Cephalalgia最新文献

{"title":"Optimising combined treatment for migraine and temporomandibular disorders (TMDs).","authors":"Marcela Romero-Reyes, Simon Akerman, Alan M Rapoport","doi":"10.1177/03331024251368882","DOIUrl":"10.1177/03331024251368882","url":null,"abstract":"<p><p>Temporomandibular disorders (TMDs) and migraine are highly prevalent, overlapping pain conditions that cause considerable burden in the population. These two disorders are of different etiology and pathophysiology, but both are mediated by the trigeminal system. Due to the interrelated anatomy and physiology of the craniofacial and cervical structures, shared molecular links and mutual feedback, there is an inherent potential for exacerbation of symptomatology, perpetuation and progression; however, on a positive note, there is good potential for developing integrated, mutually beneficial management protocols when migraine and TMDs are comorbid. Currently, there are no established protocols of management, and the literature is limited in studies exploring dual therapeutic protocols. So, the question is, how can management be optimized with the evidence available? We should start by recognizing the need for multidisciplinary management to improve patient outcomes and we must highlight the importance of the dialogue between headache medicine and dentistry. The meeting point is where the dental discipline and the specialty of orofacial pain reside. The underlying pathophysiology of this comorbidity points to the need to decrease mutual exacerbation inputs. Therefore, it is fundamental to identify contributing factors of potential sensitization, such as the presence of parafunctional behaviors, cervical spine contributors, the presence of other comorbidities and headache hygiene. Current evidence supports management recommendations that should be developed by a multidisciplinary team as an integrated plan with combination therapy including both pharmacological and non-pharmacological approaches to optimize management. This multidisciplinary team should include the medical provider (neurologist/headache medicine expertise), the dentist specialized in orofacial pain, the physical therapist and the behavioral medicine specialist. Research is needed to support evidence-based integrated protocols for the management of comorbid migraine and TMDs. Evidence has shown that calcitonin gene-related peptide (CGRP) is also involved in TMDs. CGRP-targeting therapies may hold future opportunities for pharmacological monotherapy addressing this comorbidity.</p>","PeriodicalId":10075,"journal":{"name":"Cephalalgia","volume":"45 9","pages":"3331024251368882"},"PeriodicalIF":4.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain imaging in migraine with and without aura: Similarities and differences.","authors":"Francesco Casillo, Gabriele Sebastianelli, Chiara Abagnale, Antonio Di Renzo, Lucia Ziccardi, Vincenzo Parisi, Gianluca Coppola","doi":"10.1177/03331024251365807","DOIUrl":"10.1177/03331024251365807","url":null,"abstract":"<p><p>BackgroundWhether migraine with aura (MA) is a biologically independent entity from migraine without aura (MO) is still debated. Similarities and differences between MO and MA have been extensively investigated in recent years through several neuroimaging studies, providing valuable insights into their underlying pathophysiology. To provide a better understanding of functional and structural differences between MO and MA, we conducted a narrative review of neuroimaging studies in these two conditions.MethodsA comprehensive PubMed search for neuroimaging studies in MO and MA was conducted in May 2025. We included studies that directly compared the two conditions using diffusion tensor imaging, voxel-based morphometry, surface-based morphometry, functional MRI and arterial spin labeling studies. No publication date restrictions were applied.ResultsOverall, patients with MA exhibited heightened engagement of the visual regions, cerebellum and thalamus. However, both MO and MA shared common activation of parts of the salience network and involvement of similar visual areas, including the striate and extrastriate cortices. However, contrasting results and several inconsistencies emerged from the analysis of different imaging studies. These included the lack of specification regarding the phase of the migraine cycle during which the scans were conducted, the inclusion of patients under migraine prevention, small sample sizes, and different approaches to data and statistical analysis (including a more liberal approach to interpreting results).ConclusionsAlthough several biases influence the reliability of most findings, patients with MA exhibited higher involvement of visual processing regions, decreased cerebellar antinociceptive activity and impaired thalamic information filtering. Whether this pattern represents the consequence of the recurrence of cortical spreading depression or a primary predisposition to it remains to be determined. Future studies with a rigorous and standardized approach are needed to understand the differences between MO and MA.