Headache & Migraine

Key clinical point: Atogepant (dosage 60 mg/day) may be an effective and safe treatment option in patients with difficult to treat episodic migraine who have previously failed 2-4 conventional oral preventive treatments.

Major finding: Patients receiving atogepant vs placebo had a significantly greater reduction in monthly migraine days across 12 weeks (adjusted least squares mean difference −2.4 days; P < .0001). Constipation was the most common treatment-emergent adverse event (TEAE) in the atogepant group (10%), with TEAE leading to treatment discontinuation in only 2% vs 1% of patients receiving atogepant vs placebo.

Study details: Findings are from the phase 3b ELEVATE trial including 315 patients with episodic migraine who had previously failed 2-4 classes of conventional oral migraine prevention treatments and were randomly assigned to receive 60 mg/day atogepant or placebo.

Disclosures: This study was funded by AbbVie. Five authors declared being employees of or holding stocks in AbbVie. The other authors declared ties with various sources, including AbbVie.

Source: Tassorelli C, Nagy K, Pozo-Rosich P, et al. Safety and efficacy of atogepant for the preventive treatment of episodic migraine in adults for whom conventional oral preventive treatments have failed (ELEVATE): A randomised, placebo-controlled, phase 3b trial. Lancet Neurol. 2024 (Feb 13). doi: 10.1016/S1474-4422(24)00025-5 Source

Key clinical point: Atogepant (dosage 60 mg/day) may be an effective and safe treatment option in patients with difficult to treat episodic migraine who have previously failed 2-4 conventional oral preventive treatments.

Major finding: Patients receiving atogepant vs placebo had a significantly greater reduction in monthly migraine days across 12 weeks (adjusted least squares mean difference −2.4 days; P < .0001). Constipation was the most common treatment-emergent adverse event (TEAE) in the atogepant group (10%), with TEAE leading to treatment discontinuation in only 2% vs 1% of patients receiving atogepant vs placebo.

Study details: Findings are from the phase 3b ELEVATE trial including 315 patients with episodic migraine who had previously failed 2-4 classes of conventional oral migraine prevention treatments and were randomly assigned to receive 60 mg/day atogepant or placebo.

Disclosures: This study was funded by AbbVie. Five authors declared being employees of or holding stocks in AbbVie. The other authors declared ties with various sources, including AbbVie.

Source: Tassorelli C, Nagy K, Pozo-Rosich P, et al. Safety and efficacy of atogepant for the preventive treatment of episodic migraine in adults for whom conventional oral preventive treatments have failed (ELEVATE): A randomised, placebo-controlled, phase 3b trial. Lancet Neurol. 2024 (Feb 13). doi: 10.1016/S1474-4422(24)00025-5 Source

Key clinical point: Atogepant (dosage 60 mg/day) may be an effective and safe treatment option in patients with difficult to treat episodic migraine who have previously failed 2-4 conventional oral preventive treatments.

Major finding: Patients receiving atogepant vs placebo had a significantly greater reduction in monthly migraine days across 12 weeks (adjusted least squares mean difference −2.4 days; P < .0001). Constipation was the most common treatment-emergent adverse event (TEAE) in the atogepant group (10%), with TEAE leading to treatment discontinuation in only 2% vs 1% of patients receiving atogepant vs placebo.

Study details: Findings are from the phase 3b ELEVATE trial including 315 patients with episodic migraine who had previously failed 2-4 classes of conventional oral migraine prevention treatments and were randomly assigned to receive 60 mg/day atogepant or placebo.

Disclosures: This study was funded by AbbVie. Five authors declared being employees of or holding stocks in AbbVie. The other authors declared ties with various sources, including AbbVie.

Source: Tassorelli C, Nagy K, Pozo-Rosich P, et al. Safety and efficacy of atogepant for the preventive treatment of episodic migraine in adults for whom conventional oral preventive treatments have failed (ELEVATE): A randomised, placebo-controlled, phase 3b trial. Lancet Neurol. 2024 (Feb 13). doi: 10.1016/S1474-4422(24)00025-5 Source

Key clinical point: Persistent vasomotor symptoms (VMS) and a history of migraine were associated with an increased risk for cardiovascular disease (CVD) and stroke; however, these associations were attenuated after adjustment for CVD risk factors, such as blood pressure and glucose and cholesterol levels.

Major finding: Women with vs without persistent VMS and a history of migraine had over two times higher risk for CVD (adjusted HR [aHR] 2.25; 95% CI 1.15-4.38) and three times higher risk for stroke (aHR 3.15; 95% CI 1.35-7.34; both P < .05). These associations, however, diminished after adjustment for cigarette use and levels of glucose, cholesterol, and blood pressure.

Study details: This secondary analysis of a subset of the CARDIA study included 1954 women with 15-year follow-up data.

Disclosures: This study was supported by the US National Heart, Lung, and Blood Institute. The authors declared no conflicts of interest.

Source: Kim C, Schreiner PJ, Yin Z, et al. Migraines, vasomotor symptoms, and cardiovascular disease in the Coronary Artery Risk Development in Young Adults study. Menopause. 2024;31(3):202-208 (Feb 13). doi: 10.1097/GME.0000000000002311 Source

Key clinical point: Persistent vasomotor symptoms (VMS) and a history of migraine were associated with an increased risk for cardiovascular disease (CVD) and stroke; however, these associations were attenuated after adjustment for CVD risk factors, such as blood pressure and glucose and cholesterol levels.

Major finding: Women with vs without persistent VMS and a history of migraine had over two times higher risk for CVD (adjusted HR [aHR] 2.25; 95% CI 1.15-4.38) and three times higher risk for stroke (aHR 3.15; 95% CI 1.35-7.34; both P < .05). These associations, however, diminished after adjustment for cigarette use and levels of glucose, cholesterol, and blood pressure.

Study details: This secondary analysis of a subset of the CARDIA study included 1954 women with 15-year follow-up data.

Disclosures: This study was supported by the US National Heart, Lung, and Blood Institute. The authors declared no conflicts of interest.

Source: Kim C, Schreiner PJ, Yin Z, et al. Migraines, vasomotor symptoms, and cardiovascular disease in the Coronary Artery Risk Development in Young Adults study. Menopause. 2024;31(3):202-208 (Feb 13). doi: 10.1097/GME.0000000000002311 Source

Key clinical point: Persistent vasomotor symptoms (VMS) and a history of migraine were associated with an increased risk for cardiovascular disease (CVD) and stroke; however, these associations were attenuated after adjustment for CVD risk factors, such as blood pressure and glucose and cholesterol levels.

Major finding: Women with vs without persistent VMS and a history of migraine had over two times higher risk for CVD (adjusted HR [aHR] 2.25; 95% CI 1.15-4.38) and three times higher risk for stroke (aHR 3.15; 95% CI 1.35-7.34; both P < .05). These associations, however, diminished after adjustment for cigarette use and levels of glucose, cholesterol, and blood pressure.

Study details: This secondary analysis of a subset of the CARDIA study included 1954 women with 15-year follow-up data.

Disclosures: This study was supported by the US National Heart, Lung, and Blood Institute. The authors declared no conflicts of interest.

Source: Kim C, Schreiner PJ, Yin Z, et al. Migraines, vasomotor symptoms, and cardiovascular disease in the Coronary Artery Risk Development in Young Adults study. Menopause. 2024;31(3):202-208 (Feb 13). doi: 10.1097/GME.0000000000002311 Source

Key clinical point: Shift work was associated with significantly increased risks for headache and migraine, whereas night shifts only increased the risk for headaches.

Major finding: Shift work was significantly associated with an increased risk for headaches (hazard ratio [HR] 1.32; P < .001) and migraine (HR 1.63; P < .001), with the risk for headaches being further elevated in individuals who worked night shifts (HR 1.44; P = .011).

Study details: Findings are from a meta-analysis of seven cross-sectional studies that included 422,869 participants.

Disclosures: This study was supported by the Sichuan Youth Science and Technology Innovation Research Team. The authors declared no conflicts of interest.

