From transformation to chronification of migraine: pathophysiological and clinical aspects

Torres‐Ferrús, Marta; Ursitti, Fabiana; Alpuente, Alicia; Brunello, Francesco; Chiappino, Dario; Vries, Tessa de; Marco, Salvatore Di; Ferlisi, Salvatore; Guerritore, Ludovica; González‐García, Nuria; González-Martínez, Alicia; Khutorov, Dmitrii N.; Kritsilis, Marios; Kyrou, Alexandra; Makeeva, T.; Mínguez‐Olaondo, Ane; Pilati, Laura; Serrien, Anouk; Tsurkalenko, Olena; Abbeele, Dirk Van den; Hoogstraten, Willem Sebastiaan van; Lampl, Christian

doi:10.1186/s10194-020-01111-8

Cited by 73 publications

(65 citation statements)

References 156 publications

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“…Moreover, patients with CM had volumetric changes in amygdala, hippocampus, putamen and brainstem areas [63]. These data once again prove the role of these cerebral structures in the pathogenesis of chronic migraine [64].…”

Section: Pathophysiologysupporting

confidence: 53%

“…Genetic influence on the progression from episodic to CM is yet to be established as more large-sample studies are needed [64,65]. However it looks that chronic migrain has a polygenetic background.…”

Section: Pathophysiologymentioning

confidence: 99%

“…In conclusion it is crucial that effort is made to treat migraine attacks rapidly and adequately as well as to modify other risk factors relevant to the patient so that the pathophysiological mechanisms responsible for migraine progression from episodic into chronic form could be precluded [45,64].…”

Section: Risk Factorsmentioning

confidence: 99%

“…Typical migraine attacks generally manifest as severe, usually unilateral headache of throbbing quality, increasing intensity with physical activity and a combination of associated features: nausea, vomiting, hypersensitivity to visual, auditory, olfactory and cutaneous stimuli. The headache can change sides during or between the attacks [64]. The pain in patients with CM is more commonly bilateral and the associated symptoms are less pronounced than in those with EM [93].…”

Section: Symptoms and Diagnosismentioning

confidence: 99%

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Chronic Migraine

Obelienienė¹,

Pestininkaite²,

Rastenytė³

2020

Migraine

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Chronic migraine as a disease was initially recognized in patients with a large burden of disability from frequent headaches and a history of prior migraines. Over time, this observation was operationalized into multiple diagnostic criteria with requirements for frequent headache days, typically 15 or more, which, on at least 8 days in a month, have the features of migraine headache. Chronic migraine affects 1-2% of the general population, and about 8% of patients with migraine. Understanding disease mechanisms still remains a challenge. Inflammation and central sensitization play significant role in the evolutive mechanisms of chronic migraine. Treatment of this condition should primarily focus on the prevention. The currently available evidence-based prophylactic treatment options are topiramate, valproic acid, onabotulinumtoxin A and recently developed promising anti-CGRP monoclonal antibodies. Chronic migraine research is a dynamic and rapidly advancing area. New developments in this field have the potential to improve the diagnosis, to provide more personalized treatments and to reduce burden of disability.

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Section: Pathophysiologysupporting

confidence: 53%

Section: Pathophysiologymentioning

confidence: 99%

Section: Risk Factorsmentioning

confidence: 99%

Section: Symptoms and Diagnosismentioning

confidence: 99%

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Chronic Migraine

Obelienienė¹,

Pestininkaite²,

Rastenytė³

2020

Migraine

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“…26 Chronic migraine, which causes greater disability than episodic migraine and affects ∼2% of the general population, is characterized as 15 or more headache days per month for at least 3 months with 8 or more days per month meeting migraine criteria. 60 A main symptom associated with migraine is throbbing headache, which persists for up to 72 hours and involves sensitization and activation of primary and secondary trigeminal nociceptive neurons. 22 Other commonly reported migraine symptoms are nausea, vomiting, and heightened sensitivity to light and sound.…”

