Journal of Headache and Pain最新文献

{"title":"The DRN-VLO pathway via distinct 5-HT synaptic mechanisms modulates neuropathic pain-induced depressive-like behaviors in mice.","authors":"Hai-Yan Sheng, Wei-Zhen Liu, Yan-Kai Liu, Qing-Rong Han, Dong-Yang Chen, Li-Bin Zhang, Xin-Ru Chu, Si-Han He, Jia-Xin Li, Zi-Qing Zhang, Bo-Han Duanmu, Ya-Ling Yin, Lin-Hua Jiang","doi":"10.1186/s10194-025-02110-3","DOIUrl":"10.1186/s10194-025-02110-3","url":null,"abstract":"<p><strong>Background: </strong>The neuronal activities within the dorsal raphe nucleus (DRN) and the ventrolateral orbital cortex (VLO) are strongly implicated in the development of depression, a condition comorbid with chronic pain. The goal of the present study was to determine whether and how the DRN-VLO pathway mediates chronic pain-induced depression.</p><p><strong>Methods: </strong>Trigeminal neuralgia was induced unilaterally by chronic constriction injury of the infraorbital nerve. Depressive-like behaviors were assessed by the open field test, forced swimming test and tail suspension test. Neuronal projection tracing, chemogenetic manipulations and pharmacological interventions were performed to determine the DRN-VLO pathway projection activity and pathway-mediated anti-depressant mechanism in mice with trigeminal neuralgia. The neuronal activity was assessed by measuring the c-Fos level using immunofluorescence imaging.</p><p><strong>Results: </strong>The VLO receives direct projection of the serotonergic neurons from the DRN. Anterograde or retrograde activation of the DRN-VLO pathway consistently produced anti-depressant effects in mice with neuropathic pain, whereas sustained inhibition of this pathway in healthy mice induced depressive-like behaviors. Activation of the 5-HT1A or 5-HT2A receptor in the VLO produced anti-depressant effects. Activation of the GABA_A receptors in the VLO weakened 5-HT1A receptor-mediated anti-depressant effect.</p><p><strong>Conclusions: </strong>The present study has revealed that activation of the DRN-VLO pathway exerts an anti-depressant effect in mice with neuropathic pain, through stimulating the 5-HT2A receptors in the excitatory neurons and also the 5-HT1A receptors in the GABAergic interneurons via a dis-inhibition mechanism, to enhance neuronal activity of the VLO.</p>","PeriodicalId":16013,"journal":{"name":"Journal of Headache and Pain","volume":"26 1","pages":"168"},"PeriodicalIF":7.9,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12288316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144707764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Psychological transdiagnostic factors and migraine characteristics as predictors of migraine-related disability.","authors":"Janosch Fox, Charly Gaul, Julia Ohse, Nicolina Peperkorn, Joshua Krutzki, Youssef Shiban","doi":"10.1186/s10194-025-02101-4","DOIUrl":"10.1186/s10194-025-02101-4","url":null,"abstract":"<p><strong>Background: </strong>Migraine is a prevalent primary headache disorder that significantly impairs daily life. Research on factors contributing to migraine-related disability remains limited, particularly from a biopsychosocial perspective. This study investigated whether transdiagnostic psychological factors, as proposed by the Fear Avoidance Model (FAM), contribute to migraine-related disability beyond migraine symptoms.</p><p><strong>Methods: </strong>In this cross-sectional analysis of selected baseline data from an ongoing randomized controlled trial, data from N = 158 individuals with migraine reporting ≥ 4 migraine days per month were examined. Data was collected through an online survey, including sociodemographic and clinical characteristics as well as responses to standardized questionnaires (DASS, PCS, FAMI, HIT-6). A hierarchical multiple linear regression analysis was conducted, including independent variables in two blocks: (1) sociodemographic factors and migraine symptoms, and (2) FAM factors (pain catastrophizing, fear of attacks, depressiveness). Disability, the dependent variable, was assessed using the HIT-6 questionnaire. Additionally, mediation analyses were conducted to investigate the potential mediating role of pain catastrophizing in the relationship between pain intensity or attack frequency and disability.