Headache & Migraine

Key clinical point: Ubrogepant in combination with onabotulinumtoxinA led to meaningful pain relief and return to normal function at 2 and 4 hours post-dose in patients with self-identified migraine.

Major finding: Overall, 53.3% and 76.2% of patients achieved meaningful pain relief and 25.4% and 45.9% of patients achieved returned to normal function at 2 and 4 hours post-dose after the first treated attack, respectively.

Study details: The data come from a prospective real-world study including 122 patients with migraine (age ≥ 18 years) who received ubrogepant in combination with onabotulinumtoxinA.

Disclosures: This study was funded by Allergan (prior to its acquisition by AbbVie). Some authors declared receiving research support, royalties, or honoraria from, and serving as consultants and advisory board members for various sources, including AbbVie. Three authors declared being employees of or holding stocks in AbbVie.

Source: Manack Adams A et al. Real-world effectiveness, satisfaction, and optimization of ubrogepant for the acute treatment of migraine in combination with onabotulinumtoxinA: Results from the COURAGE Study. J Headache Pain. 2023;24:102 (Aug 3). doi: 10.1186/s10194-023-01622-0

Key clinical point: Ubrogepant in combination with onabotulinumtoxinA led to meaningful pain relief and return to normal function at 2 and 4 hours post-dose in patients with self-identified migraine.

Major finding: Overall, 53.3% and 76.2% of patients achieved meaningful pain relief and 25.4% and 45.9% of patients achieved returned to normal function at 2 and 4 hours post-dose after the first treated attack, respectively.

Study details: The data come from a prospective real-world study including 122 patients with migraine (age ≥ 18 years) who received ubrogepant in combination with onabotulinumtoxinA.

Disclosures: This study was funded by Allergan (prior to its acquisition by AbbVie). Some authors declared receiving research support, royalties, or honoraria from, and serving as consultants and advisory board members for various sources, including AbbVie. Three authors declared being employees of or holding stocks in AbbVie.

Source: Manack Adams A et al. Real-world effectiveness, satisfaction, and optimization of ubrogepant for the acute treatment of migraine in combination with onabotulinumtoxinA: Results from the COURAGE Study. J Headache Pain. 2023;24:102 (Aug 3). doi: 10.1186/s10194-023-01622-0

Key clinical point: Ubrogepant in combination with onabotulinumtoxinA led to meaningful pain relief and return to normal function at 2 and 4 hours post-dose in patients with self-identified migraine.

Major finding: Overall, 53.3% and 76.2% of patients achieved meaningful pain relief and 25.4% and 45.9% of patients achieved returned to normal function at 2 and 4 hours post-dose after the first treated attack, respectively.

Study details: The data come from a prospective real-world study including 122 patients with migraine (age ≥ 18 years) who received ubrogepant in combination with onabotulinumtoxinA.

Disclosures: This study was funded by Allergan (prior to its acquisition by AbbVie). Some authors declared receiving research support, royalties, or honoraria from, and serving as consultants and advisory board members for various sources, including AbbVie. Three authors declared being employees of or holding stocks in AbbVie.

Source: Manack Adams A et al. Real-world effectiveness, satisfaction, and optimization of ubrogepant for the acute treatment of migraine in combination with onabotulinumtoxinA: Results from the COURAGE Study. J Headache Pain. 2023;24:102 (Aug 3). doi: 10.1186/s10194-023-01622-0

Key clinical point: Addition of mindfulness-based intervention (MIND) comprising 6 weekly sessions and 7-10 minutes daily self-practice to treatment as usual (TaU) led to greater improvements in clinical outcomes compared with TaU alone in patients with chronic migraine (CM) and medication-overuse headache (MOH).

Major finding: TaU-plus-MIND outperformed TaU in the achievement of ≥ 50% reduction in headache frequency at 12 months (P < .0001), percentage reduction in headache days (P  =  .0001), and reduction in intake of total medication and non-steroidal anti-inflammatory drugs (P  =  .0001).

Study details: Finding are from MIND-CM, a phase 3 trial including 177 patients with CM and MOH who were randomly assigned to receive either TaU (including withdrawal from overused drugs, education on proper medication use and lifestyle issues, and tailored prophylaxis; n = 89) or MIND added to TaU (n = 88).

Disclosures: This study was funded by the Italian Ministry of Health. The authors declared no conflicts of interest.

Source: Grazzi L at al. Efficacy of mindfulness added to treatment as usual in patients with chronic migraine and medication overuse headache: A phase-III single-blind randomized-controlled trial (the MIND-CM study). J Headache Pain. 2023;24 (Jul 14). doi:  10.1186/s10194-023-01630-0

Key clinical point: Addition of mindfulness-based intervention (MIND) comprising 6 weekly sessions and 7-10 minutes daily self-practice to treatment as usual (TaU) led to greater improvements in clinical outcomes compared with TaU alone in patients with chronic migraine (CM) and medication-overuse headache (MOH).

Major finding: TaU-plus-MIND outperformed TaU in the achievement of ≥ 50% reduction in headache frequency at 12 months (P < .0001), percentage reduction in headache days (P  =  .0001), and reduction in intake of total medication and non-steroidal anti-inflammatory drugs (P  =  .0001).

Study details: Finding are from MIND-CM, a phase 3 trial including 177 patients with CM and MOH who were randomly assigned to receive either TaU (including withdrawal from overused drugs, education on proper medication use and lifestyle issues, and tailored prophylaxis; n = 89) or MIND added to TaU (n = 88).

Disclosures: This study was funded by the Italian Ministry of Health. The authors declared no conflicts of interest.

Source: Grazzi L at al. Efficacy of mindfulness added to treatment as usual in patients with chronic migraine and medication overuse headache: A phase-III single-blind randomized-controlled trial (the MIND-CM study). J Headache Pain. 2023;24 (Jul 14). doi:  10.1186/s10194-023-01630-0

Key clinical point: Addition of mindfulness-based intervention (MIND) comprising 6 weekly sessions and 7-10 minutes daily self-practice to treatment as usual (TaU) led to greater improvements in clinical outcomes compared with TaU alone in patients with chronic migraine (CM) and medication-overuse headache (MOH).

Major finding: TaU-plus-MIND outperformed TaU in the achievement of ≥ 50% reduction in headache frequency at 12 months (P < .0001), percentage reduction in headache days (P  =  .0001), and reduction in intake of total medication and non-steroidal anti-inflammatory drugs (P  =  .0001).

Study details: Finding are from MIND-CM, a phase 3 trial including 177 patients with CM and MOH who were randomly assigned to receive either TaU (including withdrawal from overused drugs, education on proper medication use and lifestyle issues, and tailored prophylaxis; n = 89) or MIND added to TaU (n = 88).

Disclosures: This study was funded by the Italian Ministry of Health. The authors declared no conflicts of interest.

Source: Grazzi L at al. Efficacy of mindfulness added to treatment as usual in patients with chronic migraine and medication overuse headache: A phase-III single-blind randomized-controlled trial (the MIND-CM study). J Headache Pain. 2023;24 (Jul 14). doi:  10.1186/s10194-023-01630-0

Key clinical point: Migraine increased the risk for ischemic cardio-cerebrovascular diseases (CCVD), but the risk was lower in those treated with triptans or ergotamine (TE).