Source: Wang Z, Zhu T, Gong M, et al. Relationship between shift work, night work, and headache and migraine risk: A meta-analysis of observational studies. Sleep Med. 2024;115:218-225 (Feb 19). doi: 10.1016/j.sleep.2024.02.011 Source

Key clinical point: Shift work was associated with significantly increased risks for headache and migraine, whereas night shifts only increased the risk for headaches.

Major finding: Shift work was significantly associated with an increased risk for headaches (hazard ratio [HR] 1.32; P < .001) and migraine (HR 1.63; P < .001), with the risk for headaches being further elevated in individuals who worked night shifts (HR 1.44; P = .011).

Study details: Findings are from a meta-analysis of seven cross-sectional studies that included 422,869 participants.

Disclosures: This study was supported by the Sichuan Youth Science and Technology Innovation Research Team. The authors declared no conflicts of interest.

Source: Wang Z, Zhu T, Gong M, et al. Relationship between shift work, night work, and headache and migraine risk: A meta-analysis of observational studies. Sleep Med. 2024;115:218-225 (Feb 19). doi: 10.1016/j.sleep.2024.02.011 Source

Key clinical point: Shift work was associated with significantly increased risks for headache and migraine, whereas night shifts only increased the risk for headaches.

Major finding: Shift work was significantly associated with an increased risk for headaches (hazard ratio [HR] 1.32; P < .001) and migraine (HR 1.63; P < .001), with the risk for headaches being further elevated in individuals who worked night shifts (HR 1.44; P = .011).

Study details: Findings are from a meta-analysis of seven cross-sectional studies that included 422,869 participants.

Disclosures: This study was supported by the Sichuan Youth Science and Technology Innovation Research Team. The authors declared no conflicts of interest.

Source: Wang Z, Zhu T, Gong M, et al. Relationship between shift work, night work, and headache and migraine risk: A meta-analysis of observational studies. Sleep Med. 2024;115:218-225 (Feb 19). doi: 10.1016/j.sleep.2024.02.011 Source

WEST PALM BEACH, FLORIDA — Migraine, a common comorbidity in multiple sclerosis (MS), is not part of the MS prodrome, new research suggested. Investigators found that patients with MS were more likely than controls to develop migraine shortly before disease diagnosis, suggesting the headache type is not a forerunner of MS.

“The risk [of migraine] was concentrated in the year of their first [MS] symptom, or the year prior, instead of many years before,” said lead investigator Vinicius A. Schoeps, MD, MPH, postdoctoral fellow at the University of California San Francisco.

The findings were presented at the annual meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS).

Is MS a Migraine Trigger?

Worldwide up to 43% of patients with MS report migraine. Recent data point to a 3- to 5-year clinically symptomatic prodromal phase of MS and suggest migraine may be one of its potential constituents. However, the relationship between the two disorders remains unclear.

The investigators wanted to determine whether migraine is part of the MS prodrome because if this is the case, it could provide a potential opportunity for early intervention to delay or prevent the disease.

The team analyzed incidence cases of MS and matched controls in the Kaiser Permanente Southern California health system from 2011 to 2014. Participants took part in structured in-person interviews that included questions about migraine.

The 591 MS cases had an average age of onset at 36 years, with a similar index date for controls. Among the cases, 71% were women, 42% were White, 32% Hispanic, and 21% Black. Almost 40% of cases had obesity. These demographic data were similar in the control group.

In those with MS, 13% had a history of mononucleosis compared with 6% of controls. Epstein-Barr virus, which causes conditions such as mononucleosis, was considered a likely cause of MS.

Migraine was diagnosed before MS onset in 27% of cases and before the index date in 21% of controls (adjusted odds ratio [aOR], 1.36; P = .03). Migraine onset occurred later in cases versus controls (mean, 21 years vs 17 years; P = .008).

Migraine was also more likely to occur at the same time or 1 year prior to MS symptoms or the index date in cases versus controls (4.3% vs 1.3%; aOR, 3.54; P = .002).

“These findings suggest that migraine can be triggered by MS rather than part of the constellation of nonspecific symptoms that constitute the 3- to 5-year-long MS prodrome,” the investigators reported.

“The inflammatory setting of the first MS relapse might be actually triggering the migraine,” Dr. Shoeps said. He added that patients with MS developed migraines later in life.

“There could be a different pathological process in people who have traditional migraine at the most common age where people get their diagnosis of migraine — and have them throughout their lifetime — versus having a migraine at older age and a diagnosis of MS close to that period of time,” he said. However, he noted, the study design does not allow for this type of analysis.

Commenting on the findings, Anibal Chertcoff, MD, PhD, an assistant professor in the Multiple Sclerosis Research Centre at the University of Manitoba, Winnipeg, Manitoba, Canada, noted the study’s large population and well-balanced case and control groups are strengths of the study.

However, Dr. Chertcoff, who was not involved in the research, cautioned that the study is cross-sectional noting that he is “not convinced this is the best type of study design to provide insights into cause-and-effect relationships.”

Dr. Chertcoff added the findings are limited by their reliance on data from a single health system.

Disclosures were not provided. A grant from the National Institute of Neurologic Disorders and Stroke to an author helped support the study. Dr. Chertcoff received funding from MS Canada and the Michael Smith Foundation for Health Research and support from Novartis to attend a scientific meeting.

A version of this article appeared on Medscape.com.

WEST PALM BEACH, FLORIDA — Migraine, a common comorbidity in multiple sclerosis (MS), is not part of the MS prodrome, new research suggested. Investigators found that patients with MS were more likely than controls to develop migraine shortly before disease diagnosis, suggesting the headache type is not a forerunner of MS.

“The risk [of migraine] was concentrated in the year of their first [MS] symptom, or the year prior, instead of many years before,” said lead investigator Vinicius A. Schoeps, MD, MPH, postdoctoral fellow at the University of California San Francisco.

The findings were presented at the annual meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS).

Is MS a Migraine Trigger?

Worldwide up to 43% of patients with MS report migraine. Recent data point to a 3- to 5-year clinically symptomatic prodromal phase of MS and suggest migraine may be one of its potential constituents. However, the relationship between the two disorders remains unclear.

The investigators wanted to determine whether migraine is part of the MS prodrome because if this is the case, it could provide a potential opportunity for early intervention to delay or prevent the disease.

The team analyzed incidence cases of MS and matched controls in the Kaiser Permanente Southern California health system from 2011 to 2014. Participants took part in structured in-person interviews that included questions about migraine.

The 591 MS cases had an average age of onset at 36 years, with a similar index date for controls. Among the cases, 71% were women, 42% were White, 32% Hispanic, and 21% Black. Almost 40% of cases had obesity. These demographic data were similar in the control group.

In those with MS, 13% had a history of mononucleosis compared with 6% of controls. Epstein-Barr virus, which causes conditions such as mononucleosis, was considered a likely cause of MS.

Migraine was diagnosed before MS onset in 27% of cases and before the index date in 21% of controls (adjusted odds ratio [aOR], 1.36; P = .03). Migraine onset occurred later in cases versus controls (mean, 21 years vs 17 years; P = .008).

Migraine was also more likely to occur at the same time or 1 year prior to MS symptoms or the index date in cases versus controls (4.3% vs 1.3%; aOR, 3.54; P = .002).

“These findings suggest that migraine can be triggered by MS rather than part of the constellation of nonspecific symptoms that constitute the 3- to 5-year-long MS prodrome,” the investigators reported.

“The inflammatory setting of the first MS relapse might be actually triggering the migraine,” Dr. Shoeps said. He added that patients with MS developed migraines later in life.

“There could be a different pathological process in people who have traditional migraine at the most common age where people get their diagnosis of migraine — and have them throughout their lifetime — versus having a migraine at older age and a diagnosis of MS close to that period of time,” he said. However, he noted, the study design does not allow for this type of analysis.

Commenting on the findings, Anibal Chertcoff, MD, PhD, an assistant professor in the Multiple Sclerosis Research Centre at the University of Manitoba, Winnipeg, Manitoba, Canada, noted the study’s large population and well-balanced case and control groups are strengths of the study.

However, Dr. Chertcoff, who was not involved in the research, cautioned that the study is cross-sectional noting that he is “not convinced this is the best type of study design to provide insights into cause-and-effect relationships.”

Dr. Chertcoff added the findings are limited by their reliance on data from a single health system.