</p><p><strong>Results: </strong>A total of N = 158 participants were included in the analysis. Hierarchical regression analysis showed that sociodemographic and migraine symptoms accounted for 49% of the variance in disability (R²_adj = 0.49, p < 0.001). The inclusion of FAM factors significantly increased the explained variance to 62% (R²_adj = 0.62, p < 0.001; ΔR²_adj= 0.13, p < 0.001), indicative of a high goodness-of-fit. Independent predictors included gender (ß = -0.15, p = 0.007), age (ß = 0.11, p = 0.029), maximum pain intensity (ß = 0.46, p < 0.001), pain catastrophizing (ß = 0.26, p < 0.001), and depressiveness (ß = 0.13, p = 0.047). Mediation analyses revealed that pain catastrophizing (ß = 0.35, p < 0.001) mediated the relationship between pain intensity (ß = 0.47, p < 0.001) and disability (R² = 0.62, p < 0.001), whereas no mediation effect was observed for attack frequency as independent variable (X→Y: ß = -0.05, p = 0.44; X→ M: ß = -0.07, p = 0.26; M → Y: ß = 0.51, p < 0.001).</p><p><strong>Conclusion: </strong>The findings underscore the significant role of transdiagnostic psychological factors in migraine-related disability beyond migraine and sociodemographic characteristics. Pain catastrophizing emerged as an important mediator between pain experience and disability, which is in line with the assumptions of the FAM.</p><p><strong>Trial registration: </strong>German Clinical Trials Register (DRKS), DRKS-ID: DRKS00033893.</p>","PeriodicalId":16013,"journal":{"name":"Journal of Headache and Pain","volume":"26 1","pages":"167"},"PeriodicalIF":7.9,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12285010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144698654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Botulinum toxin type A inhibits microglia pyroptosis by suppressing Cblb-mediated degradation of Pdlim1 to attenuate neuropathic pain.","authors":"Sheng Tian, Lanxiang Wu, Heqing Zheng, Zhijuan Cheng, Jingjing Liu, Mingxu Liu, Xinping Yu, Jianglong Tu, Wei Wu","doi":"10.1186/s10194-025-02109-w","DOIUrl":"10.1186/s10194-025-02109-w","url":null,"abstract":"<p><strong>Background: </strong>Microglia pyroptosis, a newly identified form of inflammatory cell death, is involved in the development of neuropathic pain (NP). Botulinum toxin type A (BTX-A) has been shown to be effective in relieving NP, but the mechanisms involved have not been clarified.</p><p><strong>Methods: </strong>A mice model of NP was established with chronic constriction injury (CCI) method. The expression levels of key molecules and the extent of microglia pyroptosis were assessed using RT-qPCR, western blot, ELISA and immunofluorescence. Moreover, lipopolysaccharide (LPS) was used in vitro to induce pyroptosis of microglia to explore the potential molecular mechanisms of BTX-A.</p><p><strong>Result: </strong>In a mice model of NP, BTX-A administration increased the pain threshold and decreased the Cblb protein expression level, consistent with the results of in vitro experiments. Functional experiments and mouse models were respectively used to evaluate the severity of microglia pyroptosis. The results showed that BTX-A inhibited microglia pyroptosis through Cblb protein. Subsequently, mass spectrometry (MS) analysis and immunoprecipitation were conducted to identify proteins interacting with Cblb. The results identified Pdlim1 was a potential interacting partner of Cblb, which regulats the ubiquitination of Pdlim1. Mechanically, Cblb binds to the PDZ and LIM domains of Pdlim1 and then targets Pdlim1 at K244 for ubiquitination and proteasome-mediated degradation. Pdlim1 knockdown lentiviral plasmid was constructed and stable Pdlim1 knockdown microglial cell lines were established for rescue experiments. The results demonstrated that BTX-A suppresses microglia pyroptosis via Pdlim1/NF-κB signaling axis. Finally, intrathecal injection of adeno-associated virus overexpressing Cblb was used in rescue experiments. The results confirmed that BTX-A attenuates neuropathic pain via the Cblb/Pdlim1/NF-kB signaling axis.</p><p><strong>Conclusions: </strong>This study demonstrates that BTX-A suppresses the activity of Cblb, thereby reducing Pdlim1 protein degradation, inhibiting the NF-kB pathway, and ultimately mitigating microglia pyroptosis. Our findings suggest that Cblb could serve as a novel therapeutic target for BTX-A in the treatment of NP.</p>","PeriodicalId":16013,"journal":{"name":"Journal of Headache and Pain","volume":"26 1","pages":"165"},"PeriodicalIF":7.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12281680/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144690499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The efficacy and mechanisms of low-intensity transcranial ultrasound stimulation on pain: a systematic review of human and animal studies.","authors":"Hao-Ran Xu, Yiu-Liang Yi, Chuan Xue, Zi-Qi Guo, Li Ding, Jie Jia","doi":"10.1186/s10194-025-02096-y","DOIUrl":"10.1186/s10194-025-02096-y","url":null,"abstract":"<p><strong>Background: </strong>Low-intensity transcranial ultrasound stimulation (LITUS) is an emerging non-invasive neuromodulation technique for pain treatment, with the unique ability to modulate deep brain nuclei associated with pain. The aim of this study is to systematically review and summarize the evidence for the efficacy of LITUS in pain management and to elucidate the potential mechanisms underlying its analgesic effects.