PAIN®最新文献

{"title":"Astrocyte Orai1 signaling promotes spinal excitatory synaptic potentiation and neuropathic pain after nerve injury in male mice.","authors":"Shogo Tsujikawa, Aashutosh Shetti, Rogan A Grant, Michaela M Novakovic, Murali Prakriya","doi":"10.1097/j.pain.0000000000004136","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000004136","url":null,"abstract":"<p><strong>Abstract: </strong>Neuropathic pain after peripheral nerve injury is a multifactorial condition mediated partly by inflammation in the spinal cord that results in potentiation of excitatory synaptic transmission in nociceptive circuits. Glial cells including astrocytes are key mediators of the underlying inflammation, but the signaling checkpoints that regulate astrocyte-driven spinal cord inflammation and sensitization of nociceptive circuits are not well understood. Here, we identify Orai1-mediated store-operated Ca2+ entry (SOCE) as an important regulator of spinal astrocyte cytokine production, metabolic reprogramming, and pain hypersensitivity in mice. Conditional deletion of Orai1 in astrocytes attenuated mechanical allodynia after nerve injury in male but not female mice, despite comparable SOCE suppression in both sexes. Orai1 deficiency also attenuated production of proinflammatory cytokines after SOCE activation, including TNFα, IL-6, and IL-33, both in vivo and in vitro. Electrophysiological recordings revealed that astrocyte Orai1 deletion prevented injury-induced enhancement of glutamatergic synaptic transmission in dorsal horn neurons, linking astrocytic Ca2+ signaling to central sensitization. Metabolomic profiling showed that Orai1 loss disrupted glycolysis and TCA cycle intermediates while promoting accumulation of immunomodulatory metabolites such as itaconate, consistent with a less inflammatory astrocyte metabolic state. These findings identify Orai1 channels as integrators of astrocyte Ca2+ signaling, immunometabolism, and excitatory synaptic potentiation after nerve injury, and identify a sexually dimorphic astrocyte mechanism governing neuropathic pain pathogenesis. Targeting astrocyte Orai1 channels may provide a selective therapeutic strategy for male-predominant chronic pain.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2026-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149272107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mineralocorticoid receptor signaling reduces somatostatin expression in developing sensory neurons and drives neonatal pain after early-life stress.","authors":"Fady Eid, Elizabeth Serafin, Mezani Muniz, Samantha Woodke, Jacob Booher, Jun-Ming Zhang, Mark L Baccei","doi":"10.1097/j.pain.0000000000004139","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000004139","url":null,"abstract":"<p><strong>Abstract: </strong>Early-life stress (ELS) causes pain hypersensitivity in neonatal mice and alters the transcriptional profile of the immature dorsal root ganglia (DRG), highlighted by a marked reduction in the expression of a neuropeptide, somatostatin (Sst), which is known to constitutively suppress peripheral nociceptive transmission during adulthood. However, the mechanisms that drive plasticity in gene expression within the developing DRG and neonatal pain after ELS remain unclear. Here, we investigated the degree to which ELS-induced neonatal pain was mediated by corticosterone signaling onto sensory neurons and potential changes in peripheral Sst transmission. The conditional knockout of the mineralocorticoid receptor (MR), but not the glucocorticoid receptor, from immature DRG neurons prevented ELS-evoked neonatal pain. In contrast, the systemic administration of the selective MR antagonist eplerenone failed to acutely influence pain after ELS, thus suggesting that MR activation enhances pain during the neonatal period via canonical effects on gene transcription. Meanwhile, hind paw injection of the Sst receptor antagonist cyclo-somatostatin increased spontaneous nocifensive behaviors in control pups, but not in pups previously subjected to ELS, raising the possibility that a disruption in tonic antinociception mediated by peripheral Sst contributes to neonatal pain after ELS. Furthermore, administration of the peripherally restricted Sst analog octreotide reversed noxious cold and pressure hypersensitivity in neonatal mice after ELS. Finally, the selective deletion of MR from sensory neurons prevented the ELS-induced decrease in Sst expression. Collectively, these results provide novel mechanistic insight into the effects of chronic early-life adversity on nociceptive processing in the developing nervous system.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2026-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149272165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting GPR183 to reduce peripheral sensitization: evidence from rodent and human tissue analyses.","authors":"Kyle Oberkrom, Kathryn Braden, Evelyn Li, Samay R Shah, Dragan Maric, Andrew J Mannes, Paola Pacifico, Nirupa D Jayaraj, Christopher K Arnatt, Daniela Menichella, Matthew R Sapio, Daniela Salvemini","doi":"10.1097/j.pain.0000000000004124","DOIUrl":"10.1097/j.pain.0000000000004124","url":null,"abstract":"<p><strong>Abstract: </strong>Peripheral sensitization is a key process in the development of painful inflammatory conditions, driven in part by immune-cell mediator release following tissue injury. The G protein-coupled receptor, GPR183, predominantly expressed on immune cells, regulates