Headache & Migraine

Key clinical point: A single infusion of Lu AG09222, a humanized monoclonal antibody targeting the pituitary adenylate cyclase-activating polypeptide, was more effective than placebo in reducing migraine frequency over 4 weeks in adults with episodic or chronic migraine.

Major findings: Through week 4, a single infusion of 750 mg Lu AG09222 vs placebo led to a significantly greater reduction in monthly migraine days (−6.2 vs −4.2 days; difference −2 days; P = .02). Most adverse events were mild, with COVID-19, nasopharyngitis, and fatigue being more prevalent in those receiving 750 mg Lu AG09222 vs placebo.

Study details: This phase 2 trial included 237 adults with migraine who did not respond to two to four previous treatments and were assigned to receive either Lu AG09222 (750 mg or 100 mg) or placebo for 4 weeks.

Disclosure: The study was supported by H. Lundbeck A/S. Three authors declared being employees of H. Lundbeck A/S, of whom one held stock options. One author reported receiving consulting, speaker, and advisory board fees from various sources, including H. Lundbeck A/S.

Source: Ashina M, Phul R, Khodaie M, et al. A monoclonal antibody to PACAP for migraine prevention. N Engl J Med. 2024;391(9):800-809 (Sept 4). doi: 10.1056/NEJMoa2314577 Source

Key clinical point: A single infusion of Lu AG09222, a humanized monoclonal antibody targeting the pituitary adenylate cyclase-activating polypeptide, was more effective than placebo in reducing migraine frequency over 4 weeks in adults with episodic or chronic migraine.

Major findings: Through week 4, a single infusion of 750 mg Lu AG09222 vs placebo led to a significantly greater reduction in monthly migraine days (−6.2 vs −4.2 days; difference −2 days; P = .02). Most adverse events were mild, with COVID-19, nasopharyngitis, and fatigue being more prevalent in those receiving 750 mg Lu AG09222 vs placebo.

Study details: This phase 2 trial included 237 adults with migraine who did not respond to two to four previous treatments and were assigned to receive either Lu AG09222 (750 mg or 100 mg) or placebo for 4 weeks.

Disclosure: The study was supported by H. Lundbeck A/S. Three authors declared being employees of H. Lundbeck A/S, of whom one held stock options. One author reported receiving consulting, speaker, and advisory board fees from various sources, including H. Lundbeck A/S.

Source: Ashina M, Phul R, Khodaie M, et al. A monoclonal antibody to PACAP for migraine prevention. N Engl J Med. 2024;391(9):800-809 (Sept 4). doi: 10.1056/NEJMoa2314577 Source

Key clinical point: A single infusion of Lu AG09222, a humanized monoclonal antibody targeting the pituitary adenylate cyclase-activating polypeptide, was more effective than placebo in reducing migraine frequency over 4 weeks in adults with episodic or chronic migraine.

Major findings: Through week 4, a single infusion of 750 mg Lu AG09222 vs placebo led to a significantly greater reduction in monthly migraine days (−6.2 vs −4.2 days; difference −2 days; P = .02). Most adverse events were mild, with COVID-19, nasopharyngitis, and fatigue being more prevalent in those receiving 750 mg Lu AG09222 vs placebo.

Study details: This phase 2 trial included 237 adults with migraine who did not respond to two to four previous treatments and were assigned to receive either Lu AG09222 (750 mg or 100 mg) or placebo for 4 weeks.

Disclosure: The study was supported by H. Lundbeck A/S. Three authors declared being employees of H. Lundbeck A/S, of whom one held stock options. One author reported receiving consulting, speaker, and advisory board fees from various sources, including H. Lundbeck A/S.

Source: Ashina M, Phul R, Khodaie M, et al. A monoclonal antibody to PACAP for migraine prevention. N Engl J Med. 2024;391(9):800-809 (Sept 4). doi: 10.1056/NEJMoa2314577 Source

TOPLINE:

A history of migraine is not associated with an elevated risk for Parkinson’s disease (PD) in women, regardless of headache frequency or migraine subtype, a new study suggests.

METHODOLOGY:

• Researchers analyzed data on 39,312 women health professionals aged ≥ 45 years and having no history of PD who enrolled in the Women’s Health Study between 1992 and 1995 and were followed until 2021.
• At baseline, 7321 women (18.6%) had migraine.
• The mean follow-up duration was 22 years.
• The primary outcome was a self-reported, physician-confirmed diagnosis of PD.

TAKEAWAY:

• During the study period, 685 women self-reported a diagnosis of PD.
• Of these, 18.7% of reported cases were in women with any migraine and 81.3% in women without migraine.
• No significant association was found between PD risk and a history of migraine, migraine subtypes (with or without aura), or migraine frequency.
• Migraine was not associated with a higher risk for PD than that of nonmigraine headaches.

IN PRACTICE:

“These results are reassuring for women who have migraine, which itself causes many burdens, that they don’t have to worry about an increased risk of Parkinson’s disease in the future,” study author Tobias Kurth, Charité - Universitätsmedizin Berlin, Germany, said in a press release.

SOURCE:

The study was led by Ricarda S. Schulz, MSc, Charité - Universitätsmedizin Berlin. It was published online in Neurology.

LIMITATIONS:

The study’s findings may not be generalizable to other populations, such as men and non-White individuals. The self-reported data on migraine and PD may be subject to inaccuracies. PD is often not diagnosed until symptoms have reached an advanced stage, potentially leading to cases being underreported. Changes in the status and frequency of migraine over the study period were not accounted for, which may have affected the results.

DISCLOSURES:

The authors did not disclose any specific funding for this work. The Women’s Health Study was supported by the National Cancer Institute and National Heart, Lung, and Blood Institute. Two authors reported having financial ties outside this work. Full disclosures are available in the original article.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

A history of migraine is not associated with an elevated risk for Parkinson’s disease (PD) in women, regardless of headache frequency or migraine subtype, a new study suggests.

METHODOLOGY:

• Researchers analyzed data on 39,312 women health professionals aged ≥ 45 years and having no history of PD who enrolled in the Women’s Health Study between 1992 and 1995 and were followed until 2021.
• At baseline, 7321 women (18.6%) had migraine.
• The mean follow-up duration was 22 years.
• The primary outcome was a self-reported, physician-confirmed diagnosis of PD.