Disclosures were not provided. A grant from the National Institute of Neurologic Disorders and Stroke to an author helped support the study. Dr. Chertcoff received funding from MS Canada and the Michael Smith Foundation for Health Research and support from Novartis to attend a scientific meeting.

A version of this article appeared on Medscape.com.

WEST PALM BEACH, FLORIDA — Migraine, a common comorbidity in multiple sclerosis (MS), is not part of the MS prodrome, new research suggested. Investigators found that patients with MS were more likely than controls to develop migraine shortly before disease diagnosis, suggesting the headache type is not a forerunner of MS.

“The risk [of migraine] was concentrated in the year of their first [MS] symptom, or the year prior, instead of many years before,” said lead investigator Vinicius A. Schoeps, MD, MPH, postdoctoral fellow at the University of California San Francisco.

The findings were presented at the annual meeting held by the Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS).

Is MS a Migraine Trigger?

Worldwide up to 43% of patients with MS report migraine. Recent data point to a 3- to 5-year clinically symptomatic prodromal phase of MS and suggest migraine may be one of its potential constituents. However, the relationship between the two disorders remains unclear.

The investigators wanted to determine whether migraine is part of the MS prodrome because if this is the case, it could provide a potential opportunity for early intervention to delay or prevent the disease.

The team analyzed incidence cases of MS and matched controls in the Kaiser Permanente Southern California health system from 2011 to 2014. Participants took part in structured in-person interviews that included questions about migraine.

The 591 MS cases had an average age of onset at 36 years, with a similar index date for controls. Among the cases, 71% were women, 42% were White, 32% Hispanic, and 21% Black. Almost 40% of cases had obesity. These demographic data were similar in the control group.

In those with MS, 13% had a history of mononucleosis compared with 6% of controls. Epstein-Barr virus, which causes conditions such as mononucleosis, was considered a likely cause of MS.

Migraine was diagnosed before MS onset in 27% of cases and before the index date in 21% of controls (adjusted odds ratio [aOR], 1.36; P = .03). Migraine onset occurred later in cases versus controls (mean, 21 years vs 17 years; P = .008).

Migraine was also more likely to occur at the same time or 1 year prior to MS symptoms or the index date in cases versus controls (4.3% vs 1.3%; aOR, 3.54; P = .002).

“These findings suggest that migraine can be triggered by MS rather than part of the constellation of nonspecific symptoms that constitute the 3- to 5-year-long MS prodrome,” the investigators reported.

“The inflammatory setting of the first MS relapse might be actually triggering the migraine,” Dr. Shoeps said. He added that patients with MS developed migraines later in life.

“There could be a different pathological process in people who have traditional migraine at the most common age where people get their diagnosis of migraine — and have them throughout their lifetime — versus having a migraine at older age and a diagnosis of MS close to that period of time,” he said. However, he noted, the study design does not allow for this type of analysis.

Commenting on the findings, Anibal Chertcoff, MD, PhD, an assistant professor in the Multiple Sclerosis Research Centre at the University of Manitoba, Winnipeg, Manitoba, Canada, noted the study’s large population and well-balanced case and control groups are strengths of the study.

However, Dr. Chertcoff, who was not involved in the research, cautioned that the study is cross-sectional noting that he is “not convinced this is the best type of study design to provide insights into cause-and-effect relationships.”

Dr. Chertcoff added the findings are limited by their reliance on data from a single health system.

Disclosures were not provided. A grant from the National Institute of Neurologic Disorders and Stroke to an author helped support the study. Dr. Chertcoff received funding from MS Canada and the Michael Smith Foundation for Health Research and support from Novartis to attend a scientific meeting.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Dear colleagues, I’m Christoph Diener from the medical faculty of University Duisburg-Essen in Germany. Today I would like to tell you about five interesting studies that were published in January 2024.
 

Long COVID

I would like to start with long COVID. There is an ongoing discussion about whether this condition — which means symptoms like dizziness, vertigo, fatigue, headache, and cognitive impairment that persist for more than 6 months — is either a consequence of the infection, functional symptoms, psychosomatic disease, or a depression.

There is an important paper that came out in Science. The group investigated 39 controls and 113 patients who had COVID-19. At 6 months, 40 of them had long COVID. The researchers repeatedly measured more than 6500 proteins in serum. The patients with long COVID had a significant increase in complement activation, which persisted even beyond 6 months. These patients also showed increased tissue lesion markers in the blood and activation of the endothelium.

Also, they had increased platelet activation and autoantibodies with increased anti-cytomegalovirus and anti-Epstein-Barr virus immunoglobulins. These are very strong indicators that COVID-19 leads to long-term changes in our immune system, and different activations of complement factors could explain the variety of symptoms that these patients display. Whether this has consequences for treatment is unclear at the moment.
 

Parkinson’s Classification

Let me come to another issue, which is the future treatment of Parkinson’s disease, covered in a paper in The Lancet Neurology. I think you are all aware that once patients display symptoms like rigidity, bradykinesia, or tremor, it’s most probably too late for neuroprotective therapy because 70% of the dopaminergic neurons are already dead.

The authors propose a new biological diagnosis of the disease in the preclinical state. This early preclinical diagnosis has three components. One is to show the presence of synuclein either in skin biopsy or in serum. The second is proof of neurodegeneration either by MRI or by PET imaging. The third involves genetic markers.

On top of this, we know that we have preclinical manifestations of Parkinson’s disease, like REM sleep disorders, autonomic disturbances, and cognitive impairment. With this new classification, we should be able to identify the preclinical phase of Parkinson’s disease and include these patients in future trials for neuroprotection.
 

Niemann-Pick Disease

My third study, in The New England Journal of Medicine, deals with Niemann-Pick disease type C (Trial of N-Acetyl-l-Leucine in Niemann–Pick Disease Type C. This is a rare autosomal recessive disorder that involves impaired lysosomal storage. This disease, which manifests usually in childhood, goes along with systemic, psychiatric, and neurologic abnormalities, and in particular, ataxia. Until now, there has been only one therapy, with miglustat. which has many side effects.

The group of authors found a new therapeutic approach with N-acetyl-L-leucine, which primarily increases mitochondrial energy production. This was a small, placebo-controlled, crossover trial with 2 x 12 weeks of treatment. This new compound showed efficacy and was very well tolerated. This shows that we definitely need long-term studies with this new, well-tolerated drug in this rare disease.
 

Anticoagulation in Subclinical AF

My fourth study comes from the stroke-prevention field, published in The New England Journal of Medicine. I think you are aware of subclinical atrail fibrillation. These are high-frequency episodes in ECG, usually identified by pacemakers or ECG monitoring systems. The international ARTESIA study included more than 4000 patients randomized either to apixaban 5 mg twice daily or aspirin 81 mg.

After 3.5 years, the investigators showed a small but significant decrease in the rate of stroke, with a relative risk reduction of 37%, but also, unfortunately, a significantly increased risk for major bleeding with apixaban. This means that we need a careful discussion with the patient, the family, and the GP to decide whether these patients should be anticoagulated or not.
 

Migraine and Depression

My final study, published in the European Journal of Neurology, deals with the comorbidity of depression and migraine. This study in the Netherlands included 108 patients treated with erenumab and 90 with fremanezumab; 68 were controls.

They used two depression scales. They showed that treatment with the monoclonal antibodies improved at least one of the two depression scales. I think this is an important study because it indicates that you can improve comorbid depression in people with severe migraine, even if this study did not show a correlation between the reduction in monthly migraine days and the improvement of depression.

What we learned for clinical practice is that we have to identify depression in people with migraine and we have to deal with it. Whether it’s with the treatment of monoclonal antibodies or antidepressant therapy doesn’t really matter.

Dear colleagues, we had interesting studies this month. I think the most spectacular one was published in Science on long COVID. Thank you very much for listening and watching. I’m Christoph Diener from University Duisburg-Essen.
 

