Headache & Migraine

Optimism and pessimism are associated with migraine and migraine‐related disability. This according to a recent study that found that people with migraine were less optimistic and more pessimistic than controls and endorsed higher levels of anxious and depressive symptoms. The sample population was selected through a stratified, multi‐stage area probability sample of households. A validated questionnaire eliciting data on demographics, headache features, migraine‐related disability, depression (PHQ‐9), anxiety (GAD‐7), optimism, and pessimism was administered to people with migraine and headache‐free control participants via trained interviewers. The odds for having migraine/no headache diagnosis were calculated by binary logistic regression, and ordinal regression was performed to check associations between migraine‐related disability and optimism. Researchers found:

• Out of 600 individuals, 302 met inclusion criteria and were included (140 controls [with no history of headache disorders] and 162 people meeting criteria for migraine [29 with chronic migraine, that is, ≥15 headache days/month]).
• Pessimism and anxiety were predictors of meeting criteria for migraine, while optimism was inversely associated with migraine‐related disability.

Peres MFP, Belitardo A, Mercante JP, et al. Optimism, pessimism, and migraine: A cross‐sectional, population‐based study. [Published online ahead of print January 19, 2019]. Headache. doi:10.1111/head.13471.

Optimism and pessimism are associated with migraine and migraine‐related disability. This according to a recent study that found that people with migraine were less optimistic and more pessimistic than controls and endorsed higher levels of anxious and depressive symptoms. The sample population was selected through a stratified, multi‐stage area probability sample of households. A validated questionnaire eliciting data on demographics, headache features, migraine‐related disability, depression (PHQ‐9), anxiety (GAD‐7), optimism, and pessimism was administered to people with migraine and headache‐free control participants via trained interviewers. The odds for having migraine/no headache diagnosis were calculated by binary logistic regression, and ordinal regression was performed to check associations between migraine‐related disability and optimism. Researchers found:

• Out of 600 individuals, 302 met inclusion criteria and were included (140 controls [with no history of headache disorders] and 162 people meeting criteria for migraine [29 with chronic migraine, that is, ≥15 headache days/month]).
• Pessimism and anxiety were predictors of meeting criteria for migraine, while optimism was inversely associated with migraine‐related disability.

Peres MFP, Belitardo A, Mercante JP, et al. Optimism, pessimism, and migraine: A cross‐sectional, population‐based study. [Published online ahead of print January 19, 2019]. Headache. doi:10.1111/head.13471.

Optimism and pessimism are associated with migraine and migraine‐related disability. This according to a recent study that found that people with migraine were less optimistic and more pessimistic than controls and endorsed higher levels of anxious and depressive symptoms. The sample population was selected through a stratified, multi‐stage area probability sample of households. A validated questionnaire eliciting data on demographics, headache features, migraine‐related disability, depression (PHQ‐9), anxiety (GAD‐7), optimism, and pessimism was administered to people with migraine and headache‐free control participants via trained interviewers. The odds for having migraine/no headache diagnosis were calculated by binary logistic regression, and ordinal regression was performed to check associations between migraine‐related disability and optimism. Researchers found:

• Out of 600 individuals, 302 met inclusion criteria and were included (140 controls [with no history of headache disorders] and 162 people meeting criteria for migraine [29 with chronic migraine, that is, ≥15 headache days/month]).
• Pessimism and anxiety were predictors of meeting criteria for migraine, while optimism was inversely associated with migraine‐related disability.

Peres MFP, Belitardo A, Mercante JP, et al. Optimism, pessimism, and migraine: A cross‐sectional, population‐based study. [Published online ahead of print January 19, 2019]. Headache. doi:10.1111/head.13471.

Increased stroke risk in late life was observed in participants with late onset of migraine with aura (MA), as compared to participants with no headache in a recent ongoing, prospective, longitudinal, community‐based cohort study. Longer cumulative exposure to migraine with visual aura, however, was not associated with increased risk of ischemic stroke in late life. Participants were interviewed to ascertain migraine history at the third visit (1993–1995) and followed for ischemic stroke incidence over 20 years. Researchers performed a post hoc analysis to evaluate the association between the age of migraine onset and ischemic stroke. They found:

• There were 447 migraineurs with MA and 1128 migraineurs without aura (MO) identified among 11,592 black and white participants.
• There was an association between the age of MA onset at age ≥50 years (average duration=4.75 years) and ischemic stroke when compared to the no headache group (multivariable adjusted HR=2.17).
• MA onset at <50 years (average duration=28.17 years) was not associated with stroke (multivariable adjusted HR=1.31).
• MO was not associated with increased stroke regardless of the age of onset.

Androulakis XM, Sen S, Kodumuri N, et al. Migraine age of onset and association with ischemic stroke in late life: 20 years follow‐up in ARIC. [Published online ahead of print January 21, 2019]. Headache. doi:10.1111/head.13468.

Increased stroke risk in late life was observed in participants with late onset of migraine with aura (MA), as compared to participants with no headache in a recent ongoing, prospective, longitudinal, community‐based cohort study. Longer cumulative exposure to migraine with visual aura, however, was not associated with increased risk of ischemic stroke in late life. Participants were interviewed to ascertain migraine history at the third visit (1993–1995) and followed for ischemic stroke incidence over 20 years. Researchers performed a post hoc analysis to evaluate the association between the age of migraine onset and ischemic stroke. They found:

• There were 447 migraineurs with MA and 1128 migraineurs without aura (MO) identified among 11,592 black and white participants.
• There was an association between the age of MA onset at age ≥50 years (average duration=4.75 years) and ischemic stroke when compared to the no headache group (multivariable adjusted HR=2.17).
• MA onset at <50 years (average duration=28.17 years) was not associated with stroke (multivariable adjusted HR=1.31).
• MO was not associated with increased stroke regardless of the age of onset.

Androulakis XM, Sen S, Kodumuri N, et al. Migraine age of onset and association with ischemic stroke in late life: 20 years follow‐up in ARIC. [Published online ahead of print January 21, 2019]. Headache. doi:10.1111/head.13468.

Increased stroke risk in late life was observed in participants with late onset of migraine with aura (MA), as compared to participants with no headache in a recent ongoing, prospective, longitudinal, community‐based cohort study. Longer cumulative exposure to migraine with visual aura, however, was not associated with increased risk of ischemic stroke in late life. Participants were interviewed to ascertain migraine history at the third visit (1993–1995) and followed for ischemic stroke incidence over 20 years. Researchers performed a post hoc analysis to evaluate the association between the age of migraine onset and ischemic stroke. They found:

• There were 447 migraineurs with MA and 1128 migraineurs without aura (MO) identified among 11,592 black and white participants.
• There was an association between the age of MA onset at age ≥50 years (average duration=4.75 years) and ischemic stroke when compared to the no headache group (multivariable adjusted HR=2.17).
• MA onset at <50 years (average duration=28.17 years) was not associated with stroke (multivariable adjusted HR=1.31).
• MO was not associated with increased stroke regardless of the age of onset.

Androulakis XM, Sen S, Kodumuri N, et al. Migraine age of onset and association with ischemic stroke in late life: 20 years follow‐up in ARIC. [Published online ahead of print January 21, 2019]. Headache. doi:10.1111/head.13468.

The age at which a patient develops migraine with aura may be an important factor in assessing stroke risk, according to a prospective cohort study published in Headache.

DKart/iStockphoto

Patients who had onset of migraine with visual aura after age 50 years had an increased risk of ischemic stroke, compared with patients with no headache, the researchers found. Patients with longer exposure to migraine with visual aura – that is, onset before age 50 years – did not have significantly increased ischemic stroke risk, said X. Michelle Androulakis, MD, of the department of neurology at the University of South Carolina in Columbia, and her colleagues.

“Migraine, especially migraine with aura, is associated with increased risk of ischemic stroke,” but whether age of migraine onset affects the risk of cardiovascular disease has been unclear, the researchers said.

To examine the risk of ischemic stroke in migraineurs with and without aura with onset before and after age 50 years, the investigators conducted a post hoc analysis of data from the ongoing Atherosclerosis Risk in Communities (ARIC) study. The researchers adjusted for potential confounders, including diabetes, body mass index, hypertension, and hyperlipidemia.

