Headache & Migraine

This transcript has been edited for clarity.

Dear colleagues, I am Christoph Diener from the faculty of medicine at the University of Duisburg-Essen in Germany.

Usually in this video series, I report on interesting scientific studies in the field of neurology published in the last month. But I have to admit, June was a lousy month for new science in neurology. Therefore, this month I’d like to take a different approach and tell you about a very interesting, old drug.

We are celebrating the 125th anniversary of aspirin. Aspirin was first synthesized in Wuppertal, Germany, a city which is only 40 km from my location, by Felix Hoffmann. Hoffmann was searching for a new drug for his father who suffered from severe joint pain, and the available drugs at that time had terrible adverse events. This prompted him to work on a new drug, which was later called aspirin acetylsalicylic acid.

Aspirin has been used very successfully to the present day as therapy for joint pain or arthritis. But as you know, it’s also effective in headaches, in particular, tension-type headache. I think it’s one of the most used drugs in the world for the treatment of acute migraine attacks.

It’s also available in some European countries in intravenous form for the treatment of severe migraine attacks or in the emergency room, and it’s as effective as subcutaneous sumatriptan. It’s also an effective migraine preventive drug in a dose of 300 mg/d.
 

Discovering aspirin’s antiplatelet activity

There was an interesting observation by a dentist in the 1930s, who noted bleeding when he extracted teeth in people who took aspirin for joint pain. When he started to ask his patients about possible bleeding complications and vascular events, he observed that people who took aspirin didn’t have coronary myocardial infarctions.

It took a long time for people to discover that aspirin is not only a pain medication but also an antiplatelet agent. The first randomized study that showed that aspirin is effective in secondary prevention after myocardial infarction was published in 1974 in The New England Journal of Medicine. In 1980, aspirin was approved by the U.S. Food and Drug Administration for the secondary prevention of stroke and in 1984 for secondary prevention after myocardial infarction.

A history of efficacy

Aspirin also has a proven role in the secondary prevention of transient ischemic attack and ischemic stroke. Given early, it reduces the risk for a recurrent vascular event by 50% and long-term, compared with placebo, by 20%.

Interestingly, the doses are different in different areas of the world. In the United States, it’s either 81 mg or 325 mg. In Europe, it’s usually 100 mg. Until a few years ago, there was no single trial which used 100 mg of aspirin, compared with placebo for the secondary prevention of stroke.

If we look at dual antiplatelet therapy, the combination of aspirin and clopidogrel was not superior to aspirin alone or clopidogrel alone for long-term prevention, but the combination of dipyridamole and aspirin and the combination of cilostazol and aspirin were superior to aspirin alone for secondary stroke prevention. Short-term, within the first 30 days, the combination of aspirin and clopidogrel and the combination of ticagrelor and aspirin is superior to monotherapy but also have an increased risk for bleeding.

People with atrial fibrillation or embolic strokes need to be anticoagulated, but the addition of aspirin to anticoagulation does not increase efficacy, it only increases the risk for bleeding.

In people above the age of 75 years who have to take aspirin, there is an increased risk for upper gastrointestinal bleeding. These patients should, in addition, receive proton pump inhibitors.

The use of aspirin for the primary prevention of vascular events was promoted for almost 50 years all over the world, but in the last 5 years, a number of randomized trials clearly showed that aspirin is not effective, compared with placebo, in the primary prevention of vascular event stroke, myocardial infarction, and vascular death. It only increases the risk for bleeding.

So it’s a clear separation. Aspirin should not be used for primary prevention of vascular events, but it should be used in basically everyone who doesn’t have contraindications for secondary prevention of vascular events and vascular death.

Ladies and gentlemen, a drug that is 125 years old is also still one of the most used and affordable drugs all around the world. It’s highly effective and has only a small risk for major bleeding complications. It’s really time to celebrate aspirin for this achievement.

Dr. Diener is professor, department of neurology, Stroke Center-Headache Center, University Duisburg-Essen (Germany). A complete list of his financial disclosures is available at the link below.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Dear colleagues, I am Christoph Diener from the faculty of medicine at the University of Duisburg-Essen in Germany.

Usually in this video series, I report on interesting scientific studies in the field of neurology published in the last month. But I have to admit, June was a lousy month for new science in neurology. Therefore, this month I’d like to take a different approach and tell you about a very interesting, old drug.

We are celebrating the 125th anniversary of aspirin. Aspirin was first synthesized in Wuppertal, Germany, a city which is only 40 km from my location, by Felix Hoffmann. Hoffmann was searching for a new drug for his father who suffered from severe joint pain, and the available drugs at that time had terrible adverse events. This prompted him to work on a new drug, which was later called aspirin acetylsalicylic acid.

Aspirin has been used very successfully to the present day as therapy for joint pain or arthritis. But as you know, it’s also effective in headaches, in particular, tension-type headache. I think it’s one of the most used drugs in the world for the treatment of acute migraine attacks.

It’s also available in some European countries in intravenous form for the treatment of severe migraine attacks or in the emergency room, and it’s as effective as subcutaneous sumatriptan. It’s also an effective migraine preventive drug in a dose of 300 mg/d.
 

Discovering aspirin’s antiplatelet activity

There was an interesting observation by a dentist in the 1930s, who noted bleeding when he extracted teeth in people who took aspirin for joint pain. When he started to ask his patients about possible bleeding complications and vascular events, he observed that people who took aspirin didn’t have coronary myocardial infarctions.

