramide plus placebo (n=27).

Disclosures: This study was funded by the Canadian Institutes of Health Research through a Drug Safety and Effectiveness Network grant. The authors declared no conflicts of interest.

Source: Richer LP et al.A randomized trial of ketorolac and metoclopramide for migraine in the emergency department.Headache. 2022; 62: 681-689(Jun 7). Doi:10.1111/head.14307

Key clinical point: Patients hospitalized with refractory chronic migraine treated with continuous multiday lidocaine infusions showed a significant improvement in pain immediately after the infusion, with some patients maintaining this improvement at 1 month.

Major finding: Medianpain ratings decreased from 7.0 on admission to 1.0 at discharge (P< .001), with 87.8% of admissions being cases of acute response. Among acute responders with data on average pain, 43.2% demonstrated sustained response at 1 month.

Study details: The data come from a retrospective cohort study of 609 hospital admissions involving 537 patients with refractory chronic migraine who received continuous multiday lidocaine infusions.

Disclosures: This study did not receive any specific funding. SD Silberstein declared serving as a consultant and advisory panel member for and receiving honoraria from various sources.

Source: Schwenk ES et al. Lidocaine infusions for refractory chronic migraine: A retrospective analysis. Reg Anesth Pain Med. 2022;47:408-413(May 23). Doi:10.1136/rapm-2021-103180

Key clinical point: Patients hospitalized with refractory chronic migraine treated with continuous multiday lidocaine infusions showed a significant improvement in pain immediately after the infusion, with some patients maintaining this improvement at 1 month.

Major finding: Medianpain ratings decreased from 7.0 on admission to 1.0 at discharge (P< .001), with 87.8% of admissions being cases of acute response. Among acute responders with data on average pain, 43.2% demonstrated sustained response at 1 month.

Study details: The data come from a retrospective cohort study of 609 hospital admissions involving 537 patients with refractory chronic migraine who received continuous multiday lidocaine infusions.

Disclosures: This study did not receive any specific funding. SD Silberstein declared serving as a consultant and advisory panel member for and receiving honoraria from various sources.

Source: Schwenk ES et al. Lidocaine infusions for refractory chronic migraine: A retrospective analysis. Reg Anesth Pain Med. 2022;47:408-413(May 23). Doi:10.1136/rapm-2021-103180

Key clinical point: Patients hospitalized with refractory chronic migraine treated with continuous multiday lidocaine infusions showed a significant improvement in pain immediately after the infusion, with some patients maintaining this improvement at 1 month.

Major finding: Medianpain ratings decreased from 7.0 on admission to 1.0 at discharge (P< .001), with 87.8% of admissions being cases of acute response. Among acute responders with data on average pain, 43.2% demonstrated sustained response at 1 month.

Study details: The data come from a retrospective cohort study of 609 hospital admissions involving 537 patients with refractory chronic migraine who received continuous multiday lidocaine infusions.

Disclosures: This study did not receive any specific funding. SD Silberstein declared serving as a consultant and advisory panel member for and receiving honoraria from various sources.

Source: Schwenk ES et al. Lidocaine infusions for refractory chronic migraine: A retrospective analysis. Reg Anesth Pain Med. 2022;47:408-413(May 23). Doi:10.1136/rapm-2021-103180

Key clinical point: Cold interventions, includingcold-gel headband, cold-gel cap, and intraoral cooling, provide instant relief from pain in patients with migraine; however, their long-term effects on pain are not significant.

Major finding: The cold intervention group vs. control group led to a significant reduction in pain on a visual analog scale score at 30 minutes (standard mean difference [SMD] −3.21; P = .02) but a nonsignificant reduction in the score at 24 hours (SMD −0.44; P = .07) after the intervention.

Study details: This was a meta-analysis of 6 studies (4 randomized controlled trials and 2 quasi-experimental studies) that included adult patients with migraine who underwent a cold intervention.

Disclosures: The study was partially sponsored by the Ministry of Science and Technology, Israel. The authors declared no conflicts of interest.

Source: Hsu Y-Y et al.Cold intervention for relieving migraine symptoms: A systematic review and meta-analysis. J Clin Nurs. 2022 (May 20). Doi:10.1111/jocn.16368

Key clinical point: Cold interventions, includingcold-gel headband, cold-gel cap, and intraoral cooling, provide instant relief from pain in patients with migraine; however, their long-term effects on pain are not significant.

Major finding: The cold intervention group vs. control group led to a significant reduction in pain on a visual analog scale score at 30 minutes (standard mean difference [SMD] −3.21; P = .02) but a nonsignificant reduction in the score at 24 hours (SMD −0.44; P = .07) after the intervention.

Study details: This was a meta-analysis of 6 studies (4 randomized controlled trials and 2 quasi-experimental studies) that included adult patients with migraine who underwent a cold intervention.

Disclosures: The study was partially sponsored by the Ministry of Science and Technology, Israel. The authors declared no conflicts of interest.