In ARIC, participants completed a questionnaire about their migraine history at their third study visit (1993-1995) and were followed for ischemic stroke incidence over 20 years.

Of the 11,592 ARIC participants included in the analysis (mean age, 61 years; 76.5% white; and 55.3% female), 447 had migraine with aura, and 1,128 had migraine without aura. Onset of migraine with aura at age 50 years or older (average duration, 4.75 years) was associated with more than twofold greater risk of ischemic stroke, compared with no headache (multivariable adjusted hazard ratio = 2.17). Onset of migraine with aura before age 50 years (average duration, 28.17 years) was not significantly associated with stroke. A logistic regression model yielded consistent results.

In addition, patients with migraine without aura did not have an increased risk of stroke, regardless of the age of onset. The absolute risk for stroke in migraine with aura was 8.27%, and the absolute risk in migraine without aura was 4.25%.

“We found unexpected results suggesting that the onset of migraine with aura before age 50 is not associated with ischemic stroke. ... These results are specific to first-time ischemic stroke incidents that occurred in mid- to late life; therefore, it cannot be generalized to stroke in younger patients,” the authors wrote.

It could be that migraine with aura symptoms that start at a later age are a red flag for paradoxical emboli from a patent foramen ovale or microemboli, Dr. Androulakis and her colleagues noted. It also is possible that the degree of cortical spreading depression required to induce migraine with aura symptoms is different later in life versus earlier in life.

“This study underscores the importance of MA symptoms onset in evaluation of ischemic stroke risk in late life,” the researchers concluded.

The authors had no relevant conflicts of interest. ARIC has been funded by the National Heart, Lung, and Blood Institute.

[email protected]

SOURCE: Androulakis XM et al. Headache. 2019 Jan 21. doi: 10.1111/head.13468.

The age at which a patient develops migraine with aura may be an important factor in assessing stroke risk, according to a prospective cohort study published in Headache.

DKart/iStockphoto

Patients who had onset of migraine with visual aura after age 50 years had an increased risk of ischemic stroke, compared with patients with no headache, the researchers found. Patients with longer exposure to migraine with visual aura – that is, onset before age 50 years – did not have significantly increased ischemic stroke risk, said X. Michelle Androulakis, MD, of the department of neurology at the University of South Carolina in Columbia, and her colleagues.

“Migraine, especially migraine with aura, is associated with increased risk of ischemic stroke,” but whether age of migraine onset affects the risk of cardiovascular disease has been unclear, the researchers said.

To examine the risk of ischemic stroke in migraineurs with and without aura with onset before and after age 50 years, the investigators conducted a post hoc analysis of data from the ongoing Atherosclerosis Risk in Communities (ARIC) study. The researchers adjusted for potential confounders, including diabetes, body mass index, hypertension, and hyperlipidemia.

In ARIC, participants completed a questionnaire about their migraine history at their third study visit (1993-1995) and were followed for ischemic stroke incidence over 20 years.

Of the 11,592 ARIC participants included in the analysis (mean age, 61 years; 76.5% white; and 55.3% female), 447 had migraine with aura, and 1,128 had migraine without aura. Onset of migraine with aura at age 50 years or older (average duration, 4.75 years) was associated with more than twofold greater risk of ischemic stroke, compared with no headache (multivariable adjusted hazard ratio = 2.17). Onset of migraine with aura before age 50 years (average duration, 28.17 years) was not significantly associated with stroke. A logistic regression model yielded consistent results.

In addition, patients with migraine without aura did not have an increased risk of stroke, regardless of the age of onset. The absolute risk for stroke in migraine with aura was 8.27%, and the absolute risk in migraine without aura was 4.25%.

“We found unexpected results suggesting that the onset of migraine with aura before age 50 is not associated with ischemic stroke. ... These results are specific to first-time ischemic stroke incidents that occurred in mid- to late life; therefore, it cannot be generalized to stroke in younger patients,” the authors wrote.

It could be that migraine with aura symptoms that start at a later age are a red flag for paradoxical emboli from a patent foramen ovale or microemboli, Dr. Androulakis and her colleagues noted. It also is possible that the degree of cortical spreading depression required to induce migraine with aura symptoms is different later in life versus earlier in life.

“This study underscores the importance of MA symptoms onset in evaluation of ischemic stroke risk in late life,” the researchers concluded.

The authors had no relevant conflicts of interest. ARIC has been funded by the National Heart, Lung, and Blood Institute.

[email protected]

SOURCE: Androulakis XM et al. Headache. 2019 Jan 21. doi: 10.1111/head.13468.

The age at which a patient develops migraine with aura may be an important factor in assessing stroke risk, according to a prospective cohort study published in Headache.

DKart/iStockphoto

Patients who had onset of migraine with visual aura after age 50 years had an increased risk of ischemic stroke, compared with patients with no headache, the researchers found. Patients with longer exposure to migraine with visual aura – that is, onset before age 50 years – did not have significantly increased ischemic stroke risk, said X. Michelle Androulakis, MD, of the department of neurology at the University of South Carolina in Columbia, and her colleagues.

“Migraine, especially migraine with aura, is associated with increased risk of ischemic stroke,” but whether age of migraine onset affects the risk of cardiovascular disease has been unclear, the researchers said.

To examine the risk of ischemic stroke in migraineurs with and without aura with onset before and after age 50 years, the investigators conducted a post hoc analysis of data from the ongoing Atherosclerosis Risk in Communities (ARIC) study. The researchers adjusted for potential confounders, including diabetes, body mass index, hypertension, and hyperlipidemia.

In ARIC, participants completed a questionnaire about their migraine history at their third study visit (1993-1995) and were followed for ischemic stroke incidence over 20 years.

Of the 11,592 ARIC participants included in the analysis (mean age, 61 years; 76.5% white; and 55.3% female), 447 had migraine with aura, and 1,128 had migraine without aura. Onset of migraine with aura at age 50 years or older (average duration, 4.75 years) was associated with more than twofold greater risk of ischemic stroke, compared with no headache (multivariable adjusted hazard ratio = 2.17). Onset of migraine with aura before age 50 years (average duration, 28.17 years) was not significantly associated with stroke. A logistic regression model yielded consistent results.

In addition, patients with migraine without aura did not have an increased risk of stroke, regardless of the age of onset. The absolute risk for stroke in migraine with aura was 8.27%, and the absolute risk in migraine without aura was 4.25%.

“We found unexpected results suggesting that the onset of migraine with aura before age 50 is not associated with ischemic stroke. ... These results are specific to first-time ischemic stroke incidents that occurred in mid- to late life; therefore, it cannot be generalized to stroke in younger patients,” the authors wrote.

It could be that migraine with aura symptoms that start at a later age are a red flag for paradoxical emboli from a patent foramen ovale or microemboli, Dr. Androulakis and her colleagues noted. It also is possible that the degree of cortical spreading depression required to induce migraine with aura symptoms is different later in life versus earlier in life.

“This study underscores the importance of MA symptoms onset in evaluation of ischemic stroke risk in late life,” the researchers concluded.

The authors had no relevant conflicts of interest. ARIC has been funded by the National Heart, Lung, and Blood Institute.

[email protected]

SOURCE: Androulakis XM et al. Headache. 2019 Jan 21. doi: 10.1111/head.13468.

One-hour treatment with external trigeminal nerve stimulation resulted in significant headache pain relief compared to sham stimulation and was well tolerated, according to a recent double-blind, randomized, sham-controlled study conducted across 3 headache centers in the United States. Adult patients who were experiencing an acute migraine attack, with or without aura, were recruited on site and randomly assigned 1:1 to receive either verum or sham external trigeminal nerve stimulation treatment for 1 hour. Pain intensity was scored using a visual analog scale. Researchers found:

• One hundred and six patients were randomized and included in the intention-to-treat analysis (verum: n=52; sham: n=54).
• The primary outcome measure was significantly more reduced in the verum group than in the sham group: −3.46 ± 2.32 vs −1.78 ± 1.89, or −59% vs −30%.
• With regards to migraine subgroups, there was a significant difference in pain reduction between verum and sham for “migraine without aura” attacks.
• For “migraine with aura” attacks, pain reduction was numerically greater for verum vs sham, but did not reach significance: mean visual analog scale reduction at 1 hour was −4.3 ± 1.8 for the verum group vs −2.6 ± 1.9 for the sham group.