their migration, positioning, and mediator production. However, its role in peripheral sensitization and the specific immune cells involved remains insufficiently understood. In rats, intraplantar injection of 7α,25-dihydroxycholesterol (7α,25-OHC), the most potent endogenous GPR183 ligand, produced long-lasting nociception that was prevented by the selective GPR183 antagonist SAE-14. As GPR183 activates extracellular signal-regulated kinase signaling, which influences pain pathways including nitric oxide synthase (NOS) activity and NO formation, we used NOS inhibitors and knockout animals to test the contribution of inducible and neuronal NOS isoforms to 7α,25-OHC-induced sensitization. We found that both isoforms influence this response, independent of cyclooxygenases. In a well-characterized rat incisional injury model, GPR183 protein expression increased in injured paw tissue, and SAE-14 reversed hypersensitivity. Meta-analysis of human postsurgical skin samples similarly showed elevated GPR183 expression and transcriptional changes favoring 7α,25-OHC production after injury. We identified macrophages, Langerhans cells (LCs), and T cells as the principal GPR183-expressing cell types in human skin. Ablation of LCs and removal of mature B and T cells revealed that 7α,25-OHC-evoked hypersensitivity does not depend on these cell types, leaving GPR183+ macrophages as the most likely drivers of GPR183-induced hypersensitivity. Overall, our findings define the cellular and molecular pathways linking GPR183 to peripheral sensitization and highlight GPR183 antagonism as a promising strategy for pain management.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2026-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pain education in Brazilian medical schools: a national curriculum analysis.","authors":"Thayna Caetano Alves Silva, Felipe Maia Domingues, Daiane Lazzeri Medeiros, Ana Camila de Castro Gandolfi, Felipe J J Reis","doi":"10.1097/j.pain.0000000000004129","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000004129","url":null,"abstract":"<p><strong>Abstract: </strong>Pain is a leading cause of disability worldwide, yet undergraduate medical education remains insufficient to prepare future physicians for its assessment and management. The International Association for the Study of Pain (IASP) has proposed a competency-based curriculum framework; however, its implementation in Brazilian medical education is unclear. The aim of this study was to evaluate the availability of pain education in Brazilian medical schools and assess its alignment with the IASP Curriculum Outline on Pain for Medicine. We conducted a national cross-sectional documentary analysis of all medical schools registered in the Brazilian Ministry of Education database between May 2024 and December 2025. Institutional websites were systematically screened for publicly available curricular documentation, and data were independently extracted by 2 reviewers. Variables included the presence of pain-related content, existence of a dedicated pain course, course workload, timing within the curriculum, and type of offering. Among 447 identified schools, 277 (62.0%) provided accessible curricular information. Only 47 institutions (16.9%) offered a stand-alone pain course, and 29 had detailed syllabi for item-level analysis. Most analyzed courses were mandatory and delivered in the early years of training. Alignment with IASP competencies was incomplete across all domains, with greater coverage of neurobiological and pharmacological content and limited inclusion of pain assessment and measurement, psychosocial and behavioral management, public health, ethics, and care for special populations. Pain education in Brazil is inconsistently structured and only partially aligned with international recommendations, indicating the need of comprehensive, competency-based curricular reform.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Invisible cost of pain management by the current International Classification of Diseases coding system, a study in a tertiary care inpatient setting: erratum.","authors":"Sarasate Eiamtanasate, Kannika Smithiseth, Nantthasorn Zinboonyahgoon, Beatrice Korwisi, Antonia Barke, Winfried Rief, Rolf-Detlef Treede","doi":"10.1097/j.pain.0000000000004069","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000004069","url":null,"abstract":"","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The analgesic efficacy of opioids in different application modalities for the treatment of breakthrough cancer pain-a systematic review with network meta-analysis.","authors":"Hanns-Christian Dinges, Sophie Thiedmann, Johanna Weyland, Christian Volberg, Felix Carl Fabian Schmitt, Hinnerk Wulf, Ann-Kristin Schubert","doi":"10.1097/j.pain.0000000000004132","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000004132","url":null,"abstract":"<p><strong>Abstract: </strong>Breakthrough cancer pain episodes often require oral immediate release opioids or parenteral opioid treatment. Different formulations and application modalities have been approved for this condition. This study aimed to identify the most effective of the available substances and applications to treat breakthrough cancer pain. We conducted a comprehensive systematic review with network meta-analysis. The database search included MEDLINE, CENTRAL, Embase, and Web of Science. Eligible were randomized controlled trials comparing opioids and application modalities for the