TAKEAWAY:

• During the study period, 685 women self-reported a diagnosis of PD.
• Of these, 18.7% of reported cases were in women with any migraine and 81.3% in women without migraine.
• No significant association was found between PD risk and a history of migraine, migraine subtypes (with or without aura), or migraine frequency.
• Migraine was not associated with a higher risk for PD than that of nonmigraine headaches.

IN PRACTICE:

“These results are reassuring for women who have migraine, which itself causes many burdens, that they don’t have to worry about an increased risk of Parkinson’s disease in the future,” study author Tobias Kurth, Charité - Universitätsmedizin Berlin, Germany, said in a press release.

SOURCE:

The study was led by Ricarda S. Schulz, MSc, Charité - Universitätsmedizin Berlin. It was published online in Neurology.

LIMITATIONS:

The study’s findings may not be generalizable to other populations, such as men and non-White individuals. The self-reported data on migraine and PD may be subject to inaccuracies. PD is often not diagnosed until symptoms have reached an advanced stage, potentially leading to cases being underreported. Changes in the status and frequency of migraine over the study period were not accounted for, which may have affected the results.

DISCLOSURES:

The authors did not disclose any specific funding for this work. The Women’s Health Study was supported by the National Cancer Institute and National Heart, Lung, and Blood Institute. Two authors reported having financial ties outside this work. Full disclosures are available in the original article.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

A history of migraine is not associated with an elevated risk for Parkinson’s disease (PD) in women, regardless of headache frequency or migraine subtype, a new study suggests.

METHODOLOGY:

• Researchers analyzed data on 39,312 women health professionals aged ≥ 45 years and having no history of PD who enrolled in the Women’s Health Study between 1992 and 1995 and were followed until 2021.
• At baseline, 7321 women (18.6%) had migraine.
• The mean follow-up duration was 22 years.
• The primary outcome was a self-reported, physician-confirmed diagnosis of PD.

TAKEAWAY:

• During the study period, 685 women self-reported a diagnosis of PD.
• Of these, 18.7% of reported cases were in women with any migraine and 81.3% in women without migraine.
• No significant association was found between PD risk and a history of migraine, migraine subtypes (with or without aura), or migraine frequency.
• Migraine was not associated with a higher risk for PD than that of nonmigraine headaches.

IN PRACTICE:

“These results are reassuring for women who have migraine, which itself causes many burdens, that they don’t have to worry about an increased risk of Parkinson’s disease in the future,” study author Tobias Kurth, Charité - Universitätsmedizin Berlin, Germany, said in a press release.

SOURCE:

The study was led by Ricarda S. Schulz, MSc, Charité - Universitätsmedizin Berlin. It was published online in Neurology.

LIMITATIONS:

The study’s findings may not be generalizable to other populations, such as men and non-White individuals. The self-reported data on migraine and PD may be subject to inaccuracies. PD is often not diagnosed until symptoms have reached an advanced stage, potentially leading to cases being underreported. Changes in the status and frequency of migraine over the study period were not accounted for, which may have affected the results.

DISCLOSURES:

The authors did not disclose any specific funding for this work. The Women’s Health Study was supported by the National Cancer Institute and National Heart, Lung, and Blood Institute. Two authors reported having financial ties outside this work. Full disclosures are available in the original article.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

Earlier in 2024 the American Headache Society issued a position statement that CGRP (calcitonin gene-related peptide) agents are a first-line option for migraine prevention.

No Shinola, Sherlock.

Any of us working frontline neurology have figured that out, including me. And I was, honestly, pretty skeptical of them when they hit the pharmacy shelves. But these days, to quote The Monkees (and Neil Diamond), “I’m a Believer.”

Unfortunately, things don’t quite work out that way. Just because a drug is clearly successful doesn’t make it practical to use first line. Most insurances won’t even let family doctors prescribe them, so they have to send patients to a neurologist (which I’m not complaining about).

Then me and my neuro-brethren have to jump through hoops because of their cost. One month of any of these drugs costs the same as a few years (or more) of generic Topamax, Nortriptyline, Nadolol, etc. Granted, I shouldn’t complain about that, either. If everyone with migraines was getting them it would drive up insurance premiums across the board — including mine.

So, after patients have tried and failed at least two to four other options (depending on their plan) I can usually get a CGRP covered. This involves filling out some forms online and submitting them ... then waiting.

Even if the drug is approved, and successful, that’s still not the end of the story. Depending on the plan I have to get them reauthorized anywhere from every 3 to 12 months. There’s also the chance that in December I’ll get a letter saying the drug won’t be covered starting January, and to try one of the recommended alternatives, like generic Topamax, Nortriptyline, Nadolol, etc. Wash, rinse, repeat.

Having celebrities like Lady Gaga pushing them doesn’t help. The commercials never mention that getting the medication isn’t as easy as “ask your doctor.” Nor does it point out that Lady Gaga won’t have an issue with a CGRP agent’s price tag of $800-$1000 per month, while most of her fans need that money for rent and groceries.

The guidelines, in essence, are useful, but only apply to a perfect world where drug cost doesn’t matter. We aren’t in one. I’m not knocking the pharmaceutical companies — research and development take A LOT of money, and every drug that comes to market has to pay not only for itself, but for several others that failed. Innovation isn’t cheap.

That doesn’t make it any easier to explain to patients, who see ads, or news blurbs on Facebook, or whatever. I just wish the advertisements would have more transparency about how the pricing works.

After all, regardless of how good an automobile may be, don’t car ads show an MSRP?

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

Earlier in 2024 the American Headache Society issued a position statement that CGRP (calcitonin gene-related peptide) agents are a first-line option for migraine prevention.

No Shinola, Sherlock.

Any of us working frontline neurology have figured that out, including me. And I was, honestly, pretty skeptical of them when they hit the pharmacy shelves. But these days, to quote The Monkees (and Neil Diamond), “I’m a Believer.”

Unfortunately, things don’t quite work out that way. Just because a drug is clearly successful doesn’t make it practical to use first line. Most insurances won’t even let family doctors prescribe them, so they have to send patients to a neurologist (which I’m not complaining about).