Chou DE, Yugrakh MS, Winegarner D, Rowe V, Kuruvilla D, Schoenen. Acute migraine therapy with external trigeminal neurostimulation (ACME): A randomized controlled trial. [Published online ahead of print November 17, 2018]. Cephalalgia. doi:10.1177%2F0333102418811573.

One-hour treatment with external trigeminal nerve stimulation resulted in significant headache pain relief compared to sham stimulation and was well tolerated, according to a recent double-blind, randomized, sham-controlled study conducted across 3 headache centers in the United States. Adult patients who were experiencing an acute migraine attack, with or without aura, were recruited on site and randomly assigned 1:1 to receive either verum or sham external trigeminal nerve stimulation treatment for 1 hour. Pain intensity was scored using a visual analog scale. Researchers found:

• One hundred and six patients were randomized and included in the intention-to-treat analysis (verum: n=52; sham: n=54).
• The primary outcome measure was significantly more reduced in the verum group than in the sham group: −3.46 ± 2.32 vs −1.78 ± 1.89, or −59% vs −30%.
• With regards to migraine subgroups, there was a significant difference in pain reduction between verum and sham for “migraine without aura” attacks.
• For “migraine with aura” attacks, pain reduction was numerically greater for verum vs sham, but did not reach significance: mean visual analog scale reduction at 1 hour was −4.3 ± 1.8 for the verum group vs −2.6 ± 1.9 for the sham group.

Chou DE, Yugrakh MS, Winegarner D, Rowe V, Kuruvilla D, Schoenen. Acute migraine therapy with external trigeminal neurostimulation (ACME): A randomized controlled trial. [Published online ahead of print November 17, 2018]. Cephalalgia. doi:10.1177%2F0333102418811573.

One-hour treatment with external trigeminal nerve stimulation resulted in significant headache pain relief compared to sham stimulation and was well tolerated, according to a recent double-blind, randomized, sham-controlled study conducted across 3 headache centers in the United States. Adult patients who were experiencing an acute migraine attack, with or without aura, were recruited on site and randomly assigned 1:1 to receive either verum or sham external trigeminal nerve stimulation treatment for 1 hour. Pain intensity was scored using a visual analog scale. Researchers found:

• One hundred and six patients were randomized and included in the intention-to-treat analysis (verum: n=52; sham: n=54).
• The primary outcome measure was significantly more reduced in the verum group than in the sham group: −3.46 ± 2.32 vs −1.78 ± 1.89, or −59% vs −30%.
• With regards to migraine subgroups, there was a significant difference in pain reduction between verum and sham for “migraine without aura” attacks.
• For “migraine with aura” attacks, pain reduction was numerically greater for verum vs sham, but did not reach significance: mean visual analog scale reduction at 1 hour was −4.3 ± 1.8 for the verum group vs −2.6 ± 1.9 for the sham group.

Chou DE, Yugrakh MS, Winegarner D, Rowe V, Kuruvilla D, Schoenen. Acute migraine therapy with external trigeminal neurostimulation (ACME): A randomized controlled trial. [Published online ahead of print November 17, 2018]. Cephalalgia. doi:10.1177%2F0333102418811573.

Alcoholic beverages, especially red wine, are recognized as a migraine trigger factor by patients with migraine and have a substantial effect on alcohol consumption behavior, according to a recent study. Researchers conducted a cross‐sectional, web‐based, questionnaire study among 2197 patients with migraine from the well‐defined Leiden University MIgraine Neuro‐Analysis (LUMINA) study population. They assessed alcoholic beverage consumption and self‐reported trigger potential, reasons behind alcohol abstinence, and time between alcohol consumption and migraine attack onset. They found:

• Alcoholic beverages were reported as a trigger by 35.6% of participants with migraine.
• In addition, more than 25% of patients with migraine who had stopped consuming or never consumed alcoholic beverages did so because of presumed trigger effects.
• Wine, especially red wine (77.8% of participants), was recognized as the most common trigger among the alcoholic beverages.
• However, red wine consistently led to an attack in only 8.8% of participants.
• Time of onset was rapid (<3 hours) in one‐third of patients and almost 90% had an onset of less than 10 hours independent of beverage type.

Onderwater GLC, van Oosterhaut WPJ, Schoonman GG, Ferrari MD, Terwindt GM. Alcoholic beverages as trigger factor and the effect on alcohol consumption behavior in patients with migraine. [Published online ahead of print December 18, 2018]. Eur J Neurol. doi:10.1111/ene.13861.

Alcoholic beverages, especially red wine, are recognized as a migraine trigger factor by patients with migraine and have a substantial effect on alcohol consumption behavior, according to a recent study. Researchers conducted a cross‐sectional, web‐based, questionnaire study among 2197 patients with migraine from the well‐defined Leiden University MIgraine Neuro‐Analysis (LUMINA) study population. They assessed alcoholic beverage consumption and self‐reported trigger potential, reasons behind alcohol abstinence, and time between alcohol consumption and migraine attack onset. They found:

• Alcoholic beverages were reported as a trigger by 35.6% of participants with migraine.
• In addition, more than 25% of patients with migraine who had stopped consuming or never consumed alcoholic beverages did so because of presumed trigger effects.
• Wine, especially red wine (77.8% of participants), was recognized as the most common trigger among the alcoholic beverages.
• However, red wine consistently led to an attack in only 8.8% of participants.
• Time of onset was rapid (<3 hours) in one‐third of patients and almost 90% had an onset of less than 10 hours independent of beverage type.

Onderwater GLC, van Oosterhaut WPJ, Schoonman GG, Ferrari MD, Terwindt GM. Alcoholic beverages as trigger factor and the effect on alcohol consumption behavior in patients with migraine. [Published online ahead of print December 18, 2018]. Eur J Neurol. doi:10.1111/ene.13861.

Alcoholic beverages, especially red wine, are recognized as a migraine trigger factor by patients with migraine and have a substantial effect on alcohol consumption behavior, according to a recent study. Researchers conducted a cross‐sectional, web‐based, questionnaire study among 2197 patients with migraine from the well‐defined Leiden University MIgraine Neuro‐Analysis (LUMINA) study population. They assessed alcoholic beverage consumption and self‐reported trigger potential, reasons behind alcohol abstinence, and time between alcohol consumption and migraine attack onset. They found:

• Alcoholic beverages were reported as a trigger by 35.6% of participants with migraine.
• In addition, more than 25% of patients with migraine who had stopped consuming or never consumed alcoholic beverages did so because of presumed trigger effects.
• Wine, especially red wine (77.8% of participants), was recognized as the most common trigger among the alcoholic beverages.
• However, red wine consistently led to an attack in only 8.8% of participants.
• Time of onset was rapid (<3 hours) in one‐third of patients and almost 90% had an onset of less than 10 hours independent of beverage type.

Onderwater GLC, van Oosterhaut WPJ, Schoonman GG, Ferrari MD, Terwindt GM. Alcoholic beverages as trigger factor and the effect on alcohol consumption behavior in patients with migraine. [Published online ahead of print December 18, 2018]. Eur J Neurol. doi:10.1111/ene.13861.

Adolescents with migraine and healthy adolescents have similar inhibitory pain modulation capability despite having marked differences in pain sensitivity, according to a recent study. Although participants with a family history of migraine (Fam-His) were asymptomatic, they demonstrated alterations in pain processing, which may serve as markers for prediction of migraine development. In order to determine if inhibitory pain modulation occurs in youth as it does in adults, researchers performed a quantitative sensory testing investigation in adolescents with migraine (n=19). These patients were compared to healthy adolescents with (n=20) or without (n=29) Fam-His of migraine (eg, first degree relative with migraine). They found:

• In response to graded heat stimuli, Fam-His participants reported higher pain intensity ratings compared to migraine patients, who in turn, reported higher pain intensity ratings than the healthy controls.
• For heat- and pressure- conditioned pain modulation (CPM), there was no significant group difference in the magnitude of CPM responses.