It took a long time for people to discover that aspirin is not only a pain medication but also an antiplatelet agent. The first randomized study that showed that aspirin is effective in secondary prevention after myocardial infarction was published in 1974 in The New England Journal of Medicine. In 1980, aspirin was approved by the U.S. Food and Drug Administration for the secondary prevention of stroke and in 1984 for secondary prevention after myocardial infarction.

A history of efficacy

Aspirin also has a proven role in the secondary prevention of transient ischemic attack and ischemic stroke. Given early, it reduces the risk for a recurrent vascular event by 50% and long-term, compared with placebo, by 20%.

Interestingly, the doses are different in different areas of the world. In the United States, it’s either 81 mg or 325 mg. In Europe, it’s usually 100 mg. Until a few years ago, there was no single trial which used 100 mg of aspirin, compared with placebo for the secondary prevention of stroke.

If we look at dual antiplatelet therapy, the combination of aspirin and clopidogrel was not superior to aspirin alone or clopidogrel alone for long-term prevention, but the combination of dipyridamole and aspirin and the combination of cilostazol and aspirin were superior to aspirin alone for secondary stroke prevention. Short-term, within the first 30 days, the combination of aspirin and clopidogrel and the combination of ticagrelor and aspirin is superior to monotherapy but also have an increased risk for bleeding.

People with atrial fibrillation or embolic strokes need to be anticoagulated, but the addition of aspirin to anticoagulation does not increase efficacy, it only increases the risk for bleeding.

In people above the age of 75 years who have to take aspirin, there is an increased risk for upper gastrointestinal bleeding. These patients should, in addition, receive proton pump inhibitors.

The use of aspirin for the primary prevention of vascular events was promoted for almost 50 years all over the world, but in the last 5 years, a number of randomized trials clearly showed that aspirin is not effective, compared with placebo, in the primary prevention of vascular event stroke, myocardial infarction, and vascular death. It only increases the risk for bleeding.

So it’s a clear separation. Aspirin should not be used for primary prevention of vascular events, but it should be used in basically everyone who doesn’t have contraindications for secondary prevention of vascular events and vascular death.

Ladies and gentlemen, a drug that is 125 years old is also still one of the most used and affordable drugs all around the world. It’s highly effective and has only a small risk for major bleeding complications. It’s really time to celebrate aspirin for this achievement.

Dr. Diener is professor, department of neurology, Stroke Center-Headache Center, University Duisburg-Essen (Germany). A complete list of his financial disclosures is available at the link below.

A version of this article first appeared on Medscape.com.

This transcript has been edited for clarity.

Dear colleagues, I am Christoph Diener from the faculty of medicine at the University of Duisburg-Essen in Germany.

Usually in this video series, I report on interesting scientific studies in the field of neurology published in the last month. But I have to admit, June was a lousy month for new science in neurology. Therefore, this month I’d like to take a different approach and tell you about a very interesting, old drug.

We are celebrating the 125th anniversary of aspirin. Aspirin was first synthesized in Wuppertal, Germany, a city which is only 40 km from my location, by Felix Hoffmann. Hoffmann was searching for a new drug for his father who suffered from severe joint pain, and the available drugs at that time had terrible adverse events. This prompted him to work on a new drug, which was later called aspirin acetylsalicylic acid.

Aspirin has been used very successfully to the present day as therapy for joint pain or arthritis. But as you know, it’s also effective in headaches, in particular, tension-type headache. I think it’s one of the most used drugs in the world for the treatment of acute migraine attacks.

It’s also available in some European countries in intravenous form for the treatment of severe migraine attacks or in the emergency room, and it’s as effective as subcutaneous sumatriptan. It’s also an effective migraine preventive drug in a dose of 300 mg/d.
 

Discovering aspirin’s antiplatelet activity

There was an interesting observation by a dentist in the 1930s, who noted bleeding when he extracted teeth in people who took aspirin for joint pain. When he started to ask his patients about possible bleeding complications and vascular events, he observed that people who took aspirin didn’t have coronary myocardial infarctions.

It took a long time for people to discover that aspirin is not only a pain medication but also an antiplatelet agent. The first randomized study that showed that aspirin is effective in secondary prevention after myocardial infarction was published in 1974 in The New England Journal of Medicine. In 1980, aspirin was approved by the U.S. Food and Drug Administration for the secondary prevention of stroke and in 1984 for secondary prevention after myocardial infarction.

A history of efficacy

Aspirin also has a proven role in the secondary prevention of transient ischemic attack and ischemic stroke. Given early, it reduces the risk for a recurrent vascular event by 50% and long-term, compared with placebo, by 20%.

Interestingly, the doses are different in different areas of the world. In the United States, it’s either 81 mg or 325 mg. In Europe, it’s usually 100 mg. Until a few years ago, there was no single trial which used 100 mg of aspirin, compared with placebo for the secondary prevention of stroke.

If we look at dual antiplatelet therapy, the combination of aspirin and clopidogrel was not superior to aspirin alone or clopidogrel alone for long-term prevention, but the combination of dipyridamole and aspirin and the combination of cilostazol and aspirin were superior to aspirin alone for secondary stroke prevention. Short-term, within the first 30 days, the combination of aspirin and clopidogrel and the combination of ticagrelor and aspirin is superior to monotherapy but also have an increased risk for bleeding.