Major finding: Compared with patients having non-migraine headaches (NMH), the risk for ischemic CCVD was higher in patients with migraine receiving TE (men: adjusted hazard ratio [aHR] 1.18; 95% CI 1.01-1.39; women: aHR 1.22; 95% CI 1.09-1.37) and in those receiving neither triptans nor ergotamine (NTNE; men: aHR 1.39; 95% CI 1.28-1.50; women: aHR 1.53; 95% CI 1.42-1.65). The risk for ischemic CCVD was lower in the TE vs NTNE group (men: aHR 0.86; 95% CI 0.73-0.999; women: aHR 0.80; 95% CI 0.72-0.88).

Study details: This study included 62,272 patients with migraine or NMH. Patients with migraine were categorized into those who received ≥ 1 prescriptions for TE (n = 4959) and those who received NTNE (n = 37,624).

Disclosures: This study received no specific funding. The authors declared no conflicts of interest.

Source: Kim Y et al. Association between migraine and ischemic cardio-cerebrovascular disease (CCVD) and effects of triptans and ergotamine on the risk of ischemic CCVD in patients with migraine in the Korean NHIS-HEALS cohort. Clin Drug Investig. 2023;43(7):541-550 (Jul 17). doi:  10.1007/s40261-023-01290-7

Key clinical point: Migraine increased the risk for ischemic cardio-cerebrovascular diseases (CCVD), but the risk was lower in those treated with triptans or ergotamine (TE).

Major finding: Compared with patients having non-migraine headaches (NMH), the risk for ischemic CCVD was higher in patients with migraine receiving TE (men: adjusted hazard ratio [aHR] 1.18; 95% CI 1.01-1.39; women: aHR 1.22; 95% CI 1.09-1.37) and in those receiving neither triptans nor ergotamine (NTNE; men: aHR 1.39; 95% CI 1.28-1.50; women: aHR 1.53; 95% CI 1.42-1.65). The risk for ischemic CCVD was lower in the TE vs NTNE group (men: aHR 0.86; 95% CI 0.73-0.999; women: aHR 0.80; 95% CI 0.72-0.88).

Study details: This study included 62,272 patients with migraine or NMH. Patients with migraine were categorized into those who received ≥ 1 prescriptions for TE (n = 4959) and those who received NTNE (n = 37,624).

Disclosures: This study received no specific funding. The authors declared no conflicts of interest.

Source: Kim Y et al. Association between migraine and ischemic cardio-cerebrovascular disease (CCVD) and effects of triptans and ergotamine on the risk of ischemic CCVD in patients with migraine in the Korean NHIS-HEALS cohort. Clin Drug Investig. 2023;43(7):541-550 (Jul 17). doi:  10.1007/s40261-023-01290-7

Key clinical point: Migraine increased the risk for ischemic cardio-cerebrovascular diseases (CCVD), but the risk was lower in those treated with triptans or ergotamine (TE).

Major finding: Compared with patients having non-migraine headaches (NMH), the risk for ischemic CCVD was higher in patients with migraine receiving TE (men: adjusted hazard ratio [aHR] 1.18; 95% CI 1.01-1.39; women: aHR 1.22; 95% CI 1.09-1.37) and in those receiving neither triptans nor ergotamine (NTNE; men: aHR 1.39; 95% CI 1.28-1.50; women: aHR 1.53; 95% CI 1.42-1.65). The risk for ischemic CCVD was lower in the TE vs NTNE group (men: aHR 0.86; 95% CI 0.73-0.999; women: aHR 0.80; 95% CI 0.72-0.88).

Study details: This study included 62,272 patients with migraine or NMH. Patients with migraine were categorized into those who received ≥ 1 prescriptions for TE (n = 4959) and those who received NTNE (n = 37,624).

Disclosures: This study received no specific funding. The authors declared no conflicts of interest.

Source: Kim Y et al. Association between migraine and ischemic cardio-cerebrovascular disease (CCVD) and effects of triptans and ergotamine on the risk of ischemic CCVD in patients with migraine in the Korean NHIS-HEALS cohort. Clin Drug Investig. 2023;43(7):541-550 (Jul 17). doi:  10.1007/s40261-023-01290-7

Key clinical point: Retreatment with monoclonal antibodies (mAb) targeting the calcitonin gene-related peptide (CGRP) or its receptor was highly effective with persistent benefits in patients with high-frequency episodic migraine (HFEM) or chronic migraine (CM) who completed the first treatment year followed by 1-3 months of discontinuation.

Major finding: In the second treatment year, monthly migraine days (MMD) were lower than pre-treatment baseline levels (P < .0001), with only 23.5% presenting with same or higher MMD at the baseline of the second vs first treatment year (P  =  .207). MMD at 90-112 days after treatment initiation were also lower in the second vs first treatment year (7.2 vs 8.8; P < .001).

Study details: Findings are from a prospective observational cohort study including 226 patients with HFEM and CM who received erenumab (n = 125) and either galcanezumab or fremanezumab (n = 101).

Disclosures: This study was funded by Fondazione Policlinico Campus Bio-Medico, Italy. Some authors declared receiving travel grants, personal fees, research support, or honoraria for participation in advisory boards, speaker panels, or clinical investigation studies from various sources.

Source: Vernieri F et al. Retreating migraine patients in the second year with monoclonal antibodies anti-CGRP pathway: The multicenter prospective cohort RE-DO study. J Neurol. 2023 (Jul 19). doi: 10.1007/s00415-023-11872-2

Key clinical point: Retreatment with monoclonal antibodies (mAb) targeting the calcitonin gene-related peptide (CGRP) or its receptor was highly effective with persistent benefits in patients with high-frequency episodic migraine (HFEM) or chronic migraine (CM) who completed the first treatment year followed by 1-3 months of discontinuation.

Major finding: In the second treatment year, monthly migraine days (MMD) were lower than pre-treatment baseline levels (P < .0001), with only 23.5% presenting with same or higher MMD at the baseline of the second vs first treatment year (P  =  .207). MMD at 90-112 days after treatment initiation were also lower in the second vs first treatment year (7.2 vs 8.8; P < .001).

Study details: Findings are from a prospective observational cohort study including 226 patients with HFEM and CM who received erenumab (n = 125) and either galcanezumab or fremanezumab (n = 101).

Disclosures: This study was funded by Fondazione Policlinico Campus Bio-Medico, Italy. Some authors declared receiving travel grants, personal fees, research support, or honoraria for participation in advisory boards, speaker panels, or clinical investigation studies from various sources.

Source: Vernieri F et al. Retreating migraine patients in the second year with monoclonal antibodies anti-CGRP pathway: The multicenter prospective cohort RE-DO study. J Neurol. 2023 (Jul 19). doi: 10.1007/s00415-023-11872-2

Key clinical point: Retreatment with monoclonal antibodies (mAb) targeting the calcitonin gene-related peptide (CGRP) or its receptor was highly effective with persistent benefits in patients with high-frequency episodic migraine (HFEM) or chronic migraine (CM) who completed the first treatment year followed by 1-3 months of discontinuation.

Major finding: In the second treatment year, monthly migraine days (MMD) were lower than pre-treatment baseline levels (P < .0001), with only 23.5% presenting with same or higher MMD at the baseline of the second vs first treatment year (P  =  .207). MMD at 90-112 days after treatment initiation were also lower in the second vs first treatment year (7.2 vs 8.8; P < .001).

Study details: Findings are from a prospective observational cohort study including 226 patients with HFEM and CM who received erenumab (n = 125) and either galcanezumab or fremanezumab (n = 101).

Disclosures: This study was funded by Fondazione Policlinico Campus Bio-Medico, Italy. Some authors declared receiving travel grants, personal fees, research support, or honoraria for participation in advisory boards, speaker panels, or clinical investigation studies from various sources.