</p>","PeriodicalId":10075,"journal":{"name":"Cephalalgia","volume":"45 9","pages":"3331024251365807"},"PeriodicalIF":4.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145039294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Greater occipital nerve injection with methylprednisolone as transitional therapy in episodic cluster headache: Results from an RCT.","authors":"Roemer B Brandt, Wim M Mulleners, Emile Couturier, Johannes A Carpay, Olivier H H Gerlach, Marieke Niesters, Joost Haan, Erik W van Zwet, Michel D Ferrari, Rolf Fronczek","doi":"10.1177/03331024251370324","DOIUrl":"10.1177/03331024251370324","url":null,"abstract":"<p><p>ObjectiveWe investigated whether greater occipital nerve injection (GON injection) with 80 mg of methylprednisolone at the onset of a cluster headache episode would reduce attack frequency faster than standard therapy with verapamil alone, and reduce the need for verapamil and the risk of adverse events (AEs).MethodsThis was an investigator-initiated, randomised, double-blind, 12-week clinical trial. Participants received GON injection with 80 mg of methylprednisolone (n = 36) or placebo (n = 34) within two weeks (median) after the onset of a cluster episode, followed by standard verapamil therapy and e-diary monitoring. The primary endpoint was the mean daily dose of verapamil over the entire 12-week study period. Key secondary endpoints were reduction in the mean daily dose of verapamil over the first four weeks and attack frequency reduction in the first week.ResultsIn the verum vs. placebo group, the mean daily dose of verapamil during the total 12-week study period did not differ (232 ± 188 mg vs. 244 ± 143 mg; Δ = 12 mg, 95% confidence interval (CI) = -68 to 92; <i>p</i> = 0.230). However, exploratory analysis of the secondary endpoints showed a lower verapamil dose in the first four weeks in the methylprednisolone group compared to placebo (227 ± 126 mg vs. 287 ± 107 mg; mean Δ 60 mg; 95% CI = -4 to -116), as was the median number of attacks at week 1 (7 (interquartile range = 2-11.75) vs. 10 (interquartile range = 6-17.5); 95% CI = -1.0 to -8.0), the mean attack intensity at week 1 (5.7 ± 1.9 vs. 6.6 ± 1.8; 95% CI = 0.0-1.8) and throughout the 12-week study period (5.0 ± 1.8 vs. 5.9 ± 1.9; 95% CI = 0.01-1.8), and the number of days with adverse events (455/2520 (18%) vs. 605/2850 (21%); p < 0.01). There were no serious AEs.ComclusionsThis study failed to establish its primary endpoint. However, exploratory analysis of the secondary endpoints revealed that GON injection with 80 mg of methylprednisolone at the beginning of a cluster headache episode followed by standard therapy verapamil is a safe transitional treatment that provides faster reduction in attack frequency and intensity than verapamil alone, decreases the mean verapamil dose over the first four weeks with consequently fewer adverse events in the first four weeks after the injection.Trial RegistrationThis study is registered on Clinicaltrials.gov with registration number NCT04014634 at 08-07-2019. First inclusion was on 30-07-2019.</p>","PeriodicalId":10075,"journal":{"name":"Cephalalgia","volume":"45 9","pages":"3331024251370324"},"PeriodicalIF":4.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The \"Migraines\" epidemic: Exposing the challenges of artificial intelligence in scientific writing.","authors":"Simona Sacco","doi":"10.1177/03331024251365833","DOIUrl":"https://doi.org/10.1177/03331024251365833","url":null,"abstract":"","PeriodicalId":10075,"journal":{"name":"Cephalalgia","volume":"45 8","pages":"3331024251365833"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microglial TRPV2-mediated neuroinflammation promotes central sensitization through microglial polarization in a vestibular migraine mouse model.","authors":"Qingling Zhai, Hongyan Li, Qihui Chen, Ning Zhang, Yanan Huang, Yonghui Pan","doi":"10.1177/03331024251364753","DOIUrl":"https://doi.org/10.1177/03331024251364753","url":null,"abstract":"<p><p>BackgroundNeuroinflammation, which is mediated by microglial activation, contributes to central sensitization, a key mechanism in vestibular migraine (VM). Transient receptor potential vanilloid 2 (TRPV2)-mediated