Then me and my neuro-brethren have to jump through hoops because of their cost. One month of any of these drugs costs the same as a few years (or more) of generic Topamax, Nortriptyline, Nadolol, etc. Granted, I shouldn’t complain about that, either. If everyone with migraines was getting them it would drive up insurance premiums across the board — including mine.

So, after patients have tried and failed at least two to four other options (depending on their plan) I can usually get a CGRP covered. This involves filling out some forms online and submitting them ... then waiting.

Even if the drug is approved, and successful, that’s still not the end of the story. Depending on the plan I have to get them reauthorized anywhere from every 3 to 12 months. There’s also the chance that in December I’ll get a letter saying the drug won’t be covered starting January, and to try one of the recommended alternatives, like generic Topamax, Nortriptyline, Nadolol, etc. Wash, rinse, repeat.

Having celebrities like Lady Gaga pushing them doesn’t help. The commercials never mention that getting the medication isn’t as easy as “ask your doctor.” Nor does it point out that Lady Gaga won’t have an issue with a CGRP agent’s price tag of $800-$1000 per month, while most of her fans need that money for rent and groceries.

The guidelines, in essence, are useful, but only apply to a perfect world where drug cost doesn’t matter. We aren’t in one. I’m not knocking the pharmaceutical companies — research and development take A LOT of money, and every drug that comes to market has to pay not only for itself, but for several others that failed. Innovation isn’t cheap.

That doesn’t make it any easier to explain to patients, who see ads, or news blurbs on Facebook, or whatever. I just wish the advertisements would have more transparency about how the pricing works.

After all, regardless of how good an automobile may be, don’t car ads show an MSRP?

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

Earlier in 2024 the American Headache Society issued a position statement that CGRP (calcitonin gene-related peptide) agents are a first-line option for migraine prevention.

No Shinola, Sherlock.

Any of us working frontline neurology have figured that out, including me. And I was, honestly, pretty skeptical of them when they hit the pharmacy shelves. But these days, to quote The Monkees (and Neil Diamond), “I’m a Believer.”

Unfortunately, things don’t quite work out that way. Just because a drug is clearly successful doesn’t make it practical to use first line. Most insurances won’t even let family doctors prescribe them, so they have to send patients to a neurologist (which I’m not complaining about).

Then me and my neuro-brethren have to jump through hoops because of their cost. One month of any of these drugs costs the same as a few years (or more) of generic Topamax, Nortriptyline, Nadolol, etc. Granted, I shouldn’t complain about that, either. If everyone with migraines was getting them it would drive up insurance premiums across the board — including mine.

So, after patients have tried and failed at least two to four other options (depending on their plan) I can usually get a CGRP covered. This involves filling out some forms online and submitting them ... then waiting.

Even if the drug is approved, and successful, that’s still not the end of the story. Depending on the plan I have to get them reauthorized anywhere from every 3 to 12 months. There’s also the chance that in December I’ll get a letter saying the drug won’t be covered starting January, and to try one of the recommended alternatives, like generic Topamax, Nortriptyline, Nadolol, etc. Wash, rinse, repeat.

Having celebrities like Lady Gaga pushing them doesn’t help. The commercials never mention that getting the medication isn’t as easy as “ask your doctor.” Nor does it point out that Lady Gaga won’t have an issue with a CGRP agent’s price tag of $800-$1000 per month, while most of her fans need that money for rent and groceries.

The guidelines, in essence, are useful, but only apply to a perfect world where drug cost doesn’t matter. We aren’t in one. I’m not knocking the pharmaceutical companies — research and development take A LOT of money, and every drug that comes to market has to pay not only for itself, but for several others that failed. Innovation isn’t cheap.

That doesn’t make it any easier to explain to patients, who see ads, or news blurbs on Facebook, or whatever. I just wish the advertisements would have more transparency about how the pricing works.

After all, regardless of how good an automobile may be, don’t car ads show an MSRP?

Dr. Block has a solo neurology practice in Scottsdale, Arizona.

Migraine pathophysiology has been shown to be associated with vascular and inflammatory processes. Diet and lifestyle can have an effect on an individual's inflammatory process, and research regarding the steps between these factors and inflammation is vague and nonspecific. The Dietary Inflammation Score (DIS), which is calculated on the basis of a questionnaire, is used to score the inflammatory potential of an individual's diet. The Dietary and Lifestyle Inflammation Score (DLIS) includes the DIS questions, and also incorporates body mass index (BMI), physical activity, smoking, and alcohol consumption. A recent study, based on a secondary analysis of previous data, examined the correlation between migraine and DIS and DLIS among 285 women, 40% of whom had a chronic migraine diagnosis. Results published in Scientific Reports in July 2024 noted that participants with chronic migraine had a significantly higher DIS and DLIS than those who were not diagnosed with chronic migraine. It is important to note that migraine-associated inflammation can also result from genetic factors. A previous study, published in 2023 in Nature Genetics, described a correlation between genetic markers of inflammatory disorders, such as endometriosis, asthma, and migraine.¹ These results, consistent with our current understanding of the genetic contribution to migraine risk, emphasize that lifestyle modifications alone are not usually adequate for complete management of migraines.

Patients who experience chronic migraine may be inclined to reduce their time spent exercising and engaging in physical activity, as these activities can exacerbate migraine symptoms. Additionally, after recovering from a migraine, patients often need to catch up on tasks and responsibilities, which can squeeze out time for physical activity and exercise (often considered luxuries that can be done during leisure time). Results of a small cross-sectional retrospective study published in Scientific Reports in 2024 suggested a correlation between daily walking steps and response to calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb). According to the study, which included 22 patients who were diagnosed with migraine and treated with CGRP mAb, patients who experienced an improvement of their migraine symptoms also increased their average daily steps by almost 1000 steps per day. The authors suggested that steps can be used as a marker of treatment response in migraine.

Screen time is often blamed as a cause for a number of different ailments, including obesity, anxiety, depression, insomnia, and migraine. An article published in June 2024 in European Journal of Pain described results of a meta-analysis examining the association between sedentary lifestyle and migraine. The authors noted that time spent watching television could be causally associated with an increased risk for migraine.²Another study, with results published in July 2024 in The Journal of Headache and Pain, examined the relationship between migraine and leisure screen time. The researchers used data from 661,399 European individuals from 53 studies to look at genetically predicted leisure screen time, rather than actual leisure screen time. They reported that genetically predicted leisure screen time was associated with a 27.7% increase in migraine risk. While the results are consistent with what is already widely accepted about screen time and migraine, the inclusion of genetic predisposition to screen time is interesting in suggesting that some underlying drive could be contributing to increased screen time among patients who have migraine.