Source: Vernieri F et al. Retreating migraine patients in the second year with monoclonal antibodies anti-CGRP pathway: The multicenter prospective cohort RE-DO study. J Neurol. 2023 (Jul 19). doi: 10.1007/s00415-023-11872-2

Key clinical point: Once-monthly galcanezumab appeared to be effective and well-tolerated for up to 6 months in patients with episodic migraine.

Major finding: Patients who continued to receive galcanezumab showed sustained improvements in the least squares mean reduction in monthly migraine headache days from 4.01 at 3 months to 4.62 at 6 months, with the proportion of patients achieving ≥ 50% response increasing from 59.7% at 3 months to 70.9% at 6 months. No serious treatment-related adverse events were reported.

Study details: Findings are from a 3-month open-label extension (OLE) of the phase 3 PERSIST trial including 484 patients with episodic migraine who were previously assigned to receive galcanezumab (n = 243) or placebo (n = 241).

Disclosures: The PERSIST study was funded by Eli Lilly and Company. Three authors declared being full-time employees of Eli Lilly and Company while some other authors declared ties with various sources, including Eli Lilly.

Source: Zhou J et al. Galcanezumab in patients with episodic migraine: Results from the open-label period of the phase 3 PERSIST study. J Headache Pain. 2023;24:103 (Aug 4). doi: 10.1186/s10194-023-01613-1

Key clinical point: Once-monthly galcanezumab appeared to be effective and well-tolerated for up to 6 months in patients with episodic migraine.

Major finding: Patients who continued to receive galcanezumab showed sustained improvements in the least squares mean reduction in monthly migraine headache days from 4.01 at 3 months to 4.62 at 6 months, with the proportion of patients achieving ≥ 50% response increasing from 59.7% at 3 months to 70.9% at 6 months. No serious treatment-related adverse events were reported.

Study details: Findings are from a 3-month open-label extension (OLE) of the phase 3 PERSIST trial including 484 patients with episodic migraine who were previously assigned to receive galcanezumab (n = 243) or placebo (n = 241).

Disclosures: The PERSIST study was funded by Eli Lilly and Company. Three authors declared being full-time employees of Eli Lilly and Company while some other authors declared ties with various sources, including Eli Lilly.

Source: Zhou J et al. Galcanezumab in patients with episodic migraine: Results from the open-label period of the phase 3 PERSIST study. J Headache Pain. 2023;24:103 (Aug 4). doi: 10.1186/s10194-023-01613-1

Key clinical point: Once-monthly galcanezumab appeared to be effective and well-tolerated for up to 6 months in patients with episodic migraine.

Major finding: Patients who continued to receive galcanezumab showed sustained improvements in the least squares mean reduction in monthly migraine headache days from 4.01 at 3 months to 4.62 at 6 months, with the proportion of patients achieving ≥ 50% response increasing from 59.7% at 3 months to 70.9% at 6 months. No serious treatment-related adverse events were reported.

Study details: Findings are from a 3-month open-label extension (OLE) of the phase 3 PERSIST trial including 484 patients with episodic migraine who were previously assigned to receive galcanezumab (n = 243) or placebo (n = 241).

Disclosures: The PERSIST study was funded by Eli Lilly and Company. Three authors declared being full-time employees of Eli Lilly and Company while some other authors declared ties with various sources, including Eli Lilly.

Source: Zhou J et al. Galcanezumab in patients with episodic migraine: Results from the open-label period of the phase 3 PERSIST study. J Headache Pain. 2023;24:103 (Aug 4). doi: 10.1186/s10194-023-01613-1

Key clinical point: Treatment with calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) did not increase the risk for SARS-CoV‑2 infection or its severe clinical outcomes in veterans with migraine.

Major finding: Over a 28-month follow-up, 12.5% vs 9.6% of CGRP mAb initiators vs non-initiators tested positive for SARS-CoV-2, respectively, with the incidence of SARS-CoV-2 infection (P  =  .08) and hospitalization (P  =  .45), requirement for supplemental oxygen (P  =  .27) or mechanical ventilation (P  =  .96), and death (P  =  .37) among those testing positive for SARS-CoV-2 not being significantly different between CGRP mAb initiators and non-initiators.

Study details: The data come from a retrospective cohort study including 354,294 veterans (8,178,652 person-trials) with migraine who were at risk for COVID-19, of whom 9382 initiated a CGRP mAb.

Disclosures: This study was supported by the special purpose medical service award from the US Department of Veterans Affairs. Dr. Schindler, Prof. Lipton, and Dr. Seng declared receiving grants, personal fees, or paid royalties from various sources.

Source: Wang K et al. Calcitonin gene-related peptide monoclonal antibodies and risk of SARS-CoV-2 infection and severe COVID-19 outcomes among veterans with migraine disorder. JAMA Netw Open. 2023;6(7):e2326371 (Jul 31). doi: 10.1001/jamanetworkopen.2023.26371

Key clinical point: Treatment with calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) did not increase the risk for SARS-CoV‑2 infection or its severe clinical outcomes in veterans with migraine.

Major finding: Over a 28-month follow-up, 12.5% vs 9.6% of CGRP mAb initiators vs non-initiators tested positive for SARS-CoV-2, respectively, with the incidence of SARS-CoV-2 infection (P  =  .08) and hospitalization (P  =  .45), requirement for supplemental oxygen (P  =  .27) or mechanical ventilation (P  =  .96), and death (P  =  .37) among those testing positive for SARS-CoV-2 not being significantly different between CGRP mAb initiators and non-initiators.

Study details: The data come from a retrospective cohort study including 354,294 veterans (8,178,652 person-trials) with migraine who were at risk for COVID-19, of whom 9382 initiated a CGRP mAb.

Disclosures: This study was supported by the special purpose medical service award from the US Department of Veterans Affairs. Dr. Schindler, Prof. Lipton, and Dr. Seng declared receiving grants, personal fees, or paid royalties from various sources.

Source: Wang K et al. Calcitonin gene-related peptide monoclonal antibodies and risk of SARS-CoV-2 infection and severe COVID-19 outcomes among veterans with migraine disorder. JAMA Netw Open. 2023;6(7):e2326371 (Jul 31). doi: 10.1001/jamanetworkopen.2023.26371

Key clinical point: Treatment with calcitonin gene-related peptide (CGRP) monoclonal antibodies (mAb) did not increase the risk for SARS-CoV‑2 infection or its severe clinical outcomes in veterans with migraine.

Major finding: Over a 28-month follow-up, 12.5% vs 9.6% of CGRP mAb initiators vs non-initiators tested positive for SARS-CoV-2, respectively, with the incidence of SARS-CoV-2 infection (P  =  .08) and hospitalization (P  =  .45), requirement for supplemental oxygen (P  =  .27) or mechanical ventilation (P  =  .96), and death (P  =  .37) among those testing positive for SARS-CoV-2 not being significantly different between CGRP mAb initiators and non-initiators.

Study details: The data come from a retrospective cohort study including 354,294 veterans (8,178,652 person-trials) with migraine who were at risk for COVID-19, of whom 9382 initiated a CGRP mAb.

Disclosures: This study was supported by the special purpose medical service award from the US Department of Veterans Affairs. Dr. Schindler, Prof. Lipton, and Dr. Seng declared receiving grants, personal fees, or paid royalties from various sources.