Dr. Diener is Professor, Department of Neurology, Stroke Center-Headache Center, University Duisburg-Essen, Essen, Germany. He disclosed ties with Abbott; Addex Pharma; Alder; Allergan; Almirall; Amgen; Autonomic Technology; AstraZeneca; Bayer Vital; Berlin Chemie; Bristol-Myers Squibb; Boehringer Ingelheim; Chordate; CoAxia; Corimmun; Covidien; Coherex; CoLucid; Daiichi-Sankyo; D-Pharml Electrocore; Fresenius; GlaxoSmithKline; Grunenthal; Janssen-Cilag; Labrys Biologics Lilly; La Roche; 3M Medica; MSD; Medtronic; Menarini; MindFrame; Minster; Neuroscore; Neurobiological Technologies; Novartis; Novo-Nordisk; Johnson & Johnson; Knoll; Paion; Parke-Davis; Pierre Fabre; Pfizer Inc; Schaper and Brummer; sanofi-aventis; Schering-Plough; Servier; Solvay; Syngis; St. Jude; Talecris; Thrombogenics; WebMD Global; Weber and Weber; Wyeth; and Yamanouchi.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Dear colleagues, I’m Christoph Diener from the medical faculty of University Duisburg-Essen in Germany. Today I would like to tell you about five interesting studies that were published in January 2024.
 

Long COVID

I would like to start with long COVID. There is an ongoing discussion about whether this condition — which means symptoms like dizziness, vertigo, fatigue, headache, and cognitive impairment that persist for more than 6 months — is either a consequence of the infection, functional symptoms, psychosomatic disease, or a depression.

There is an important paper that came out in Science. The group investigated 39 controls and 113 patients who had COVID-19. At 6 months, 40 of them had long COVID. The researchers repeatedly measured more than 6500 proteins in serum. The patients with long COVID had a significant increase in complement activation, which persisted even beyond 6 months. These patients also showed increased tissue lesion markers in the blood and activation of the endothelium.

Also, they had increased platelet activation and autoantibodies with increased anti-cytomegalovirus and anti-Epstein-Barr virus immunoglobulins. These are very strong indicators that COVID-19 leads to long-term changes in our immune system, and different activations of complement factors could explain the variety of symptoms that these patients display. Whether this has consequences for treatment is unclear at the moment.
 

Parkinson’s Classification

Let me come to another issue, which is the future treatment of Parkinson’s disease, covered in a paper in The Lancet Neurology. I think you are all aware that once patients display symptoms like rigidity, bradykinesia, or tremor, it’s most probably too late for neuroprotective therapy because 70% of the dopaminergic neurons are already dead.

The authors propose a new biological diagnosis of the disease in the preclinical state. This early preclinical diagnosis has three components. One is to show the presence of synuclein either in skin biopsy or in serum. The second is proof of neurodegeneration either by MRI or by PET imaging. The third involves genetic markers.

On top of this, we know that we have preclinical manifestations of Parkinson’s disease, like REM sleep disorders, autonomic disturbances, and cognitive impairment. With this new classification, we should be able to identify the preclinical phase of Parkinson’s disease and include these patients in future trials for neuroprotection.
 

Niemann-Pick Disease

My third study, in The New England Journal of Medicine, deals with Niemann-Pick disease type C (Trial of N-Acetyl-l-Leucine in Niemann–Pick Disease Type C. This is a rare autosomal recessive disorder that involves impaired lysosomal storage. This disease, which manifests usually in childhood, goes along with systemic, psychiatric, and neurologic abnormalities, and in particular, ataxia. Until now, there has been only one therapy, with miglustat. which has many side effects.

The group of authors found a new therapeutic approach with N-acetyl-L-leucine, which primarily increases mitochondrial energy production. This was a small, placebo-controlled, crossover trial with 2 x 12 weeks of treatment. This new compound showed efficacy and was very well tolerated. This shows that we definitely need long-term studies with this new, well-tolerated drug in this rare disease.
 

Anticoagulation in Subclinical AF

My fourth study comes from the stroke-prevention field, published in The New England Journal of Medicine. I think you are aware of subclinical atrail fibrillation. These are high-frequency episodes in ECG, usually identified by pacemakers or ECG monitoring systems. The international ARTESIA study included more than 4000 patients randomized either to apixaban 5 mg twice daily or aspirin 81 mg.

After 3.5 years, the investigators showed a small but significant decrease in the rate of stroke, with a relative risk reduction of 37%, but also, unfortunately, a significantly increased risk for major bleeding with apixaban. This means that we need a careful discussion with the patient, the family, and the GP to decide whether these patients should be anticoagulated or not.
 

Migraine and Depression

My final study, published in the European Journal of Neurology, deals with the comorbidity of depression and migraine. This study in the Netherlands included 108 patients treated with erenumab and 90 with fremanezumab; 68 were controls.

They used two depression scales. They showed that treatment with the monoclonal antibodies improved at least one of the two depression scales. I think this is an important study because it indicates that you can improve comorbid depression in people with severe migraine, even if this study did not show a correlation between the reduction in monthly migraine days and the improvement of depression.

What we learned for clinical practice is that we have to identify depression in people with migraine and we have to deal with it. Whether it’s with the treatment of monoclonal antibodies or antidepressant therapy doesn’t really matter.

Dear colleagues, we had interesting studies this month. I think the most spectacular one was published in Science on long COVID. Thank you very much for listening and watching. I’m Christoph Diener from University Duisburg-Essen.
 

Dr. Diener is Professor, Department of Neurology, Stroke Center-Headache Center, University Duisburg-Essen, Essen, Germany. He disclosed ties with Abbott; Addex Pharma; Alder; Allergan; Almirall; Amgen; Autonomic Technology; AstraZeneca; Bayer Vital; Berlin Chemie; Bristol-Myers Squibb; Boehringer Ingelheim; Chordate; CoAxia; Corimmun; Covidien; Coherex; CoLucid; Daiichi-Sankyo; D-Pharml Electrocore; Fresenius; GlaxoSmithKline; Grunenthal; Janssen-Cilag; Labrys Biologics Lilly; La Roche; 3M Medica; MSD; Medtronic; Menarini; MindFrame; Minster; Neuroscore; Neurobiological Technologies; Novartis; Novo-Nordisk; Johnson & Johnson; Knoll; Paion; Parke-Davis; Pierre Fabre; Pfizer Inc; Schaper and Brummer; sanofi-aventis; Schering-Plough; Servier; Solvay; Syngis; St. Jude; Talecris; Thrombogenics; WebMD Global; Weber and Weber; Wyeth; and Yamanouchi.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity.

Dear colleagues, I’m Christoph Diener from the medical faculty of University Duisburg-Essen in Germany. Today I would like to tell you about five interesting studies that were published in January 2024.
 

Long COVID

I would like to start with long COVID. There is an ongoing discussion about whether this condition — which means symptoms like dizziness, vertigo, fatigue, headache, and cognitive impairment that persist for more than 6 months — is either a consequence of the infection, functional symptoms, psychosomatic disease, or a depression.

There is an important paper that came out in Science. The group investigated 39 controls and 113 patients who had COVID-19. At 6 months, 40 of them had long COVID. The researchers repeatedly measured more than 6500 proteins in serum. The patients with long COVID had a significant increase in complement activation, which persisted even beyond 6 months. These patients also showed increased tissue lesion markers in the blood and activation of the endothelium.

Also, they had increased platelet activation and autoantibodies with increased anti-cytomegalovirus and anti-Epstein-Barr virus immunoglobulins. These are very strong indicators that COVID-19 leads to long-term changes in our immune system, and different activations of complement factors could explain the variety of symptoms that these patients display. Whether this has consequences for treatment is unclear at the moment.
 

Parkinson’s Classification

Let me come to another issue, which is the future treatment of Parkinson’s disease, covered in a paper in The Lancet Neurology. I think you are all aware that once patients display symptoms like rigidity, bradykinesia, or tremor, it’s most probably too late for neuroprotective therapy because 70% of the dopaminergic neurons are already dead.

The authors propose a new biological diagnosis of the disease in the preclinical state. This early preclinical diagnosis has three components. One is to show the presence of synuclein either in skin biopsy or in serum. The second is proof of neurodegeneration either by MRI or by PET imaging. The third involves genetic markers.

On top of this, we know that we have preclinical manifestations of Parkinson’s disease, like REM sleep disorders, autonomic disturbances, and cognitive impairment. With this new classification, we should be able to identify the preclinical phase of Parkinson’s disease and include these patients in future trials for neuroprotection.
 