The results of these studies reemphasize the importance of the link between lifestyle factors and migraine but warn against oversimplifying the correlation. There is a bidirectional relationship between migraine and inflammation. We know that inflammation is mediated by diet as well as physical activity. During a migraine, patients may turn to foods that have a high inflammatory potential. Furthermore, migraine can influence a person's inclination to participate in physical activity, as the pain and discomfort can make it difficult engage in exercise. During a migraine, patients may prefer sedentary activities. Screen time can be appealing or relaxing while recovering from a migraine. Genetic predisposition is an interesting additional contributor to this link. Acknowledging genetic predisposition to inflammation or sedentary activity can be a step in helping patients recognize that it could be challenging to overcome these genetically inherent drives or conditions, while providing encouragement regarding the potential benefits of doing so.

Additional References

1. Rahmioglu N, Mortlock S, Ghiasi M, et al. The genetic basis of endometriosis and comorbidity with other pain and inflammatory conditions. Nat Genet. 2023;55(3):423-436. Doi: 10.1038/s41588-023-01323-z Source

2. Li P, Li J, Zhu H, et al. Causal effects of sedentary behaviours on the risk of migraine: A univariable and multivariable Mendelian randomization study. Eur J Pain. 2024 (Jun 4). Doi: 10.1002/ejp.2296  Source

Migraine pathophysiology has been shown to be associated with vascular and inflammatory processes. Diet and lifestyle can have an effect on an individual's inflammatory process, and research regarding the steps between these factors and inflammation is vague and nonspecific. The Dietary Inflammation Score (DIS), which is calculated on the basis of a questionnaire, is used to score the inflammatory potential of an individual's diet. The Dietary and Lifestyle Inflammation Score (DLIS) includes the DIS questions, and also incorporates body mass index (BMI), physical activity, smoking, and alcohol consumption. A recent study, based on a secondary analysis of previous data, examined the correlation between migraine and DIS and DLIS among 285 women, 40% of whom had a chronic migraine diagnosis. Results published in Scientific Reports in July 2024 noted that participants with chronic migraine had a significantly higher DIS and DLIS than those who were not diagnosed with chronic migraine. It is important to note that migraine-associated inflammation can also result from genetic factors. A previous study, published in 2023 in Nature Genetics, described a correlation between genetic markers of inflammatory disorders, such as endometriosis, asthma, and migraine.¹ These results, consistent with our current understanding of the genetic contribution to migraine risk, emphasize that lifestyle modifications alone are not usually adequate for complete management of migraines.

Patients who experience chronic migraine may be inclined to reduce their time spent exercising and engaging in physical activity, as these activities can exacerbate migraine symptoms. Additionally, after recovering from a migraine, patients often need to catch up on tasks and responsibilities, which can squeeze out time for physical activity and exercise (often considered luxuries that can be done during leisure time). Results of a small cross-sectional retrospective study published in Scientific Reports in 2024 suggested a correlation between daily walking steps and response to calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb). According to the study, which included 22 patients who were diagnosed with migraine and treated with CGRP mAb, patients who experienced an improvement of their migraine symptoms also increased their average daily steps by almost 1000 steps per day. The authors suggested that steps can be used as a marker of treatment response in migraine.

Screen time is often blamed as a cause for a number of different ailments, including obesity, anxiety, depression, insomnia, and migraine. An article published in June 2024 in European Journal of Pain described results of a meta-analysis examining the association between sedentary lifestyle and migraine. The authors noted that time spent watching television could be causally associated with an increased risk for migraine.²Another study, with results published in July 2024 in The Journal of Headache and Pain, examined the relationship between migraine and leisure screen time. The researchers used data from 661,399 European individuals from 53 studies to look at genetically predicted leisure screen time, rather than actual leisure screen time. They reported that genetically predicted leisure screen time was associated with a 27.7% increase in migraine risk. While the results are consistent with what is already widely accepted about screen time and migraine, the inclusion of genetic predisposition to screen time is interesting in suggesting that some underlying drive could be contributing to increased screen time among patients who have migraine.

The results of these studies reemphasize the importance of the link between lifestyle factors and migraine but warn against oversimplifying the correlation. There is a bidirectional relationship between migraine and inflammation. We know that inflammation is mediated by diet as well as physical activity. During a migraine, patients may turn to foods that have a high inflammatory potential. Furthermore, migraine can influence a person's inclination to participate in physical activity, as the pain and discomfort can make it difficult engage in exercise. During a migraine, patients may prefer sedentary activities. Screen time can be appealing or relaxing while recovering from a migraine. Genetic predisposition is an interesting additional contributor to this link. Acknowledging genetic predisposition to inflammation or sedentary activity can be a step in helping patients recognize that it could be challenging to overcome these genetically inherent drives or conditions, while providing encouragement regarding the potential benefits of doing so.

Additional References

1. Rahmioglu N, Mortlock S, Ghiasi M, et al. The genetic basis of endometriosis and comorbidity with other pain and inflammatory conditions. Nat Genet. 2023;55(3):423-436. Doi: 10.1038/s41588-023-01323-z Source

2. Li P, Li J, Zhu H, et al. Causal effects of sedentary behaviours on the risk of migraine: A univariable and multivariable Mendelian randomization study. Eur J Pain. 2024 (Jun 4). Doi: 10.1002/ejp.2296  Source

Migraine pathophysiology has been shown to be associated with vascular and inflammatory processes. Diet and lifestyle can have an effect on an individual's inflammatory process, and research regarding the steps between these factors and inflammation is vague and nonspecific. The Dietary Inflammation Score (DIS), which is calculated on the basis of a questionnaire, is used to score the inflammatory potential of an individual's diet. The Dietary and Lifestyle Inflammation Score (DLIS) includes the DIS questions, and also incorporates body mass index (BMI), physical activity, smoking, and alcohol consumption. A recent study, based on a secondary analysis of previous data, examined the correlation between migraine and DIS and DLIS among 285 women, 40% of whom had a chronic migraine diagnosis. Results published in Scientific Reports in July 2024 noted that participants with chronic migraine had a significantly higher DIS and DLIS than those who were not diagnosed with chronic migraine. It is important to note that migraine-associated inflammation can also result from genetic factors. A previous study, published in 2023 in Nature Genetics, described a correlation between genetic markers of inflammatory disorders, such as endometriosis, asthma, and migraine.¹ These results, consistent with our current understanding of the genetic contribution to migraine risk, emphasize that lifestyle modifications alone are not usually adequate for complete management of migraines.

