Pub Date : 2024-09-01Epub Date: 2024-01-02DOI: 10.1097/j.pain.0000000000003167
Rolf-Detlef Treede
{"title":"Interactions between 2 subtypes of central sensitization in rats and humans: spinal long-term potentiation and brainstem controls.","authors":"Rolf-Detlef Treede","doi":"10.1097/j.pain.0000000000003167","DOIUrl":"10.1097/j.pain.0000000000003167","url":null,"abstract":"","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139417715","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}
Pub Date : 2024-09-01Epub Date: 2024-03-05DOI: 10.1097/j.pain.0000000000003209
Anders Pedersen Årnes, Mats Kirkeby Fjeld, Hein Stigum, Christopher Sivert Nielsen, Audun Stubhaug, Aslak Johansen, Laila Arnesdatter Hopstock, Bente Morseth, Tom Wilsgaard, Ólöf Anna Steingrímsdóttir
Abstract: Knowledge is needed regarding mechanisms acting between physical activity (PA) and chronic pain. We investigated whether cold pain tolerance mediates an effect of leisure-time physical activity on the risk of chronic pain 7 to 8 years later using consecutive surveys of the population-based Tromsø Study. We included participants with information on baseline leisure-time PA (LTPA) and the level of cold pressor-assessed cold pain tolerance, who reported chronic pain status at follow-up as any of the following: chronic pain for ≥3 months, widespread chronic pain, moderate-to-severe chronic pain, or widespread moderate-to-severe chronic pain. We included 6834 participants (52% women; mean age, 55 years) in counterfactual mediation analyses. Prevalence decreased with severity, for example, 60% for chronic pain vs 5% for widespread moderate-to-severe chronic pain. People with one level higher LTPA rating (light to moderate or moderate to vigorous) at baseline had lower relative risk (RR) of 4 chronic pain states 7 to 8 years later. Total RR effect of a 1-level LTPA increase was 0.95 (0.91-1.00), that is, -5% decreased risk. Total effect RR for widespread chronic pain was 0.84 (0.73-0.97). Indirect effect for moderate-to-severe chronic pain was statistically significant at RR 0.993 (0.988-0.999); total effect RR was 0.91 (0.83-0.98). Statistically significantly mediated RR for widespread moderate-to-severe chronic pain was 0.988 (0.977-0.999); total effect RR was 0.77 (0.64-0.94). This shows small mediation of the effect of LTPA through pain tolerance on 2 moderate-to-severe chronic pain types. This suggests pain tolerance to be one possible mechanism through which PA modifies the risk of moderate-to-severe chronic pain types with and without widespread pain.
{"title":"Does pain tolerance mediate the effect of physical activity on chronic pain in the general population? The Tromsø Study.","authors":"Anders Pedersen Årnes, Mats Kirkeby Fjeld, Hein Stigum, Christopher Sivert Nielsen, Audun Stubhaug, Aslak Johansen, Laila Arnesdatter Hopstock, Bente Morseth, Tom Wilsgaard, Ólöf Anna Steingrímsdóttir","doi":"10.1097/j.pain.0000000000003209","DOIUrl":"10.1097/j.pain.0000000000003209","url":null,"abstract":"<p><strong>Abstract: </strong>Knowledge is needed regarding mechanisms acting between physical activity (PA) and chronic pain. We investigated whether cold pain tolerance mediates an effect of leisure-time physical activity on the risk of chronic pain 7 to 8 years later using consecutive surveys of the population-based Tromsø Study. We included participants with information on baseline leisure-time PA (LTPA) and the level of cold pressor-assessed cold pain tolerance, who reported chronic pain status at follow-up as any of the following: chronic pain for ≥3 months, widespread chronic pain, moderate-to-severe chronic pain, or widespread moderate-to-severe chronic pain. We included 6834 participants (52% women; mean age, 55 years) in counterfactual mediation analyses. Prevalence decreased with severity, for example, 60% for chronic pain vs 5% for widespread moderate-to-severe chronic pain. People with one level higher LTPA rating (light to moderate or moderate to vigorous) at baseline had lower relative risk (RR) of 4 chronic pain states 7 to 8 years later. Total