Source: Wang K et al. Calcitonin gene-related peptide monoclonal antibodies and risk of SARS-CoV-2 infection and severe COVID-19 outcomes among veterans with migraine disorder. JAMA Netw Open. 2023;6(7):e2326371 (Jul 31). doi: 10.1001/jamanetworkopen.2023.26371

Key clinical point: Atogepant showed clinically relevant benefits in patients with chronic migraine (CM), making it the first calcitonin gene-related peptide (CGRP)-targeted, efficacious, and safe oral preventive treatment option for CM.

Major finding: Compared with placebo, the reduction in mean monthly migraine days at week 12 was significantly higher in patients who received 30 mg atogepant twice daily (adjusted least squares mean difference from placebo [LSMD] −2.4; P < .0001) and 60 mg once daily (adjusted LSMD −1.8; P  =  .0009). Constipation and nausea were the most common adverse events in both atogepant groups.

Study details: This phase 3 PROGRESS trial included 755 patients with CM who were randomly assigned to receive atogepant (30 mg twice daily or 60 mg once daily) or placebo.

Disclosures: This study was funded by Allergan (now AbbVie). Some authors declared receiving research support and personal and institutional fees from various sources, including AbbVie. Eleven authors declared being current or former employees or stockholders of AbbVie.

Source: Pozo-Rosich P et al. Atogepant for the preventive treatment of chronic migraine (PROGRESS): A randomised, double-blind, placebo-controlled, phase 3 trial. Lancet. 2023 (Jul 26). doi: 10.1016/S0140-6736(23)01049-8

Key clinical point: Atogepant showed clinically relevant benefits in patients with chronic migraine (CM), making it the first calcitonin gene-related peptide (CGRP)-targeted, efficacious, and safe oral preventive treatment option for CM.

Major finding: Compared with placebo, the reduction in mean monthly migraine days at week 12 was significantly higher in patients who received 30 mg atogepant twice daily (adjusted least squares mean difference from placebo [LSMD] −2.4; P < .0001) and 60 mg once daily (adjusted LSMD −1.8; P  =  .0009). Constipation and nausea were the most common adverse events in both atogepant groups.

Study details: This phase 3 PROGRESS trial included 755 patients with CM who were randomly assigned to receive atogepant (30 mg twice daily or 60 mg once daily) or placebo.

Disclosures: This study was funded by Allergan (now AbbVie). Some authors declared receiving research support and personal and institutional fees from various sources, including AbbVie. Eleven authors declared being current or former employees or stockholders of AbbVie.

Source: Pozo-Rosich P et al. Atogepant for the preventive treatment of chronic migraine (PROGRESS): A randomised, double-blind, placebo-controlled, phase 3 trial. Lancet. 2023 (Jul 26). doi: 10.1016/S0140-6736(23)01049-8

Key clinical point: Atogepant showed clinically relevant benefits in patients with chronic migraine (CM), making it the first calcitonin gene-related peptide (CGRP)-targeted, efficacious, and safe oral preventive treatment option for CM.

Major finding: Compared with placebo, the reduction in mean monthly migraine days at week 12 was significantly higher in patients who received 30 mg atogepant twice daily (adjusted least squares mean difference from placebo [LSMD] −2.4; P < .0001) and 60 mg once daily (adjusted LSMD −1.8; P  =  .0009). Constipation and nausea were the most common adverse events in both atogepant groups.

Study details: This phase 3 PROGRESS trial included 755 patients with CM who were randomly assigned to receive atogepant (30 mg twice daily or 60 mg once daily) or placebo.

Disclosures: This study was funded by Allergan (now AbbVie). Some authors declared receiving research support and personal and institutional fees from various sources, including AbbVie. Eleven authors declared being current or former employees or stockholders of AbbVie.

Source: Pozo-Rosich P et al. Atogepant for the preventive treatment of chronic migraine (PROGRESS): A randomised, double-blind, placebo-controlled, phase 3 trial. Lancet. 2023 (Jul 26). doi: 10.1016/S0140-6736(23)01049-8

Migraine is well known as a vascular phenomenon, but research over time has shown that vasodilation is a secondary feature of headache rather than the cause of headache pain. Calcitonin gene-related peptide (CGRP) and other vasoactive inflammatory proteins transmit nociceptive signals through the trigeminal system, and although vasodilation occurs, it is not essential for migraine attacks to occur. White matter changes on MRI are a common finding in people with migraine, and the burden of migraine often correlates with the amount of white matter changes seen. This connection highlights the indirect connection between migraine and vascular risks factors, and this study attempts to better quantify this, specifically with respect to stroke and myocardial infarction (MI).

The study by Fuglsang and colleagues was a registry-based nationwide population-based cohort study that included over 200,000 individuals with migraine, using data collected from 1996 to 2018. Participants were differentiated as having or not having migraine on the basis of prescriptions of preventive or acute migraine medications. Male and female participants were further subdivided, and these groups were compared to healthy controls. The primary endpoints were hazard ratio and absolute risk differences for developing hemorrhagic or ischemic stroke or MI among all groups.

The researchers found an increased risk for ischemic stroke that was equal among male and female participants. Hemorrhagic stroke and MI were seen to be increased in migraine, but primarily among women with migraine. This study specifically investigated what the researchers termed "premature" stroke and MI, and there remains a likelihood that estrogen could be the differentiating factor between the difference in risk between male and female participants with migraine. I have recently highlighted a number of studies investigating vascular risk factors associated with migraine; this study will help clinicians appropriately educate their patients with migraine regarding vascular risk.

The first medications reported as helpful preventively for migraine were antihypertensives, specifically beta-blockers (BB). A number of other medications in other antihypertensive subclasses have also subsequently been shown to be helpful for migraine prevention. These include angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARB), calcium channel blockers (CCB), and alpha-blockers (AB). Carcel and colleagues conducted a meta-analysis that investigated a wide variety of antihypertensive medications in multiple classes and compared the reduction in headache frequency as defined as headache days per month.

This analysis reviewed 50 studies involving over 4000 participants. The majority of the studies (35 out 50 [70%]) had a cross-over design. The medications evaluated included clonidine (an alpha agonist), candesartan (an ARB), telmisartan (an ARB), propranolol (a BB), timolol (a BB), pindolol (a BB), metoprolol (a BB), bisoprolol (a BB), atenolol (a BB), alprenolol (a BB), nimodipine (a CCB), nifedipine (a CCB), verapamil (a CCB), nicardipine (a CCB), enalapril (an ACE inhibitor), and lisinopril (an ACE inhibitor). For each class of antihypertensive, there was a lower number of monthly headache days with treatment compared with placebo; the greatest reduction was for the CCB with a mean difference of about 2 days per month. BB on average decreased headache days per month by 0.7 days. For BB, there was no clear trend to increased efficacy with increased dose. Only six trials reported the difference in blood pressure: On average, there was a 9.3 mm Hg drop in systolic and 3.0 mm Hg drop in diastolic pressure.

The authors showed that there is statistical significance for the use of antihypertensive medications for decreasing migraine days per month, and this was statistically significant separately for numerous specific drugs within the classes: clonidine, candesartan, atenolol, bisoprolol, propranolol, timolol, nicardipine, and verapamil. Antihypertensive medications remain some of the most popular first-line preventive options for migraine, and although the benefit of this class as a whole is mild (slightly more than 1 day per month), it can be an excellent option for many patients

The relationship between migraine and caffeine is necessarily controversial. Caffeine is included as a component of many over-the-counter migraine treatments, and the beneficial effect of caffeine as an acute treatment for migraine has been documented for decades. Reduction in caffeine, however, has also been established as a helpful lifestyle modification for prevention of migraine attacks. Zhang and colleagues used data from the National Health and Nutrition Examination Survey database, a program conducted by the Centers for Disease Control and Prevention to assess the health and nutritional status of adults and children in the United States.