treatment of breakthrough cancer pain episodes. Primary end points were the pain intensity difference (PID) at 15 and 30 minutes. Secondary end points were side effects and adverse events, as well as dichotomous outcomes of treatment success. Frequentist network meta-analysis was conducted using the package netmeta in R. From 5133 records initially identified by the literature review, 23 studies were eligible for quantitative analysis. Compared with placebo, the most effective interventions at 15 minutes (PID) were intravenous or subcutaneous applications of morphine, and intranasal fentanyl or sublingual fentanyl tablets. After 30 minutes (PID), the most effective interventions were still subcutaneous and intravenous morphine, but also sublingual fentanyl tablets. Intranasal fentanyl spray was equally effective as buccal and other transmucosal applications by 30 minutes. The quality of evidence on the topic is poor as most studies are phase III trials for drug approval. The risk of publication bias is therefore high. Sublingual fentanyl tablets were as effective as intravenous or subcutaneous morphine and are a practical modality for self-administration.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":""},"PeriodicalIF":5.8,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149183873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evoked alpha oscillatory activity is suppressed by prolonged elbow pain and modulated by repetitive transcranial magnetic stimulation","authors":"Nahian S. Chowdhury,Joshua D. Hoddinott,Wei-Ju Chang,Donovan Cheng,Naveen Manivasagan,Siobhan M. Schabrun,David A. Seminowicz","doi":"10.1097/j.pain.0000000000004126","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000004126","url":null,"abstract":"Abstract Alpha-band oscillatory activity, assessed using electroencephalography (EEG), is among the most widely studied neurophysiological markers of pain. However, the literature has focused predominantly on resting-state measures, leaving unclear whether pain also alters evoked alpha-band dynamics, measured via cortical perturbation using transcranial magnetic stimulation (TMS). Here, we examined whether prolonged pain alters TMS-evoked alpha event-related spectral perturbation (ERSP) and intertrial coherence (ITC), reflecting cortical reactivity and phase consistency, and whether 10-Hz repetitive TMS (rTMS) modulates these responses. We performed a secondary analysis on 2 previous experiments, which used nerve growth factor (NGF) injection to induce prolonged elbow muscle pain. In experiment 1, participants underwent primary motor cortex (M1) TMS-EEG at baseline (day 0) pre-NGF injection and day 2 (peak pain) and day 7 (pain resolution) post-injection. In experiment 2, M1-TMS-EEG was assessed on day 0 before NGF injection and again on day 4 after injection, with active or sham 10-Hz rTMS delivered to M1 between these assessments. In experiment 1, M1 TMS-EEG showed reductions in alpha ERSP ( P = 0.014) and alpha ITC ( P = 0.041) from day 0 to day 2. In experiment 2, active rTMS produced a more positive pre-to-post change in alpha ERSP ( P = 0.006) relative to sham but did not alter alpha ITC ( P = 0.804). Our findings suggest that prolonged experimental pain is associated with diminished evoked alpha oscillatory activity, whereas high-frequency rTMS modulates this activity in the positive direction. These findings suggest that perturbation-evoked alpha metrics warrant further investigation as candidate biomarkers of pain state and response to neuromodulation.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"1 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149089162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain gray matter changes across chronic pain trajectories: MRI evidence from 35,000 individuals","authors":"Katerina Zorina-Lichtenwalter,Carmen I. Bango,Bogdan Petre,Lydia Rader,Marta Čeko,Martin A. Lindquist,Naomi P. Friedman,Tor D. Wager","doi":"10.1097/j.pain.0000000000004125","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000004125","url":null,"abstract":"Abstract Chronic pain affects brain gray matter structure, but the magnitude, pattern, and reversibility of brain changes upon pain recovery remain unclear because of inconsistent findings from small-scale studies. We analyzed data from 35,052 UK Biobank participants who completed chronic pain assessments at 2 time points, approximately 9 years apart, evaluating pain lasting 3 months or more, across 8 body sites. Brain magnetic resonance imaging data were available from the second time point. Participants were grouped into 4 categories: Pain-free controls, New chronic pain, Persistent chronic pain, and Resolved chronic pain. We examined relationships between these categories and 313 brain-wide measures across cortical surface area, cortical thickness, and subcortical volume. New chronic pain was associated with surface area reductions in sensorimotor, temporo-parietal, and medial and lateral prefrontal cortices. Persistent chronic pain showed larger and more widespread area reductions and mixed changes in cortical thickness and subcortical volumes, including cerebellar atrophy and hypertrophy in the thalamus and basal ganglia. Resolved pain demonstrated reversibility of most brain changes, except sustained surface area reductions in the primary somatosensory cortex. No areas showed effects consistent with a predisposition to pain. Brain structural changes in chronic pain reflect adaptive neuroplasticity