People with atrial fibrillation or embolic strokes need to be anticoagulated, but the addition of aspirin to anticoagulation does not increase efficacy, it only increases the risk for bleeding.

In people above the age of 75 years who have to take aspirin, there is an increased risk for upper gastrointestinal bleeding. These patients should, in addition, receive proton pump inhibitors.

The use of aspirin for the primary prevention of vascular events was promoted for almost 50 years all over the world, but in the last 5 years, a number of randomized trials clearly showed that aspirin is not effective, compared with placebo, in the primary prevention of vascular event stroke, myocardial infarction, and vascular death. It only increases the risk for bleeding.

So it’s a clear separation. Aspirin should not be used for primary prevention of vascular events, but it should be used in basically everyone who doesn’t have contraindications for secondary prevention of vascular events and vascular death.

Ladies and gentlemen, a drug that is 125 years old is also still one of the most used and affordable drugs all around the world. It’s highly effective and has only a small risk for major bleeding complications. It’s really time to celebrate aspirin for this achievement.

Dr. Diener is professor, department of neurology, Stroke Center-Headache Center, University Duisburg-Essen (Germany). A complete list of his financial disclosures is available at the link below.

A version of this article first appeared on Medscape.com.

Key clinical point: External concurrent occipital and trigeminal neurostimulation (eCOT-NS) was well tolerated, safe, and an effective treatment that provided fast and durable relief and freedom from pain in patients with migraine with or without aura.

Major finding: A significantly higher proportion of patients in the active vs sham eCOT-NS arm reported pain relief after 2 hours of treatment initiation (60% vs 37%; P  =  .018), freedom from pain at 2 hours after treatment initiation without any rescue medication (46% vs 12%; P < .001), and improvement in their most bothersome symptom (81% vs 60%; P  =  .047). No serious adverse events were reported.

Study details: Findings are from the RIME study, a randomized, double-blind, sham-controlled study including 187 adults with migraine with or without aura who were randomly assigned to receive active (n = 94) or sham (n = 93) eCOT-NS.

Disclosures: This study was supported by Neurolief Ltd. Several authors reported receiving research grants or honoraria or serving as consultants or advisory board members for various sources, including Neurolief Ltd.

Source: Tepper SJ et al. Migraine treatment with external concurrent occipital and trigeminal neurostimulation—A randomized controlled trial. Headache. 2022 (Jun 24). Doi:  10.1111/head.14350

Key clinical point: External concurrent occipital and trigeminal neurostimulation (eCOT-NS) was well tolerated, safe, and an effective treatment that provided fast and durable relief and freedom from pain in patients with migraine with or without aura.

Major finding: A significantly higher proportion of patients in the active vs sham eCOT-NS arm reported pain relief after 2 hours of treatment initiation (60% vs 37%; P  =  .018), freedom from pain at 2 hours after treatment initiation without any rescue medication (46% vs 12%; P < .001), and improvement in their most bothersome symptom (81% vs 60%; P  =  .047). No serious adverse events were reported.

Study details: Findings are from the RIME study, a randomized, double-blind, sham-controlled study including 187 adults with migraine with or without aura who were randomly assigned to receive active (n = 94) or sham (n = 93) eCOT-NS.

Disclosures: This study was supported by Neurolief Ltd. Several authors reported receiving research grants or honoraria or serving as consultants or advisory board members for various sources, including Neurolief Ltd.

Source: Tepper SJ et al. Migraine treatment with external concurrent occipital and trigeminal neurostimulation—A randomized controlled trial. Headache. 2022 (Jun 24). Doi:  10.1111/head.14350

Key clinical point: External concurrent occipital and trigeminal neurostimulation (eCOT-NS) was well tolerated, safe, and an effective treatment that provided fast and durable relief and freedom from pain in patients with migraine with or without aura.

Major finding: A significantly higher proportion of patients in the active vs sham eCOT-NS arm reported pain relief after 2 hours of treatment initiation (60% vs 37%; P  =  .018), freedom from pain at 2 hours after treatment initiation without any rescue medication (46% vs 12%; P < .001), and improvement in their most bothersome symptom (81% vs 60%; P  =  .047). No serious adverse events were reported.

Study details: Findings are from the RIME study, a randomized, double-blind, sham-controlled study including 187 adults with migraine with or without aura who were randomly assigned to receive active (n = 94) or sham (n = 93) eCOT-NS.

Disclosures: This study was supported by Neurolief Ltd. Several authors reported receiving research grants or honoraria or serving as consultants or advisory board members for various sources, including Neurolief Ltd.

Source: Tepper SJ et al. Migraine treatment with external concurrent occipital and trigeminal neurostimulation—A randomized controlled trial. Headache. 2022 (Jun 24). Doi:  10.1111/head.14350

Key clinical point: Vitamin D3 (5000 IU daily) supplementation as an adjuvant therapy to topiramate was well tolerated and safe, and an effective strategy for pediatric migraine prophylaxis.

Major finding: After 16 weeks of treatment, the monthly headache frequency (6.23 vs 9.79 attacks/month; P  =  .01) and disability from headache score (17.56 vs 25.18; P  =  .04) were significantly lower in the vitamin D3 supplementation vs placebo group, with >50% decrease in the monthly headache attack frequency being reported by a significantly higher proportion of patients receiving vitamin D3 supplementation vs placebo (75.0% vs 53.5%; P  =  .01) and no serious adverse events being reported.

