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The field of headache medicine has changed significantly since 2018 with the advent of calcitonin gene-related peptide (CGRP)–targeted medications. Although many patients improve after their first injection, and there is even a significant portion of "super responders" who can revert to nearly zero headache days per month, the majority of patients have a moderate response. Many patients who have not had a significant decrease in the frequency and severity of migraine attacks over 12 weeks wonder whether they will eventually achieve this on a CGRP medication. Barbanti and colleagues looked specifically at the subpopulation of late responders to CGRP treatments.
This was a multicenter, prospective study lasting 24 weeks, defining the differences in responders to CGRP treatments. Participants in this study had failed three or more prior preventive medications and had high-frequency, episodic, or chronic migraine. Their response rate was determined as follows: "responder" patients had a more than 50% reduction in baseline monthly migraine days between weeks 9 and 12, and "late responder" patients achieved that reduction after 12 weeks. All three injectable CGRP monoclonal antibodies were included in this trial.
Nearly 66% of patients treated with a CGRP monoclonal antibody had a 50% or greater response at 12 weeks. Of the study participants, 34% were considered nonresponders at 12 weeks, and 55% of those nonresponders did become responders between 13 and 24 weeks. This subpopulation of late responders was noted to have higher body mass index (BMI), more frequent prior treatment failures, as well as other pain and psychiatric comorbidities. Allodynia and unilateral cranial autonomic symptoms were also noted to be significantly higher in this population.
This study helps better determine the length of a CGRP trial for prevention. Patients with more treatment failures and comorbidities should be given additional time for this class of medications to work, even beyond the initial 12 weeks.
The COVID-19 pandemic has changed the way of life for everyone, and this is especially true for people with chronic medical conditions. Hrytsenko and colleagues sought to quantify the effect that COVID-19 had on patients with a history of episodic or chronic migraine. They used a scale to determine "psycho-emotional state deterioration" in patients with migraine with and without a history of COVID-19.
The investigators included 133 participants with a prior diagnosis of migraine, either chronic or episodic. Of these, 95 had a positive polymerase chain reaction (PCR) test for COVID-19, indicating SARS-CoV-2 infection; 38 did not. The Hamilton Anxiety Rating Scale (HARS) was used to assess the severity of perceived anxiety symptoms and was used to determine psycho-emotional state. The Migraine Disability Assessment test (MIDAS) was used to determine their quality of life and degree of disability related to migraine. Patients with a history of COVID-19 had an increased usage of antimigraine medications, increased frequency of attacks, and higher HARS ratings. The average MIDAS score also increased significantly.
Many of our patients who were struggling prior to the COVID-19 pandemic unfortunately have done much worse after SARS-CoV-2 infection. A number of potential explanations exist for this, including worsening neuroinflammation in the context of COVID-19, which can specifically increase the propagation of inflammatory neurotransmitters, such as CGRP. Patients with a history of migraine respond to this with heightened frequency and severity of migraine.
There is a notable growing connection between certain neurologic conditions and vasomotor symptoms. Specifically, there appears to be an increased incidence of migraine and certain hypertensive or tachycardic conditions. Migraine is well known to be a vascular risk factor and migraine with aura even more so. Faubion and colleagues sought to quantify this in a specific menopausal population.
This was a large cross-sectional study, with an older median age compared with average migraine studies: 52.8 years. Nearly 60% of participants were postmenopausal and were recruited from a Mayo Clinic menopause registry. Participants were evaluated for a history of migraine based on The International Classification of Headache Disorders, third edition (ICHD3), criteria. They also had their symptoms measured on a menopause rating scale (the symptoms measured included hot flashes, sleep problems, physical and mental exhaustion, joint and muscular discomfort, and mood). Additional information was cross-referenced, including BMI, race, ethnicity, education, marital status, hypertension, and menopause status.
A diagnosis of migraine was associated with hypertension. There was no association between hypertension and hot flash severity, and there was a suggestion that hot flash severity and migraine history were not associated. The presence of other pain disorders also did not correlate with any other vasomotor symptoms.
This study does again link vasomotor issues with migraines. This connection remains well-founded and relevant. Antihypertensive medications have been some of the first preventive options ever offered to people with migraine. CGRP medications may actually lead to an increase in the risk for hypertension. Disconnection remains relevant and is something to discuss with patients with migraine, especially if they are at a higher risk.