</p><p><strong>Methods: </strong>A systematic search was conducted across five databases up to Mar 31st, 2025. Controlled studies in both human and animal subjects were included. Two independent reviewers completed the screening and risk of bias assessment process following predefined inclusion and exclusion criteria.</p><p><strong>Results: </strong>A total of thirteen studies were included in the review. These studies demonstrated LITUS's potential in managing various types of pain among different populations and animal models, particularly targeting the anterior cingulate cortex, thalamus, insular cortex, primary sensorimotor cortex, and periaqueductal gray. Most included studies showed positive effects and verified the safety of LITUS on pain, reporting few adverse effects.</p><p><strong>Conclusions: </strong>LITUS is an effective and non-invasive tool for pain regulation in animals and humans, enabling precise modulation of deep brain circuits. Analgesic effects may be affected by pain-related risk factors, insufficient dosage, suboptimal protocols, and target selection. Initial evidence has highlighted the direct link between LITUS parameters, brain region responses, and pain behavior. Modulation of brain excitatory, nociceptive circuit, electrophysiological response, autonomic response, biochemistry, neuroinflammation, and psychology are proposed as the potential mechanisms underlying the efficacy of LITUS. More high-quality research is urgently needed to advance clinical LITUS use and reveal its mechanisms.</p>","PeriodicalId":16013,"journal":{"name":"Journal of Headache and Pain","volume":"26 1","pages":"166"},"PeriodicalIF":7.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12281706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144690500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hallmarks of primary headache: part 2- Tension-type headache.","authors":"Li-Ling Hope Pan, Yu-Hsiang Ling, Shuu-Jiun Wang, Linda Al-Hassany, Wei-Ta Chen, Chia-Chun Chiang, Soo-Jin Cho, Min Kyung Chu, Gianluca Coppola, Adriana Della Pietra, Zhao Dong, Esme Ekizoglu, Charl Els, Fatemeh Farham, David Garcia-Azorin, Woo-Seok Ha, Fu-Jung Hsiao, Ryotaro Ishii, Byung-Kun Kim, Najib Kissani, Alejandro Labastida-Ramirez, Kristin Sophie Lange, Ellina Lytvyak, Dilara Onan, Aynur Ozge, Laura Papetti, Lanfranco Pellesi, Bianca Raffaelli, Alberto Raggi, Sebastian Straube, Tsubasa Takizawa, Surat Tanprawate, Derya Uğurlu Uludüz, Kiratikorn Vongvaivanich, Marta Waliszewska-Prosół, Yonggang Wang, Tissa Wijeratne, Jr-Wei Wu, Sophie Merve Yener, Paolo Martelletti","doi":"10.1186/s10194-025-02098-w","DOIUrl":"10.1186/s10194-025-02098-w","url":null,"abstract":"<p><strong>Background and aim: </strong>Tension-type headache is the most prevalent primary headache disorder. While the episodic subtype is more common, chronic tension-type headache significantly impacts health-related quality of life and contribute to increased healthcare utilization and disability. Despite considerable advances in the understanding of tension-type headache, critical gaps persist. This paper aims to provide a comprehensive review of the hallmarks of tension-type headache, from its pathophysiology, comorbidities, treatment options, to psychosocial impact.</p><p><strong>Main results: </strong>Multiple factors are associated with tension-type headache, including peripheral mechanisms (increased muscle tenderness and myofascial trigger points), central sensitization, genetic predisposition, and psychological comorbidities such as anxiety and depression. Neuroimaging and neurophysiological studies demonstrated altered pain processing in cortical and subcortical regions in patients with tension-type headache. Regarding treatment strategy, in addition to pharmacological treatment, novel insights into non-pharmacological interventions such as cognitive behavioral therapy, neuromodulation techniques, physical therapy, mindfulness, lifestyle management, and patient education were highlighted as valuable components of comprehensive management strategies.</p><p><strong>Conclusions: </strong>A complex interplay between peripheral and central mechanisms and psychosocial stressors underpins tension-type headache. Integrated multidisciplinary approaches combining pharmacological and non-pharmacological interventions are critical for optimal patient outcomes. Further research should continue to refine the understanding of these mechanisms to improve targeted therapeutic strategies and reduce the global burden of tension-type headache.