Study details: The findings are from a double-blind, prospective case-control study including 60 children and adolescents (aged 5-14 years) with migraine who were randomly assigned to receive topiramate with vitamin D3 supplementation or placebo.

Disclosures: This study did not receive any financial support. The authors declared no competing interests.

Source: Elmala MK et al. The impact of vitamin D₃ supplementation to topiramate therapy on pediatric migraine prophylaxis. J Child Neurol. 2022 (Jun 22). Doi: 10.1177/08830738221092882

Key clinical point: Vitamin D3 (5000 IU daily) supplementation as an adjuvant therapy to topiramate was well tolerated and safe, and an effective strategy for pediatric migraine prophylaxis.

Major finding: After 16 weeks of treatment, the monthly headache frequency (6.23 vs 9.79 attacks/month; P  =  .01) and disability from headache score (17.56 vs 25.18; P  =  .04) were significantly lower in the vitamin D3 supplementation vs placebo group, with >50% decrease in the monthly headache attack frequency being reported by a significantly higher proportion of patients receiving vitamin D3 supplementation vs placebo (75.0% vs 53.5%; P  =  .01) and no serious adverse events being reported.

Study details: The findings are from a double-blind, prospective case-control study including 60 children and adolescents (aged 5-14 years) with migraine who were randomly assigned to receive topiramate with vitamin D3 supplementation or placebo.

Disclosures: This study did not receive any financial support. The authors declared no competing interests.

Source: Elmala MK et al. The impact of vitamin D₃ supplementation to topiramate therapy on pediatric migraine prophylaxis. J Child Neurol. 2022 (Jun 22). Doi: 10.1177/08830738221092882

Key clinical point: Vitamin D3 (5000 IU daily) supplementation as an adjuvant therapy to topiramate was well tolerated and safe, and an effective strategy for pediatric migraine prophylaxis.

Major finding: After 16 weeks of treatment, the monthly headache frequency (6.23 vs 9.79 attacks/month; P  =  .01) and disability from headache score (17.56 vs 25.18; P  =  .04) were significantly lower in the vitamin D3 supplementation vs placebo group, with >50% decrease in the monthly headache attack frequency being reported by a significantly higher proportion of patients receiving vitamin D3 supplementation vs placebo (75.0% vs 53.5%; P  =  .01) and no serious adverse events being reported.

Study details: The findings are from a double-blind, prospective case-control study including 60 children and adolescents (aged 5-14 years) with migraine who were randomly assigned to receive topiramate with vitamin D3 supplementation or placebo.

Disclosures: This study did not receive any financial support. The authors declared no competing interests.

Source: Elmala MK et al. The impact of vitamin D₃ supplementation to topiramate therapy on pediatric migraine prophylaxis. J Child Neurol. 2022 (Jun 22). Doi: 10.1177/08830738221092882

Key clinical point: Oral calcitonin gene-related peptide (CGRP) receptor antagonists appeared to be safer and better tolerated than triptans for the treatment of acute migraine and could be a viable option for patients who experience overall triptan-associated adverse events (AE).

Major finding: Oral CGRP receptor antagonists were safer than triptans in terms of any AE (risk ratio [RR] 0.78; P  =  .03) and treatment-related AE (RR 0.68; P < .00001), with the incidence of dizziness (RR 0.69; P  =  .01), dry mouth (RR 0.72; P  =  .02), fatigue (RR 0.52; P  =  .001), paresthesia (RR 0.34; P < .0001), and somnolence (RR 0.65; P  =  .004) being lower with oral CGRP receptor antagonists vs triptans.

Study details: The data come from a meta-analysis of 15 trials including 13,270 patients who received oral CGRP receptor antagonists (n = 8240), placebo (n = 4253), or triptans (n = 777) for the treatment of acute migraine.

Disclosures: This study was funded by a National Research Foundation of Korea grant funded by the Korea government. The authors declared no competing interests.

Source: Lee S et al. Safety evaluation of oral calcitonin-gene–related peptide receptor antagonists in patients with acute migraine: A systematic review and meta-analysis. Eur J Clin Pharmacol. 2022 (Jun 22). Doi: 10.1007/s00228-022-03347-6

Key clinical point: Oral calcitonin gene-related peptide (CGRP) receptor antagonists appeared to be safer and better tolerated than triptans for the treatment of acute migraine and could be a viable option for patients who experience overall triptan-associated adverse events (AE).

Major finding: Oral CGRP receptor antagonists were safer than triptans in terms of any AE (risk ratio [RR] 0.78; P  =  .03) and treatment-related AE (RR 0.68; P < .00001), with the incidence of dizziness (RR 0.69; P  =  .01), dry mouth (RR 0.72; P  =  .02), fatigue (RR 0.52; P  =  .001), paresthesia (RR 0.34; P < .0001), and somnolence (RR 0.65; P  =  .004) being lower with oral CGRP receptor antagonists vs triptans.

Study details: The data come from a meta-analysis of 15 trials including 13,270 patients who received oral CGRP receptor antagonists (n = 8240), placebo (n = 4253), or triptans (n = 777) for the treatment of acute migraine.