Source: Hsu Y-Y et al.Cold intervention for relieving migraine symptoms: A systematic review and meta-analysis. J Clin Nurs. 2022 (May 20). Doi:10.1111/jocn.16368

Key clinical point: Cold interventions, includingcold-gel headband, cold-gel cap, and intraoral cooling, provide instant relief from pain in patients with migraine; however, their long-term effects on pain are not significant.

Major finding: The cold intervention group vs. control group led to a significant reduction in pain on a visual analog scale score at 30 minutes (standard mean difference [SMD] −3.21; P = .02) but a nonsignificant reduction in the score at 24 hours (SMD −0.44; P = .07) after the intervention.

Study details: This was a meta-analysis of 6 studies (4 randomized controlled trials and 2 quasi-experimental studies) that included adult patients with migraine who underwent a cold intervention.

Disclosures: The study was partially sponsored by the Ministry of Science and Technology, Israel. The authors declared no conflicts of interest.

Source: Hsu Y-Y et al.Cold intervention for relieving migraine symptoms: A systematic review and meta-analysis. J Clin Nurs. 2022 (May 20). Doi:10.1111/jocn.16368

Key clinical point: As a migraine preventive agent, fremanezumab is effective across the full patient spectrum, including those with episodic migraine (EM), chronic migraine (CM), and difficult-to-treat (DTT) migraine (patients with medication overuse [MO], major depressive disorder [MDD], generalized anxiety disorder [GAD], or exposure to a different calcitonin gene-related peptide monoclonal antibody [CGRP mAb]).

Major finding: At month 6,the mean monthly migraine days reduced in patients with EM (−7.7 days), CM (−10.1 days), MO (−10.8 days), MDD (−9.9 days), GAD (−9.5 days), and prior CGRP mAb exposure (−9.0 days).

Study details: Findings are from aretrospective, online chart review study that collected data from 1003 patients with EM/CM aged ≥18 years at fremanezumab initiation, including those with DTT migraine, and 421 clinicians treating patients with EM/CM in a US-based practice.

Disclosures: This study was funded by Teva Pharmaceuticals. All authors declared being current or former employees of Teva Pharmaceuticals or Analysis Group, which performed these analyses funded by Teva.

Source: Driessen MT et al.Real-world effectiveness after initiating fremanezumab treatment in US patients with episodic and chronic migraine or difficult-to-treat migraine. J Headache Pain. 2022;23:56(May 16). Doi:10.1186/s10194-022-01415-x

Key clinical point: As a migraine preventive agent, fremanezumab is effective across the full patient spectrum, including those with episodic migraine (EM), chronic migraine (CM), and difficult-to-treat (DTT) migraine (patients with medication overuse [MO], major depressive disorder [MDD], generalized anxiety disorder [GAD], or exposure to a different calcitonin gene-related peptide monoclonal antibody [CGRP mAb]).

Major finding: At month 6,the mean monthly migraine days reduced in patients with EM (−7.7 days), CM (−10.1 days), MO (−10.8 days), MDD (−9.9 days), GAD (−9.5 days), and prior CGRP mAb exposure (−9.0 days).

Study details: Findings are from aretrospective, online chart review study that collected data from 1003 patients with EM/CM aged ≥18 years at fremanezumab initiation, including those with DTT migraine, and 421 clinicians treating patients with EM/CM in a US-based practice.

Disclosures: This study was funded by Teva Pharmaceuticals. All authors declared being current or former employees of Teva Pharmaceuticals or Analysis Group, which performed these analyses funded by Teva.

Source: Driessen MT et al.Real-world effectiveness after initiating fremanezumab treatment in US patients with episodic and chronic migraine or difficult-to-treat migraine. J Headache Pain. 2022;23:56(May 16). Doi:10.1186/s10194-022-01415-x

Key clinical point: As a migraine preventive agent, fremanezumab is effective across the full patient spectrum, including those with episodic migraine (EM), chronic migraine (CM), and difficult-to-treat (DTT) migraine (patients with medication overuse [MO], major depressive disorder [MDD], generalized anxiety disorder [GAD], or exposure to a different calcitonin gene-related peptide monoclonal antibody [CGRP mAb]).

Major finding: At month 6,the mean monthly migraine days reduced in patients with EM (−7.7 days), CM (−10.1 days), MO (−10.8 days), MDD (−9.9 days), GAD (−9.5 days), and prior CGRP mAb exposure (−9.0 days).

Study details: Findings are from aretrospective, online chart review study that collected data from 1003 patients with EM/CM aged ≥18 years at fremanezumab initiation, including those with DTT migraine, and 421 clinicians treating patients with EM/CM in a US-based practice.

Disclosures: This study was funded by Teva Pharmaceuticals. All authors declared being current or former employees of Teva Pharmaceuticals or Analysis Group, which performed these analyses funded by Teva.

Source: Driessen MT et al.Real-world effectiveness after initiating fremanezumab treatment in US patients with episodic and chronic migraine or difficult-to-treat migraine. J Headache Pain. 2022;23:56(May 16). Doi:10.1186/s10194-022-01415-x