Niemann-Pick Disease

My third study, in The New England Journal of Medicine, deals with Niemann-Pick disease type C (Trial of N-Acetyl-l-Leucine in Niemann–Pick Disease Type C. This is a rare autosomal recessive disorder that involves impaired lysosomal storage. This disease, which manifests usually in childhood, goes along with systemic, psychiatric, and neurologic abnormalities, and in particular, ataxia. Until now, there has been only one therapy, with miglustat. which has many side effects.

The group of authors found a new therapeutic approach with N-acetyl-L-leucine, which primarily increases mitochondrial energy production. This was a small, placebo-controlled, crossover trial with 2 x 12 weeks of treatment. This new compound showed efficacy and was very well tolerated. This shows that we definitely need long-term studies with this new, well-tolerated drug in this rare disease.
 

Anticoagulation in Subclinical AF

My fourth study comes from the stroke-prevention field, published in The New England Journal of Medicine. I think you are aware of subclinical atrail fibrillation. These are high-frequency episodes in ECG, usually identified by pacemakers or ECG monitoring systems. The international ARTESIA study included more than 4000 patients randomized either to apixaban 5 mg twice daily or aspirin 81 mg.

After 3.5 years, the investigators showed a small but significant decrease in the rate of stroke, with a relative risk reduction of 37%, but also, unfortunately, a significantly increased risk for major bleeding with apixaban. This means that we need a careful discussion with the patient, the family, and the GP to decide whether these patients should be anticoagulated or not.
 

Migraine and Depression

My final study, published in the European Journal of Neurology, deals with the comorbidity of depression and migraine. This study in the Netherlands included 108 patients treated with erenumab and 90 with fremanezumab; 68 were controls.

They used two depression scales. They showed that treatment with the monoclonal antibodies improved at least one of the two depression scales. I think this is an important study because it indicates that you can improve comorbid depression in people with severe migraine, even if this study did not show a correlation between the reduction in monthly migraine days and the improvement of depression.

What we learned for clinical practice is that we have to identify depression in people with migraine and we have to deal with it. Whether it’s with the treatment of monoclonal antibodies or antidepressant therapy doesn’t really matter.

Dear colleagues, we had interesting studies this month. I think the most spectacular one was published in Science on long COVID. Thank you very much for listening and watching. I’m Christoph Diener from University Duisburg-Essen.
 

Dr. Diener is Professor, Department of Neurology, Stroke Center-Headache Center, University Duisburg-Essen, Essen, Germany. He disclosed ties with Abbott; Addex Pharma; Alder; Allergan; Almirall; Amgen; Autonomic Technology; AstraZeneca; Bayer Vital; Berlin Chemie; Bristol-Myers Squibb; Boehringer Ingelheim; Chordate; CoAxia; Corimmun; Covidien; Coherex; CoLucid; Daiichi-Sankyo; D-Pharml Electrocore; Fresenius; GlaxoSmithKline; Grunenthal; Janssen-Cilag; Labrys Biologics Lilly; La Roche; 3M Medica; MSD; Medtronic; Menarini; MindFrame; Minster; Neuroscore; Neurobiological Technologies; Novartis; Novo-Nordisk; Johnson & Johnson; Knoll; Paion; Parke-Davis; Pierre Fabre; Pfizer Inc; Schaper and Brummer; sanofi-aventis; Schering-Plough; Servier; Solvay; Syngis; St. Jude; Talecris; Thrombogenics; WebMD Global; Weber and Weber; Wyeth; and Yamanouchi.

A version of this article appeared on Medscape.com.

Additionally, several recently published reviews have examined the risks of comorbidities that are not neurologic or cardiovascular, such as allergies, inflammatory bowel disease, obesity, and diabetes. Although these types of associations are not inherently obvious in terms of migraine pathophysiology, determining whether there is a link may help shed a light on some contributing factors that could play a role in migraine or in the comorbid disorders.

Authors of a study published in the January 2024 issue of the European Journal of Medical Research sought to examine the relationship between allergic rhinitis and migraine. They noted that several studies, as well as a statement from the American Migraine Prevalence and Prevention Study, published in 2013, reported an increased frequency of migraines in patients with allergic rhinitis. The researchers used data extracted from the UK Biobank, comprising 25,486 patients diagnosed with allergic rhinitis and 87,097 controls and 8547 migraine cases and 176,107 controls. They performed statistical analysis using bidirectional two-sample Mendelian randomization with publicly available summary-level statistics of large genome-wide association studies to estimate the possible causal effects. The researchers did not find any clear causal or genetic association between allergic rhinitis and migraine risk. However, the lack of causation between migraine and allergic rhinitis does not contradict previous studies that point to the prevalence of comorbidity of the two conditions. It's also important to note that congestion is a known migraine trigger, and the results of the study do not contradict that relationship. Given the variability of results from different research studies, the authors suggested that more research is warranted to help untangle the complex association between allergic rhinitis and migraine.

Inflammatory bowel disease (IBD) is another condition with a higher prevalence in patients who have migraine. A January 2024 article in Scientific Reports described the results of a nationwide population-based study that was conducted using data from the Korean National Health Insurance Service database. This study included 10,131,193 individuals. The researchers found that the risk for development of IBD in patients with migraine was significantly higher, by 1.3 times, compared with the general population. These results are similar to previous studies, such as a meta-analysis published in May 2023 in the International Journal of Preventive Medicine, which reported a pooled prevalence of migraine in IBD cases of 19%, with 1.5-fold higher odds of developing migraine in IBD cases when compared with controls.^[3] These studies were both aimed at examining epidemiologic data rather than uncovering a physiologic or genetic cause of the link, and neither study described an explanation for this connection.

A Mendelian randomization study published in May 2023 in Headache investigated potential genetic links between migraine and IBD. As with the January 2024 European Journal of Medical Research study that was done to search for a genetic association between migraine and allergic rhinitis, the authors stated that there was no evidence of a shared genetic basis or of a causal association between migraine and either IBD or celiac disease.^[4] Although the evidence doesn't point to a causal relationship, it's important to note that diet plays a role in migraine management, and diet is especially important in managing IBD. Consideration of dietary factors could be beneficial for preventing symptoms — and is even more important for avoiding exacerbation of symptoms.

A high body mass index (BMI) is correlated with migraine. A study published in January 2024 in BMC Geriatrics analyzed data from people who participated in the National Health and Nutrition Examination Survey between 1999 and 2004 by the Centers for Disease Control and the National Center for Health Statistics, comprising a total of 31,126 participants. The researchers found a linear association between BMI and migraine. They also noted that increased BMI was related to a significantly higher risk for migraine in the group with diabetes, but this positive relationship between BMI and migraine seemed to be smaller in the group without diabetes. The authors considered inflammation associated with obesity as a possible contributing factor for this link but acknowledged that the pathophysiologic mechanism is unknown and suggested that there is a high likelihood of confounding factors. Given that diabetes and obesity are both correlated with an increased risk for vascular disease and migraine is associated with a slight increase in cardiovascular risk, it could be especially important to identify these comorbidities in individual patients.

Migraine is common, and many comorbidities have been verified with population studies. Although there are some explanations for the links between migraine and vascular or neurologic conditions, the cause of associations between migraine and other conditions is not known. Some theories that have begun to be investigated include inflammation and genetics. Eventually, further research and understanding of contributing factors could potentially provide explanations that may help in diagnosing migraine or associated disorders at an early stage — and might even be used to help guide treatment.

Additional References

1. Ashina M, Katsarava Z, Do TP, et al. Migraine: Epidemiology and systems of care. Lancet. 2021;397:1485-1495. doi: 10.1016/S0140-6736(20)32160-7 Source

2. Burch RC, Buse DC, Lipton RB. Migraine: Epidemiology, burden, and comorbidity. Neurol Clin. 2019;37:631-649. doi: 10.1016/j.ncl.2019.06.001 Source

3. Olfati H, Mirmosayyeb O, Hosseinabadi AM, Ghajarzadeh M. The prevalence of migraine in inflammatory bowel disease, a systematic review and meta-analysis. Int J Prev Med. 2023;14:66. doi: 10.4103/ijpvm.ijpvm_413_21 Source

4. Welander NZ, Rukh G, Rask-Andersen M, Harder AV, et al and International Headache Genetics Consortium. Migraine, inflammatory bowel disease and celiac disease: A Mendelian randomization study. Headache. 2023;63:642-651. doi: 10.1111/head.14470 Source

Additionally, several recently published reviews have examined the risks of comorbidities that are not neurologic or cardiovascular, such as allergies, inflammatory bowel disease, obesity, and diabetes. Although these types of associations are not inherently obvious in terms of migraine pathophysiology, determining whether there is a link may help shed a light on some contributing factors that could play a role in migraine or in the comorbid disorders.