Disclosures: This study was funded by a National Research Foundation of Korea grant funded by the Korea government. The authors declared no competing interests.

Source: Lee S et al. Safety evaluation of oral calcitonin-gene–related peptide receptor antagonists in patients with acute migraine: A systematic review and meta-analysis. Eur J Clin Pharmacol. 2022 (Jun 22). Doi: 10.1007/s00228-022-03347-6

Key clinical point: Oral calcitonin gene-related peptide (CGRP) receptor antagonists appeared to be safer and better tolerated than triptans for the treatment of acute migraine and could be a viable option for patients who experience overall triptan-associated adverse events (AE).

Major finding: Oral CGRP receptor antagonists were safer than triptans in terms of any AE (risk ratio [RR] 0.78; P  =  .03) and treatment-related AE (RR 0.68; P < .00001), with the incidence of dizziness (RR 0.69; P  =  .01), dry mouth (RR 0.72; P  =  .02), fatigue (RR 0.52; P  =  .001), paresthesia (RR 0.34; P < .0001), and somnolence (RR 0.65; P  =  .004) being lower with oral CGRP receptor antagonists vs triptans.

Study details: The data come from a meta-analysis of 15 trials including 13,270 patients who received oral CGRP receptor antagonists (n = 8240), placebo (n = 4253), or triptans (n = 777) for the treatment of acute migraine.

Disclosures: This study was funded by a National Research Foundation of Korea grant funded by the Korea government. The authors declared no competing interests.

Source: Lee S et al. Safety evaluation of oral calcitonin-gene–related peptide receptor antagonists in patients with acute migraine: A systematic review and meta-analysis. Eur J Clin Pharmacol. 2022 (Jun 22). Doi: 10.1007/s00228-022-03347-6

Key clinical point: Levetiracetam reduced attack frequency, headache days, and days with acute drug intake as the prophylactic treatment for episodic migraine along with an overall tolerable safety profile.

Major finding: During the last 4 weeks of treatment, levetiracetam significantly reduced the number of migraine attacks (P < .001), days with migraine (P  =  .001), and use of acute drugs for migraine attack (P < .001), with 46.0% of patients showing at least 50% reduction in migraine attack frequency and the mean number of migraine attacks decreasing from 5.2 ± 2.1 to 3.4 ± 2.7.

Study details: The data come from a prospective, open-label study including 50 patients with episodic migraine who received 1000 mg levetiracetam (starting dose 500 mg) twice a day for 12 weeks.

Disclosures: This study was supported by UCB Chemie GmbH Germany. Some authors declared serving as consultants for various sources.

Source: Evers S et al. Levetiracetam in the prophylactic treatment of episodic migraine: A prospective open label study. Cephalalgia. 2022 (May 27). Doi: 10.1177/03331024221103815

Key clinical point: Levetiracetam reduced attack frequency, headache days, and days with acute drug intake as the prophylactic treatment for episodic migraine along with an overall tolerable safety profile.

Major finding: During the last 4 weeks of treatment, levetiracetam significantly reduced the number of migraine attacks (P < .001), days with migraine (P  =  .001), and use of acute drugs for migraine attack (P < .001), with 46.0% of patients showing at least 50% reduction in migraine attack frequency and the mean number of migraine attacks decreasing from 5.2 ± 2.1 to 3.4 ± 2.7.

Study details: The data come from a prospective, open-label study including 50 patients with episodic migraine who received 1000 mg levetiracetam (starting dose 500 mg) twice a day for 12 weeks.

Disclosures: This study was supported by UCB Chemie GmbH Germany. Some authors declared serving as consultants for various sources.

Source: Evers S et al. Levetiracetam in the prophylactic treatment of episodic migraine: A prospective open label study. Cephalalgia. 2022 (May 27). Doi: 10.1177/03331024221103815

Key clinical point: Levetiracetam reduced attack frequency, headache days, and days with acute drug intake as the prophylactic treatment for episodic migraine along with an overall tolerable safety profile.

Major finding: During the last 4 weeks of treatment, levetiracetam significantly reduced the number of migraine attacks (P < .001), days with migraine (P  =  .001), and use of acute drugs for migraine attack (P < .001), with 46.0% of patients showing at least 50% reduction in migraine attack frequency and the mean number of migraine attacks decreasing from 5.2 ± 2.1 to 3.4 ± 2.7.

Study details: The data come from a prospective, open-label study including 50 patients with episodic migraine who received 1000 mg levetiracetam (starting dose 500 mg) twice a day for 12 weeks.

Disclosures: This study was supported by UCB Chemie GmbH Germany. Some authors declared serving as consultants for various sources.

Source: Evers S et al. Levetiracetam in the prophylactic treatment of episodic migraine: A prospective open label study. Cephalalgia. 2022 (May 27). Doi: 10.1177/03331024221103815

Key clinical point: Once-daily oral atogepant was overall safe and effective for the prevention of episodic migraine in adults.

Major finding: The reduction in the mean number of migraine days across the 12-week treatment period was significantly greater with 10 mg atogepant (mean difference [MD] −1.16; P < .001), 30 mg (MD −1.15; P < .001), or 60 mg (MD −1.20; P  =  .016) vs placebo. Overall, the relative risk for any adverse event with atogepant vs placebo treatment was 1.07 (P  =  .630).