Nahman-Averbuch H, Leon E, Hunter BM, et al. Increased pain sensitivity but normal pain modulation in adolescents with migraine. [Published online ahead of print January 7, 2019]. Pain. doi:10.1097/j.pain.0000000000001477.

Adolescents with migraine and healthy adolescents have similar inhibitory pain modulation capability despite having marked differences in pain sensitivity, according to a recent study. Although participants with a family history of migraine (Fam-His) were asymptomatic, they demonstrated alterations in pain processing, which may serve as markers for prediction of migraine development. In order to determine if inhibitory pain modulation occurs in youth as it does in adults, researchers performed a quantitative sensory testing investigation in adolescents with migraine (n=19). These patients were compared to healthy adolescents with (n=20) or without (n=29) Fam-His of migraine (eg, first degree relative with migraine). They found:

• In response to graded heat stimuli, Fam-His participants reported higher pain intensity ratings compared to migraine patients, who in turn, reported higher pain intensity ratings than the healthy controls.
• For heat- and pressure- conditioned pain modulation (CPM), there was no significant group difference in the magnitude of CPM responses.

Nahman-Averbuch H, Leon E, Hunter BM, et al. Increased pain sensitivity but normal pain modulation in adolescents with migraine. [Published online ahead of print January 7, 2019]. Pain. doi:10.1097/j.pain.0000000000001477.

Adolescents with migraine and healthy adolescents have similar inhibitory pain modulation capability despite having marked differences in pain sensitivity, according to a recent study. Although participants with a family history of migraine (Fam-His) were asymptomatic, they demonstrated alterations in pain processing, which may serve as markers for prediction of migraine development. In order to determine if inhibitory pain modulation occurs in youth as it does in adults, researchers performed a quantitative sensory testing investigation in adolescents with migraine (n=19). These patients were compared to healthy adolescents with (n=20) or without (n=29) Fam-His of migraine (eg, first degree relative with migraine). They found:

• In response to graded heat stimuli, Fam-His participants reported higher pain intensity ratings compared to migraine patients, who in turn, reported higher pain intensity ratings than the healthy controls.
• For heat- and pressure- conditioned pain modulation (CPM), there was no significant group difference in the magnitude of CPM responses.

Nahman-Averbuch H, Leon E, Hunter BM, et al. Increased pain sensitivity but normal pain modulation in adolescents with migraine. [Published online ahead of print January 7, 2019]. Pain. doi:10.1097/j.pain.0000000000001477.

Children exposed to valproate in utero were 48% more likely to be diagnosed with ADHD when compared with unexposed children in a population-based cohort study of more than 900,000 children in Denmark.

Antiepileptic drug exposure is associated with an increased risk of various congenital malformations, but its role in the development of ADHD in children has not been well documented, first author Jakob Christensen, MD, PhD, DrMedSci, of Aarhus (Denmark) University Hospital, and his colleagues wrote in their paper, published online Jan. 4 in JAMA Network Open.

The researchers identified 913,302 singleton births in Denmark from 1997 through 2011, with children followed through 2015.

Overall, children who were prenatally exposed to valproate had a 48% increased risk of ADHD. Antiepileptic drug exposure was defined as 30 days before the estimated day of conception to the day of birth, and included valproate, clobazam, and other antiepileptic drugs. The average age of the children at the study’s end was 10 years, and approximately half were male.

A total of 580 children were exposed to valproate in utero; of these, 8.4% were later diagnosed with ADHD, compared with 3.2% of 912,722 children who were not exposed to valproate. In addition, the absolute 15-year risk of ADHD was 11% in valproate-exposed children vs. 4.6% in unexposed children. No significant associations appeared between ADHD and other antiepileptic drugs.

The study findings were limited by several factors, including the contraindication of valproate for use in pregnancy, which may mean that the women taking valproate had more severe disease, the researchers noted.

“Due to the observational nature of this study, we cannot rule out that the observed risk increase for ADHD is at least in part explained by the mother’s health condition that triggered the prescription of valproate during pregnancy,” they said. Other limitations included a lack of data on the exact amounts of valproate taken during pregnancy and the potential impact of nonepilepsy medications, they noted.

However, the results were strengthened by the large size and population-based cohort, and support warnings by professional medical organizations against valproate use in pregnancy, the researchers said. “As randomized clinical trials of valproate use during pregnancy are neither feasible nor ethical, our study provides clinical information on the risk of ADHD associated with valproate use during pregnancy,” they concluded.

The study was supported by grants to various authors from the Danish Epilepsy Association Central Denmark Region, the Aarhus University Research Foundation, the Lundbeck Foundation, the National Institutes of Health, the Novo Nordisk Foundation, and the European Commission.

SOURCE: Christensen J et al. JAMA Network Open. 2019;2(1):e186606. doi: 10.1001/jamanetworkopen.2018.6606.

Children exposed to valproate in utero were 48% more likely to be diagnosed with ADHD when compared with unexposed children in a population-based cohort study of more than 900,000 children in Denmark.

Antiepileptic drug exposure is associated with an increased risk of various congenital malformations, but its role in the development of ADHD in children has not been well documented, first author Jakob Christensen, MD, PhD, DrMedSci, of Aarhus (Denmark) University Hospital, and his colleagues wrote in their paper, published online Jan. 4 in JAMA Network Open.

The researchers identified 913,302 singleton births in Denmark from 1997 through 2011, with children followed through 2015.

Overall, children who were prenatally exposed to valproate had a 48% increased risk of ADHD. Antiepileptic drug exposure was defined as 30 days before the estimated day of conception to the day of birth, and included valproate, clobazam, and other antiepileptic drugs. The average age of the children at the study’s end was 10 years, and approximately half were male.

A total of 580 children were exposed to valproate in utero; of these, 8.4% were later diagnosed with ADHD, compared with 3.2% of 912,722 children who were not exposed to valproate. In addition, the absolute 15-year risk of ADHD was 11% in valproate-exposed children vs. 4.6% in unexposed children. No significant associations appeared between ADHD and other antiepileptic drugs.

The study findings were limited by several factors, including the contraindication of valproate for use in pregnancy, which may mean that the women taking valproate had more severe disease, the researchers noted.

“Due to the observational nature of this study, we cannot rule out that the observed risk increase for ADHD is at least in part explained by the mother’s health condition that triggered the prescription of valproate during pregnancy,” they said. Other limitations included a lack of data on the exact amounts of valproate taken during pregnancy and the potential impact of nonepilepsy medications, they noted.

However, the results were strengthened by the large size and population-based cohort, and support warnings by professional medical organizations against valproate use in pregnancy, the researchers said. “As randomized clinical trials of valproate use during pregnancy are neither feasible nor ethical, our study provides clinical information on the risk of ADHD associated with valproate use during pregnancy,” they concluded.

The study was supported by grants to various authors from the Danish Epilepsy Association Central Denmark Region, the Aarhus University Research Foundation, the Lundbeck Foundation, the National Institutes of Health, the Novo Nordisk Foundation, and the European Commission.

SOURCE: Christensen J et al. JAMA Network Open. 2019;2(1):e186606. doi: 10.1001/jamanetworkopen.2018.6606.

Children exposed to valproate in utero were 48% more likely to be diagnosed with ADHD when compared with unexposed children in a population-based cohort study of more than 900,000 children in Denmark.

Antiepileptic drug exposure is associated with an increased risk of various congenital malformations, but its role in the development of ADHD in children has not been well documented, first author Jakob Christensen, MD, PhD, DrMedSci, of Aarhus (Denmark) University Hospital, and his colleagues wrote in their paper, published online Jan. 4 in JAMA Network Open.

The researchers identified 913,302 singleton births in Denmark from 1997 through 2011, with children followed through 2015.