rather than irreversible damage or preexisting vulnerability. Most changes appear reversible with pain resolution, underscoring the importance of effective pain treatment to alleviate symptoms and support recovery of brain structure and function.","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":"8 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149089163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methodological considerations for designing and conducting open-label placebo trials.","authors":"Helena Hartmann, Diana Müßgens, Livia Asan, Aleksandrina Skvortsova, Julian Kleine-Borgmann, Katharina Schmidt, Aurore Fernandez, Jules Phalip, Johannes Wessels, Marco Valerio, Meike Shedden-Mora, Ulrike Bingel, Jana L Aulenkamp","doi":"10.1097/j.pain.0000000000004071","DOIUrl":"10.1097/j.pain.0000000000004071","url":null,"abstract":"<p><strong>Abstract: </strong>In pain and other research fields, placebos have traditionally been associated with deception, although harnessing placebo effects does not necessarily require deception. Open-label placebos (OLPs) represent a novel approach in which inert treatments are administered openly and transparently, allowing patients to knowingly receive an inert treatment while still experiencing therapeutic benefits (eg, pain relief). As OLP research grows, concerns have been raised regarding methodological rigor and the unique challenges posed by unblinded designs in both experimental and clinical contexts. Given the inherent transparency regarding treatment group allocation in OLP trials, particular attention is needed when defining appropriate control groups, implementing feasible blinding strategies, and providing a treatment rationale to adequately explain OLPs. Addressing these challenges is crucial to advancing both the scientific understanding of the psychoneurobiological mechanisms underlying OLP effects and their clinical relevance in pain. In this review, we outline key methodological considerations for designing and conducting OLP studies in pain research and beyond, providing guidance on control group selection, blinding strategies, and reporting standards. In addition, we integrate insights from the patient advisory board of the transregional Collaborative Research Center (CRC/TRR) 289 \"Treatment Expectation\" to incorporate patient perspectives on the feasibility and acceptability of OLPs. Aligning study designs with patient needs and expectations may foster a more meaningful, patient-centered approach to OLP research. By combining methodological guidance and emphasizing patient-centered insights, this review aims to enhance the quality, relevance, and clinical translation of OLP research in pain.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":"2248-2262"},"PeriodicalIF":5.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580221/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148707402","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":"Centrally mediated pain features predict persistent pain in early inflammatory arthritis: a 2-year prospective study.","authors":"Zoe Rutter-Locher, Sam Norton, Bina Menon, Tom Esterine, Ruth Williams, Leonie S Taams, Bruce W Kirkham, Kirsty Bannister","doi":"10.1097/j.pain.0000000000004099","DOIUrl":"10.1097/j.pain.0000000000004099","url":null,"abstract":"<p><strong>Abstract: </strong>Patients with inflammatory arthritis (IA) often report pain not necessarily coupled to active inflammation. We previously demonstrated that a significant subset of patients with newly diagnosed IA report features of centrally mediated pain. In this prospective study following the same IA cohort, we tracked the relative contributions of inflammatory/noninflammatory mechanisms to pain over 2 years. We used patient-reported outcome measures (PROMs), clinical data (including ultrasound), and standardised quantitative sensory testing. Mixed-effects regression models examined longitudinal associations. We recruited 66 patients. At 6, 12, and 24 months, 62%, 57%, and 49% of individuals, respectively, reported persistent pain (numerical rating scale ≥3). Using factor-derived composite scores, baseline and longitudinal inflammation was not associated with subsequent pain ( b -0.05, P = 0.87), whereas higher centrally mediated pain markers predicted less pain reduction ( b 1.41, 95%, P < 0.001). Baseline PROMs of centrally mediated pain (fibromyalgia severity average marginal effect [AME]: 0.94, P < 0.001, painDETECT AME: 1.03, P < 0.001) and mental health (eg, Generalised Anxiety Disorder-7 AME: 1.08, P < 0.001) were the strongest predictors of persistent pain. Baseline trapezius pressure pain threshold (PPT) and conditioned pain modulation (CPM) pain detection threshold (PDT) effect showed modest association (trapezius PPT AME: -0.51, P = 0.054, CPM PDT effect AME: -0.49, P = 0.051) whereas temporal summation of pain (AME: 0.09, P = 0.756) and CPM pain tolerance threshold effect (AME: -0.01, P = 0.964) did not. In our cohort, persistent pain was associated with higher baseline and longitudinal scores for centrally mediated pain according to PROMs rather than inflammation according to joint ultrasound. In IA, early identification and treatment of features of centrally mediated pain may improve pain-related outcomes.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":" ","pages":"2365-2374"},"PeriodicalIF":5.8,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148905810","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}