RR effect of a 1-level LTPA increase was 0.95 (0.91-1.00), that is, -5% decreased risk. Total effect RR for widespread chronic pain was 0.84 (0.73-0.97). Indirect effect for moderate-to-severe chronic pain was statistically significant at RR 0.993 (0.988-0.999); total effect RR was 0.91 (0.83-0.98). Statistically significantly mediated RR for widespread moderate-to-severe chronic pain was 0.988 (0.977-0.999); total effect RR was 0.77 (0.64-0.94). This shows small mediation of the effect of LTPA through pain tolerance on 2 moderate-to-severe chronic pain types. This suggests pain tolerance to be one possible mechanism through which PA modifies the risk of moderate-to-severe chronic pain types with and without widespread pain.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140040060","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}
Pub Date : 2024-09-01Epub Date: 2024-03-06DOI: 10.1097/j.pain.0000000000003205
Amelia K Mardon, K Jane Chalmers, Lauren C Heathcote, Lee-Anne Curtis, Lesley Freedman, Rinkle Malani, Romy Parker, Patricia B Neumann, G Lorimer Moseley, Hayley B Leake
Abstract: Pain science education (PSE) provides people with an understanding of "how pain works" grounded in the biopsychosocial model of pain; it has been demonstrated to improve outcomes in musculoskeletal pain conditions. Preliminary evidence suggests PSE may be effective for female individuals with persistent pelvic pain, but how the content of PSE needs to be modified for this group remains to be determined. A reflexive thematic analysis of qualitative data was performed to identify PSE concepts that female individuals with persistent pelvic pain consider important and why. Twenty individual, semistructured interviews were conducted with adult females who had engaged with PSE and had self-identified as having "improved" pelvic pain. Most participants had been diagnosed with endometriosis (n = 16). Four themes were generated capturing PSE concepts considered important by female individuals with "improved" pelvic pain: (1) "A sensitised nervous system leads to overprotective pain" validated their pelvic pain as being real; (2) "Pain does not have to mean the body is damaged (although sometimes it does)" provided reassurance that pelvic pain does not mean their condition is worsening; (3) "How I think, feel, and 'see' my pain can make it worse" enabled participants to find optimal ways to manage their pain; and (4) "I can change my pain… slowly" provided hope that pelvic pain can improve and empowered them to pursue pain improvement as a viable goal. This study generated 4 PSE learning concepts that were important to female individuals with improved pelvic pain and may be incorporated into PSE curricula for female individuals with pelvic pain.
摘要:疼痛科学教育(PSE)以疼痛的生物-心理-社会模型为基础,让人们了解 "疼痛是如何产生的";它已被证明能改善肌肉骨骼疼痛的治疗效果。初步证据表明,PSE 可能对患有持续性骨盆疼痛的女性患者有效,但 PSE 的内容如何针对这一群体进行调整仍有待确定。我们对定性数据进行了反思性主题分析,以确定持续性骨盆疼痛女性患者认为重要的 PSE 概念及其原因。我们对参与过 PSE 并自认为盆腔疼痛得到 "改善 "的成年女性进行了 20 次个人半结构式访谈。大多数参与者被诊断出患有子宫内膜异位症(n = 16)。通过对盆腔疼痛 "得到改善 "的女性进行 PSE 研究,我们发现了四个主题,这些主题体现了 PSE 的重要理念:(1) "敏感的神经系统导致过度保护性疼痛 "证实了她们的盆腔疼痛是真实存在的;(2) "疼痛不一定意味着身体受损(尽管有时确实如此)"为盆腔疼痛并不意味着病情恶化提供了保证;(3) "我是如何思考、感受和'看待'我的疼痛的 "使参与者能够找到控制疼痛的最佳方法;以及 (4) "我可以慢慢改变我的疼痛...... "为盆腔疼痛患者提供了希望。我可以慢慢地改变我的疼痛 "为盆腔疼痛的改善提供了希望,并使他们有能力将疼痛的改善作为一个可行的目标。本研究提出了 4 个 PSE 学习概念,这些概念对于盆腔疼痛得到改善的女性患者非常重要,可将其纳入针对盆腔疼痛女性患者的 PSE 课程中。
{"title":"\"I wish I knew then what I know now\" - pain science education concepts important for female persistent pelvic pain: a reflexive thematic analysis.","authors":"Amelia K Mardon, K Jane Chalmers, Lauren C Heathcote, Lee-Anne Curtis, Lesley Freedman, Rinkle Malani, Romy Parker, Patricia B Neumann, G Lorimer Moseley, Hayley B Leake","doi":"10.1097/j.pain.0000000000003205","DOIUrl":"10.1097/j.pain.0000000000003205","url":null,"abstract":"<p><strong>Abstract: </strong>Pain science education (PSE) provides people with an understanding of \"how pain works\" grounded in the biopsychosocial model of pain; it has been demonstrated to improve outcomes in musculoskeletal pain conditions. Preliminary evidence