Cephalalgia最新文献

BackgroundNeck pain is common in migraine patients, occurring during all migraine phases and between attacks. It can be a migraine symptom, trigger or a coexisting condition, and is associated with greater disability and poorer treatment response. There is evidence that neck pain associated with headaches can be frequently incorrectly diagnosed as a cervical disorder rather than migraine, resulting in a lack of appropriate treatment. Accurately assessing the connection between neck pain and migraine is crucial for effective treatment.MethodsThis narrative review aims to summarise existing research on the role and contribution of neck pain in migraine, both as a symptom and a trigger, and outlines future research needed to deepen our understanding of this relationship. It also proposes a structured approach for assessing neck pain in migraine and a treatment algorithm, offering guidance for clinical evaluation and treatment. For this purpose, a comprehensive narrative review was conducted using PubMed, covering preclinical, clinical, neurophysiological and imaging evidence on migraine and neck pain.ResultsMigraine patients frequently exhibit cervical dysfunction, tenderness and altered posture, with overlapping neuroanatomical pathways of the neck and trigeminal systems, suggesting shared mechanisms of nociception and migraine initiation. Clinical assessment involves a thorough history, physical exam and exclusion of secondary causes. Standard migraine therapies, such as amitriptyline and onabotulinumtoxinA, may help reduce neck pain and non-pharmacological treatments, such as physical therapy, acupuncture and behavioural strategies, show some promise. However, evidence on neck pain relief is limited.ConclusionsAccurately distinguishing whether neck pain is a symptom, trigger or comorbid condition in migraine is essential for guiding effective treatment strategies. Both pharmacological and non-pharmacological approaches may help manage migraine-associated neck pain. However, few studies have assessed the effects of acute or preventive migraine therapies, particularly calcitonin gene-related peptide-targeted treatments, on neck pain, highlighting a significant gap in our current knowledge. Future research should evaluate the effectiveness of these therapies on neck pain, both alone and in combination with non-pharmacological interventions.

BackgroundThis study evaluated the long-term safety, tolerability and effectiveness of rimegepant, 75 mg orally disintegrating tablet, for the acute treatment of migraine in Chinese adults.MethodsThis phase 3, multicenter, open-label, single-arm study enrolled Chinese adults with a ≥1 year history of migraine (with or without aura), 6-18 moderate-to-severe migraine attacks/month within three months before a screening visit and at least six migraine days during a 30-day observation phase (OP). After the OP, eligible participants took rimegepant as needed (maximum one tablet per day) at the onset of mild-to-severe migraine attack for a long-term treatment (LTT) of 52 weeks.ResultsOverall, 240 participants were treated and 208 (86.3%) completed the study. During LTT, 203 (84.6%) participants reported ≥1 treatment-emergent adverse event (TEAE) and 46 (19.2%) reported ≥1 TEAE considered to be rimegepant-related. There were no rimegepant-related serious AEs or rimegepant-related TEAEs that led to treatment interruption or discontinuation. Mean reduction from the OP in monthly migraine days was observed as early as the first four weeks (-1.7; 95% confidence interval = -2.2 to -1.2), with an overall mean reduction of -4.4 (95% confidence interval = -4.9 to -3.9) days across LTT.ConclusionsRimegepant had a favorable long-term safety profile, was well tolerated in Chinese participants, and a reduction in the number of monthly migraine days was observed during the LLT.Trial registration: ClinicalTrials.gov identifier: NCT05371652.

Aim: To investigate the effect of different cannabinoid compounds on the periorbital mechanical allodynia and photosensitivity in acute and chronic migraine models.

Methods: Female Wistar rats were treated systemically with different cannabinoid compounds (cannabidiol, CBD, 30 mg/kg; CBD and cannabigerol, CBD/CBG - 2:1; CBD and 0.3% tetrahydrocannabinol (CBD/THC); or CBD/CBG/THC) followed by injection of calcitonin-gene-related peptide (CGRP) or pituitary adenylate cyclase-activating polypeptide (PACAP) into the trigeminal ganglion to induced immediate periorbital mechanical allodynia and late photosensitivity. The effect of CBD and CBD/THC was also assessed on periorbital mechanical allodynia and photosensitivity in the chronic migraine model induced by repeated nitroglycerin (NTG) injections.

Results: Periorbital mechanical allodynia induced by CGRP was significantly reduced by CBD alone and combined with THC or CBG. CBD/THC was the most effective treatment in this condition since it presented the longer effect (up to three hours) and was the only treatment capable of reducing late photosensitivity associated with CGRP. All four compounds presented antinociceptive effect on acute migraine-like responses induced by PACAP, with CBD alone presenting the longer effect (from 30 minutes up to two hours). Except for CBD/CBG, all compounds also reduced (up to two hours) late photosensitivity associated with PACAP. In the chronic migraine model induced by NTG, CBD reduced periorbital mechanical allodynia on days 5, 7 and 11, while CBD/THC suppressed the development of periorbital allodynia up to day 13 and significantly reduced photosensitivity up to three hours.

Conclusion: Altogether, these results suggest that cannabinoid compounds may represent effective alternatives for the treatment of episodic and chronic migraine.