This study sought to quantify the relationship between dietary caffeine and "severe headache." For this study, "severe headache" was defined as answering yes to the question: During the past 3 months, did you have severe headaches or migraines? Dietary caffeine intake was collected through two 24-hour dietary recall interviews, one in person and one 3-10 days later via telephone. The amount of caffeine consumed was estimated in mg/day from all caffeine-containing foods and beverages, including coffee, tea, soda, and chocolate, using the US Department of Agriculture's Food and Nutrient Database. Each participant's mean caffeine intake was defined as the difference between the first and second dietary recalls.

A large number of covariates were assessed as well, including age, race/ethnicity, body mass index, poverty-income ratio, educational level, marital status, hypertension, cancer, energy intake, protein intake, calcium intake, magnesium intake, iron intake, sodium intake, alcohol status, smoking status, and triglyceride level. A total of 8993 participants were included. Caffeine intake was divided into four groups: ≥ 0 to < 40 mg/day, ≥ 40 to < 200 mg/day, ≥ 200 to < 400 mg/day, and ≥ 400 mg/day. After adjusting for confounders, a significant association between dietary caffeine intake and severe headaches or migraines was detected.

Curiously, in this study, only male participants were included. The authors found a clear correlation between the amount of caffeine consumed over a 24-hour period and severe migraine attacks. Further evaluation should investigate the frequency of attacks rather than just individual experience over a 3-month period. Although caffeine is helpful acutely, higher dose consumption is a risk factor for worsening migraine.

Migraine is well known as a vascular phenomenon, but research over time has shown that vasodilation is a secondary feature of headache rather than the cause of headache pain. Calcitonin gene-related peptide (CGRP) and other vasoactive inflammatory proteins transmit nociceptive signals through the trigeminal system, and although vasodilation occurs, it is not essential for migraine attacks to occur. White matter changes on MRI are a common finding in people with migraine, and the burden of migraine often correlates with the amount of white matter changes seen. This connection highlights the indirect connection between migraine and vascular risks factors, and this study attempts to better quantify this, specifically with respect to stroke and myocardial infarction (MI).

The study by Fuglsang and colleagues was a registry-based nationwide population-based cohort study that included over 200,000 individuals with migraine, using data collected from 1996 to 2018. Participants were differentiated as having or not having migraine on the basis of prescriptions of preventive or acute migraine medications. Male and female participants were further subdivided, and these groups were compared to healthy controls. The primary endpoints were hazard ratio and absolute risk differences for developing hemorrhagic or ischemic stroke or MI among all groups.

The researchers found an increased risk for ischemic stroke that was equal among male and female participants. Hemorrhagic stroke and MI were seen to be increased in migraine, but primarily among women with migraine. This study specifically investigated what the researchers termed "premature" stroke and MI, and there remains a likelihood that estrogen could be the differentiating factor between the difference in risk between male and female participants with migraine. I have recently highlighted a number of studies investigating vascular risk factors associated with migraine; this study will help clinicians appropriately educate their patients with migraine regarding vascular risk.

The first medications reported as helpful preventively for migraine were antihypertensives, specifically beta-blockers (BB). A number of other medications in other antihypertensive subclasses have also subsequently been shown to be helpful for migraine prevention. These include angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARB), calcium channel blockers (CCB), and alpha-blockers (AB). Carcel and colleagues conducted a meta-analysis that investigated a wide variety of antihypertensive medications in multiple classes and compared the reduction in headache frequency as defined as headache days per month.

This analysis reviewed 50 studies involving over 4000 participants. The majority of the studies (35 out 50 [70%]) had a cross-over design. The medications evaluated included clonidine (an alpha agonist), candesartan (an ARB), telmisartan (an ARB), propranolol (a BB), timolol (a BB), pindolol (a BB), metoprolol (a BB), bisoprolol (a BB), atenolol (a BB), alprenolol (a BB), nimodipine (a CCB), nifedipine (a CCB), verapamil (a CCB), nicardipine (a CCB), enalapril (an ACE inhibitor), and lisinopril (an ACE inhibitor). For each class of antihypertensive, there was a lower number of monthly headache days with treatment compared with placebo; the greatest reduction was for the CCB with a mean difference of about 2 days per month. BB on average decreased headache days per month by 0.7 days. For BB, there was no clear trend to increased efficacy with increased dose. Only six trials reported the difference in blood pressure: On average, there was a 9.3 mm Hg drop in systolic and 3.0 mm Hg drop in diastolic pressure.

The authors showed that there is statistical significance for the use of antihypertensive medications for decreasing migraine days per month, and this was statistically significant separately for numerous specific drugs within the classes: clonidine, candesartan, atenolol, bisoprolol, propranolol, timolol, nicardipine, and verapamil. Antihypertensive medications remain some of the most popular first-line preventive options for migraine, and although the benefit of this class as a whole is mild (slightly more than 1 day per month), it can be an excellent option for many patients

The relationship between migraine and caffeine is necessarily controversial. Caffeine is included as a component of many over-the-counter migraine treatments, and the beneficial effect of caffeine as an acute treatment for migraine has been documented for decades. Reduction in caffeine, however, has also been established as a helpful lifestyle modification for prevention of migraine attacks. Zhang and colleagues used data from the National Health and Nutrition Examination Survey database, a program conducted by the Centers for Disease Control and Prevention to assess the health and nutritional status of adults and children in the United States.

This study sought to quantify the relationship between dietary caffeine and "severe headache." For this study, "severe headache" was defined as answering yes to the question: During the past 3 months, did you have severe headaches or migraines? Dietary caffeine intake was collected through two 24-hour dietary recall interviews, one in person and one 3-10 days later via telephone. The amount of caffeine consumed was estimated in mg/day from all caffeine-containing foods and beverages, including coffee, tea, soda, and chocolate, using the US Department of Agriculture's Food and Nutrient Database. Each participant's mean caffeine intake was defined as the difference between the first and second dietary recalls.

A large number of covariates were assessed as well, including age, race/ethnicity, body mass index, poverty-income ratio, educational level, marital status, hypertension, cancer, energy intake, protein intake, calcium intake, magnesium intake, iron intake, sodium intake, alcohol status, smoking status, and triglyceride level. A total of 8993 participants were included. Caffeine intake was divided into four groups: ≥ 0 to < 40 mg/day, ≥ 40 to < 200 mg/day, ≥ 200 to < 400 mg/day, and ≥ 400 mg/day. After adjusting for confounders, a significant association between dietary caffeine intake and severe headaches or migraines was detected.

Curiously, in this study, only male participants were included. The authors found a clear correlation between the amount of caffeine consumed over a 24-hour period and severe migraine attacks. Further evaluation should investigate the frequency of attacks rather than just individual experience over a 3-month period. Although caffeine is helpful acutely, higher dose consumption is a risk factor for worsening migraine.

Migraine is well known as a vascular phenomenon, but research over time has shown that vasodilation is a secondary feature of headache rather than the cause of headache pain. Calcitonin gene-related peptide (CGRP) and other vasoactive inflammatory proteins transmit nociceptive signals through the trigeminal system, and although vasodilation occurs, it is not essential for migraine attacks to occur. White matter changes on MRI are a common finding in people with migraine, and the burden of migraine often correlates with the amount of white matter changes seen. This connection highlights the indirect connection between migraine and vascular risks factors, and this study attempts to better quantify this, specifically with respect to stroke and myocardial infarction (MI).