suggests PSE may be effective for female individuals with persistent pelvic pain, but how the content of PSE needs to be modified for this group remains to be determined. A reflexive thematic analysis of qualitative data was performed to identify PSE concepts that female individuals with persistent pelvic pain consider important and why. Twenty individual, semistructured interviews were conducted with adult females who had engaged with PSE and had self-identified as having \"improved\" pelvic pain. Most participants had been diagnosed with endometriosis (n = 16). Four themes were generated capturing PSE concepts considered important by female individuals with \"improved\" pelvic pain: (1) \"A sensitised nervous system leads to overprotective pain\" validated their pelvic pain as being real; (2) \"Pain does not have to mean the body is damaged (although sometimes it does)\" provided reassurance that pelvic pain does not mean their condition is worsening; (3) \"How I think, feel, and 'see' my pain can make it worse\" enabled participants to find optimal ways to manage their pain; and (4) \"I can change my pain… slowly\" provided hope that pelvic pain can improve and empowered them to pursue pain improvement as a viable goal. This study generated 4 PSE learning concepts that were important to female individuals with improved pelvic pain and may be incorporated into PSE curricula for female individuals with pelvic pain.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140060158","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}
Pub Date : 2024-09-01Epub Date: 2024-03-06DOI: 10.1097/j.pain.0000000000003224
Jay Karri, Steven P Cohen
{"title":"Dilemmas with denervation: to do or not to do (that is the question).","authors":"Jay Karri, Steven P Cohen","doi":"10.1097/j.pain.0000000000003224","DOIUrl":"10.1097/j.pain.0000000000003224","url":null,"abstract":"","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142004984","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}
Pub Date : 2024-09-01Epub Date: 2024-01-09DOI: 10.1097/j.pain.0000000000003166
Ryan Patel, Joseph L Taylor, Anthony H Dickenson, Stephen B McMahon, Kirsty Bannister
Abstract: In humans and animals, high-frequency electrocutaneous stimulation (HFS) induces an "early long-term potentiation-like" sensitisation, where synaptic plasticity is underpinned by an ill-defined interaction between peripheral input and central modulatory processes. The relative contributions of these processes to the initial pain or nociceptive response likely differ from those that underpin development of the heightened response. To investigate the impact of HFS-induced hyperalgesia on pain and nociception in perception and neural terms, respectively, and to explore the impact of descending inhibitory pathway activation on the development of HFS-induced hyperalgesia, we performed parallel studies utilising identical stimuli to apply HFS concurrent to (1) a conditioned pain modulation paradigm during psychophysical testing in healthy humans or (2) a diffuse noxious inhibitory controls paradigm during in vivo electrophysiological recording of spinal neurones in healthy anaesthetised rats. High-frequency electrocutaneous stimulation alone induced enhanced perceptual responses to pinprick stimuli in cutaneous areas secondary to the area of electrical stimulation in humans and increased the excitability of spinal neurones which exhibited stimulus intensity-dependent coded responses to pinprick stimulation in a manner that tracked with human psychophysics, supporting their translational validity. Application of a distant noxious conditioning stimulus during HFS did not alter perceived primary or secondary hyperalgesia in humans or the development of primary or secondary neuronal hyperexcitability in rats compared with HFS alone, suggesting that, upon HFS-response initiation in a healthy nervous system, excitatory signalling escapes inhibitory control. Therefore, in this model, dampening facilitatory mechanisms rather than augmenting top-down inhibitions could prevent pain development.