</p>","PeriodicalId":16013,"journal":{"name":"Journal of Headache and Pain","volume":"26 1","pages":"164"},"PeriodicalIF":7.9,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12273213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144659391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of lacosamide on cortical spreading depolarization in mice.","authors":"Chisato Iba, Miyuki Unekawa, Keiko Ihara, Yoshikane Izawa, Jin Nakahara, Tsubasa Takizawa","doi":"10.1186/s10194-025-02099-9","DOIUrl":"10.1186/s10194-025-02099-9","url":null,"abstract":"<p><strong>Background: </strong>Antiseizure medications are often used as preventive treatment of migraine in appropriate cases; however, the efficacy of lacosamide (LCM), a sodium channel blocker, in preventing migraine attacks remains unclear. Cortical spreading depolarization (CSD) refers to a wave of slowly propagating depolarization across the cerebral cortex. CSD animal models have been extensively used to investigate migraine attacks and evaluate the effects of migraine medication. Herein, we examined the effects of single dose LCM (40 mg/kg) on CSD sensitivity in a mouse model.</p><p><strong>Findings: </strong>Thirty-two C57BL/6 mice (male, n = 16; female, n = 16) were intraperitoneally injected with either LCM (40 mg/kg) or saline before CSD sensitivity testing. Potassium chloride (KCl) was administered to induce CSD, and the CSD threshold, frequency, and propagation velocity were determined. The average CSD frequency induced by 1 M KCl was significantly lower (p = 0.030) and the CSD propagation velocity tended to be lower in the female LCM group than in the saline group. However, no significant differences were observed in any of the three CSD parameters in male mice.</p><p><strong>Conclusions: </strong>In female mice, single dose LCM treatment significantly reduced CSD frequency induced by KCl. Further investigations are warranted to assess the clinical potential of LCM in preventing migraine.</p>","PeriodicalId":16013,"journal":{"name":"Journal of Headache and Pain","volume":"26 1","pages":"163"},"PeriodicalIF":7.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269239/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural alterations in occipital cortices in trigeminal neuralgia: a voxel- and surface-based morphometric MRI study.","authors":"Francesca Caramia, Antonio Di Renzo, Marco Fiorelli, Gianfranco De Stefano, Giulia Di Stefano, Maddalena Boccia, Maria Giulia Tullo, Gaia Cartocci, Costanza Gianni, Andrea Truini","doi":"10.1186/s10194-025-02104-1","DOIUrl":"10.1186/s10194-025-02104-1","url":null,"abstract":"","PeriodicalId":16013,"journal":{"name":"Journal of Headache and Pain","volume":"26 1","pages":"162"},"PeriodicalIF":7.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Promoter demethylation of cerebellin 2 by ten-eleven translocation 3 contributes to peripheral sensitization in trigeminal neuropathic pain of mice.","authors":"Xin-Ying Guan, Bao-Tong Yuan, Meng-Na Li, Tian Wang, Lin-Peng Zhu, Si-Yuan Song, Lu-Lu Ji, Yong-Jing Gao, Ling-Jie Ma","doi":"10.1186/s10194-025-02093-1","DOIUrl":"10.1186/s10194-025-02093-1","url":null,"abstract":"<p><strong>Background: </strong>Chronic neuropathic pain involves complex molecular adaptations, and emerging evidence indicates that cerebellins (CBLNs) play a role in sensory processing. This study investigates the role of CBLN2 in trigeminal neuropathic pain (TNP) and examines its regulation through epigenetic mechanisms.</p><p><strong>Methods: </strong>Bioinformatics analyses of CBLNs were performed using publicly available expression data from the trigeminal ganglion (TG). A mouse model of TNP was established through partial infraorbital nerve transection (pIONT). Facial allodynia in mice was assessed using the von Frey test. Quantitative real-time PCR (qRT-PCR), Western blotting and enzyme-linked immunosorbent assay (ELISA) were performed to evaluate the expression of CBLN2. Immunofluorescence was used to determine CBLN2's cellular localization. DNA methylation of Cbln2's promoter region was examined using methylation-specific PCR (MSP) and bisulfite sequencing PCR (BSP). Neuronal excitability was assessed through whole-cell patch-clamp recordings.