Study details: The data come from a systematic review and meta-analysis of 2 randomized controlled trials including 1550 patients with episodic migraine who were randomly assigned to receive 10 mg atopegant (n = 314), 30 mg atogepant (n = 411), 60 mg atopegant (n = 417), or placebo (n = 408).

Disclosures: This study did not receive any funding. Some authors declared receiving grants or serving as speakers, consultants, or on advisory boards for various sources.

Source: Lattanzi S et al. Atogepant for the prevention of episodic migraine in adults: A systematic review and meta-analysis of efficacy and safety. Neurol Ther. 2022 (Jun 15). Doi:  10.1007/s40120-022-00370-8

Key clinical point: Once-daily oral atogepant was overall safe and effective for the prevention of episodic migraine in adults.

Major finding: The reduction in the mean number of migraine days across the 12-week treatment period was significantly greater with 10 mg atogepant (mean difference [MD] −1.16; P < .001), 30 mg (MD −1.15; P < .001), or 60 mg (MD −1.20; P  =  .016) vs placebo. Overall, the relative risk for any adverse event with atogepant vs placebo treatment was 1.07 (P  =  .630).

Study details: The data come from a systematic review and meta-analysis of 2 randomized controlled trials including 1550 patients with episodic migraine who were randomly assigned to receive 10 mg atopegant (n = 314), 30 mg atogepant (n = 411), 60 mg atopegant (n = 417), or placebo (n = 408).

Disclosures: This study did not receive any funding. Some authors declared receiving grants or serving as speakers, consultants, or on advisory boards for various sources.

Source: Lattanzi S et al. Atogepant for the prevention of episodic migraine in adults: A systematic review and meta-analysis of efficacy and safety. Neurol Ther. 2022 (Jun 15). Doi:  10.1007/s40120-022-00370-8

Key clinical point: Once-daily oral atogepant was overall safe and effective for the prevention of episodic migraine in adults.

Major finding: The reduction in the mean number of migraine days across the 12-week treatment period was significantly greater with 10 mg atogepant (mean difference [MD] −1.16; P < .001), 30 mg (MD −1.15; P < .001), or 60 mg (MD −1.20; P  =  .016) vs placebo. Overall, the relative risk for any adverse event with atogepant vs placebo treatment was 1.07 (P  =  .630).

Study details: The data come from a systematic review and meta-analysis of 2 randomized controlled trials including 1550 patients with episodic migraine who were randomly assigned to receive 10 mg atopegant (n = 314), 30 mg atogepant (n = 411), 60 mg atopegant (n = 417), or placebo (n = 408).

Disclosures: This study did not receive any funding. Some authors declared receiving grants or serving as speakers, consultants, or on advisory boards for various sources.

Source: Lattanzi S et al. Atogepant for the prevention of episodic migraine in adults: A systematic review and meta-analysis of efficacy and safety. Neurol Ther. 2022 (Jun 15). Doi:  10.1007/s40120-022-00370-8

Key clinical point: Calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating polypeptide-38 (PACAP-38) could serve as effective diagnostic biomarkers for pediatric migraine.

Major finding: The plasma levels of CGRP and PACAP-38 were significantly higher in patients with migraine in the ictal and interictal periods and with and without aura compared with healthy controls (P < .001), with PACAP-38 (adjusted odds ratio [aOR] 1.331; P < .001) and CGRP (aOR 1.113; P < .001) being independent risk factors for the diagnosis of pediatric migraine.

Study details: This was a prospective study of 76 patients aged 4-18 years with migraine and 77 age-matched healthy controls.

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

Source: Liu J et al. CGRP and PACAP-38 play an important role in diagnosing pediatric migraine. J Headache Pain. 2022;23:68 (Jun 13). Doi: 10.1186/s10194-022-01435-7

Key clinical point: Calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating polypeptide-38 (PACAP-38) could serve as effective diagnostic biomarkers for pediatric migraine.

Major finding: The plasma levels of CGRP and PACAP-38 were significantly higher in patients with migraine in the ictal and interictal periods and with and without aura compared with healthy controls (P < .001), with PACAP-38 (adjusted odds ratio [aOR] 1.331; P < .001) and CGRP (aOR 1.113; P < .001) being independent risk factors for the diagnosis of pediatric migraine.

Study details: This was a prospective study of 76 patients aged 4-18 years with migraine and 77 age-matched healthy controls.

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

Source: Liu J et al. CGRP and PACAP-38 play an important role in diagnosing pediatric migraine. J Headache Pain. 2022;23:68 (Jun 13). Doi: 10.1186/s10194-022-01435-7

Key clinical point: Calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase-activating polypeptide-38 (PACAP-38) could serve as effective diagnostic biomarkers for pediatric migraine.

Major finding: The plasma levels of CGRP and PACAP-38 were significantly higher in patients with migraine in the ictal and interictal periods and with and without aura compared with healthy controls (P < .001), with PACAP-38 (adjusted odds ratio [aOR] 1.331; P < .001) and CGRP (aOR 1.113; P < .001) being independent risk factors for the diagnosis of pediatric migraine.

Study details: This was a prospective study of 76 patients aged 4-18 years with migraine and 77 age-matched healthy controls.

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

Source: Liu J et al. CGRP and PACAP-38 play an important role in diagnosing pediatric migraine. J Headache Pain. 2022;23:68 (Jun 13). Doi: 10.1186/s10194-022-01435-7

Key clinical point: Migraine was significantly associated with the incidence of ocular motor cranial nerve palsy (OMCNP), with the risk being particularly high among patients with migraine who smoked or had diabetes mellitus.