Overall, children who were prenatally exposed to valproate had a 48% increased risk of ADHD. Antiepileptic drug exposure was defined as 30 days before the estimated day of conception to the day of birth, and included valproate, clobazam, and other antiepileptic drugs. The average age of the children at the study’s end was 10 years, and approximately half were male.

A total of 580 children were exposed to valproate in utero; of these, 8.4% were later diagnosed with ADHD, compared with 3.2% of 912,722 children who were not exposed to valproate. In addition, the absolute 15-year risk of ADHD was 11% in valproate-exposed children vs. 4.6% in unexposed children. No significant associations appeared between ADHD and other antiepileptic drugs.

The study findings were limited by several factors, including the contraindication of valproate for use in pregnancy, which may mean that the women taking valproate had more severe disease, the researchers noted.

“Due to the observational nature of this study, we cannot rule out that the observed risk increase for ADHD is at least in part explained by the mother’s health condition that triggered the prescription of valproate during pregnancy,” they said. Other limitations included a lack of data on the exact amounts of valproate taken during pregnancy and the potential impact of nonepilepsy medications, they noted.

However, the results were strengthened by the large size and population-based cohort, and support warnings by professional medical organizations against valproate use in pregnancy, the researchers said. “As randomized clinical trials of valproate use during pregnancy are neither feasible nor ethical, our study provides clinical information on the risk of ADHD associated with valproate use during pregnancy,” they concluded.

The study was supported by grants to various authors from the Danish Epilepsy Association Central Denmark Region, the Aarhus University Research Foundation, the Lundbeck Foundation, the National Institutes of Health, the Novo Nordisk Foundation, and the European Commission.

SOURCE: Christensen J et al. JAMA Network Open. 2019;2(1):e186606. doi: 10.1001/jamanetworkopen.2018.6606.

CHICAGO—Child neurologists differ in their approach to diagnosing and managing posttraumatic headache, according to survey results presented at the 47th Annual Meeting of the Child Neurology Society.

For example, practice differs as to when posttraumatic headaches are considered persistent and when to recommend preventive therapy.

“As there are no established guidelines on management of posttraumatic headache, it is not surprising that diagnosis and management vary considerably,” said Rachel Pearson, MD, a child neurology resident at Children’s Hospital of Orange County in Orange, California, and colleagues. “Further studies are needed to define the best evidence-based practices for pediatric posttraumatic headache.”

Research indicates that about 7% of children ages 3 to 17 experience a significant head injury, and headache is the most common postconcussive symptom. Headache persists at three months in as much as 43% of cases, according to current studies. To better understand the current clinical practices of child neurologists in the diagnosis and treatment of posttraumatic headache, Dr. Pearson and colleagues sent all active, nonresident members of the Child Neurology Society a link to an online survey. The survey covered diagnosis, management, and return-to-play guidelines. Ninety-five members responded to the survey.

Persistence Threshold: Four Weeks or Three Months?

Although 39% of respondents reported that they always use ICHD diagnostic criteria to diagnose posttraumatic headache, and 31% sometimes use ICHD criteria, “only 19% of respondents correctly defined persistent posttraumatic headache per ICHD diagnostic criteria” as lasting more than three months, the researchers said. “The largest number of participants considered posttraumatic headache to be persistent at four weeks,” they said. “This may have implications for when prophylactic headache medications are considered.”

More than 90% recommend NSAIDs as abortive therapy. One-third consider starting preventive headache therapy within one month, and one-third between one and two months.

The most commonly used preventive medications are amitriptyline and nortriptyline (93.7%) and topiramate (71.6%). Amitriptyline and nortriptyline may be widely used because they “can also address other postconcussive symptoms, such as sleep or mood disturbance,” the investigators noted.

Treatment Options

In addition, 59% of providers use vitamins and supplements (eg, magnesium, riboflavin, melatonin, and CoQ10) as preventive treatments. “These are considered generally safe and have few adverse effects,” and “families may prefer these treatment options as they are perceived as ‘natural,’” Dr. Pearson and colleagues said. More than half of respondents use nonmedicinal therapies such as physical therapy, pain-focused cognitive behavioral therapy, and biofeedback.

Thirty-eight percent use injection-based therapies (eg, nerve blocks, botulinum toxin, and trigger point injections), and 14% of providers administer injections themselves.

One-third of respondents recommend cognitive and physical rest for one to three days, followed by a progressive return to activities, consistent with evidence-based recommendations. Approximately one-third advise patients to rest for seven to 14 days before returning to play.

“As a whole, these findings can guide additional research in this area and serve as a platform on which to base future randomized controlled trials,” said Dr. Pearson and colleagues.

—Jake Remaly

Suggested Reading

Blume HK, Vavilala MS, Jaffe KM, et al. Headache after pediatric traumatic brain injury: a cohort study. Pediatrics. 2012;129(1):e31-e39.

Blume HK. Headaches after concussion in pediatrics: a review. Curr Pain Headache Rep. 2015;19(9):42.

Choe MC, Blume HK. Pediatric posttraumatic headache: a review. J Child Neurol. 2016;31(1): 76-85.

CHICAGO—Child neurologists differ in their approach to diagnosing and managing posttraumatic headache, according to survey results presented at the 47th Annual Meeting of the Child Neurology Society.

For example, practice differs as to when posttraumatic headaches are considered persistent and when to recommend preventive therapy.

“As there are no established guidelines on management of posttraumatic headache, it is not surprising that diagnosis and management vary considerably,” said Rachel Pearson, MD, a child neurology resident at Children’s Hospital of Orange County in Orange, California, and colleagues. “Further studies are needed to define the best evidence-based practices for pediatric posttraumatic headache.”

Research indicates that about 7% of children ages 3 to 17 experience a significant head injury, and headache is the most common postconcussive symptom. Headache persists at three months in as much as 43% of cases, according to current studies. To better understand the current clinical practices of child neurologists in the diagnosis and treatment of posttraumatic headache, Dr. Pearson and colleagues sent all active, nonresident members of the Child Neurology Society a link to an online survey. The survey covered diagnosis, management, and return-to-play guidelines. Ninety-five members responded to the survey.

Persistence Threshold: Four Weeks or Three Months?

Although 39% of respondents reported that they always use ICHD diagnostic criteria to diagnose posttraumatic headache, and 31% sometimes use ICHD criteria, “only 19% of respondents correctly defined persistent posttraumatic headache per ICHD diagnostic criteria” as lasting more than three months, the researchers said. “The largest number of participants considered posttraumatic headache to be persistent at four weeks,” they said. “This may have implications for when prophylactic headache medications are considered.”

More than 90% recommend NSAIDs as abortive therapy. One-third consider starting preventive headache therapy within one month, and one-third between one and two months.

The most commonly used preventive medications are amitriptyline and nortriptyline (93.7%) and topiramate (71.6%). Amitriptyline and nortriptyline may be widely used because they “can also address other postconcussive symptoms, such as sleep or mood disturbance,” the investigators noted.

Treatment Options

In addition, 59% of providers use vitamins and supplements (eg, magnesium, riboflavin, melatonin, and CoQ10) as preventive treatments. “These are considered generally safe and have few adverse effects,” and “families may prefer these treatment options as they are perceived as ‘natural,’” Dr. Pearson and colleagues said. More than half of respondents use nonmedicinal therapies such as physical therapy, pain-focused cognitive behavioral therapy, and biofeedback.

Thirty-eight percent use injection-based therapies (eg, nerve blocks, botulinum toxin, and trigger point injections), and 14% of providers administer injections themselves.

One-third of respondents recommend cognitive and physical rest for one to three days, followed by a progressive return to activities, consistent with evidence-based recommendations. Approximately one-third advise patients to rest for seven to 14 days before returning to play.

“As a whole, these findings can guide additional research in this area and serve as a platform on which to base future randomized controlled trials,” said Dr. Pearson and colleagues.

—Jake Remaly

Suggested Reading

Blume HK, Vavilala MS, Jaffe KM, et al. Headache after pediatric traumatic brain injury: a cohort study. Pediatrics. 2012;129(1):e31-e39.