Authors of a study published in the January 2024 issue of the European Journal of Medical Research sought to examine the relationship between allergic rhinitis and migraine. They noted that several studies, as well as a statement from the American Migraine Prevalence and Prevention Study, published in 2013, reported an increased frequency of migraines in patients with allergic rhinitis. The researchers used data extracted from the UK Biobank, comprising 25,486 patients diagnosed with allergic rhinitis and 87,097 controls and 8547 migraine cases and 176,107 controls. They performed statistical analysis using bidirectional two-sample Mendelian randomization with publicly available summary-level statistics of large genome-wide association studies to estimate the possible causal effects. The researchers did not find any clear causal or genetic association between allergic rhinitis and migraine risk. However, the lack of causation between migraine and allergic rhinitis does not contradict previous studies that point to the prevalence of comorbidity of the two conditions. It's also important to note that congestion is a known migraine trigger, and the results of the study do not contradict that relationship. Given the variability of results from different research studies, the authors suggested that more research is warranted to help untangle the complex association between allergic rhinitis and migraine.

Inflammatory bowel disease (IBD) is another condition with a higher prevalence in patients who have migraine. A January 2024 article in Scientific Reports described the results of a nationwide population-based study that was conducted using data from the Korean National Health Insurance Service database. This study included 10,131,193 individuals. The researchers found that the risk for development of IBD in patients with migraine was significantly higher, by 1.3 times, compared with the general population. These results are similar to previous studies, such as a meta-analysis published in May 2023 in the International Journal of Preventive Medicine, which reported a pooled prevalence of migraine in IBD cases of 19%, with 1.5-fold higher odds of developing migraine in IBD cases when compared with controls.^[3] These studies were both aimed at examining epidemiologic data rather than uncovering a physiologic or genetic cause of the link, and neither study described an explanation for this connection.

A Mendelian randomization study published in May 2023 in Headache investigated potential genetic links between migraine and IBD. As with the January 2024 European Journal of Medical Research study that was done to search for a genetic association between migraine and allergic rhinitis, the authors stated that there was no evidence of a shared genetic basis or of a causal association between migraine and either IBD or celiac disease.^[4] Although the evidence doesn't point to a causal relationship, it's important to note that diet plays a role in migraine management, and diet is especially important in managing IBD. Consideration of dietary factors could be beneficial for preventing symptoms — and is even more important for avoiding exacerbation of symptoms.

A high body mass index (BMI) is correlated with migraine. A study published in January 2024 in BMC Geriatrics analyzed data from people who participated in the National Health and Nutrition Examination Survey between 1999 and 2004 by the Centers for Disease Control and the National Center for Health Statistics, comprising a total of 31,126 participants. The researchers found a linear association between BMI and migraine. They also noted that increased BMI was related to a significantly higher risk for migraine in the group with diabetes, but this positive relationship between BMI and migraine seemed to be smaller in the group without diabetes. The authors considered inflammation associated with obesity as a possible contributing factor for this link but acknowledged that the pathophysiologic mechanism is unknown and suggested that there is a high likelihood of confounding factors. Given that diabetes and obesity are both correlated with an increased risk for vascular disease and migraine is associated with a slight increase in cardiovascular risk, it could be especially important to identify these comorbidities in individual patients.

Migraine is common, and many comorbidities have been verified with population studies. Although there are some explanations for the links between migraine and vascular or neurologic conditions, the cause of associations between migraine and other conditions is not known. Some theories that have begun to be investigated include inflammation and genetics. Eventually, further research and understanding of contributing factors could potentially provide explanations that may help in diagnosing migraine or associated disorders at an early stage — and might even be used to help guide treatment.

Additional References

1. Ashina M, Katsarava Z, Do TP, et al. Migraine: Epidemiology and systems of care. Lancet. 2021;397:1485-1495. doi: 10.1016/S0140-6736(20)32160-7 Source

2. Burch RC, Buse DC, Lipton RB. Migraine: Epidemiology, burden, and comorbidity. Neurol Clin. 2019;37:631-649. doi: 10.1016/j.ncl.2019.06.001 Source

3. Olfati H, Mirmosayyeb O, Hosseinabadi AM, Ghajarzadeh M. The prevalence of migraine in inflammatory bowel disease, a systematic review and meta-analysis. Int J Prev Med. 2023;14:66. doi: 10.4103/ijpvm.ijpvm_413_21 Source

4. Welander NZ, Rukh G, Rask-Andersen M, Harder AV, et al and International Headache Genetics Consortium. Migraine, inflammatory bowel disease and celiac disease: A Mendelian randomization study. Headache. 2023;63:642-651. doi: 10.1111/head.14470 Source

Additionally, several recently published reviews have examined the risks of comorbidities that are not neurologic or cardiovascular, such as allergies, inflammatory bowel disease, obesity, and diabetes. Although these types of associations are not inherently obvious in terms of migraine pathophysiology, determining whether there is a link may help shed a light on some contributing factors that could play a role in migraine or in the comorbid disorders.

Authors of a study published in the January 2024 issue of the European Journal of Medical Research sought to examine the relationship between allergic rhinitis and migraine. They noted that several studies, as well as a statement from the American Migraine Prevalence and Prevention Study, published in 2013, reported an increased frequency of migraines in patients with allergic rhinitis. The researchers used data extracted from the UK Biobank, comprising 25,486 patients diagnosed with allergic rhinitis and 87,097 controls and 8547 migraine cases and 176,107 controls. They performed statistical analysis using bidirectional two-sample Mendelian randomization with publicly available summary-level statistics of large genome-wide association studies to estimate the possible causal effects. The researchers did not find any clear causal or genetic association between allergic rhinitis and migraine risk. However, the lack of causation between migraine and allergic rhinitis does not contradict previous studies that point to the prevalence of comorbidity of the two conditions. It's also important to note that congestion is a known migraine trigger, and the results of the study do not contradict that relationship. Given the variability of results from different research studies, the authors suggested that more research is warranted to help untangle the complex association between allergic rhinitis and migraine.

Inflammatory bowel disease (IBD) is another condition with a higher prevalence in patients who have migraine. A January 2024 article in Scientific Reports described the results of a nationwide population-based study that was conducted using data from the Korean National Health Insurance Service database. This study included 10,131,193 individuals. The researchers found that the risk for development of IBD in patients with migraine was significantly higher, by 1.3 times, compared with the general population. These results are similar to previous studies, such as a meta-analysis published in May 2023 in the International Journal of Preventive Medicine, which reported a pooled prevalence of migraine in IBD cases of 19%, with 1.5-fold higher odds of developing migraine in IBD cases when compared with controls.^[3] These studies were both aimed at examining epidemiologic data rather than uncovering a physiologic or genetic cause of the link, and neither study described an explanation for this connection.

A Mendelian randomization study published in May 2023 in Headache investigated potential genetic links between migraine and IBD. As with the January 2024 European Journal of Medical Research study that was done to search for a genetic association between migraine and allergic rhinitis, the authors stated that there was no evidence of a shared genetic basis or of a causal association between migraine and either IBD or celiac disease.^[4] Although the evidence doesn't point to a causal relationship, it's important to note that diet plays a role in migraine management, and diet is especially important in managing IBD. Consideration of dietary factors could be beneficial for preventing symptoms — and is even more important for avoiding exacerbation of symptoms.

