Migraine: disease characterisation, biomarkers, and precision medicine

Ashina, Messoud; Terwindt, Gisela M.; Al‐Karagholi, Mohammad Al‐Mahdi; Boer, Irene de; Lee, Mi Ji; Hay, Debbie L.; Schulte, Laura H.; Hadjikhani, Nouchine; Sinclair, Alexandra J; Ashina, Håkan; Schwedt, Todd J.; Goadsby, PJ

doi:10.1016/s0140-6736(20)32162-0

Cited by 182 publications

(181 citation statements)

References 117 publications

(122 reference statements)

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“…Furthermore, a minority of those affected develop chronic migraine, in which attacks become highly frequent 7 . The pathogenesis of migraine is widely believed to involve peripheral and central activation of the trigeminovascular system 8 , and cortical spreading depression is thought to be the underlying neurophysiological substrate of migraine aura 9 . However, much remains unknown about specific pathogenic processes and few mechanism-based treatment options currently exist 10 .…”

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confidence: 99%

Diagnosis and management of migraine in ten steps

et al. 2021

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Migraine is a disabling primary headache disorder that directly affects more than one billion people worldwide. Despite its widespread prevalence, migraine remains under-diagnosed and under-treated. To support clinical decision-making, we convened a European panel of experts to develop a ten-step approach to the diagnosis and management of migraine. Each step was established by expert consensus and supported by a review of current literature, and the Consensus Statement is endorsed by the European Headache Federation and the European Academy of Neurology. In this Consensus Statement, we introduce typical clinical features, diagnostic criteria and differential diagnoses of migraine. We then emphasize the value of patient centricity and patient education to ensure treatment adherence and satisfaction with care provision. Further, we outline best practices for acute and preventive treatment of migraine in various patient populations, including adults, children and adolescents, pregnant and breastfeeding women, and older people. In addition, we provide recommendations for evaluating treatment response and managing treatment failure. Lastly, we discuss the management of complications and comorbidities as well as the importance of planning long-term follow-up.

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confidence: 99%

Diagnosis and management of migraine in ten steps

et al. 2021

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“…Binding of CGRP to the CGRP-receptor complex on vascular smooth muscle cells (VSMCs) (Eftekhari et al, 2013;Edvinsson et al, 2018) mediates an activation of the cyclic adenosine monophosphate-protein kinase A (cAMP-PKA) pathway resulting in potassium efflux through K ATP channels, hyperpolarization, and eventually relaxation and vasodilation (Hong et al, 1996;Williams et al, 1998;Ashina et al, 2021). K ATP channels consist of different isoforms of sulfonylurea receptor subunits (SUR1, SUR2A, and SUR2B) (Kokoti et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

“…Calcitonin gene-related peptide (CGRP) is a potent vasodilator of cranial arteries (Brain et al, 1985;Falkenberg et al, 2020) and intravenous infusion of CGRP causes headache in healthy volunteers (Petersen et al, 2005b;Falkenberg et al, 2020) and migraine attacks in migraine patients (Lassen et al, 2002;Hansen et al, 2010;Ashina, 2020;Iljazi et al, 2020;Ashina et al, 2021). The molecular mechanisms by which CGRP mediates head pain are still unclear (Ashina et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

The Effect of KATP Channel Blocker Glibenclamide on CGRP-Induced Headache and Hemodynamic in Healthy Volunteers

et al. 2021

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BackgroundCalcitonin gene-related peptide (CGRP) dilates cranial arteries and triggers headache. The CGRP signaling pathway is partly dependent on activation of ATP-sensitive potassium (KATP) channels. Here, we investigated the effect of the KATP channel blocker glibenclamide on CGRP-induced headache and vascular changes in healthy volunteers.MethodsIn a randomized, double-blind, placebo-controlled, cross-over study, 20 healthy volunteers aged 18–27 years were randomly allocated to receive an intravenous infusion of 1.5 μg/min CGRP after oral pretreatment with glibenclamide (glibenclamide-CGRP day) or placebo (placebo-CGRP day). The primary endpoints were the difference in incidence of headache and the difference in area under the curve (AUC) for headache intensity scores (0–14 h) between glibenclamide and placebo. The secondary endpoints were the difference in AUC for middle cerebral artery blood flow velocity (VMCA), superficial temporal artery (STA) and radial artery (RA) diameter, facial flushing, heart rate (HR) and mean arterial blood pressure (MAP) (0–4 h) between glibenclamide and placebo.ResultsWe found no significant difference in the incidence of headache between glibenclamide-CGRP day (14/20, 70%) and placebo-CGRP day (19/20, 95%) (P = 0.06). The AUC for headache intensity, VMCA, STA, RA, facial skin blood flow, HR, and MAP did not differ between glibenclamide-CGRP day compared to placebo-CGRP day (P > 0.05).ConclusionPretreatment with a non-selective KATP channel inhibitor glibenclamide did not attenuate CGRP-induced headache and hemodynamic changes in healthy volunteers. We suggest that CGRP-induced responses could be mediated via activation of specific isoforms of sulfonylurea receptor subunits of KATP channel.

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“…However, our study was not designed to prove any biological hypothesis, as it was not interventional, and we did not measure any level of female sex hormones or CGRP in the study population. The measurement of functional biomarkers of migraine in humans is an emerging trend ( 28 ) and could provide useful insights when assessing the effect of anti-migraine drugs.…”

Section: Discussionmentioning

confidence: 99%

Gender Differences in 3-Month Outcomes of Erenumab Treatment—Study on Efficacy and Safety of Treatment With Erenumab in Men

et al. 2021

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Objective: We reported gender-specific data on the efficacy and safety of erenumab, a monoclonal antibody antagonizing the calcitonin gene-related peptide (CGRP) receptor.Methods: Our pooled patient-level analysis of real-world data included patients treated with erenumab and followed up for 12 weeks. We considered the following outcomes at weeks 9–12 of treatment compared with baseline: 0–29%, 30–49%, 50–75%, and ≥75% responder rates, according to the decrease in monthly headache days (MHDs), rate of treatment stopping, change in MHDs, monthly migraine days (MMDs), monthly days of acute medication and triptan use, and Headache Impact Test-6 (HIT-6) score from baseline to weeks 9–12. Outcomes were compared between men and women by the chi-squared test or t-test, as appropriate. An analysis of covariance (ANCOVA) was performed to identify factors influencing the efficacy outcomes.Results: We included 1,410 patients from 16 centers, of which 256 (18.2%) were men. Men were older than women and had a lower number of MHDs at baseline. At weeks 9–12, compared with baseline, 46 (18.0%) men had a ≥75% response, 75 (29.3%) had a 50–74% response, 35 (13.7%) had a 30–49% response, and 86 (33.6%) had a 0–29% response, while 14 (5.5%) stopped the treatment. The corresponding numbers for women were 220 (19.1%), 314 (27.2%), 139 (12.0%), 402 (34.8%), and 79 (6.8%). No gender difference was found in any of the outcomes. The ANCOVA showed that gender did not influence the efficacy of outcomes.Conclusion: We found that erenumab is equally safe and effective in men compared with women after 12 weeks.

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Migraine: disease characterisation, biomarkers, and precision medicine

Cited by 182 publications

References 117 publications

Diagnosis and management of migraine in ten steps

Diagnosis and management of migraine in ten steps

The Effect of KATP Channel Blocker Glibenclamide on CGRP-Induced Headache and Hemodynamic in Healthy Volunteers

Gender Differences in 3-Month Outcomes of Erenumab Treatment—Study on Efficacy and Safety of Treatment With Erenumab in Men

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