</p><p><strong>Results: </strong>Integration of cross-species single-nucleus RNA sequencing (snRNA-seq) datasets identified dominant CBLN2 expression in Aδ, Aβ and c-fiber low-threshold mechanoreceptors (LTMRs), with significant upregulation observed in a murine model of inflammatory migraine. Consistently, CBLN2 expression was upregulated in the TG of pIONT-induced TNP mice and localized to neurons with myelinated axons, peptidergic and nonpeptidergic nociceptors. siRNA-mediated Cbln2 knockdown attenuated mechanical allodynia, confirming its role in pain initiation and maintenance. Notably, Cbln2 expression was partially dependent on promoter demethylation. MSP and BSP analyses revealed significantly reduced methylation of the Cbln2 promoter in pIONT mice compared to sham controls. Furthermore, pIONT induced persistent upregulation of ten-eleven translocation 3 (TET3) in the TG, while Tet3 knockdown alleviated neuropathic pain and downregulated both Tet3 and Cbln2 expression. Additionally, exogenous CBLN2 potentiated neuronal excitability and activated extracellular signal-regulated kinase (ERK) signaling. Inhibition of the mitogen-activated protein kinase (MAPK)/ERK kinase (MEK) pathway abolished CBLN2-induced hypersensitivity and suppressed the expression of proinflammatory cytokines, including Cxcl1, Cxcr2, Cxcl9, Cxcl10, and Il-6.</p><p><strong>Conclusions: </strong>TET3-mediated demethylation of the Cbln2 promoter drives ERK-dependent neuronal hyperexcitability and neuroinflammation following pIONT. The dual regulatory effects on neuroinflammatory cascades establish CBLN2 as a novel therapeutic target for the treatment of TNP.</p>","PeriodicalId":16013,"journal":{"name":"Journal of Headache and Pain","volume":"26 1","pages":"160"},"PeriodicalIF":7.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12261730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Headaches and family planning: insights from a Japanese school-based survey.","authors":"Masahito Katsuki, Naomichi Wada, Keiko Iijima, Noriyuki Yoshizawa, Yoshizumi Toya, Yasuko Hanaoka, Kazuma Kaneko, Shoji Kajikawa","doi":"10.1186/s10194-025-02102-3","DOIUrl":"10.1186/s10194-025-02102-3","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effect of headaches on women's pregnancy plans and fertility intentions.</p><p><strong>Methods: </strong>We prospectively performed a school-based online survey for students' parents in Suwa city, Japan, in 2023. We asked their age, sex, the number of children, the presence of headache attacks, the use of acute and prophylactic medications, monthly headache days (MHD), monthly acute medication intake days (AMD), headache impact test-6 (HIT-6), and whether or not headaches worsen during menstruation. We also examined headache's effect on pregnancy plans and asked about how headaches would affect pregnancy, the ability to raise a child, and the child's health.Of 5558 students' households, we retrieved 1142 (20.1%) answers, and 717 (12.9%) responses from parents with headaches.</p><p><strong>Results: </strong>Of 5558 students' households, we retrieved 1142 (20.1%) answers, and 717 (12.9%) responses from parents with headaches were finally analyzed. The median (first quartile-third quartile) age was 43 (37-46) years, and 653 (91.1%) were female. Median MHD, AMD, and HIT-6 were 3 (1-6), 3 (1.5-6), and 62 (58-65), respectively. Twenty-four (3.3%) used prophylactic medications and 562 (78.4%) used acute medications for headache attacks. The median number of children was 2 (1-2). Avoid pregnancy group consisted of 39/717 (5.4%) respondents. They were younger (median 39 years; first quartile-third quartile 33-42 years), with more respondents with headaches worsening during menstruation (28/35; 80.0%), with acute medication use (36/39; 92.3%), and had more MHD (5; 3-10), more AMD (5; 2-11), and high HIT-6 score (66; 60-67), compared to the no impact group. They tended to think that headaches would be worse during pregnancy (16/39; 41.0%) and that headaches negatively affect pregnancy (28/39; 71.8%), raising a child (20/39; 51.3%), and the child's development (31/39; 79.5%) and risk of having a headache (28/39; 71.8%) compared to the no impact group.</p><p><strong>Conclusions: </strong>Some of the respondents avoided pregnancy because of their headaches. Those in avoid pregnancy group had severe headaches and felt that headaches negatively affected family planning.</p>","PeriodicalId":16013,"journal":{"name":"Journal of Headache and Pain","volume":"26 1","pages":"161"},"PeriodicalIF":7.3,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12265367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparing eptinezumab with onabotulinumtoxinA in the treatment of chronic migraine: a real-world evidence study.","authors":"Damiana Scuteri, Martina Pagliaro, Rosario Iannacchero, Michele Trimboli, Gary W Lawrence, Giacinto Bagetta, Maria Tiziana Corasaniti","doi":"10.1186/s10194-025-02106-z","DOIUrl":"10.1186/s10194-025-02106-z","url":null,"abstract":"","PeriodicalId":16013,"journal":{"name":"Journal of Headache and Pain","volume":"26 1","pages":"159"},"PeriodicalIF":7.3,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12261790/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}