calcium influx enhances nucleotide-binding oligomerization domain; leucine-rich repeat, and pyrin domain-containing protein 3 (NLRP3) inflammasome assembly, potentially driving inflammation. This study investigated the role of TRPV2 in VM pathogenesis.MethodsA VM model was established via repeated intraperitoneal injections of nitroglycerin and kainic acid-induced vestibular nerve terminal impairment. Periorbital thresholds and vestibular scores were measured to assess allodynia and vestibular dysfunction. Western blotting and immunofluorescence were used to evaluate TRPV2, ionized calcium-binding adapter molecule 1 (IBA1), interleukin-1β and NLRP3 expression in the spinal trigeminal nucleus caudalis (Sp5c) region. <i>In vitro</i>, BV2 cells treated with lipopolysaccharide and interferon-γ were transfected with TRPV2 small interfering RNA. TRPV2 activity was analyzed via patch-clamp electrophysiology. Microglial polarization and morphology were examined via flow cytometry and immunofluorescence, with a focus on CD16, CD63, CD206 and CD163 markers. NLRP3 inflammasome activation was assessed through western blotting and immunofluorescence.ResultsVM-related behaviors, including allodynia and dizziness, were successfully reproduced. Central sensitization in the Sp5c was marked by increased TRPV2 expression in microglia, as demonstrated by co-localization with the microglial marker IBA1. <i>In vitro</i>, TRPV2 inhibition in BV2 cells shifted microglial polarization from the pro-inflammatory M1 state to the anti-inflammatory M2 state. Additionally, TRPV2 blockade significantly reduced NLRP3 inflammasome activation and the levels of proinflammatory cytokines.ConclusionsTRPV2 regulates microglial activation and NLRP3 inflammasome activity via polarization mechanisms, contributing to central sensitization in VM. These findings highlight the critical role of TRPV2 in VM pathogenesis and its potential as a therapeutic target.</p>","PeriodicalId":10075,"journal":{"name":"Cephalalgia","volume":"45 8","pages":"3331024251364753"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145112289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasma adrenomedullin levels in migraine: A registry for migraine (REFORM) study.","authors":"Rogelio Dominguez-Moreno, William K Karlsson, Haidar M Al-Khazali, Rune H Christensen, Håkan Ashina, Messoud Ashina","doi":"10.1177/03331024251360234","DOIUrl":"10.1177/03331024251360234","url":null,"abstract":"<p><p>ObjectiveTo compare plasma adrenomedullin (AM) levels between adults with migraine and healthy controls (HCs), assessing subgroup differences and clinical associations.MethodsThis cross-sectional, observational single-center study was carried out from September 2020 to June 2022. Adults with migraine and HCs were enrolled and underwent blood sampling. Migraine subgroups included episodic migraine, chronic migraine, migraine without aura and migraine with aura. Plasma AM concentrations were quantified using a validated immunoluminometric assay by trained personnel who were blinded to group status.ResultsIn total, 667 participants with migraine and 147 HCs provided data eligible for analysis. Plasma AM concentrations did not differ significantly between the migraine and HC group (18.2 ± 9.1 pg/ml vs. 18.5 ± 8.4 pg/ml; <i>p</i> = 0.08). However, participants with episodic migraine exhibited lower AM levels than HCs (16.9 ± 7.7 pg/ml vs. 18.5 ± 8.4 pg/ml; <i>p</i> = 0.04). Multivariate regression models showed that plasma AM concentrations are positively associated with body mass index (4.2% increase in AM per kg/m²; 3.6 to 4.8%; <i>p</i> < 0.001) and monthly migraine days (0.6% increase in AM per MMD; 0.2 to 1.0%; <i>p</i> = 0.006).ConclusionsPlasma AM concentrations were comparable between participants with migraine and HCs; however, those with episodic migraine exhibited slightly lower levels. Future studies should investigate other candidate blood-based biomarkers for migraine.</p>","PeriodicalId":10075,"journal":{"name":"Cephalalgia","volume":"45 8","pages":"3331024251360234"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144815910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding PACAP signaling: Splice variants, pathways and designer drugs.","authors":"Zoe Tasma, Debbie L Hay","doi":"10.1177/03331024251363560","DOIUrl":"https://doi.org/10.1177/03331024251363560","url":null,"abstract":"<p><p>The neuropeptides pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP) play roles in vasodilation, the immune response and neuronal signaling, with recent links to headache disorders. This association has resulted in considerable interest in targeting this family