The field of headache medicine has changed significantly since 2018 with the advent of calcitonin gene-related peptide (CGRP)–targeted medications. Although many patients improve after their first injection, and there is even a significant portion of "super responders" who can revert to nearly zero headache days per month, the majority of patients have a moderate response. Many patients who have not had a significant decrease in the frequency and severity of migraine attacks over 12 weeks wonder whether they will eventually achieve this on a CGRP medication. Barbanti and colleagues looked specifically at the subpopulation of late responders to CGRP treatments.
This was a multicenter, prospective study lasting 24 weeks, defining the differences in responders to CGRP treatments. Participants in this study had failed three or more prior preventive medications and had high-frequency, episodic, or chronic migraine. Their response rate was determined as follows: "responder" patients had a more than 50% reduction in baseline monthly migraine days between weeks 9 and 12, and "late responder" patients achieved that reduction after 12 weeks. All three injectable CGRP monoclonal antibodies were included in this trial.
Nearly 66% of patients treated with a CGRP monoclonal antibody had a 50% or greater response at 12 weeks. Of the study participants, 34% were considered nonresponders at 12 weeks, and 55% of those nonresponders did become responders between 13 and 24 weeks. This subpopulation of late responders was noted to have higher body mass index (BMI), more frequent prior treatment failures, as well as other pain and psychiatric comorbidities. Allodynia and unilateral cranial autonomic symptoms were also noted to be significantly higher in this population.
This study helps better determine the length of a CGRP trial for prevention. Patients with more treatment failures and comorbidities should be given additional time for this class of medications to work, even beyond the initial 12 weeks.
The COVID-19 pandemic has changed the way of life for everyone, and this is especially true for people with chronic medical conditions. Hrytsenko and colleagues sought to quantify the effect that COVID-19 had on patients with a history of episodic or chronic migraine. They used a scale to determine "psycho-emotional state deterioration" in patients with migraine with and without a history of COVID-19.
The investigators included 133 participants with a prior diagnosis of migraine, either chronic or episodic. Of these, 95 had a positive polymerase chain reaction (PCR) test for COVID-19, indicating SARS-CoV-2 infection; 38 did not. The Hamilton Anxiety Rating Scale (HARS) was used to assess the severity of perceived anxiety symptoms and was used to determine psycho-emotional state. The Migraine Disability Assessment test (MIDAS) was used to determine their quality of life and degree of disability related to migraine. Patients with a history of COVID-19 had an increased usage of antimigraine medications, increased frequency of attacks, and higher HARS ratings. The average MIDAS score also increased significantly.
Many of our patients who were struggling prior to the COVID-19 pandemic unfortunately have done much worse after SARS-CoV-2 infection. A number of potential explanations exist for this, including worsening neuroinflammation in the context of COVID-19, which can specifically increase the propagation of inflammatory neurotransmitters, such as CGRP. Patients with a history of migraine respond to this with heightened frequency and severity of migraine.
There is a notable growing connection between certain neurologic conditions and vasomotor symptoms. Specifically, there appears to be an increased incidence of migraine and certain hypertensive or tachycardic conditions. Migraine is well known to be a vascular risk factor and migraine with aura even more so. Faubion and colleagues sought to quantify this in a specific menopausal population.
This was a large cross-sectional study, with an older median age compared with average migraine studies: 52.8 years. Nearly 60% of participants were postmenopausal and were recruited from a Mayo Clinic menopause registry. Participants were evaluated for a history of migraine based on The International Classification of Headache Disorders, third edition (ICHD3), criteria. They also had their symptoms measured on a menopause rating scale (the symptoms measured included hot flashes, sleep problems, physical and mental exhaustion, joint and muscular discomfort, and mood). Additional information was cross-referenced, including BMI, race, ethnicity, education, marital status, hypertension, and menopause status.
A diagnosis of migraine was associated with hypertension. There was no association between hypertension and hot flash severity, and there was a suggestion that hot flash severity and migraine history were not associated. The presence of other pain disorders also did not correlate with any other vasomotor symptoms.
This study does again link vasomotor issues with migraines. This connection remains well-founded and relevant. Antihypertensive medications have been some of the first preventive options ever offered to people with migraine. CGRP medications may actually lead to an increase in the risk for hypertension. Disconnection remains relevant and is something to discuss with patients with migraine, especially if they are at a higher risk.