Blume HK. Headaches after concussion in pediatrics: a review. Curr Pain Headache Rep. 2015;19(9):42.

Choe MC, Blume HK. Pediatric posttraumatic headache: a review. J Child Neurol. 2016;31(1): 76-85.

CHICAGO—Child neurologists differ in their approach to diagnosing and managing posttraumatic headache, according to survey results presented at the 47th Annual Meeting of the Child Neurology Society.

For example, practice differs as to when posttraumatic headaches are considered persistent and when to recommend preventive therapy.

“As there are no established guidelines on management of posttraumatic headache, it is not surprising that diagnosis and management vary considerably,” said Rachel Pearson, MD, a child neurology resident at Children’s Hospital of Orange County in Orange, California, and colleagues. “Further studies are needed to define the best evidence-based practices for pediatric posttraumatic headache.”

Research indicates that about 7% of children ages 3 to 17 experience a significant head injury, and headache is the most common postconcussive symptom. Headache persists at three months in as much as 43% of cases, according to current studies. To better understand the current clinical practices of child neurologists in the diagnosis and treatment of posttraumatic headache, Dr. Pearson and colleagues sent all active, nonresident members of the Child Neurology Society a link to an online survey. The survey covered diagnosis, management, and return-to-play guidelines. Ninety-five members responded to the survey.

Persistence Threshold: Four Weeks or Three Months?

Although 39% of respondents reported that they always use ICHD diagnostic criteria to diagnose posttraumatic headache, and 31% sometimes use ICHD criteria, “only 19% of respondents correctly defined persistent posttraumatic headache per ICHD diagnostic criteria” as lasting more than three months, the researchers said. “The largest number of participants considered posttraumatic headache to be persistent at four weeks,” they said. “This may have implications for when prophylactic headache medications are considered.”

More than 90% recommend NSAIDs as abortive therapy. One-third consider starting preventive headache therapy within one month, and one-third between one and two months.

The most commonly used preventive medications are amitriptyline and nortriptyline (93.7%) and topiramate (71.6%). Amitriptyline and nortriptyline may be widely used because they “can also address other postconcussive symptoms, such as sleep or mood disturbance,” the investigators noted.

Treatment Options

In addition, 59% of providers use vitamins and supplements (eg, magnesium, riboflavin, melatonin, and CoQ10) as preventive treatments. “These are considered generally safe and have few adverse effects,” and “families may prefer these treatment options as they are perceived as ‘natural,’” Dr. Pearson and colleagues said. More than half of respondents use nonmedicinal therapies such as physical therapy, pain-focused cognitive behavioral therapy, and biofeedback.

Thirty-eight percent use injection-based therapies (eg, nerve blocks, botulinum toxin, and trigger point injections), and 14% of providers administer injections themselves.

One-third of respondents recommend cognitive and physical rest for one to three days, followed by a progressive return to activities, consistent with evidence-based recommendations. Approximately one-third advise patients to rest for seven to 14 days before returning to play.

“As a whole, these findings can guide additional research in this area and serve as a platform on which to base future randomized controlled trials,” said Dr. Pearson and colleagues.

—Jake Remaly

Suggested Reading

Blume HK, Vavilala MS, Jaffe KM, et al. Headache after pediatric traumatic brain injury: a cohort study. Pediatrics. 2012;129(1):e31-e39.

Blume HK. Headaches after concussion in pediatrics: a review. Curr Pain Headache Rep. 2015;19(9):42.

Choe MC, Blume HK. Pediatric posttraumatic headache: a review. J Child Neurol. 2016;31(1): 76-85.

Steven M. Baskin, PhD, a clinical psychologist at the New England Institute for Neurology and Headache in Stamford, Connecticut, recently answered the Migraine Resource Center’s questions about the benefits of behavioral therapy in the treatment of migraine and tension-type headache.
 

Alan M. Rapoport, MD: Could you please give a brief description of the 5 best modalities of behavioral therapy for migraine and tension-type headache? 
 

Steven M. Baskin, PhD: The most researched modalities that have a good evidence base for both migraine and tension-type headache (TTHA) are relaxation therapies that often combine abdominal breathing with some form of progressive relaxation, electromyography (EMG) biofeedback therapy where headache patients learn to decrease scalp and neck muscle tension utilizing muscular biofeedback, thermal biofeedback where migraine sufferers learn a way to warm their hands which often creates a low arousal state that may reduce brain hyperexcitability, and cognitive behavioral therapy (CBT) techniques to learn stress management. The combination of behavioral medicine techniques plus preventive pharmacological treatment has been showed to be more efficacious than either treatment alone. (Holroyd KA, et al. Effect of preventive (β blocker) treatment, behavioural migraine management, or their combination on outcomes of optimised acute treatment in frequent migraine: randomised controlled trial. BMJ. 2010;1-12)

CBT to treat insomnia has also been shown to reverse many chronic migraine sufferers back to episodic migraine. (Smitherman TA, et al. Cognitive-Behavioral Therapy for Insomnia to Reduce Chronic Migraine: A Sequential Bayesian Analysis. Headache 2018;58:1052-1059)
 

Dr. Rapoport: How do you identify a patient who may benefit from behavioral therapy over acute medication, and what is the first step that you suggest?
 

Dr. Baskin: Behavioral therapies for migraine management are typically preventive therapies that can and should be combined with medications to control acute attacks. There are behavioral principles that can maximize adherence to abortive agents in order to optimize acute care.
 

Dr. Rapoport: Which tends to work the best for migraine?
 

Dr. Baskin: What works best is to first do a good behavioral assessment of the frequency, duration, intensity, and disability level of their headaches as well as current stress levels, history, and adherence to drug and nondrug therapies, and psychiatric comorbidities. A program should then be developed that includes some combination of pharmacological and behavioral interventions to address these issues. It is important to increase self-efficacy: patients’ belief in the ability to control the headache, belief in the ability to manage emotional reactivity to pain, and belief that they can achieve functionality in the presence of a significant headache disorder.
 

Dr. Rapoport: Who should not have biofeedback therapy?
 

Dr. Baskin: Biofeedback has shown to be effective in treating migraine and TTHA. It has not been shown to be effective in treating trigeminal autonomic cephalgias (TACs) such as cluster headache. Like pharmacological therapies, it is less effective in chronic migraine that is daily and constant. A patient with severe psychiatric disorder should be treated for their psychiatric disorder before beginning biofeedback therapy.
 

Dr. Rapoport: Some doctors see patients twice per week for several months. What is your typical routine for behavioral therapy?
 

Dr. Baskin: We have a variety of programs. For complicated patients, we tend to see them weekly and have a very systematic program of biofeedback and CBT for approximately 12 to 15 sessions. This may include treating psychiatric comorbidities. We see many other patients for 1 or 2 sessions of biofeedback to try to effect physiological learning and for 1 or 2 sessions of CBT to help them manage stressors and learn coping skills that they can use to help manage migraines and life stress.
 

Dr. Rapoport: Does behavioral medicine work best in conjunction with preventive medications, or on its own?

Dr. Baskin: Many patients do well with a behavioral treatment as a preventive therapy and a pharmacologic agent to optimize acute care. I believe that many patients with higher frequency migraine with psychological issues or ongoing stressors do best with a combination of preventive pharmacologic therapy and behavior therapy. Any migraine patient with sleep issues should learn CBT for insomnia. 

Dr. Rapoport: Is there evidence that suggests behavioral therapy can help patients at various ages manage their migraines?

Dr. Baskin: There is both adult and child data on behavioral therapy for migraine.  An excellent study was done in children and adolescents by Powers et al. It showed that adding 10 sessions of CBT to preventive amitriptyline therapy, compared to adding headache education, significantly reduced the number of headache days, level of disability, and kids with a better than 50% decrease in days of headache compared to amitriptyline, plus headache education control in chronic migraine patients.  (Powers SW et al. Cognitive Behavioral Therapy Plus Amitriptyline for Chronic Migraine in Children and Adolescents: A Randomized Clinical Trial. JAMA 2013;310(24):2622-2630)

Dr. Rapoport: A recent MedPage Today article noted that “anxiety may complicate migraine more than depression with greater long-term persistence, greater headache-related disability, and reduced satisfaction with acute therapies.” Could you please elaborate on why this may be the case? 