Major finding: The incidence of OMCNP was significantly higher in patients with vs without migraine (adjusted hazard ratio [aHR] 1.166; 95% CI 1.013-1.343), with the association being strongest among those who smoked (aHR 1.426; 95% CI 1.127-1.803) and had diabetes mellitus (aHR 1.378; 95% CI 1.045-1.378).

Study details: This was a population-based, observational, retrospective cohort study including 4,053,824 medical beneficiaries; of which 5806 developed OMCNP and 4,048,018 did not develop OMCNP (control population). A subgroup of 111,853 patients had migraine.

Disclosures: This study was supported by a National Research Foundation of Korea grant funded by the Korea government and others. The authors declared no conflicts of interest.

Source: Rhiu S et al. Association between migraine and risk of ocular motor cranial nerve palsy. Sci Rep. 2022;12:10512 (Jun 22). Doi: 10.1038/s41598-022-14621-z

Key clinical point: Migraine was significantly associated with the incidence of ocular motor cranial nerve palsy (OMCNP), with the risk being particularly high among patients with migraine who smoked or had diabetes mellitus.

Major finding: The incidence of OMCNP was significantly higher in patients with vs without migraine (adjusted hazard ratio [aHR] 1.166; 95% CI 1.013-1.343), with the association being strongest among those who smoked (aHR 1.426; 95% CI 1.127-1.803) and had diabetes mellitus (aHR 1.378; 95% CI 1.045-1.378).

Study details: This was a population-based, observational, retrospective cohort study including 4,053,824 medical beneficiaries; of which 5806 developed OMCNP and 4,048,018 did not develop OMCNP (control population). A subgroup of 111,853 patients had migraine.

Disclosures: This study was supported by a National Research Foundation of Korea grant funded by the Korea government and others. The authors declared no conflicts of interest.

Source: Rhiu S et al. Association between migraine and risk of ocular motor cranial nerve palsy. Sci Rep. 2022;12:10512 (Jun 22). Doi: 10.1038/s41598-022-14621-z

Key clinical point: Migraine was significantly associated with the incidence of ocular motor cranial nerve palsy (OMCNP), with the risk being particularly high among patients with migraine who smoked or had diabetes mellitus.

Major finding: The incidence of OMCNP was significantly higher in patients with vs without migraine (adjusted hazard ratio [aHR] 1.166; 95% CI 1.013-1.343), with the association being strongest among those who smoked (aHR 1.426; 95% CI 1.127-1.803) and had diabetes mellitus (aHR 1.378; 95% CI 1.045-1.378).

Study details: This was a population-based, observational, retrospective cohort study including 4,053,824 medical beneficiaries; of which 5806 developed OMCNP and 4,048,018 did not develop OMCNP (control population). A subgroup of 111,853 patients had migraine.

Disclosures: This study was supported by a National Research Foundation of Korea grant funded by the Korea government and others. The authors declared no conflicts of interest.

Source: Rhiu S et al. Association between migraine and risk of ocular motor cranial nerve palsy. Sci Rep. 2022;12:10512 (Jun 22). Doi: 10.1038/s41598-022-14621-z

Key clinical point: Treatment of a single migraine attack with 200 mg lasmiditan demonstrated a strong association between achieving freedom from pain and central nervous system common treatment-emergent adverse events (CTEAE).

Major finding: Significantly higher proportion of patients treated with 200 mg lasmiditan who were pain-free vs those who experienced moderate-to-severe pain at 2 hours post-dose reported ≥1 CTEAE (48.2% vs 28.7%; P < .001). A significantly higher proportion of patients reporting ≥1 vs 0 CTEAE were pain-free at 2 hours (39.0% vs 30.2%; P < .001). However, the absence of CTAE did not translate to the lack of efficacy.

Study details: This was a post hoc analysis of 4 randomized phase 2/3 trials including 6602 patients with migraine with or without aura who received lasmiditan (50, 100, or 200 mg) or placebo.

Disclosures: This study was funded by Eli Lilly and Company. Six authors reported being employees and minor stockholders of Eli Lilly. RB Lipton reported ties with Eli Lilly and other sources and owning stock or stock options in 3 companies.

Source: Doty EG et al. The association between the occurrence of common treatment-emergent adverse events and efficacy outcomes after lasmiditan treatment of a single migraine attack: Secondary analyses from four pooled randomized clinical trials. CNS Drugs. 2022;36:771–783 (Jul 2). Doi: 10.1007/s40263-022-00928-y

Key clinical point: Treatment of a single migraine attack with 200 mg lasmiditan demonstrated a strong association between achieving freedom from pain and central nervous system common treatment-emergent adverse events (CTEAE).

Major finding: Significantly higher proportion of patients treated with 200 mg lasmiditan who were pain-free vs those who experienced moderate-to-severe pain at 2 hours post-dose reported ≥1 CTEAE (48.2% vs 28.7%; P < .001). A significantly higher proportion of patients reporting ≥1 vs 0 CTEAE were pain-free at 2 hours (39.0% vs 30.2%; P < .001). However, the absence of CTAE did not translate to the lack of efficacy.