Patients who experience chronic migraine may be inclined to reduce their time spent exercising and engaging in physical activity, as these activities can exacerbate migraine symptoms. Additionally, after recovering from a migraine, patients often need to catch up on tasks and responsibilities, which can squeeze out time for physical activity and exercise (often considered luxuries that can be done during leisure time). Results of a small cross-sectional retrospective study published in Scientific Reports in 2024 suggested a correlation between daily walking steps and response to calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb). According to the study, which included 22 patients who were diagnosed with migraine and treated with CGRP mAb, patients who experienced an improvement of their migraine symptoms also increased their average daily steps by almost 1000 steps per day. The authors suggested that steps can be used as a marker of treatment response in migraine.

Screen time is often blamed as a cause for a number of different ailments, including obesity, anxiety, depression, insomnia, and migraine. An article published in June 2024 in European Journal of Pain described results of a meta-analysis examining the association between sedentary lifestyle and migraine. The authors noted that time spent watching television could be causally associated with an increased risk for migraine.²Another study, with results published in July 2024 in The Journal of Headache and Pain, examined the relationship between migraine and leisure screen time. The researchers used data from 661,399 European individuals from 53 studies to look at genetically predicted leisure screen time, rather than actual leisure screen time. They reported that genetically predicted leisure screen time was associated with a 27.7% increase in migraine risk. While the results are consistent with what is already widely accepted about screen time and migraine, the inclusion of genetic predisposition to screen time is interesting in suggesting that some underlying drive could be contributing to increased screen time among patients who have migraine.

The results of these studies reemphasize the importance of the link between lifestyle factors and migraine but warn against oversimplifying the correlation. There is a bidirectional relationship between migraine and inflammation. We know that inflammation is mediated by diet as well as physical activity. During a migraine, patients may turn to foods that have a high inflammatory potential. Furthermore, migraine can influence a person's inclination to participate in physical activity, as the pain and discomfort can make it difficult engage in exercise. During a migraine, patients may prefer sedentary activities. Screen time can be appealing or relaxing while recovering from a migraine. Genetic predisposition is an interesting additional contributor to this link. Acknowledging genetic predisposition to inflammation or sedentary activity can be a step in helping patients recognize that it could be challenging to overcome these genetically inherent drives or conditions, while providing encouragement regarding the potential benefits of doing so.

Additional References

1. Rahmioglu N, Mortlock S, Ghiasi M, et al. The genetic basis of endometriosis and comorbidity with other pain and inflammatory conditions. Nat Genet. 2023;55(3):423-436. Doi: 10.1038/s41588-023-01323-z Source

2. Li P, Li J, Zhu H, et al. Causal effects of sedentary behaviours on the risk of migraine: A univariable and multivariable Mendelian randomization study. Eur J Pain. 2024 (Jun 4). Doi: 10.1002/ejp.2296  Source

Key clinical point: Rimegepant was more effective than placebo in reducing pain and most bothersome symptoms in patients with moderate to severe migraine, while also showing favorable safety and tolerability.

Major findings: At 2 hours post dose, rimegepant was more effective than placebo in providing freedom from pain (risk difference 4.9; P = .0298) and the most bothersome symptoms (risk difference 8.9; P = .0016). Similar proportions of participants in the rimegepant vs placebo group experienced at least one adverse event (12.6% vs 10.7%), with nausea (0.9% vs 1.1%) and dizziness (0.7% vs 0.4%) being the most common adverse events.

Study details: This randomized, double-blind, placebo-controlled trial (Safety and Efficacy Study in Adult Subjects With Acute Migraines, NCT03235479)  included 1084 patients with migraine with or without aura who were randomly assigned to receive 75 mg rimegepant (n = 543) or placebo (n = 541).

Disclosures: This study was supported by Biohaven Pharmaceuticals (acquired by Pfizer, Inc.). Four authors declared being employees or stockholders of Biohaven Pharmaceuticals, Pfizer, or having other ties with various sources.

Source: Lipton RB, Thiry A, Morris BA, Croop R. Efficacy and safety of rimegepant 75 mg oral tablet, a CGRP receptor antagonist, for the acute treatment of migraine: A randomized, double-blind, placebo-controlled trial. J Pain Res. 2024;17:2431-2441 (Jul 22). Doi: 10.2147/JPR.S453806 Source

Key clinical point: Rimegepant was more effective than placebo in reducing pain and most bothersome symptoms in patients with moderate to severe migraine, while also showing favorable safety and tolerability.

Major findings: At 2 hours post dose, rimegepant was more effective than placebo in providing freedom from pain (risk difference 4.9; P = .0298) and the most bothersome symptoms (risk difference 8.9; P = .0016). Similar proportions of participants in the rimegepant vs placebo group experienced at least one adverse event (12.6% vs 10.7%), with nausea (0.9% vs 1.1%) and dizziness (0.7% vs 0.4%) being the most common adverse events.

Study details: This randomized, double-blind, placebo-controlled trial (Safety and Efficacy Study in Adult Subjects With Acute Migraines, NCT03235479)  included 1084 patients with migraine with or without aura who were randomly assigned to receive 75 mg rimegepant (n = 543) or placebo (n = 541).

Disclosures: This study was supported by Biohaven Pharmaceuticals (acquired by Pfizer, Inc.). Four authors declared being employees or stockholders of Biohaven Pharmaceuticals, Pfizer, or having other ties with various sources.