Migraine is one of the most disabling diseases worldwide, especially when it transforms into chronic migraine, which is often associated with medication overuse and can become resistant or even refractory to treatments. Molecular, neuroimaging and neurophysiological changes have been described in chronic migraine, some of which might not be fully reversible with preventive treatment. For these reasons, we should aim to prevent this transition, and initiate preventive treatment before disease becomes refractory and burden increases. Preventive migraine treatments are often delayed because of access to care, stigma leading to undertreatment and patients' reluctance as a result of fear of side effects and, in some cases, fear of being labeled as chronically ill. With the availability of effective and well-tolerated preventive treatments, we must shift our mindset and take advantage of new opportunities to initiate preventive treatment earlier. In this International Headache Society position statement, we propose a migraine preventive strategy under the idea of shifting from reactive treatment once disability is established (prevention of attacks), to proactive, individualized prevention initiated early with safe, effective and tolerable therapies (prevention of disease progression). This approach is based on 1) promoting the early initiation of effective and tolerable preventive therapies, starting from two to four monthly migraine days in line with the majority of current guidelines and recommendations and 2) fostering longitudinal studies to gather more evidence on the potential benefit of early prevention, with the final goal of improving patient outcomes, promoting excellent migraine care, enhancing individual and social well-being, and, ultimately, preventing migraine progression and preserving brain health.

AimMigraine with aura is a risk factor for ischemic stroke. To further assess this risk factor in relation to ischemic stroke, along with other risk factors, we created the migraine associated risk of stroke score (MARS+), making it applicable to migraineurs. The risk score includes vascular risk factors, migraine characteristics and medications used in migraine patients.MethodsWe prospectively evaluated participants in Atherosclerosis Risk in Communities Cohort (ARIC) with a history of migraine. In this population, we tested the association of potential risk factors for ischemic stroke using a Cox proportional hazards model. The coefficient of each variable was divided by the lowest β value and rounded to the nearest integer. The sum of the weighted score of the reported risk factors was found and categorized into two prognostic groups.ResultsWe assessed migraine characteristics (aura, migraine frequency and duration) and medications that were in current use by participants, mean ± SD age 58 ± 5.5 years, 86% white, 14% black and 77% women (ergot alkaloids, triptans, hormone replacement therapy, sympathomimetics, steroids, selective serotonin reuptake inhibitors and opioids), in addition to traditional risk factors. Based on the points derived from the significant factors we assigned age ≥65 years = 1, non-white race = 2, hypertension = 2, diabetes = 3, body mass index ≥30 = 2, atrial fibrillation = 2, use of steroid medications = 3, use of selective serotonin reuptake inhibitor medications = 1, opioids = 2, presence of aura = 2 and duration <5 years = 1 to total 21 points. A cut-off of MARS+ ≥5 was considered as a lifetime high risk for ischemic stroke based on receiver operating characteristic curve and Youden's index. Of the 1485 participants with migraine, 112 had an ischemic stroke. MARS+ ≥5 revealed a hazard ratio of 4.09 (95% confidence interval = 2.67-6.26).ConclusionsThe MARS+ score is used to predict ischemic stroke in middle-aged migraine sufferers. This risk score, in addition to generalizability, includes factors such as migraine characteristics and medications that may increase stroke risk.

BackgroundMigraine is a common neurological disorder with a strong genetic component, yet the precise mechanisms underlying its genetic susceptibility remain largely unknown. Genome-wide association studies (GWAS) have identified multiple risk loci, but monogenic forms of migraine, particularly Familial Hemiplegic Migraine (FHM), have provided deeper insights into the pathophysiology of migraine. Studying monogenic disorders that present migraine as a symptom could help identify novel therapeutic targets by uncovering shared molecular pathways.MethodsA narrative literature review was conducted using a stepwise approach in the PubMed database. Reviewers were divided into three groups, each focusing on different aspects of migraine genetics. The first group analyzed monogenic migraine syndromes, including FHM and related ion-channelopathies. The second group examined clinical manifestations and phenotypic spectrum of FHM-related genes. The third group expanded the search to other monogenic disorders associated with migraine, such as Cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS), and Familial Advanced Sleep Phase Syndrome (FASPS). Additional searches were conducted using the Compendium of Causative Genes for Monogenic Disorders.ResultsThe review identified multiple monogenic disorders associated with migraine, revealing distinct but interconnected mechanisms. Ion-channel dysfunction (CACNA1A, SCN1A, ATP1A2), vascular impairment (NOTCH3, TREX1), mitochondrial dysfunction (MT-TL1), and circadian dysregulation (CSNK1D) emerged as critical contributors to migraine pathophysiology. These findings highlight the roles of neuronal excitability, cortical spreading depression, trigeminal sensitization, and neurovascular dysfunction in migraine.ConclusionsMonogenic migraine disorders offer valuable insights into migraine pathogenesis, emphasizing the importance of ion homeostasis, vascular function, and circadian regulation. Although genetic studies have not yet directly translated into new therapeutic targets, the study and knowledge of these rare conditions is pivotal for neurologists and migraine specialists, as it might improve diagnosis and care, and provide new insights into migraine pathophysiology that may ultimately inform future treatments.