The study by Fuglsang and colleagues was a registry-based nationwide population-based cohort study that included over 200,000 individuals with migraine, using data collected from 1996 to 2018. Participants were differentiated as having or not having migraine on the basis of prescriptions of preventive or acute migraine medications. Male and female participants were further subdivided, and these groups were compared to healthy controls. The primary endpoints were hazard ratio and absolute risk differences for developing hemorrhagic or ischemic stroke or MI among all groups.

The researchers found an increased risk for ischemic stroke that was equal among male and female participants. Hemorrhagic stroke and MI were seen to be increased in migraine, but primarily among women with migraine. This study specifically investigated what the researchers termed "premature" stroke and MI, and there remains a likelihood that estrogen could be the differentiating factor between the difference in risk between male and female participants with migraine. I have recently highlighted a number of studies investigating vascular risk factors associated with migraine; this study will help clinicians appropriately educate their patients with migraine regarding vascular risk.

The first medications reported as helpful preventively for migraine were antihypertensives, specifically beta-blockers (BB). A number of other medications in other antihypertensive subclasses have also subsequently been shown to be helpful for migraine prevention. These include angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARB), calcium channel blockers (CCB), and alpha-blockers (AB). Carcel and colleagues conducted a meta-analysis that investigated a wide variety of antihypertensive medications in multiple classes and compared the reduction in headache frequency as defined as headache days per month.

This analysis reviewed 50 studies involving over 4000 participants. The majority of the studies (35 out 50 [70%]) had a cross-over design. The medications evaluated included clonidine (an alpha agonist), candesartan (an ARB), telmisartan (an ARB), propranolol (a BB), timolol (a BB), pindolol (a BB), metoprolol (a BB), bisoprolol (a BB), atenolol (a BB), alprenolol (a BB), nimodipine (a CCB), nifedipine (a CCB), verapamil (a CCB), nicardipine (a CCB), enalapril (an ACE inhibitor), and lisinopril (an ACE inhibitor). For each class of antihypertensive, there was a lower number of monthly headache days with treatment compared with placebo; the greatest reduction was for the CCB with a mean difference of about 2 days per month. BB on average decreased headache days per month by 0.7 days. For BB, there was no clear trend to increased efficacy with increased dose. Only six trials reported the difference in blood pressure: On average, there was a 9.3 mm Hg drop in systolic and 3.0 mm Hg drop in diastolic pressure.

The authors showed that there is statistical significance for the use of antihypertensive medications for decreasing migraine days per month, and this was statistically significant separately for numerous specific drugs within the classes: clonidine, candesartan, atenolol, bisoprolol, propranolol, timolol, nicardipine, and verapamil. Antihypertensive medications remain some of the most popular first-line preventive options for migraine, and although the benefit of this class as a whole is mild (slightly more than 1 day per month), it can be an excellent option for many patients

The relationship between migraine and caffeine is necessarily controversial. Caffeine is included as a component of many over-the-counter migraine treatments, and the beneficial effect of caffeine as an acute treatment for migraine has been documented for decades. Reduction in caffeine, however, has also been established as a helpful lifestyle modification for prevention of migraine attacks. Zhang and colleagues used data from the National Health and Nutrition Examination Survey database, a program conducted by the Centers for Disease Control and Prevention to assess the health and nutritional status of adults and children in the United States.

This study sought to quantify the relationship between dietary caffeine and "severe headache." For this study, "severe headache" was defined as answering yes to the question: During the past 3 months, did you have severe headaches or migraines? Dietary caffeine intake was collected through two 24-hour dietary recall interviews, one in person and one 3-10 days later via telephone. The amount of caffeine consumed was estimated in mg/day from all caffeine-containing foods and beverages, including coffee, tea, soda, and chocolate, using the US Department of Agriculture's Food and Nutrient Database. Each participant's mean caffeine intake was defined as the difference between the first and second dietary recalls.

A large number of covariates were assessed as well, including age, race/ethnicity, body mass index, poverty-income ratio, educational level, marital status, hypertension, cancer, energy intake, protein intake, calcium intake, magnesium intake, iron intake, sodium intake, alcohol status, smoking status, and triglyceride level. A total of 8993 participants were included. Caffeine intake was divided into four groups: ≥ 0 to < 40 mg/day, ≥ 40 to < 200 mg/day, ≥ 200 to < 400 mg/day, and ≥ 400 mg/day. After adjusting for confounders, a significant association between dietary caffeine intake and severe headaches or migraines was detected.

Curiously, in this study, only male participants were included. The authors found a clear correlation between the amount of caffeine consumed over a 24-hour period and severe migraine attacks. Further evaluation should investigate the frequency of attacks rather than just individual experience over a 3-month period. Although caffeine is helpful acutely, higher dose consumption is a risk factor for worsening migraine.

What types of headache and other illnesses respond to biofeedback training?

Migraine affects about 12% of the US and most Western populations, and is 3 times more common in women than men. Migraine can be treated with a variety of strategies that include medications and nonpharmacologic therapies such as biofeedback, as well as other behavioral therapies and devices. Biofeedback refers to the use of instrumentation to monitor and display physiologic responses that the patient may not be aware of so that they can be “modified” in a more adaptive direction. Feedback gives immediate objective information and is usually combined with a relaxation-based therapy. The most common biofeedback treatments for migraine include feeding back muscle activity in the face and neck to help people relax contracted muscles and teach them a “low-arousal” response; they learn to increase finger temperature, which coincides with modifying the “stress” nervous system. Biofeedback has been shown to be helpful for migraine and tension-type headache. It is also helpful to decrease anxiety and stress levels and lower blood pressure.

Can patients use biofeedback treatments in conjunction with migraine medication?

Research has shown that migraine, in particular higher-frequency migraine, is best treated by a combination of medications and behavioral strategies. Biofeedback is a good option for use in conjunction with medication for migraine.

Who is trained to provide biofeedback treatments?

Biofeedback for migraine is something usually performed by psychologists and other professionals with specialized training. Many practitioners are certified by the Biofeedback Certification Institute of America (BCIA). It is important to find an experienced biofeedback practitioner who also has some expertise in treating headache disorders. 

How are biofeedback treatments performed?

Biofeedback is a therapy that follows a learning model whereby the patient gradually learns a self-regulation skill that impacts their headaches. 

Patients come to an office, typically once per week, where they are attached to instruments that measure physical responses associated with migraine. The patient typically sits in a comfortable chair or recliner, and numerous physiologic responses are monitored with surface electrodes. 

When treating headache, sensors are typically placed on the head and neck to monitor muscle responses and a thermistor is placed on a finger to measure temperature. Feedback is given via visual cues (computer graphics) or a change in auditory tone as the patient is taught various relaxation techniques.  

Patients use the feedback to learn a physiologic relaxation response that may be beneficial for their headache management. Most of the research on biofeedback is related to treatment to prevent migraine; however, these techniques can be helpful to use during an acute attack, ideally paired with an acute care migraine medication. 

Can children with migraine have biofeedback treatments as well?

 Most children typically have a lower frequency of migraine than adults, although some have frequent migraines with associated disability and are candidates for preventive medication (although no medications are yet approved for children by the US Food and Drug Association). Most children are good candidates for behavioral therapies such as biofeedback. There are many computer games utilized in biofeedback training that children easily learn to modify physical responses. There are some fairly recent data suggesting that behavioral treatments, some of which include biofeedback, are effective strategies for children and may be more effective than preventive medication.  

What other types of illnesses could benefit from biofeedback training?    