of peptides and their receptors for drug development, and, notably, an anti-PACAP antibody has reported clinical efficacy in reducing migraine frequency. The PACAP/VIP ligands act at G protein-coupled receptors (GPCRs). PAC₁, VPAC₁ and VPAC₂ are the officially-recognized canonical receptors. Each of these has the potential to generate receptor variants through exon splicing. These variants may exhibit altered function, significantly increasing the diversity of PACAP-responsive receptors. In addition to these canonical receptors, PACAP is proposed to activate other unrelated receptors, GPR55 and MRGPRX2. Altogether, any of these canonical and proposed receptors may mediate the biological actions of PACAP, including migraine-relevant behaviors. However, we have a limited understanding of how these receptors function, such as their capacity to activate downstream signaling, the cellular and subcellular location of that signaling, and whether accessory protein interactions may alter these responses, especially in migraine-relevant contexts. The complex nature of the PACAP/VIP system therefore provides not only numerous considerations for target design and validation, but also unique opportunities for \"designer\" drugs. This narrative review provides an overview of the complex PACAP/VIP system, exploring peptide, receptor and downstream signaling behaviors that may be potential targets for the treatment of headache disorders and beyond.</p>","PeriodicalId":10075,"journal":{"name":"Cephalalgia","volume":"45 8","pages":"3331024251363560"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Opening of ATP-sensitive potassium channels activates meningeal nociceptors: Implications for the origin of migraine headache.","authors":"Rune H Christensen, Andrew M Strassman, Messoud Ashina, Håkan Ashina, Rami Burstein","doi":"10.1177/03331024251359237","DOIUrl":"https://doi.org/10.1177/03331024251359237","url":null,"abstract":"<p><p>AimMeningeal nociceptors within the trigeminal ganglion are important contributors to migraine pathogenesis because they transmit pain signals from the dura mater to the central nervous system. As such, pharmacological interventions that target these peripheral neurons might offer new avenues for migraine treatment. In this context, ATP-sensitive potassium (K_ATP) channels have garnered increasing attention as potential modulators of meningeal nociception. Human experimental studies support this hypothesis, showing that intravenous infusion of levcromakalim, a K_ATP channel opener, induces migraine attacks in people with migraine and mild, transient headache in healthy adults. However, the precise anatomical site and mechanism of action remain incompletely understood.MethodsTo address these gaps, we conducted <i>in vivo</i> single-unit electrophysiological recordings of 36 meningeal nociceptors (23 Aδ- and 13 C-fibers) in the trigeminal ganglion of anesthetized male and female rats. We measured spontaneous firing rates before and up to four hours after a 20-minute continuous intracarotid infusion of levcromakalim (1.43 mg/kg or 0.14 mg/kg) or vehicle (71.4% ethanol).ResultsLevcromakalim at 1.43 mg/kg activated nine (69%) of 13 nociceptors, compared with one (11%) of nine in the vehicle group (<i>p</i> = 0.012). Activation rates did not differ between Aδ-fibers (6 of 8, 69%) and C-fibers (3 of 6; 50%; <i>p</i> = 1.00), or between male (6 of 8; 75%) and female animals (3 of 5; 60%; <i>p</i> = 0.61). Moreover, levcromakalim at 0.14 mg/kg activated only three (21%) of 14 nociceptors.ConclusionsTaken together, our findings demonstrate that K_ATP channel opening mediates activation of meningeal nociceptors, providing a mechanistic basis for previous observations in humans. The development of K_ATP channel blockers might therefore hold therapeutic promise for migraine by inhibiting meningeal nociceptors.</p>","PeriodicalId":10075,"journal":{"name":"Cephalalgia","volume":"45 8","pages":"3331024251359237"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144815909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Invisible burdens: Gender-specific associations between migraine and work-family conflict: Insights from the SMILE project - a cohort study.","authors":"Ido Peles, Shaked Sharvit, Yana Mechnik Steen, Michal Gordon, Victor Novack, Ronit Waismel-Manor, Gal Ifergane","doi":"10.1177/03331024251352533","DOIUrl":"10.1177/03331024251352533","url":null,"abstract":"<p><p>BackgroundMigraine, a neurovascular disorder that affects quality of life, with peak prevalence during individuals' most productive working years. Work-family conflict (WFC), a well-documented source of stress, occurs