{"title":"A back-translational study of descending interactions with the induction of hyperalgesia by high-frequency electrical stimulation in rats and humans.","authors":"Ryan Patel, Joseph L Taylor, Anthony H Dickenson, Stephen B McMahon, Kirsty Bannister","doi":"10.1097/j.pain.0000000000003166","DOIUrl":"10.1097/j.pain.0000000000003166","url":null,"abstract":"<p><strong>Abstract: </strong>In humans and animals, high-frequency electrocutaneous stimulation (HFS) induces an \"early long-term potentiation-like\" sensitisation, where synaptic plasticity is underpinned by an ill-defined interaction between peripheral input and central modulatory processes. The relative contributions of these processes to the initial pain or nociceptive response likely differ from those that underpin development of the heightened response. To investigate the impact of HFS-induced hyperalgesia on pain and nociception in perception and neural terms, respectively, and to explore the impact of descending inhibitory pathway activation on the development of HFS-induced hyperalgesia, we performed parallel studies utilising identical stimuli to apply HFS concurrent to (1) a conditioned pain modulation paradigm during psychophysical testing in healthy humans or (2) a diffuse noxious inhibitory controls paradigm during in vivo electrophysiological recording of spinal neurones in healthy anaesthetised rats. High-frequency electrocutaneous stimulation alone induced enhanced perceptual responses to pinprick stimuli in cutaneous areas secondary to the area of electrical stimulation in humans and increased the excitability of spinal neurones which exhibited stimulus intensity-dependent coded responses to pinprick stimulation in a manner that tracked with human psychophysics, supporting their translational validity. Application of a distant noxious conditioning stimulus during HFS did not alter perceived primary or secondary hyperalgesia in humans or the development of primary or secondary neuronal hyperexcitability in rats compared with HFS alone, suggesting that, upon HFS-response initiation in a healthy nervous system, excitatory signalling escapes inhibitory control. Therefore, in this model, dampening facilitatory mechanisms rather than augmenting top-down inhibitions could prevent pain development.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11331830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139417712","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}
Pub Date : 2024-09-01Epub Date: 2024-05-07DOI: 10.1097/j.pain.0000000000003259
Pietro Falco, Daniel Litewczuk, Giulia Di Stefano, Eleonora Galosi, Caterina Leone, Gianfranco De Stefano, Giuseppe Di Pietro, Lorenzo Tramontana, Maria Rosa Ciardi, Patrizia Pasculli, Maria Antonella Zingaropoli, Lars Arendt-Nielsen, Andrea Truini
Abstract: Approximately 10% to 20% of individuals with previous SARS-CoV-2 infection may develop long-COVID syndrome, characterized by various physical and mental health issues, including pain. Previous studies suggested an association between small fibre neuropathy and pain in long-COVID cases. In this case-control study, our aim was to identify small fibre neuropathy in patients experiencing painful long-COVID syndrome. Clinical data, quantitative sensory testing, and skin biopsies were collected from 26 selected patients with painful long-COVID syndrome. We also examined 100 individuals with past COVID-19 infection, selecting 33 patients with painless long-COVID syndrome, characterized mainly by symptoms such as brain fog and fatigue, and 30 asymptomatic post-COVID-19 controls. Demographic and clinical variables were compared among these groups. Among the 26 patients with painful long-COVID syndrome, 12 had skin biopsy and/or quantitative sensory testing abnormalities compatible with small fibre neuropathy. Demographic and clinical data did not differ across patients with small fibre neuropathy, patients with painless long-COVID syndrome, and asymptomatic post-COVID-19 controls. This case-control study showed that approximately 50% of patients experiencing painful long-COVID syndrome had small fibre neuropathy. However, in our patient cohort, this specific post-COVID-19 complication was unrelated to demographic and COVID-19 clinical variables. Approximately half of our sample of patients with painful long-COVID symptoms met diagnostic criteria for small fibre neuropathy.