Dr. Baskin: Anxiety disorders are often based on feeling threat. They are always associated with avoidance behaviors. Headache sufferers with significant anxiety tend to overestimate the probability of danger (migraine) and perceive it as more unmanageable and threatening than objective reality. They are often very sensitive to medication side effects and benign somatic sensations. They sometimes take medications pre-emptively, because of their fear of getting a migraine, which may lead to medication misuse or overuse. The lifetime prevalence of anxiety disorders in migraineurs (ranging from 51-58%) is almost twice that of major depression.

Please write to us at Neurology Reviews Migraine Resource Center ([email protected]) with your opinions.

Alan M. Rapoport, M.D.

Editor-in-Chief

Migraine Resource Center

Clinical Professor of Neurology

The David Geffen School of Medicine at UCLA

Los Angeles, California

Steven M. Baskin, PhD, a clinical psychologist at the New England Institute for Neurology and Headache in Stamford, Connecticut, recently answered the Migraine Resource Center’s questions about the benefits of behavioral therapy in the treatment of migraine and tension-type headache.
 

Alan M. Rapoport, MD: Could you please give a brief description of the 5 best modalities of behavioral therapy for migraine and tension-type headache? 
 

Steven M. Baskin, PhD: The most researched modalities that have a good evidence base for both migraine and tension-type headache (TTHA) are relaxation therapies that often combine abdominal breathing with some form of progressive relaxation, electromyography (EMG) biofeedback therapy where headache patients learn to decrease scalp and neck muscle tension utilizing muscular biofeedback, thermal biofeedback where migraine sufferers learn a way to warm their hands which often creates a low arousal state that may reduce brain hyperexcitability, and cognitive behavioral therapy (CBT) techniques to learn stress management. The combination of behavioral medicine techniques plus preventive pharmacological treatment has been showed to be more efficacious than either treatment alone. (Holroyd KA, et al. Effect of preventive (β blocker) treatment, behavioural migraine management, or their combination on outcomes of optimised acute treatment in frequent migraine: randomised controlled trial. BMJ. 2010;1-12)

CBT to treat insomnia has also been shown to reverse many chronic migraine sufferers back to episodic migraine. (Smitherman TA, et al. Cognitive-Behavioral Therapy for Insomnia to Reduce Chronic Migraine: A Sequential Bayesian Analysis. Headache 2018;58:1052-1059)
 

Dr. Rapoport: How do you identify a patient who may benefit from behavioral therapy over acute medication, and what is the first step that you suggest?
 

Dr. Baskin: Behavioral therapies for migraine management are typically preventive therapies that can and should be combined with medications to control acute attacks. There are behavioral principles that can maximize adherence to abortive agents in order to optimize acute care.
 

Dr. Rapoport: Which tends to work the best for migraine?
 

Dr. Baskin: What works best is to first do a good behavioral assessment of the frequency, duration, intensity, and disability level of their headaches as well as current stress levels, history, and adherence to drug and nondrug therapies, and psychiatric comorbidities. A program should then be developed that includes some combination of pharmacological and behavioral interventions to address these issues. It is important to increase self-efficacy: patients’ belief in the ability to control the headache, belief in the ability to manage emotional reactivity to pain, and belief that they can achieve functionality in the presence of a significant headache disorder.
 

Dr. Rapoport: Who should not have biofeedback therapy?
 

Dr. Baskin: Biofeedback has shown to be effective in treating migraine and TTHA. It has not been shown to be effective in treating trigeminal autonomic cephalgias (TACs) such as cluster headache. Like pharmacological therapies, it is less effective in chronic migraine that is daily and constant. A patient with severe psychiatric disorder should be treated for their psychiatric disorder before beginning biofeedback therapy.
 

Dr. Rapoport: Some doctors see patients twice per week for several months. What is your typical routine for behavioral therapy?
 

Dr. Baskin: We have a variety of programs. For complicated patients, we tend to see them weekly and have a very systematic program of biofeedback and CBT for approximately 12 to 15 sessions. This may include treating psychiatric comorbidities. We see many other patients for 1 or 2 sessions of biofeedback to try to effect physiological learning and for 1 or 2 sessions of CBT to help them manage stressors and learn coping skills that they can use to help manage migraines and life stress.
 

Dr. Rapoport: Does behavioral medicine work best in conjunction with preventive medications, or on its own?

Dr. Baskin: Many patients do well with a behavioral treatment as a preventive therapy and a pharmacologic agent to optimize acute care. I believe that many patients with higher frequency migraine with psychological issues or ongoing stressors do best with a combination of preventive pharmacologic therapy and behavior therapy. Any migraine patient with sleep issues should learn CBT for insomnia. 

Dr. Rapoport: Is there evidence that suggests behavioral therapy can help patients at various ages manage their migraines?

Dr. Baskin: There is both adult and child data on behavioral therapy for migraine.  An excellent study was done in children and adolescents by Powers et al. It showed that adding 10 sessions of CBT to preventive amitriptyline therapy, compared to adding headache education, significantly reduced the number of headache days, level of disability, and kids with a better than 50% decrease in days of headache compared to amitriptyline, plus headache education control in chronic migraine patients.  (Powers SW et al. Cognitive Behavioral Therapy Plus Amitriptyline for Chronic Migraine in Children and Adolescents: A Randomized Clinical Trial. JAMA 2013;310(24):2622-2630)

Dr. Rapoport: A recent MedPage Today article noted that “anxiety may complicate migraine more than depression with greater long-term persistence, greater headache-related disability, and reduced satisfaction with acute therapies.” Could you please elaborate on why this may be the case? 

Dr. Baskin: Anxiety disorders are often based on feeling threat. They are always associated with avoidance behaviors. Headache sufferers with significant anxiety tend to overestimate the probability of danger (migraine) and perceive it as more unmanageable and threatening than objective reality. They are often very sensitive to medication side effects and benign somatic sensations. They sometimes take medications pre-emptively, because of their fear of getting a migraine, which may lead to medication misuse or overuse. The lifetime prevalence of anxiety disorders in migraineurs (ranging from 51-58%) is almost twice that of major depression.

Please write to us at Neurology Reviews Migraine Resource Center ([email protected]) with your opinions.

Alan M. Rapoport, M.D.

Editor-in-Chief

Migraine Resource Center

Clinical Professor of Neurology

The David Geffen School of Medicine at UCLA

Los Angeles, California

Steven M. Baskin, PhD, a clinical psychologist at the New England Institute for Neurology and Headache in Stamford, Connecticut, recently answered the Migraine Resource Center’s questions about the benefits of behavioral therapy in the treatment of migraine and tension-type headache.
 

Alan M. Rapoport, MD: Could you please give a brief description of the 5 best modalities of behavioral therapy for migraine and tension-type headache? 
 

Steven M. Baskin, PhD: The most researched modalities that have a good evidence base for both migraine and tension-type headache (TTHA) are relaxation therapies that often combine abdominal breathing with some form of progressive relaxation, electromyography (EMG) biofeedback therapy where headache patients learn to decrease scalp and neck muscle tension utilizing muscular biofeedback, thermal biofeedback where migraine sufferers learn a way to warm their hands which often creates a low arousal state that may reduce brain hyperexcitability, and cognitive behavioral therapy (CBT) techniques to learn stress management. The combination of behavioral medicine techniques plus preventive pharmacological treatment has been showed to be more efficacious than either treatment alone. (Holroyd KA, et al. Effect of preventive (β blocker) treatment, behavioural migraine management, or their combination on outcomes of optimised acute treatment in frequent migraine: randomised controlled trial. BMJ. 2010;1-12)

CBT to treat insomnia has also been shown to reverse many chronic migraine sufferers back to episodic migraine. (Smitherman TA, et al. Cognitive-Behavioral Therapy for Insomnia to Reduce Chronic Migraine: A Sequential Bayesian Analysis. Headache 2018;58:1052-1059)
 

Dr. Rapoport: How do you identify a patient who may benefit from behavioral therapy over acute medication, and what is the first step that you suggest?
 