There are data showing that biofeedback therapy can be helpful for anxiety disorders, insomnia, and functional bowel disorders and may help in modifying high blood pressure. It can also be a very effective stress-management strategy.  

Do you refer some of your patients with migraine to a psychologist for biofeedback treatments?      

 Yes, but it is always good for the referring physician to check on the credentials of the person performing the biofeedback treatment. Some headache specialists might do it themselves, but we do not. It takes a while—at least several sessions—and psychologists are better at it. Patients’ perspectives are also important. We communicate with the referred biofeedback treatment specialist to get more insight on the patient. For example, some patients are anxious and depressed, and they are not sleeping at night. The doctor we referred the patient to may recommend an antidepressant for the patient to help address those issues. It is a team effort.

What is the average cost per treatment?      
The costs vary throughout the country and range from $75 to $400 per session. Insurance coverage varies.  

How many times should a patient go in for treatment?    

Most protocols are about 10 to 12 sessions, depending on patient response. 

Have there been clinical trials on biofeedback treatments/devices?  

There have been many clinical trials that have been positive, so there is good evidence that biofeedback can be an effective treatment for migraine and tension-type headache. There are many types of biofeedback devices that measure different modalities. The most common one used in migraine is measuring scalp muscle contraction with surface electromyography or measuring peripheral blood flow with a temperature gauge. The goals are to relax muscles and learn to increase finger temperature, which is related to decreased arousal of the sympathetic nervous system or stress system. Other modalities include learning to modulate brain waves (electroencephalography or neurofeedback) and certain cardiovascular measures that reduce the stress response by a different mechanism. The goal is for patients to learn a low arousal response that they can utilize in their natural environment. Certain breathing techniques and visualization exercises are also helpful, but biofeedback refers to using physiologic recording equipment to help learn to change physical responses related to headache disorder. 

Over our years of experience, we have found that biofeedback can help a large percentage of our patients with migraine and tension-type headache, and it is associated with almost no adverse events.

What types of headache and other illnesses respond to biofeedback training?

Migraine affects about 12% of the US and most Western populations, and is 3 times more common in women than men. Migraine can be treated with a variety of strategies that include medications and nonpharmacologic therapies such as biofeedback, as well as other behavioral therapies and devices. Biofeedback refers to the use of instrumentation to monitor and display physiologic responses that the patient may not be aware of so that they can be “modified” in a more adaptive direction. Feedback gives immediate objective information and is usually combined with a relaxation-based therapy. The most common biofeedback treatments for migraine include feeding back muscle activity in the face and neck to help people relax contracted muscles and teach them a “low-arousal” response; they learn to increase finger temperature, which coincides with modifying the “stress” nervous system. Biofeedback has been shown to be helpful for migraine and tension-type headache. It is also helpful to decrease anxiety and stress levels and lower blood pressure.

Can patients use biofeedback treatments in conjunction with migraine medication?

Research has shown that migraine, in particular higher-frequency migraine, is best treated by a combination of medications and behavioral strategies. Biofeedback is a good option for use in conjunction with medication for migraine.

Who is trained to provide biofeedback treatments?

Biofeedback for migraine is something usually performed by psychologists and other professionals with specialized training. Many practitioners are certified by the Biofeedback Certification Institute of America (BCIA). It is important to find an experienced biofeedback practitioner who also has some expertise in treating headache disorders. 

How are biofeedback treatments performed?

Biofeedback is a therapy that follows a learning model whereby the patient gradually learns a self-regulation skill that impacts their headaches. 

Patients come to an office, typically once per week, where they are attached to instruments that measure physical responses associated with migraine. The patient typically sits in a comfortable chair or recliner, and numerous physiologic responses are monitored with surface electrodes. 

When treating headache, sensors are typically placed on the head and neck to monitor muscle responses and a thermistor is placed on a finger to measure temperature. Feedback is given via visual cues (computer graphics) or a change in auditory tone as the patient is taught various relaxation techniques.  

Patients use the feedback to learn a physiologic relaxation response that may be beneficial for their headache management. Most of the research on biofeedback is related to treatment to prevent migraine; however, these techniques can be helpful to use during an acute attack, ideally paired with an acute care migraine medication. 

Can children with migraine have biofeedback treatments as well?

 Most children typically have a lower frequency of migraine than adults, although some have frequent migraines with associated disability and are candidates for preventive medication (although no medications are yet approved for children by the US Food and Drug Association). Most children are good candidates for behavioral therapies such as biofeedback. There are many computer games utilized in biofeedback training that children easily learn to modify physical responses. There are some fairly recent data suggesting that behavioral treatments, some of which include biofeedback, are effective strategies for children and may be more effective than preventive medication.  

What other types of illnesses could benefit from biofeedback training?    

There are data showing that biofeedback therapy can be helpful for anxiety disorders, insomnia, and functional bowel disorders and may help in modifying high blood pressure. It can also be a very effective stress-management strategy.  

Do you refer some of your patients with migraine to a psychologist for biofeedback treatments?      

 Yes, but it is always good for the referring physician to check on the credentials of the person performing the biofeedback treatment. Some headache specialists might do it themselves, but we do not. It takes a while—at least several sessions—and psychologists are better at it. Patients’ perspectives are also important. We communicate with the referred biofeedback treatment specialist to get more insight on the patient. For example, some patients are anxious and depressed, and they are not sleeping at night. The doctor we referred the patient to may recommend an antidepressant for the patient to help address those issues. It is a team effort.

What is the average cost per treatment?      
The costs vary throughout the country and range from $75 to $400 per session. Insurance coverage varies.  

How many times should a patient go in for treatment?    

Most protocols are about 10 to 12 sessions, depending on patient response. 

Have there been clinical trials on biofeedback treatments/devices?  

There have been many clinical trials that have been positive, so there is good evidence that biofeedback can be an effective treatment for migraine and tension-type headache. There are many types of biofeedback devices that measure different modalities. The most common one used in migraine is measuring scalp muscle contraction with surface electromyography or measuring peripheral blood flow with a temperature gauge. The goals are to relax muscles and learn to increase finger temperature, which is related to decreased arousal of the sympathetic nervous system or stress system. Other modalities include learning to modulate brain waves (electroencephalography or neurofeedback) and certain cardiovascular measures that reduce the stress response by a different mechanism. The goal is for patients to learn a low arousal response that they can utilize in their natural environment. Certain breathing techniques and visualization exercises are also helpful, but biofeedback refers to using physiologic recording equipment to help learn to change physical responses related to headache disorder. 

Over our years of experience, we have found that biofeedback can help a large percentage of our patients with migraine and tension-type headache, and it is associated with almost no adverse events.

What types of headache and other illnesses respond to biofeedback training?

Migraine affects about 12% of the US and most Western populations, and is 3 times more common in women than men. Migraine can be treated with a variety of strategies that include medications and nonpharmacologic therapies such as biofeedback, as well as other behavioral therapies and devices. Biofeedback refers to the use of instrumentation to monitor and display physiologic responses that the patient may not be aware of so that they can be “modified” in a more adaptive direction. Feedback gives immediate objective information and is usually combined with a relaxation-based therapy. The most common biofeedback treatments for migraine include feeding back muscle activity in the face and neck to help people relax contracted muscles and teach them a “low-arousal” response; they learn to increase finger temperature, which coincides with modifying the “stress” nervous system. Biofeedback has been shown to be helpful for migraine and tension-type headache. It is also helpful to decrease anxiety and stress levels and lower blood pressure.

Can patients use biofeedback treatments in conjunction with migraine medication?