{"title":"Small fibre neuropathy frequently underlies the painful long-COVID syndrome.","authors":"Pietro Falco, Daniel Litewczuk, Giulia Di Stefano, Eleonora Galosi, Caterina Leone, Gianfranco De Stefano, Giuseppe Di Pietro, Lorenzo Tramontana, Maria Rosa Ciardi, Patrizia Pasculli, Maria Antonella Zingaropoli, Lars Arendt-Nielsen, Andrea Truini","doi":"10.1097/j.pain.0000000000003259","DOIUrl":"10.1097/j.pain.0000000000003259","url":null,"abstract":"<p><strong>Abstract: </strong>Approximately 10% to 20% of individuals with previous SARS-CoV-2 infection may develop long-COVID syndrome, characterized by various physical and mental health issues, including pain. Previous studies suggested an association between small fibre neuropathy and pain in long-COVID cases. In this case-control study, our aim was to identify small fibre neuropathy in patients experiencing painful long-COVID syndrome. Clinical data, quantitative sensory testing, and skin biopsies were collected from 26 selected patients with painful long-COVID syndrome. We also examined 100 individuals with past COVID-19 infection, selecting 33 patients with painless long-COVID syndrome, characterized mainly by symptoms such as brain fog and fatigue, and 30 asymptomatic post-COVID-19 controls. Demographic and clinical variables were compared among these groups. Among the 26 patients with painful long-COVID syndrome, 12 had skin biopsy and/or quantitative sensory testing abnormalities compatible with small fibre neuropathy. Demographic and clinical data did not differ across patients with small fibre neuropathy, patients with painless long-COVID syndrome, and asymptomatic post-COVID-19 controls. This case-control study showed that approximately 50% of patients experiencing painful long-COVID syndrome had small fibre neuropathy. However, in our patient cohort, this specific post-COVID-19 complication was unrelated to demographic and COVID-19 clinical variables. Approximately half of our sample of patients with painful long-COVID symptoms met diagnostic criteria for small fibre neuropathy.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899032","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}
Pub Date : 2024-09-01Epub Date: 2024-03-05DOI: 10.1097/j.pain.0000000000003200
Jessica J Wong, Pierre Côté, Andrea C Tricco, Tristan Watson, Laura C Rosella
Abstract: Some patients with back pain contribute disproportionately to high healthcare costs; however, characteristics of high-cost users with back pain are not well defined. We described high-cost healthcare users based on total costs among a population-based cohort of adults with back pain within the Ontario government's single-payer health system across sociodemographic, health, and behavioural characteristics. We conducted a population-based cohort study of Ontario adult (aged 18 years or older) respondents of the Canadian Community Health Survey (CCHS) with back pain (2003-2012), linked to administrative data (n = 36,605; weighted n = 2,076,937, representative of Ontario). Respondents were ranked based on gradients of total healthcare costs (top 1%, top 2%-5%, top 6%-50%, and bottom 50%) for 1 year following the CCHS survey, with high-cost users as top 5%. We used multinomial logistic regression to investigate characteristics associated with the 4 cost groups. Top 5% of cost users accounted for 49% ($4 billion CAD) of total healthcare spending, with inpatient hospital care as the largest contributing service type (approximately 40% of costs). Top 5% high-cost users were more likely aged 65 years or older (OR top1% = 16.6; OR top2-5% = 44.2), with lower income (OR top1% = 3.6; OR top 2-5% = 1.8), chronic disease(s) (OR top1% = 3.8; OR top2-5% = 1.6), Aggregated Diagnosis Groups measuring comorbidities (OR top1% = 25.4; OR top2-5% = 13.9), and fair/poor self-rated general health (OR top1% = 6.7; OR top2-5% = 4.6) compared with bottom 50% users. High-cost users tended to be current/former smokers, obese, and report fair/poor mental health. High-cost users (based on total costs) among adults with back pain account for nearly half of all healthcare spending over a 1-year period and are associated with older age, lower income, comorbidities, and fair/poor general health. Findings identify characteristics associated with a high-risk group for back pain to inform healthcare and public health strategies that target upstream determinants.