Source: Lipton RB, Thiry A, Morris BA, Croop R. Efficacy and safety of rimegepant 75 mg oral tablet, a CGRP receptor antagonist, for the acute treatment of migraine: A randomized, double-blind, placebo-controlled trial. J Pain Res. 2024;17:2431-2441 (Jul 22). Doi: 10.2147/JPR.S453806 Source

Key clinical point: Rimegepant was more effective than placebo in reducing pain and most bothersome symptoms in patients with moderate to severe migraine, while also showing favorable safety and tolerability.

Major findings: At 2 hours post dose, rimegepant was more effective than placebo in providing freedom from pain (risk difference 4.9; P = .0298) and the most bothersome symptoms (risk difference 8.9; P = .0016). Similar proportions of participants in the rimegepant vs placebo group experienced at least one adverse event (12.6% vs 10.7%), with nausea (0.9% vs 1.1%) and dizziness (0.7% vs 0.4%) being the most common adverse events.

Study details: This randomized, double-blind, placebo-controlled trial (Safety and Efficacy Study in Adult Subjects With Acute Migraines, NCT03235479)  included 1084 patients with migraine with or without aura who were randomly assigned to receive 75 mg rimegepant (n = 543) or placebo (n = 541).

Disclosures: This study was supported by Biohaven Pharmaceuticals (acquired by Pfizer, Inc.). Four authors declared being employees or stockholders of Biohaven Pharmaceuticals, Pfizer, or having other ties with various sources.

Source: Lipton RB, Thiry A, Morris BA, Croop R. Efficacy and safety of rimegepant 75 mg oral tablet, a CGRP receptor antagonist, for the acute treatment of migraine: A randomized, double-blind, placebo-controlled trial. J Pain Res. 2024;17:2431-2441 (Jul 22). Doi: 10.2147/JPR.S453806 Source

Key clinical point: This Mendelian randomization study showed that leisure screen time (LST) worsens migraine, whereas moderate to vigorous physical activity (MVPA) alleviates it, with hypertension and diastolic blood pressure (DBP) being responsible for the effects of MVPA or LST on migraine.

Major findings: Genetically predicted LST was associated with a significantly increased risk for migraine (odds ratio [OR] 1.28; P < .001), whereas MVPA was linked to a significantly reduced risk (OR 0.73; P = .000006). Hypertension mediated 4.86% and 24.81% of the effects of MVPA and LST on migraine risk, respectively, and DBP accounted for 4.66% of the effects of MVPA on migraine risk.

Study details: This study included 18,477 patients with migraine and 287,837 control individuals without migraine from the FinnGen consortium and 26,052 patients with migraine and 487,214 control individuals without migraine from the large-scale genome-wide association studies.

Disclosures: This study was supported by grants from the National Natural Science Foundation of China and others. The authors declared no conflicts of interest.

Source: Gan Q, Song E, Zhang L, et al. The role of hypertension in the relationship between leisure screen time, physical activity and migraine: A 2-sample Mendelian randomization study. J Headache Pain. 2024;25:122 (Jul 24). Doi: 10.1186/s10194-024-01820-4 Source

Key clinical point: This Mendelian randomization study showed that leisure screen time (LST) worsens migraine, whereas moderate to vigorous physical activity (MVPA) alleviates it, with hypertension and diastolic blood pressure (DBP) being responsible for the effects of MVPA or LST on migraine.

Major findings: Genetically predicted LST was associated with a significantly increased risk for migraine (odds ratio [OR] 1.28; P < .001), whereas MVPA was linked to a significantly reduced risk (OR 0.73; P = .000006). Hypertension mediated 4.86% and 24.81% of the effects of MVPA and LST on migraine risk, respectively, and DBP accounted for 4.66% of the effects of MVPA on migraine risk.

Study details: This study included 18,477 patients with migraine and 287,837 control individuals without migraine from the FinnGen consortium and 26,052 patients with migraine and 487,214 control individuals without migraine from the large-scale genome-wide association studies.

Disclosures: This study was supported by grants from the National Natural Science Foundation of China and others. The authors declared no conflicts of interest.

Source: Gan Q, Song E, Zhang L, et al. The role of hypertension in the relationship between leisure screen time, physical activity and migraine: A 2-sample Mendelian randomization study. J Headache Pain. 2024;25:122 (Jul 24). Doi: 10.1186/s10194-024-01820-4 Source

Key clinical point: This Mendelian randomization study showed that leisure screen time (LST) worsens migraine, whereas moderate to vigorous physical activity (MVPA) alleviates it, with hypertension and diastolic blood pressure (DBP) being responsible for the effects of MVPA or LST on migraine.

Major findings: Genetically predicted LST was associated with a significantly increased risk for migraine (odds ratio [OR] 1.28; P < .001), whereas MVPA was linked to a significantly reduced risk (OR 0.73; P = .000006). Hypertension mediated 4.86% and 24.81% of the effects of MVPA and LST on migraine risk, respectively, and DBP accounted for 4.66% of the effects of MVPA on migraine risk.

Study details: This study included 18,477 patients with migraine and 287,837 control individuals without migraine from the FinnGen consortium and 26,052 patients with migraine and 487,214 control individuals without migraine from the large-scale genome-wide association studies.

Disclosures: This study was supported by grants from the National Natural Science Foundation of China and others. The authors declared no conflicts of interest.

Source: Gan Q, Song E, Zhang L, et al. The role of hypertension in the relationship between leisure screen time, physical activity and migraine: A 2-sample Mendelian randomization study. J Headache Pain. 2024;25:122 (Jul 24). Doi: 10.1186/s10194-024-01820-4 Source

Key clinical point: The meta-analysis showed that atogepant was effective and well tolerated in patients with migraine in a non–dose-dependent manner, with rare incidences of serious treatment-emergent adverse events (TEAE) reported.

Major findings: Atogepant vs placebo led to a significant reduction in monthly migraine days (standardized mean difference [SMD] −0.40; P = .00001) and headache days (SMD −0.39; P = .00001), with consistent results observed across all dosage groups. The risk for TEAE (relative risk [RR] 1.11; P = .02) was significantly higher in the atogepant vs placebo group, with constipation (RR 2.55; P < .00001), nausea (RR 2.19; P < .00001), and urinary tract infection (RR 1.49; P = .03) being the most common.

Study details: This meta-analysis of four randomized controlled trials included 2813 patients with migraine who were treated with atogepant (10 mg, 30 mg, or 60 mg).