A high body mass index (BMI) is correlated with migraine. A study published in January 2024 in BMC Geriatrics analyzed data from people who participated in the National Health and Nutrition Examination Survey between 1999 and 2004 by the Centers for Disease Control and the National Center for Health Statistics, comprising a total of 31,126 participants. The researchers found a linear association between BMI and migraine. They also noted that increased BMI was related to a significantly higher risk for migraine in the group with diabetes, but this positive relationship between BMI and migraine seemed to be smaller in the group without diabetes. The authors considered inflammation associated with obesity as a possible contributing factor for this link but acknowledged that the pathophysiologic mechanism is unknown and suggested that there is a high likelihood of confounding factors. Given that diabetes and obesity are both correlated with an increased risk for vascular disease and migraine is associated with a slight increase in cardiovascular risk, it could be especially important to identify these comorbidities in individual patients.

Migraine is common, and many comorbidities have been verified with population studies. Although there are some explanations for the links between migraine and vascular or neurologic conditions, the cause of associations between migraine and other conditions is not known. Some theories that have begun to be investigated include inflammation and genetics. Eventually, further research and understanding of contributing factors could potentially provide explanations that may help in diagnosing migraine or associated disorders at an early stage — and might even be used to help guide treatment.

Additional References

1. Ashina M, Katsarava Z, Do TP, et al. Migraine: Epidemiology and systems of care. Lancet. 2021;397:1485-1495. doi: 10.1016/S0140-6736(20)32160-7 Source

2. Burch RC, Buse DC, Lipton RB. Migraine: Epidemiology, burden, and comorbidity. Neurol Clin. 2019;37:631-649. doi: 10.1016/j.ncl.2019.06.001 Source

3. Olfati H, Mirmosayyeb O, Hosseinabadi AM, Ghajarzadeh M. The prevalence of migraine in inflammatory bowel disease, a systematic review and meta-analysis. Int J Prev Med. 2023;14:66. doi: 10.4103/ijpvm.ijpvm_413_21 Source

4. Welander NZ, Rukh G, Rask-Andersen M, Harder AV, et al and International Headache Genetics Consortium. Migraine, inflammatory bowel disease and celiac disease: A Mendelian randomization study. Headache. 2023;63:642-651. doi: 10.1111/head.14470 Source

Key clinical point: Calcitonin gene-related peptide-antagonists, such as rimegepant and Ubrogepant, can be used for treating acute migraine due to their favorable efficacy and safety, whereas lasmiditan, despite showing promising efficacy, may increase the risk for adverse events (AE).

Major finding: Compared with other drugs, 100 mg ubrogepant showed the highest surface under the cumulative ranking curve (SUCRA) for providing quick pain freedom at 2 hours (0.79) and sustained pain freedom for over 24 hours (0.74), and 75 mg rimegepant showed the highest SUCRA for providing freedom from photophobia within 2 hours (0.96). Although both 100 mg and 200 mg lasmiditan provided relief from headache pain at 2 hours, they increased the risk for AE.

Study details: Findings are from a network meta-analysis of 18 studies including 22,429 patients with migraine who received lasmiditan, rimegepant, ubrogepant, and zavegepant.

Disclosures: This study was supported by the Fundamental Research Funds for the Central Universities, China. The authors declared no conflicts of interest.

Source: Deng X, Zhou L, Liang C et al. Comparison of effectiveness and safety of lasmiditan and CGRP-antagonists for the acute treatment of migraine in adults: Systematic review and network meta-analysis of randomised trials. J Headache Pain. 2024;25:16. doi: 10.1186/s10194-024-01723-4 Source

Key clinical point: Calcitonin gene-related peptide-antagonists, such as rimegepant and Ubrogepant, can be used for treating acute migraine due to their favorable efficacy and safety, whereas lasmiditan, despite showing promising efficacy, may increase the risk for adverse events (AE).

Major finding: Compared with other drugs, 100 mg ubrogepant showed the highest surface under the cumulative ranking curve (SUCRA) for providing quick pain freedom at 2 hours (0.79) and sustained pain freedom for over 24 hours (0.74), and 75 mg rimegepant showed the highest SUCRA for providing freedom from photophobia within 2 hours (0.96). Although both 100 mg and 200 mg lasmiditan provided relief from headache pain at 2 hours, they increased the risk for AE.

Study details: Findings are from a network meta-analysis of 18 studies including 22,429 patients with migraine who received lasmiditan, rimegepant, ubrogepant, and zavegepant.

Disclosures: This study was supported by the Fundamental Research Funds for the Central Universities, China. The authors declared no conflicts of interest.

Source: Deng X, Zhou L, Liang C et al. Comparison of effectiveness and safety of lasmiditan and CGRP-antagonists for the acute treatment of migraine in adults: Systematic review and network meta-analysis of randomised trials. J Headache Pain. 2024;25:16. doi: 10.1186/s10194-024-01723-4 Source

Key clinical point: Calcitonin gene-related peptide-antagonists, such as rimegepant and Ubrogepant, can be used for treating acute migraine due to their favorable efficacy and safety, whereas lasmiditan, despite showing promising efficacy, may increase the risk for adverse events (AE).

Major finding: Compared with other drugs, 100 mg ubrogepant showed the highest surface under the cumulative ranking curve (SUCRA) for providing quick pain freedom at 2 hours (0.79) and sustained pain freedom for over 24 hours (0.74), and 75 mg rimegepant showed the highest SUCRA for providing freedom from photophobia within 2 hours (0.96). Although both 100 mg and 200 mg lasmiditan provided relief from headache pain at 2 hours, they increased the risk for AE.

Study details: Findings are from a network meta-analysis of 18 studies including 22,429 patients with migraine who received lasmiditan, rimegepant, ubrogepant, and zavegepant.

Disclosures: This study was supported by the Fundamental Research Funds for the Central Universities, China. The authors declared no conflicts of interest.

Source: Deng X, Zhou L, Liang C et al. Comparison of effectiveness and safety of lasmiditan and CGRP-antagonists for the acute treatment of migraine in adults: Systematic review and network meta-analysis of randomised trials. J Headache Pain. 2024;25:16. doi: 10.1186/s10194-024-01723-4 Source

Key clinical point: Habitual intake of caffeinated beverages may not increase headache frequency, duration, or intensity in patients with episodic migraine, contrary to popular belief.

Major finding: Compared with patients having episodic migraine who did not habitually consume caffeinated beverages, those who consumed 1-2 servings per day reported 0.3 (95% CI −2.0 to 2.5) more headache days per month, whereas those who consumed 3-4 servings per day reported 1.3 (95% CI −4.5 to 1.9) fewer headache days per month. Moreover, the headache duration and intensity did not differ across levels of caffeinated beverage intake.

Study details: This prospective cohort study evaluated the association between habitual caffeinated beverages intake and headache outcomes among 97 patients with episodic migraine (age ≥ 18 years).

Disclosures: This study was funded by US National Institute of Neurological Disorders and Stroke, the American Sleep Medicine Foundation, Harvard Catalyst—The Harvard Clinical and Translational Science Center. Suzanne M. Bertisch declared serving as a consultant for Idorsia and ResMed. The other authors declared no conflicts of interest.

Source: Mittleman MR, Mostofsky E, Vgontzas A, Bertisch SM. Habitual caffeinated beverage consumption and headaches among adults with episodic migraine: A prospective cohort study. Headache. 2024 (Feb 6). doi: 10.1111/head.14673 Source

Key clinical point: Habitual intake of caffeinated beverages may not increase headache frequency, duration, or intensity in patients with episodic migraine, contrary to popular belief.

Major finding: Compared with patients having episodic migraine who did not habitually consume caffeinated beverages, those who consumed 1-2 servings per day reported 0.3 (95% CI −2.0 to 2.5) more headache days per month, whereas those who consumed 3-4 servings per day reported 1.3 (95% CI −4.5 to 1.9) fewer headache days per month. Moreover, the headache duration and intensity did not differ across levels of caffeinated beverage intake.

Study details: This prospective cohort study evaluated the association between habitual caffeinated beverages intake and headache outcomes among 97 patients with episodic migraine (age ≥ 18 years).

Disclosures: This study was funded by US National Institute of Neurological Disorders and Stroke, the American Sleep Medicine Foundation, Harvard Catalyst—The Harvard Clinical and Translational Science Center. Suzanne M. Bertisch declared serving as a consultant for Idorsia and ResMed. The other authors declared no conflicts of interest.