{"title":"Characterizing high-cost healthcare users among adults with back pain in Ontario, Canada: a population-based cohort study.","authors":"Jessica J Wong, Pierre Côté, Andrea C Tricco, Tristan Watson, Laura C Rosella","doi":"10.1097/j.pain.0000000000003200","DOIUrl":"10.1097/j.pain.0000000000003200","url":null,"abstract":"<p><strong>Abstract: </strong>Some patients with back pain contribute disproportionately to high healthcare costs; however, characteristics of high-cost users with back pain are not well defined. We described high-cost healthcare users based on total costs among a population-based cohort of adults with back pain within the Ontario government's single-payer health system across sociodemographic, health, and behavioural characteristics. We conducted a population-based cohort study of Ontario adult (aged 18 years or older) respondents of the Canadian Community Health Survey (CCHS) with back pain (2003-2012), linked to administrative data (n = 36,605; weighted n = 2,076,937, representative of Ontario). Respondents were ranked based on gradients of total healthcare costs (top 1%, top 2%-5%, top 6%-50%, and bottom 50%) for 1 year following the CCHS survey, with high-cost users as top 5%. We used multinomial logistic regression to investigate characteristics associated with the 4 cost groups. Top 5% of cost users accounted for 49% ($4 billion CAD) of total healthcare spending, with inpatient hospital care as the largest contributing service type (approximately 40% of costs). Top 5% high-cost users were more likely aged 65 years or older (OR top1% = 16.6; OR top2-5% = 44.2), with lower income (OR top1% = 3.6; OR top 2-5% = 1.8), chronic disease(s) (OR top1% = 3.8; OR top2-5% = 1.6), Aggregated Diagnosis Groups measuring comorbidities (OR top1% = 25.4; OR top2-5% = 13.9), and fair/poor self-rated general health (OR top1% = 6.7; OR top2-5% = 4.6) compared with bottom 50% users. High-cost users tended to be current/former smokers, obese, and report fair/poor mental health. High-cost users (based on total costs) among adults with back pain account for nearly half of all healthcare spending over a 1-year period and are associated with older age, lower income, comorbidities, and fair/poor general health. Findings identify characteristics associated with a high-risk group for back pain to inform healthcare and public health strategies that target upstream determinants.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11331817/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140040059","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}
Pub Date : 2024-09-01Epub Date: 2024-03-26DOI: 10.1097/j.pain.0000000000003220
Ying Liu, Junfeng Sun, Chaomin Wu, Jinxuan Ren, Yanni He, Na Sun, Hao Huang, QunShan Chen, Dan Liu, Yangyuxin Huang, Feng Xu, Lina Yu, Bernadette M Fitzgibbon, Robin F H Cash, Paul B Fitzgerald, Min Yan, Xianwei Che
Abstract: Repetitive transcranial magnetic stimulation (rTMS) is a promising technology to reduce chronic pain. Investigating the mechanisms of rTMS analgesia holds the potential to improve treatment efficacy. Using a double-blind and placebo-controlled design at both stimulation and pharmacologic ends, this study investigated the opioidergic mechanisms of rTMS analgesia by abolishing and recovering analgesia in 2 separate stages across brain regions and TMS doses. A group of 45 healthy participants were equally randomized to the primary motor cortex (M1), the dorsolateral prefrontal cortex (DLPFC), and the Sham group. In each session, participants received an intravenous infusion of naloxone or saline before the first rTMS session. Participants then received a second dose of rTMS session after the drugs were metabolized at 90 minutes. M1-rTMS-induced analgesia was abolished by naloxone compared with saline and was recovered by the second rTMS run when naloxone was metabolized. In the DLPFC, double but not the first TMS session induced significant pain reduction in the saline condition, resulting in less pain compared with the naloxone condition. In addition, TMS over the M1 or DLPFC selectively increased plasma concentrations of β-endorphin or encephalin, respectively. Overall, we present causal evidence that opioidergic mechanisms are involved in both M1-induced and DLPFC-rTMS-induced analgesia; however, these are shaped by rTMS dosage and the release of different endogenous opioids.