Section: Introductionmentioning

confidence: 99%

Noninvasive vagus nerve stimulation and morphine transiently inhibit trigeminal pain signaling in a chronic headache model

Cornelison

Hawkins

Woodman

et al. 2020

PR9

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Effects of Intravenous Eptinezumab vs Placebo on Headache Pain and Most Bothersome Symptom When Initiated During a Migraine Attack

Winner

McAllister

Chakhava

et al. 2021

JAMA

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an anti-calcitonin gene-related peptide antibody, is approved for migraine prevention in adults. It has established onset of preventive efficacy on day 1 after infusion. OBJECTIVE To evaluate the efficacy of and adverse events related to eptinezumab when initiated during a migraine attack.DESIGN, SETTING, AND PARTICIPANTS Phase 3, multicenter, parallel-group, double-blind, randomized, placebo-controlled trial conducted from November 4, 2019, to July 8, 2020, at 47 sites in the United States and the country of Georgia. Participants (aged 18-75 years) with a greater than 1-year history of migraine and migraine on 4 to 15 days per month in the 3 months prior to screening were treated during a moderate to severe migraine attack.INTERVENTIONS Eptinezumab, 100 mg (n = 238), or placebo (n = 242), administered intravenously within 1 to 6 hours of onset of a qualifying moderate to severe migraine. MAIN OUTCOMES AND MEASURESCo-primary efficacy end points were time to headache pain freedom and time to absence of most bothersome symptom (nausea, photophobia, or phonophobia). Key secondary end points were headache pain freedom and absence of most bothersome symptom at 2 hours after start of infusion. Additional secondary end points were headache pain freedom and absence of most bothersome symptom at 4 hours and use of rescue medication within 24 hours. RESULTSOf 480 randomized and treated patients (mean age, 44 years; 84% female), 476 completed the study. Patients treated with eptinezumab vs placebo, respectively, achieved statistically significantly faster headache pain freedom (median, 4 hours vs 9 hours; hazard ratio, 1.54 [P < .001]) and absence of most bothersome symptom (median, 2 hours vs 3 hours; hazard ratio, 1.75 [P < .001]). At 2 hours after infusion, in the respective eptinezumab and placebo groups, headache pain freedom was achieved by 23.5% and 12.0% (between-group difference, 11.6% [95% CI, 4.78%-18.31%]; odds ratio, 2.27 [95% CI, 1.39-3.72]; P < .001) and absence of most bothersome symptom by 55. 5% and 35.8% (between-group difference, 19.6% [95% CI, 10.87%-28.39%]; odds ratio, 2.25 [95% CI, 1.55-3.25]; P < .001). Results remained statistically significant at 4 hours after infusion. Statistically significantly fewer eptinezumab-treated patients used rescue medication within 24 hours than did placebo patients (31.5% vs 59.9%, respectively; between-group difference, −28.4% [95% CI, −36.95% to −19.86%]; odds ratio, 0.31 [95% CI, 0.21-0.45]; P < .001). Treatment-emergent adverse events occurred in 10.9% of the eptinezumab group and 10.3% of the placebo group; the most common was hypersensitivity (eptinezumab, 2.1%; placebo, 0%). No treatment-emergent serious adverse events occurred.CONCLUSIONS AND RELEVANCE Among patients eligible for preventive migraine therapy experiencing a moderate to severe migraine attack, treatment with intravenous eptinezumab vs placebo shortened time to headache and symptom resolution. Feasibility of administering eptinezumab treatment during a migraine attack and comparison with alterna...

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From transformation to chronification of migraine: pathophysiological and clinical aspects

Cited by 73 publications

References 156 publications

Chronic Migraine

Chronic Migraine

Noninvasive vagus nerve stimulation and morphine transiently inhibit trigeminal pain signaling in a chronic headache model

Effects of Intravenous Eptinezumab vs Placebo on Headache Pain and Most Bothersome Symptom When Initiated During a Migraine Attack

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