Disclosures: This study was supported by the Chongqing Clinical Pharmacy Key Specialties Construction Project, China. The authors declared no conflicts of interest.

Source: Hou M, Luo X, He S, et al. Efficacy and safety of atogepant, a small molecule CGRP receptor antagonist, for the preventive treatment of migraine: A systematic review and meta-analysis. J Headache Pain. 2024;25:116 (Jul 19). Doi: 10.1186/s10194-024-01822-2 Source

Key clinical point: The meta-analysis showed that atogepant was effective and well tolerated in patients with migraine in a non–dose-dependent manner, with rare incidences of serious treatment-emergent adverse events (TEAE) reported.

Major findings: Atogepant vs placebo led to a significant reduction in monthly migraine days (standardized mean difference [SMD] −0.40; P = .00001) and headache days (SMD −0.39; P = .00001), with consistent results observed across all dosage groups. The risk for TEAE (relative risk [RR] 1.11; P = .02) was significantly higher in the atogepant vs placebo group, with constipation (RR 2.55; P < .00001), nausea (RR 2.19; P < .00001), and urinary tract infection (RR 1.49; P = .03) being the most common.

Study details: This meta-analysis of four randomized controlled trials included 2813 patients with migraine who were treated with atogepant (10 mg, 30 mg, or 60 mg).

Disclosures: This study was supported by the Chongqing Clinical Pharmacy Key Specialties Construction Project, China. The authors declared no conflicts of interest.

Source: Hou M, Luo X, He S, et al. Efficacy and safety of atogepant, a small molecule CGRP receptor antagonist, for the preventive treatment of migraine: A systematic review and meta-analysis. J Headache Pain. 2024;25:116 (Jul 19). Doi: 10.1186/s10194-024-01822-2 Source

Key clinical point: The meta-analysis showed that atogepant was effective and well tolerated in patients with migraine in a non–dose-dependent manner, with rare incidences of serious treatment-emergent adverse events (TEAE) reported.

Major findings: Atogepant vs placebo led to a significant reduction in monthly migraine days (standardized mean difference [SMD] −0.40; P = .00001) and headache days (SMD −0.39; P = .00001), with consistent results observed across all dosage groups. The risk for TEAE (relative risk [RR] 1.11; P = .02) was significantly higher in the atogepant vs placebo group, with constipation (RR 2.55; P < .00001), nausea (RR 2.19; P < .00001), and urinary tract infection (RR 1.49; P = .03) being the most common.

Study details: This meta-analysis of four randomized controlled trials included 2813 patients with migraine who were treated with atogepant (10 mg, 30 mg, or 60 mg).

Disclosures: This study was supported by the Chongqing Clinical Pharmacy Key Specialties Construction Project, China. The authors declared no conflicts of interest.

Source: Hou M, Luo X, He S, et al. Efficacy and safety of atogepant, a small molecule CGRP receptor antagonist, for the preventive treatment of migraine: A systematic review and meta-analysis. J Headache Pain. 2024;25:116 (Jul 19). Doi: 10.1186/s10194-024-01822-2 Source

Key clinical point: The presence of migraine aura exacerbated migraine-related disability, mainly due to concurrent non-pain symptoms of migraine rather than the aura itself.

Major findings: The presence of aura on the first day of the migraine episode was significantly associated with increased odds of disability across all migraine days (odds ratio [OR] 1.40; P < .001); and non-pain symptoms, such as allodynia, photophobia, phonophobia, and nausea or vomiting (P < .001 for all). No association was observed between aura and headache-related migraine symptoms.

Study details: This observational prospective cohort study included 554 adults with episodic migraine, with complete data on migraine symptoms and psychological variables collected daily for 90 days using the N-1 Headache™ digital app (N = 11,156 total migraine days).

Disclosures: This study did not receive funding from any sources. The authors declared no conflicts of interest.

Source: Denney DE, Lee AA, Landy SH, Smitherman TA. Headache-related disability as a function of migraine aura: A daily diary study. Headache. 2024 (Aug 1). Doi: 10.1111/head.14796 Source

Key clinical point: The presence of migraine aura exacerbated migraine-related disability, mainly due to concurrent non-pain symptoms of migraine rather than the aura itself.

Major findings: The presence of aura on the first day of the migraine episode was significantly associated with increased odds of disability across all migraine days (odds ratio [OR] 1.40; P < .001); and non-pain symptoms, such as allodynia, photophobia, phonophobia, and nausea or vomiting (P < .001 for all). No association was observed between aura and headache-related migraine symptoms.

Study details: This observational prospective cohort study included 554 adults with episodic migraine, with complete data on migraine symptoms and psychological variables collected daily for 90 days using the N-1 Headache™ digital app (N = 11,156 total migraine days).

Disclosures: This study did not receive funding from any sources. The authors declared no conflicts of interest.

Source: Denney DE, Lee AA, Landy SH, Smitherman TA. Headache-related disability as a function of migraine aura: A daily diary study. Headache. 2024 (Aug 1). Doi: 10.1111/head.14796 Source

Key clinical point: The presence of migraine aura exacerbated migraine-related disability, mainly due to concurrent non-pain symptoms of migraine rather than the aura itself.

Major findings: The presence of aura on the first day of the migraine episode was significantly associated with increased odds of disability across all migraine days (odds ratio [OR] 1.40; P < .001); and non-pain symptoms, such as allodynia, photophobia, phonophobia, and nausea or vomiting (P < .001 for all). No association was observed between aura and headache-related migraine symptoms.

Study details: This observational prospective cohort study included 554 adults with episodic migraine, with complete data on migraine symptoms and psychological variables collected daily for 90 days using the N-1 Headache™ digital app (N = 11,156 total migraine days).

Disclosures: This study did not receive funding from any sources. The authors declared no conflicts of interest.

Source: Denney DE, Lee AA, Landy SH, Smitherman TA. Headache-related disability as a function of migraine aura: A daily diary study. Headache. 2024 (Aug 1). Doi: 10.1111/head.14796 Source

Key clinical point: Patients with migraine and a history of abuse had a greater migraine burden than those without a history of abuse, with this association being mediated by depression and anxiety.