Study details: This was a post hoc analysis of 4 randomized phase 2/3 trials including 6602 patients with migraine with or without aura who received lasmiditan (50, 100, or 200 mg) or placebo.

Disclosures: This study was funded by Eli Lilly and Company. Six authors reported being employees and minor stockholders of Eli Lilly. RB Lipton reported ties with Eli Lilly and other sources and owning stock or stock options in 3 companies.

Source: Doty EG et al. The association between the occurrence of common treatment-emergent adverse events and efficacy outcomes after lasmiditan treatment of a single migraine attack: Secondary analyses from four pooled randomized clinical trials. CNS Drugs. 2022;36:771–783 (Jul 2). Doi: 10.1007/s40263-022-00928-y

Key clinical point: Treatment of a single migraine attack with 200 mg lasmiditan demonstrated a strong association between achieving freedom from pain and central nervous system common treatment-emergent adverse events (CTEAE).

Major finding: Significantly higher proportion of patients treated with 200 mg lasmiditan who were pain-free vs those who experienced moderate-to-severe pain at 2 hours post-dose reported ≥1 CTEAE (48.2% vs 28.7%; P < .001). A significantly higher proportion of patients reporting ≥1 vs 0 CTEAE were pain-free at 2 hours (39.0% vs 30.2%; P < .001). However, the absence of CTAE did not translate to the lack of efficacy.

Study details: This was a post hoc analysis of 4 randomized phase 2/3 trials including 6602 patients with migraine with or without aura who received lasmiditan (50, 100, or 200 mg) or placebo.

Disclosures: This study was funded by Eli Lilly and Company. Six authors reported being employees and minor stockholders of Eli Lilly. RB Lipton reported ties with Eli Lilly and other sources and owning stock or stock options in 3 companies.

Source: Doty EG et al. The association between the occurrence of common treatment-emergent adverse events and efficacy outcomes after lasmiditan treatment of a single migraine attack: Secondary analyses from four pooled randomized clinical trials. CNS Drugs. 2022;36:771–783 (Jul 2). Doi: 10.1007/s40263-022-00928-y

Key clinical point: Long-term treatment with galcanezumab led to three-quarters of patients with chronic migraine (CM) reverting to episodic migraine (EM), with more than half persistently reverting to episodic migraine (EM) under real-life conditions.

Major finding: Over 1 year, approximately ≥75% of patients reverted from CM to EM at each visit, with persistent reversion from CM to EM and medium-to-low frequency EM being reported by 52.3% and 20.6% of patients, respectively. Older age at onset (P  =  .01) and less frequent baseline monthly migraine days (P  =  .005) significantly increased the reversion frequency to EM.

Study details: Findings are from a 12-month observational, longitudinal cohort study, GARLIT, including 155 patients with CM who received galcanezumab.

Disclosures: This study did not receive any specific funding. Several authors reported receiving grants or honoraria from various sources.

Source: Altamura C et al for the GARLIT Study Group. Conversion from chronic to episodic migraine in patients treated with galcanezumab in real life in Italy: The 12-month observational, longitudinal, cohort multicenter GARLIT experience. J Neurol. 2022 (Jun 28). Doi: 10.1007/s00415-022-11226-4

Key clinical point: Long-term treatment with galcanezumab led to three-quarters of patients with chronic migraine (CM) reverting to episodic migraine (EM), with more than half persistently reverting to episodic migraine (EM) under real-life conditions.

Major finding: Over 1 year, approximately ≥75% of patients reverted from CM to EM at each visit, with persistent reversion from CM to EM and medium-to-low frequency EM being reported by 52.3% and 20.6% of patients, respectively. Older age at onset (P  =  .01) and less frequent baseline monthly migraine days (P  =  .005) significantly increased the reversion frequency to EM.

Study details: Findings are from a 12-month observational, longitudinal cohort study, GARLIT, including 155 patients with CM who received galcanezumab.

Disclosures: This study did not receive any specific funding. Several authors reported receiving grants or honoraria from various sources.

Source: Altamura C et al for the GARLIT Study Group. Conversion from chronic to episodic migraine in patients treated with galcanezumab in real life in Italy: The 12-month observational, longitudinal, cohort multicenter GARLIT experience. J Neurol. 2022 (Jun 28). Doi: 10.1007/s00415-022-11226-4

Key clinical point: Long-term treatment with galcanezumab led to three-quarters of patients with chronic migraine (CM) reverting to episodic migraine (EM), with more than half persistently reverting to episodic migraine (EM) under real-life conditions.

Major finding: Over 1 year, approximately ≥75% of patients reverted from CM to EM at each visit, with persistent reversion from CM to EM and medium-to-low frequency EM being reported by 52.3% and 20.6% of patients, respectively. Older age at onset (P  =  .01) and less frequent baseline monthly migraine days (P  =  .005) significantly increased the reversion frequency to EM.

Study details: Findings are from a 12-month observational, longitudinal cohort study, GARLIT, including 155 patients with CM who received galcanezumab.

Disclosures: This study did not receive any specific funding. Several authors reported receiving grants or honoraria from various sources.

Source: Altamura C et al for the GARLIT Study Group. Conversion from chronic to episodic migraine in patients treated with galcanezumab in real life in Italy: The 12-month observational, longitudinal, cohort multicenter GARLIT experience. J Neurol. 2022 (Jun 28). Doi: 10.1007/s00415-022-11226-4