The field of headache medicine has changed significantly since 2018 with the advent of calcitonin gene-related peptide (CGRP)–targeted medications. Although many patients improve after their first injection, and there is even a significant portion of "super responders" who can revert to nearly zero headache days per month, the majority of patients have a moderate response. Many patients who have not had a significant decrease in the frequency and severity of migraine attacks over 12 weeks wonder whether they will eventually achieve this on a CGRP medication. Barbanti and colleagues looked specifically at the subpopulation of late responders to CGRP treatments.
This was a multicenter, prospective study lasting 24 weeks, defining the differences in responders to CGRP treatments. Participants in this study had failed three or more prior preventive medications and had high-frequency, episodic, or chronic migraine. Their response rate was determined as follows: "responder" patients had a more than 50% reduction in baseline monthly migraine days between weeks 9 and 12, and "late responder" patients achieved that reduction after 12 weeks. All three injectable CGRP monoclonal antibodies were included in this trial.
Nearly 66% of patients treated with a CGRP monoclonal antibody had a 50% or greater response at 12 weeks. Of the study participants, 34% were considered nonresponders at 12 weeks, and 55% of those nonresponders did become responders between 13 and 24 weeks. This subpopulation of late responders was noted to have higher body mass index (BMI), more frequent prior treatment failures, as well as other pain and psychiatric comorbidities. Allodynia and unilateral cranial autonomic symptoms were also noted to be significantly higher in this population.
This study helps better determine the length of a CGRP trial for prevention. Patients with more treatment failures and comorbidities should be given additional time for this class of medications to work, even beyond the initial 12 weeks.
The COVID-19 pandemic has changed the way of life for everyone, and this is especially true for people with chronic medical conditions. Hrytsenko and colleagues sought to quantify the effect that COVID-19 had on patients with a history of episodic or chronic migraine. They used a scale to determine "psycho-emotional state deterioration" in patients with migraine with and without a history of COVID-19.
The investigators included 133 participants with a prior diagnosis of migraine, either chronic or episodic. Of these, 95 had a positive polymerase chain reaction (PCR) test for COVID-19, indicating SARS-CoV-2 infection; 38 did not. The Hamilton Anxiety Rating Scale (HARS) was used to assess the severity of perceived anxiety symptoms and was used to determine psycho-emotional state. The Migraine Disability Assessment test (MIDAS) was used to determine their quality of life and degree of disability related to migraine. Patients with a history of COVID-19 had an increased usage of antimigraine medications, increased frequency of attacks, and higher HARS ratings. The average MIDAS score also increased significantly.
Many of our patients who were struggling prior to the COVID-19 pandemic unfortunately have done much worse after SARS-CoV-2 infection. A number of potential explanations exist for this, including worsening neuroinflammation in the context of COVID-19, which can specifically increase the propagation of inflammatory neurotransmitters, such as CGRP. Patients with a history of migraine respond to this with heightened frequency and severity of migraine.
There is a notable growing connection between certain neurologic conditions and vasomotor symptoms. Specifically, there appears to be an increased incidence of migraine and certain hypertensive or tachycardic conditions. Migraine is well known to be a vascular risk factor and migraine with aura even more so. Faubion and colleagues sought to quantify this in a specific menopausal population.
This was a large cross-sectional study, with an older median age compared with average migraine studies: 52.8 years. Nearly 60% of participants were postmenopausal and were recruited from a Mayo Clinic menopause registry. Participants were evaluated for a history of migraine based on The International Classification of Headache Disorders, third edition (ICHD3), criteria. They also had their symptoms measured on a menopause rating scale (the symptoms measured included hot flashes, sleep problems, physical and mental exhaustion, joint and muscular discomfort, and mood). Additional information was cross-referenced, including BMI, race, ethnicity, education, marital status, hypertension, and menopause status.
A diagnosis of migraine was associated with hypertension. There was no association between hypertension and hot flash severity, and there was a suggestion that hot flash severity and migraine history were not associated. The presence of other pain disorders also did not correlate with any other vasomotor symptoms.
This study does again link vasomotor issues with migraines. This connection remains well-founded and relevant. Antihypertensive medications have been some of the first preventive options ever offered to people with migraine. CGRP medications may actually lead to an increase in the risk for hypertension. Disconnection remains relevant and is something to discuss with patients with migraine, especially if they are at a higher risk.