Major findings: Patients with migraine who did vs did not have a history of abuse had significantly higher migraine-specific disability (68 vs 49), subjective cognitive impairment (10 vs 7), and pain interference (65 vs 62.5) scores, as well as greater overall work impairment (47.6% vs 38.6%) and activity impairment (49.3% vs 39.3%; all P < .001). Depression and anxiety mediated the association between history of abuse and migraine burden.

Study details: This cross-sectional study included 866 patients with migraine from the American Registry for Migraine Research, of whom 316 (36.5 %) had a history of abuse.

Disclosures: This study was supported by the American Migraine Foundation and American Academy of Neurology. Some authors declared receiving research funding from or having other ties with various sources.

Source: Trivedi M, Dumkrieger G, Chong CD, et al. A history of abuse is associated with more severe migraine- and pain-related disability: Results from the American Registry for Migraine Research. Headache. 2024 (Jul 25). Doi: 10.1111/head.14787 Source

Key clinical point: Patients with migraine and a history of abuse had a greater migraine burden than those without a history of abuse, with this association being mediated by depression and anxiety.

Major findings: Patients with migraine who did vs did not have a history of abuse had significantly higher migraine-specific disability (68 vs 49), subjective cognitive impairment (10 vs 7), and pain interference (65 vs 62.5) scores, as well as greater overall work impairment (47.6% vs 38.6%) and activity impairment (49.3% vs 39.3%; all P < .001). Depression and anxiety mediated the association between history of abuse and migraine burden.

Study details: This cross-sectional study included 866 patients with migraine from the American Registry for Migraine Research, of whom 316 (36.5 %) had a history of abuse.

Disclosures: This study was supported by the American Migraine Foundation and American Academy of Neurology. Some authors declared receiving research funding from or having other ties with various sources.

Source: Trivedi M, Dumkrieger G, Chong CD, et al. A history of abuse is associated with more severe migraine- and pain-related disability: Results from the American Registry for Migraine Research. Headache. 2024 (Jul 25). Doi: 10.1111/head.14787 Source

Key clinical point: Patients with migraine and a history of abuse had a greater migraine burden than those without a history of abuse, with this association being mediated by depression and anxiety.

Major findings: Patients with migraine who did vs did not have a history of abuse had significantly higher migraine-specific disability (68 vs 49), subjective cognitive impairment (10 vs 7), and pain interference (65 vs 62.5) scores, as well as greater overall work impairment (47.6% vs 38.6%) and activity impairment (49.3% vs 39.3%; all P < .001). Depression and anxiety mediated the association between history of abuse and migraine burden.

Study details: This cross-sectional study included 866 patients with migraine from the American Registry for Migraine Research, of whom 316 (36.5 %) had a history of abuse.

Disclosures: This study was supported by the American Migraine Foundation and American Academy of Neurology. Some authors declared receiving research funding from or having other ties with various sources.

Source: Trivedi M, Dumkrieger G, Chong CD, et al. A history of abuse is associated with more severe migraine- and pain-related disability: Results from the American Registry for Migraine Research. Headache. 2024 (Jul 25). Doi: 10.1111/head.14787 Source

Key clinical point: Anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) were effective and showed a similar time to onset in patients with chronic migraine (CM), irrespective of disease duration.

Major findings: At 10-12 months of follow-up, anti-CGRP mAb reduced monthly migraine days by an average of 12 days across all tertiles of CM duration (P = .946). Additionally, monthly headache days and acute medication use significantly decreased from baseline to 10-12 months (P < .001) across all tertiles of CM duration, indicating no difference in the time to onset of anti-CGRP mAb across tertiles.

Study details: This cohort study included 335 patients with CM treated with anti-CGRP mAb for at least 12 months. Patients were categorized into different tertiles of CM duration: 0-7 years, 8-18 years, and 18-60 years.

Disclosures: This study did not disclose any funding sources. Four authors declared receiving personal fees from or having other ties with various sources.

Source: Ornello R, Baldini F, Onofri A, et al. Impact of duration of chronic migraine on long-term effectiveness of monoclonal antibodies targeting the calcitonin gene-related peptide pathway-A real-world study. Headache. 2024 (Jul 16). Doi: 10.1111/head.14788 Source

Key clinical point: Anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) were effective and showed a similar time to onset in patients with chronic migraine (CM), irrespective of disease duration.

Major findings: At 10-12 months of follow-up, anti-CGRP mAb reduced monthly migraine days by an average of 12 days across all tertiles of CM duration (P = .946). Additionally, monthly headache days and acute medication use significantly decreased from baseline to 10-12 months (P < .001) across all tertiles of CM duration, indicating no difference in the time to onset of anti-CGRP mAb across tertiles.

Study details: This cohort study included 335 patients with CM treated with anti-CGRP mAb for at least 12 months. Patients were categorized into different tertiles of CM duration: 0-7 years, 8-18 years, and 18-60 years.

Disclosures: This study did not disclose any funding sources. Four authors declared receiving personal fees from or having other ties with various sources.

Source: Ornello R, Baldini F, Onofri A, et al. Impact of duration of chronic migraine on long-term effectiveness of monoclonal antibodies targeting the calcitonin gene-related peptide pathway-A real-world study. Headache. 2024 (Jul 16). Doi: 10.1111/head.14788 Source

Key clinical point: Anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) were effective and showed a similar time to onset in patients with chronic migraine (CM), irrespective of disease duration.

Major findings: At 10-12 months of follow-up, anti-CGRP mAb reduced monthly migraine days by an average of 12 days across all tertiles of CM duration (P = .946). Additionally, monthly headache days and acute medication use significantly decreased from baseline to 10-12 months (P < .001) across all tertiles of CM duration, indicating no difference in the time to onset of anti-CGRP mAb across tertiles.

Study details: This cohort study included 335 patients with CM treated with anti-CGRP mAb for at least 12 months. Patients were categorized into different tertiles of CM duration: 0-7 years, 8-18 years, and 18-60 years.

Disclosures: This study did not disclose any funding sources. Four authors declared receiving personal fees from or having other ties with various sources.

Source: Ornello R, Baldini F, Onofri A, et al. Impact of duration of chronic migraine on long-term effectiveness of monoclonal antibodies targeting the calcitonin gene-related peptide pathway-A real-world study. Headache. 2024 (Jul 16). Doi: 10.1111/head.14788 Source