when work and family responsibilities interfere with each other. While migraine has been associated with occupational impairment, its association with WFC remains underexplored. The present study examines the association between migraine diagnosis, severity and WFC, stratified by gender.MethodsThis study analyzed data from the SMILE cohort, a subset of the Negev Migraine Cohort. Participants with and without migraine were recruited and completed a structured questionnaire assessing WFC. The main exposures were migraine diagnosis and severity, measured using the Migraine Disability Assessment (MIDAS) score. The primary outcome was WFC. Covariates included sociodemographic characteristics, employment factors, and psychological distress (Depression, Anxiety and Stress Scale - 21 Items (DASS-21)). Statistical analyses involved multivariable gamma generalized linear mode regression models and quantile regression to examine associations, adjust for potential confounders and effect modification by gender.ResultsIn total, 675 migraine patients and 232 non-migraine participants were included in the study; 80.6% of migraine patients were female. Severe disability (MIDAS score ≥21) was reported by 65.0% of migraine patients, with employment rates of 89.2% for females and 93.1% for males. Migraine patients worked longer hours per week (median 40.0 vs. 36.0 hours for females, and 48.0 vs. 42.0 hours for males), and were more likely to work over 42 hours per week (18.2% vs. 7.0% for females and 32.8% vs. 8.7% for males, standardized mean difference = 0.487). Migraine diagnosis was associated with higher Work To Family and Family To Work strain-based conflict scores among males (β = 0.43, 95% confidence interval = 0.06-0.78, <i>p</i> = 0.03 and β = 0.35, 95% 95% confidence interval = 0.03-0.66, <i>p</i> = 0.04, respectively); however, no statistically significant associations were observed among female. Higher migraine severity (MIDAS) was correlated with greater WFC, with the effect more pronounced at higher levels of migraine disability and more strongly associated with men (<i>p</i> < 0.01 for all).ConclusionsMigraine is associated with higher WFC, especially in strain-based domains, with a stronger effect in men. Greater migraine severity further amplifies this conflict. These findings emphasize the need for workplace and clinical strategies to support migraine patients in managing work-life balance.</p>","PeriodicalId":10075,"journal":{"name":"Cephalalgia","volume":"45 8","pages":"3331024251352533"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differences in cortical morphometry between persistent post-traumatic headache, migraine and healthy controls.","authors":"Rune Häckert Christensen, Haidar Muhsen Al-Khazali, Messoud Ashina, Nina Vashchenko, Rogelio Dominguez-Moreno, Daniel Tolnai, Håkan Ashina","doi":"10.1177/03331024251362830","DOIUrl":"https://doi.org/10.1177/03331024251362830","url":null,"abstract":"<p><p>BackgroundPersistent post-traumatic headache (PTH) is a prevalent and disabling neurological disorder, often attributed to mild traumatic brain injury and resembling migraine in clinical features. The underlying cortical morphometric changes and their relevance to persistent PTH remain unclear.MethodsThis cross-sectional magnetic resonance imaging (MRI) investigation enrolled 103 adults with persistent PTH, 296 with migraine and 155 healthy controls (HC), to undergo structural MRI at 3T. Cortical surface area, thickness and volume were evaluated in FreeSurfer. The analyses applied cluster-determining thresholds of <i>p</i> < 0.001 and cluster-wise thresholds of <i>p</i> < 0.05, adjusted for age, sex and total intracranial volume.ResultsParticipants with persistent PTH exhibited larger surface area in the right anterior and posterior cingulate cortex (<i>p</i>_cluster = 0.003), as well as the right superior parietal cortex/postcentral gyrus, compared to HC (<i>p</i>_cluster < 0.035). No morphometric differences were observed between participants with persistent PTH and migraine (including subgroups: episodic, chronic, with aura without aura).ConclusionsThese findings reveal morphometric alterations in persistent PTH, specifically within pain processing regions of the mid-cingulate and somatosensory cortex. Similar changes have been reported in migraine, suggesting a shared neurobiological substrate. These enlargements might reflect adaptations to recurrent nociceptive stimuli that sustain persistent PTH.</p>","PeriodicalId":10075,"journal":{"name":"Cephalalgia","volume":"45 8","pages":"3331024251362830"},"PeriodicalIF":4.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}