Source: Mittleman MR, Mostofsky E, Vgontzas A, Bertisch SM. Habitual caffeinated beverage consumption and headaches among adults with episodic migraine: A prospective cohort study. Headache. 2024 (Feb 6). doi: 10.1111/head.14673 Source

Key clinical point: Habitual intake of caffeinated beverages may not increase headache frequency, duration, or intensity in patients with episodic migraine, contrary to popular belief.

Major finding: Compared with patients having episodic migraine who did not habitually consume caffeinated beverages, those who consumed 1-2 servings per day reported 0.3 (95% CI −2.0 to 2.5) more headache days per month, whereas those who consumed 3-4 servings per day reported 1.3 (95% CI −4.5 to 1.9) fewer headache days per month. Moreover, the headache duration and intensity did not differ across levels of caffeinated beverage intake.

Study details: This prospective cohort study evaluated the association between habitual caffeinated beverages intake and headache outcomes among 97 patients with episodic migraine (age ≥ 18 years).

Disclosures: This study was funded by US National Institute of Neurological Disorders and Stroke, the American Sleep Medicine Foundation, Harvard Catalyst—The Harvard Clinical and Translational Science Center. Suzanne M. Bertisch declared serving as a consultant for Idorsia and ResMed. The other authors declared no conflicts of interest.

Source: Mittleman MR, Mostofsky E, Vgontzas A, Bertisch SM. Habitual caffeinated beverage consumption and headaches among adults with episodic migraine: A prospective cohort study. Headache. 2024 (Feb 6). doi: 10.1111/head.14673 Source

Key clinical point: Anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) were more effective than onabotulinumtoxinA (BoNT-A) in reducing monthly headache days (MHD) in patients with chronic migraine (CM), although the safety profile of both treatments was comparable.

Major finding: Anti-CGRP mAb vs BoNT-A led to a significantly greater reduction in MHD at 6 months (adjusted mean difference ‒7.1; P < .001) and 12 months(adjusted mean difference ‒6.2; P < .001). Both treatments had favorable and comparable safety profiles.

Study details: Findings are from an observational, retrospective, multicenter, cohort study including 183 patients with CM who had at least two oral preventive treatment failures and received anti-CGRP mAb (n = 86) and BoNT-A (n = 97).

Disclosures: This study was supported by Italian Ministry of Health. Four authors declared receiving consultancy and advisory fees, travel grants, honoraria, or personal fees for participating in advisory boards, speaker panels, or clinical investigation studies from various sources.

Source: Grazzi L, Giossi R, Montisano DA et al. Real-world effectiveness of anti-CGRP monoclonal antibodies compared to onabotulinumtoxinA (RAMO) in chronic migraine: A retrospective, observational, multicenter, cohort study. J Headache Pain. 2024;25:14. doi: 10.1186/s10194-024-01721-6 Source

Key clinical point: Anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) were more effective than onabotulinumtoxinA (BoNT-A) in reducing monthly headache days (MHD) in patients with chronic migraine (CM), although the safety profile of both treatments was comparable.

Major finding: Anti-CGRP mAb vs BoNT-A led to a significantly greater reduction in MHD at 6 months (adjusted mean difference ‒7.1; P < .001) and 12 months(adjusted mean difference ‒6.2; P < .001). Both treatments had favorable and comparable safety profiles.

Study details: Findings are from an observational, retrospective, multicenter, cohort study including 183 patients with CM who had at least two oral preventive treatment failures and received anti-CGRP mAb (n = 86) and BoNT-A (n = 97).

Disclosures: This study was supported by Italian Ministry of Health. Four authors declared receiving consultancy and advisory fees, travel grants, honoraria, or personal fees for participating in advisory boards, speaker panels, or clinical investigation studies from various sources.

Source: Grazzi L, Giossi R, Montisano DA et al. Real-world effectiveness of anti-CGRP monoclonal antibodies compared to onabotulinumtoxinA (RAMO) in chronic migraine: A retrospective, observational, multicenter, cohort study. J Headache Pain. 2024;25:14. doi: 10.1186/s10194-024-01721-6 Source

Key clinical point: Anti-calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) were more effective than onabotulinumtoxinA (BoNT-A) in reducing monthly headache days (MHD) in patients with chronic migraine (CM), although the safety profile of both treatments was comparable.

Major finding: Anti-CGRP mAb vs BoNT-A led to a significantly greater reduction in MHD at 6 months (adjusted mean difference ‒7.1; P < .001) and 12 months(adjusted mean difference ‒6.2; P < .001). Both treatments had favorable and comparable safety profiles.

Study details: Findings are from an observational, retrospective, multicenter, cohort study including 183 patients with CM who had at least two oral preventive treatment failures and received anti-CGRP mAb (n = 86) and BoNT-A (n = 97).

Disclosures: This study was supported by Italian Ministry of Health. Four authors declared receiving consultancy and advisory fees, travel grants, honoraria, or personal fees for participating in advisory boards, speaker panels, or clinical investigation studies from various sources.

Source: Grazzi L, Giossi R, Montisano DA et al. Real-world effectiveness of anti-CGRP monoclonal antibodies compared to onabotulinumtoxinA (RAMO) in chronic migraine: A retrospective, observational, multicenter, cohort study. J Headache Pain. 2024;25:14. doi: 10.1186/s10194-024-01721-6 Source

and migraine or its subtypes, and vice versa.

Major finding: Genetic predispositions to AR were not casually associated with a higher risk for migraine (odds ratio [OR] 0.816; P = .394), both with aura (OR 0.690; P = .384) and without aura (OR 1.022; P = .954). Reciprocally, genetic predispositions to migraine or its subtypes showed no casual association with AR.

Study details: This two-sample Mendelian randomization analysis included 25,486 patients with AR and 87,907 control individuals without AR along with 3541 patients with migraine with aura, 3215 patients with migraine without aura, and 176,107 controls individuals without migraine.

Disclosures: This study was supported by grants from the National Natural Science Foundation of China and the Fundamental Research Funds for the Central Universities. The authors declared no conflicts of interest.

Source: Lv H, Liu K, Xie Y et al. No causal association between allergic rhinitis and migraine: A Mendelian randomization study. Eur J Med Res. 2024;29:78. doi: 10.1186/s40001-024-01682-1 Source

and migraine or its subtypes, and vice versa.

Major finding: Genetic predispositions to AR were not casually associated with a higher risk for migraine (odds ratio [OR] 0.816; P = .394), both with aura (OR 0.690; P = .384) and without aura (OR 1.022; P = .954). Reciprocally, genetic predispositions to migraine or its subtypes showed no casual association with AR.

Study details: This two-sample Mendelian randomization analysis included 25,486 patients with AR and 87,907 control individuals without AR along with 3541 patients with migraine with aura, 3215 patients with migraine without aura, and 176,107 controls individuals without migraine.

Disclosures: This study was supported by grants from the National Natural Science Foundation of China and the Fundamental Research Funds for the Central Universities. The authors declared no conflicts of interest.

Source: Lv H, Liu K, Xie Y et al. No causal association between allergic rhinitis and migraine: A Mendelian randomization study. Eur J Med Res. 2024;29:78. doi: 10.1186/s40001-024-01682-1 Source

and migraine or its subtypes, and vice versa.

Major finding: Genetic predispositions to AR were not casually associated with a higher risk for migraine (odds ratio [OR] 0.816; P = .394), both with aura (OR 0.690; P = .384) and without aura (OR 1.022; P = .954). Reciprocally, genetic predispositions to migraine or its subtypes showed no casual association with AR.

Study details: This two-sample Mendelian randomization analysis included 25,486 patients with AR and 87,907 control individuals without AR along with 3541 patients with migraine with aura, 3215 patients with migraine without aura, and 176,107 controls individuals without migraine.

Disclosures: This study was supported by grants from the National Natural Science Foundation of China and the Fundamental Research Funds for the Central Universities. The authors declared no conflicts of interest.

Source: Lv H, Liu K, Xie Y et al. No causal association between allergic rhinitis and migraine: A Mendelian randomization study. Eur J Med Res. 2024;29:78. doi: 10.1186/s40001-024-01682-1 Source