Research has shown that migraine, in particular higher-frequency migraine, is best treated by a combination of medications and behavioral strategies. Biofeedback is a good option for use in conjunction with medication for migraine.

Who is trained to provide biofeedback treatments?

Biofeedback for migraine is something usually performed by psychologists and other professionals with specialized training. Many practitioners are certified by the Biofeedback Certification Institute of America (BCIA). It is important to find an experienced biofeedback practitioner who also has some expertise in treating headache disorders. 

How are biofeedback treatments performed?

Biofeedback is a therapy that follows a learning model whereby the patient gradually learns a self-regulation skill that impacts their headaches. 

Patients come to an office, typically once per week, where they are attached to instruments that measure physical responses associated with migraine. The patient typically sits in a comfortable chair or recliner, and numerous physiologic responses are monitored with surface electrodes. 

When treating headache, sensors are typically placed on the head and neck to monitor muscle responses and a thermistor is placed on a finger to measure temperature. Feedback is given via visual cues (computer graphics) or a change in auditory tone as the patient is taught various relaxation techniques.  

Patients use the feedback to learn a physiologic relaxation response that may be beneficial for their headache management. Most of the research on biofeedback is related to treatment to prevent migraine; however, these techniques can be helpful to use during an acute attack, ideally paired with an acute care migraine medication. 

Can children with migraine have biofeedback treatments as well?

 Most children typically have a lower frequency of migraine than adults, although some have frequent migraines with associated disability and are candidates for preventive medication (although no medications are yet approved for children by the US Food and Drug Association). Most children are good candidates for behavioral therapies such as biofeedback. There are many computer games utilized in biofeedback training that children easily learn to modify physical responses. There are some fairly recent data suggesting that behavioral treatments, some of which include biofeedback, are effective strategies for children and may be more effective than preventive medication.  

What other types of illnesses could benefit from biofeedback training?    

There are data showing that biofeedback therapy can be helpful for anxiety disorders, insomnia, and functional bowel disorders and may help in modifying high blood pressure. It can also be a very effective stress-management strategy.  

Do you refer some of your patients with migraine to a psychologist for biofeedback treatments?      

 Yes, but it is always good for the referring physician to check on the credentials of the person performing the biofeedback treatment. Some headache specialists might do it themselves, but we do not. It takes a while—at least several sessions—and psychologists are better at it. Patients’ perspectives are also important. We communicate with the referred biofeedback treatment specialist to get more insight on the patient. For example, some patients are anxious and depressed, and they are not sleeping at night. The doctor we referred the patient to may recommend an antidepressant for the patient to help address those issues. It is a team effort.

What is the average cost per treatment?      
The costs vary throughout the country and range from $75 to $400 per session. Insurance coverage varies.  

How many times should a patient go in for treatment?    

Most protocols are about 10 to 12 sessions, depending on patient response. 

Have there been clinical trials on biofeedback treatments/devices?  

There have been many clinical trials that have been positive, so there is good evidence that biofeedback can be an effective treatment for migraine and tension-type headache. There are many types of biofeedback devices that measure different modalities. The most common one used in migraine is measuring scalp muscle contraction with surface electromyography or measuring peripheral blood flow with a temperature gauge. The goals are to relax muscles and learn to increase finger temperature, which is related to decreased arousal of the sympathetic nervous system or stress system. Other modalities include learning to modulate brain waves (electroencephalography or neurofeedback) and certain cardiovascular measures that reduce the stress response by a different mechanism. The goal is for patients to learn a low arousal response that they can utilize in their natural environment. Certain breathing techniques and visualization exercises are also helpful, but biofeedback refers to using physiologic recording equipment to help learn to change physical responses related to headache disorder. 

Over our years of experience, we have found that biofeedback can help a large percentage of our patients with migraine and tension-type headache, and it is associated with almost no adverse events.

Key clinical point: Nearly one third of patients with treatment-refractory chronic migraine (CM) who did not respond to anti-calcitonin gene-related peptide (CGRP) receptor monoclonal antibodies (mAb) showed a meaningful response to anti-CGRP ligand mAb.

Major finding: Overall, 25.6% of patients achieved ≥30% reduction in monthly migraine days (MMD) after 3 months of initiating fremanezumab and were considered responders, with the mean MMD significantly reducing from 21.4 days at baseline to 15.0 days at 3 months (P = .007), 8.6 days at 6 months (P = .007), and 8.6 days at the last follow-up (P = .001). Treatment-related side effects were generally mild.

Study details: This long-term prospective real-world analysis included 39 patients with treatment-refractory CM who did not achieve a meaningful response to erenumab and switched to fremanezumab.

Disclosures: This study did not disclose the funding source. Some authors declared receiving research grants, funding for travel, personal fees as speakers or advisors, or honoraria for participation in advisory boards from various sources.

Source: Lambru G et al. Long-term effect of switching from an anti-CGRP receptor to an anti-CGRP ligand antibody in treatment-refractory chronic migraine: A prospective real-world analysis. Neurotherapeutics. 2023 (Jul 10). Doi: 10.1007/s13311-023-01394-0

Key clinical point: Nearly one third of patients with treatment-refractory chronic migraine (CM) who did not respond to anti-calcitonin gene-related peptide (CGRP) receptor monoclonal antibodies (mAb) showed a meaningful response to anti-CGRP ligand mAb.

Major finding: Overall, 25.6% of patients achieved ≥30% reduction in monthly migraine days (MMD) after 3 months of initiating fremanezumab and were considered responders, with the mean MMD significantly reducing from 21.4 days at baseline to 15.0 days at 3 months (P = .007), 8.6 days at 6 months (P = .007), and 8.6 days at the last follow-up (P = .001). Treatment-related side effects were generally mild.

Study details: This long-term prospective real-world analysis included 39 patients with treatment-refractory CM who did not achieve a meaningful response to erenumab and switched to fremanezumab.

Disclosures: This study did not disclose the funding source. Some authors declared receiving research grants, funding for travel, personal fees as speakers or advisors, or honoraria for participation in advisory boards from various sources.

Source: Lambru G et al. Long-term effect of switching from an anti-CGRP receptor to an anti-CGRP ligand antibody in treatment-refractory chronic migraine: A prospective real-world analysis. Neurotherapeutics. 2023 (Jul 10). Doi: 10.1007/s13311-023-01394-0

Key clinical point: Nearly one third of patients with treatment-refractory chronic migraine (CM) who did not respond to anti-calcitonin gene-related peptide (CGRP) receptor monoclonal antibodies (mAb) showed a meaningful response to anti-CGRP ligand mAb.

Major finding: Overall, 25.6% of patients achieved ≥30% reduction in monthly migraine days (MMD) after 3 months of initiating fremanezumab and were considered responders, with the mean MMD significantly reducing from 21.4 days at baseline to 15.0 days at 3 months (P = .007), 8.6 days at 6 months (P = .007), and 8.6 days at the last follow-up (P = .001). Treatment-related side effects were generally mild.

Study details: This long-term prospective real-world analysis included 39 patients with treatment-refractory CM who did not achieve a meaningful response to erenumab and switched to fremanezumab.

Disclosures: This study did not disclose the funding source. Some authors declared receiving research grants, funding for travel, personal fees as speakers or advisors, or honoraria for participation in advisory boards from various sources.

Source: Lambru G et al. Long-term effect of switching from an anti-CGRP receptor to an anti-CGRP ligand antibody in treatment-refractory chronic migraine: A prospective real-world analysis. Neurotherapeutics. 2023 (Jul 10). Doi: 10.1007/s13311-023-01394-0