{"title":"Characterizing the opioidergic mechanisms of repetitive transcranial magnetic stimulation-induced analgesia: a randomized controlled trial.","authors":"Ying Liu, Junfeng Sun, Chaomin Wu, Jinxuan Ren, Yanni He, Na Sun, Hao Huang, QunShan Chen, Dan Liu, Yangyuxin Huang, Feng Xu, Lina Yu, Bernadette M Fitzgibbon, Robin F H Cash, Paul B Fitzgerald, Min Yan, Xianwei Che","doi":"10.1097/j.pain.0000000000003220","DOIUrl":"10.1097/j.pain.0000000000003220","url":null,"abstract":"<p><strong>Abstract: </strong>Repetitive transcranial magnetic stimulation (rTMS) is a promising technology to reduce chronic pain. Investigating the mechanisms of rTMS analgesia holds the potential to improve treatment efficacy. Using a double-blind and placebo-controlled design at both stimulation and pharmacologic ends, this study investigated the opioidergic mechanisms of rTMS analgesia by abolishing and recovering analgesia in 2 separate stages across brain regions and TMS doses. A group of 45 healthy participants were equally randomized to the primary motor cortex (M1), the dorsolateral prefrontal cortex (DLPFC), and the Sham group. In each session, participants received an intravenous infusion of naloxone or saline before the first rTMS session. Participants then received a second dose of rTMS session after the drugs were metabolized at 90 minutes. M1-rTMS-induced analgesia was abolished by naloxone compared with saline and was recovered by the second rTMS run when naloxone was metabolized. In the DLPFC, double but not the first TMS session induced significant pain reduction in the saline condition, resulting in less pain compared with the naloxone condition. In addition, TMS over the M1 or DLPFC selectively increased plasma concentrations of β-endorphin or encephalin, respectively. Overall, we present causal evidence that opioidergic mechanisms are involved in both M1-induced and DLPFC-rTMS-induced analgesia; however, these are shaped by rTMS dosage and the release of different endogenous opioids.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11331833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140306405","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}
Pub Date : 2024-08-30DOI: 10.1097/j.pain.0000000000003374
James Gerhart, John W Burns, Beverly Thorn, Mark Jensen, James Carmody, Francis Keefe
Abstract: Findings suggest that cognitive therapy (CT), mindfulness-based stress reduction (MBSR), and behavior therapy (BT) for chronic pain produce improvements through changes in putative mechanisms. Evidence supporting this notion is largely based on findings showing significant associations between treatment mechanism variables and outcomes. An alternative view is that treatments may work by reducing or decoupling the impact of changes in mechanism variables on changes in outcomes. We examined the degree to which relationships between previous changes in potential treatment mechanisms and subsequent changes in outcomes changed as treatment progressed and vice versa. Cognitive therapy, MBSR, BT, and treatment as usual (TAU) were compared in people with chronic low back pain (N = 521). Eight individual sessions were administered with weekly assessments of putative treatment mechanisms and outcomes. Lagged analyses revealed mechanism × session number interactions and outcome × session number interactions, such that associations between mechanism and outcome variables were strong and significant in the first third of treatment, but weakened over time and became nonsignificant by the last third of treatment. These effects were similar across treatment conditions but did not emerge among people undergoing TAU. Results suggest that during the course of CT, MBSR, and BT, the links between changes in treatment mechanism variables became decoupled from subsequent changes in outcomes and vice versa. Thus, starting by midtreatment and continuing into late treatment, participants may have learned through participation in the treatments that episodes of maladaptive pain-related thoughts and/or spikes in pain need not have detrimental consequences on their subsequent experience.