Dr. Baskin: Behavioral therapies for migraine management are typically preventive therapies that can and should be combined with medications to control acute attacks. There are behavioral principles that can maximize adherence to abortive agents in order to optimize acute care.
 

Dr. Rapoport: Which tends to work the best for migraine?
 

Dr. Baskin: What works best is to first do a good behavioral assessment of the frequency, duration, intensity, and disability level of their headaches as well as current stress levels, history, and adherence to drug and nondrug therapies, and psychiatric comorbidities. A program should then be developed that includes some combination of pharmacological and behavioral interventions to address these issues. It is important to increase self-efficacy: patients’ belief in the ability to control the headache, belief in the ability to manage emotional reactivity to pain, and belief that they can achieve functionality in the presence of a significant headache disorder.
 

Dr. Rapoport: Who should not have biofeedback therapy?
 

Dr. Baskin: Biofeedback has shown to be effective in treating migraine and TTHA. It has not been shown to be effective in treating trigeminal autonomic cephalgias (TACs) such as cluster headache. Like pharmacological therapies, it is less effective in chronic migraine that is daily and constant. A patient with severe psychiatric disorder should be treated for their psychiatric disorder before beginning biofeedback therapy.
 

Dr. Rapoport: Some doctors see patients twice per week for several months. What is your typical routine for behavioral therapy?
 

Dr. Baskin: We have a variety of programs. For complicated patients, we tend to see them weekly and have a very systematic program of biofeedback and CBT for approximately 12 to 15 sessions. This may include treating psychiatric comorbidities. We see many other patients for 1 or 2 sessions of biofeedback to try to effect physiological learning and for 1 or 2 sessions of CBT to help them manage stressors and learn coping skills that they can use to help manage migraines and life stress.
 

Dr. Rapoport: Does behavioral medicine work best in conjunction with preventive medications, or on its own?

Dr. Baskin: Many patients do well with a behavioral treatment as a preventive therapy and a pharmacologic agent to optimize acute care. I believe that many patients with higher frequency migraine with psychological issues or ongoing stressors do best with a combination of preventive pharmacologic therapy and behavior therapy. Any migraine patient with sleep issues should learn CBT for insomnia. 

Dr. Rapoport: Is there evidence that suggests behavioral therapy can help patients at various ages manage their migraines?

Dr. Baskin: There is both adult and child data on behavioral therapy for migraine.  An excellent study was done in children and adolescents by Powers et al. It showed that adding 10 sessions of CBT to preventive amitriptyline therapy, compared to adding headache education, significantly reduced the number of headache days, level of disability, and kids with a better than 50% decrease in days of headache compared to amitriptyline, plus headache education control in chronic migraine patients.  (Powers SW et al. Cognitive Behavioral Therapy Plus Amitriptyline for Chronic Migraine in Children and Adolescents: A Randomized Clinical Trial. JAMA 2013;310(24):2622-2630)

Dr. Rapoport: A recent MedPage Today article noted that “anxiety may complicate migraine more than depression with greater long-term persistence, greater headache-related disability, and reduced satisfaction with acute therapies.” Could you please elaborate on why this may be the case? 

Dr. Baskin: Anxiety disorders are often based on feeling threat. They are always associated with avoidance behaviors. Headache sufferers with significant anxiety tend to overestimate the probability of danger (migraine) and perceive it as more unmanageable and threatening than objective reality. They are often very sensitive to medication side effects and benign somatic sensations. They sometimes take medications pre-emptively, because of their fear of getting a migraine, which may lead to medication misuse or overuse. The lifetime prevalence of anxiety disorders in migraineurs (ranging from 51-58%) is almost twice that of major depression.

Please write to us at Neurology Reviews Migraine Resource Center ([email protected]) with your opinions.

Alan M. Rapoport, M.D.

Editor-in-Chief

Migraine Resource Center

Clinical Professor of Neurology

The David Geffen School of Medicine at UCLA

Los Angeles, California

In order to provide healthcare professionals with updated guidance in the use of novel preventive and acute treatments for migraine in adults, a recent position statement released by the American Headache Society updates prior recommendations and outlines the indications for initiating, continuing, combining, and switching preventive and acute treatments. Input was sought from health insurance providers, employers, pharmacy benefit service companies, device manufacturers, pharmaceutical and biotechnology companies, patients, and patient advocates. In addition, expert clinicians and researchers in the field of headache medicine from across North America and the European Union provided input and feedback.

The principles of pharmacologic preventive treatment of migraine with oral treatments have been as follows:

• Use evidence‐based treatments when possible and appropriate.
• Start with a low dose and titrate slowly; newer injectable treatments may work faster and may not need titration.
• Reach a therapeutic dose if possible.
• Allow for an adequate treatment trial duration.
• Establish expectations of therapeutic response and adverse events and maximize adherence.

The principles of acute treatment include:

• Use evidence‐based treatments when possible and appropriate.
• Treat early after the onset of a migraine attack.
• Choose a non-oral route of administration for selected patients.
• Account for tolerability and safety issues.
• Consider self‐administered rescue treatments.
• Avoid overuse of acute medications.

American Headache Society. The American Headache Society position statement on integrating new migraine treatments into clinical practice. [Published online ahead of print December 10, 2018]. Headache. doi:10.1111/head.13456.

In order to provide healthcare professionals with updated guidance in the use of novel preventive and acute treatments for migraine in adults, a recent position statement released by the American Headache Society updates prior recommendations and outlines the indications for initiating, continuing, combining, and switching preventive and acute treatments. Input was sought from health insurance providers, employers, pharmacy benefit service companies, device manufacturers, pharmaceutical and biotechnology companies, patients, and patient advocates. In addition, expert clinicians and researchers in the field of headache medicine from across North America and the European Union provided input and feedback.

The principles of pharmacologic preventive treatment of migraine with oral treatments have been as follows:

• Use evidence‐based treatments when possible and appropriate.
• Start with a low dose and titrate slowly; newer injectable treatments may work faster and may not need titration.
• Reach a therapeutic dose if possible.
• Allow for an adequate treatment trial duration.
• Establish expectations of therapeutic response and adverse events and maximize adherence.

The principles of acute treatment include:

• Use evidence‐based treatments when possible and appropriate.
• Treat early after the onset of a migraine attack.
• Choose a non-oral route of administration for selected patients.
• Account for tolerability and safety issues.
• Consider self‐administered rescue treatments.
• Avoid overuse of acute medications.

American Headache Society. The American Headache Society position statement on integrating new migraine treatments into clinical practice. [Published online ahead of print December 10, 2018]. Headache. doi:10.1111/head.13456.

In order to provide healthcare professionals with updated guidance in the use of novel preventive and acute treatments for migraine in adults, a recent position statement released by the American Headache Society updates prior recommendations and outlines the indications for initiating, continuing, combining, and switching preventive and acute treatments. Input was sought from health insurance providers, employers, pharmacy benefit service companies, device manufacturers, pharmaceutical and biotechnology companies, patients, and patient advocates. In addition, expert clinicians and researchers in the field of headache medicine from across North America and the European Union provided input and feedback.

The principles of pharmacologic preventive treatment of migraine with oral treatments have been as follows:

• Use evidence‐based treatments when possible and appropriate.
• Start with a low dose and titrate slowly; newer injectable treatments may work faster and may not need titration.
• Reach a therapeutic dose if possible.
• Allow for an adequate treatment trial duration.
• Establish expectations of therapeutic response and adverse events and maximize adherence.

The principles of acute treatment include:

• Use evidence‐based treatments when possible and appropriate.
• Treat early after the onset of a migraine attack.
• Choose a non-oral route of administration for selected patients.
• Account for tolerability and safety issues.
• Consider self‐administered rescue treatments.
• Avoid overuse of acute medications.

American Headache Society. The American Headache Society position statement on integrating new migraine treatments into clinical practice. [Published online ahead of print December 10, 2018]. Headache. doi:10.1111/head.13456.