摘要:研究结果表明,认知疗法(CT)、正念减压疗法(MBSR)和行为疗法(BT)通过改变假定机制来改善慢性疼痛。支持这一观点的证据主要基于治疗机制变量与治疗结果之间存在显著关联的研究结果。另一种观点认为,治疗方法可能通过减少或解除机制变量变化对结果变化的影响而发挥作用。我们研究了潜在治疗机制的先前变化与后续结果变化之间的关系随治疗进展而变化的程度,反之亦然。我们对慢性腰背痛患者(521 人)的认知疗法、MBSR、BT 和常规治疗(TAU)进行了比较。共进行了八次单独治疗,每周对假定的治疗机制和结果进行评估。滞后分析显示了机制×疗程数交互作用和结果×疗程数交互作用,因此机制和结果变量之间的关联在治疗的前三分之一时间内是强烈和显著的,但随着时间的推移逐渐减弱,到治疗的最后三分之一时间变得不显著。这些效应在不同的治疗条件下相似,但在接受 TAU 治疗的人群中没有出现。结果表明,在 CT、MBSR 和 BT 治疗过程中,治疗机制变量的变化与后续结果变化之间的联系变得不相关,反之亦然。因此,从治疗中期开始,一直到治疗后期,参与者通过参与治疗可能已经了解到,与疼痛相关的适应不良想法和/或疼痛峰值的发作不一定会对他们随后的经历产生不利影响。
{"title":"Treatment mechanism and outcome decoupling effects in cognitive therapy, mindfulness-based stress reduction, and behavior therapy for chronic pain.","authors":"James Gerhart, John W Burns, Beverly Thorn, Mark Jensen, James Carmody, Francis Keefe","doi":"10.1097/j.pain.0000000000003374","DOIUrl":"https://doi.org/10.1097/j.pain.0000000000003374","url":null,"abstract":"<p><strong>Abstract: </strong>Findings suggest that cognitive therapy (CT), mindfulness-based stress reduction (MBSR), and behavior therapy (BT) for chronic pain produce improvements through changes in putative mechanisms. Evidence supporting this notion is largely based on findings showing significant associations between treatment mechanism variables and outcomes. An alternative view is that treatments may work by reducing or decoupling the impact of changes in mechanism variables on changes in outcomes. We examined the degree to which relationships between previous changes in potential treatment mechanisms and subsequent changes in outcomes changed as treatment progressed and vice versa. Cognitive therapy, MBSR, BT, and treatment as usual (TAU) were compared in people with chronic low back pain (N = 521). Eight individual sessions were administered with weekly assessments of putative treatment mechanisms and outcomes. Lagged analyses revealed mechanism × session number interactions and outcome × session number interactions, such that associations between mechanism and outcome variables were strong and significant in the first third of treatment, but weakened over time and became nonsignificant by the last third of treatment. These effects were similar across treatment conditions but did not emerge among people undergoing TAU. Results suggest that during the course of CT, MBSR, and BT, the links between changes in treatment mechanism variables became decoupled from subsequent changes in outcomes and vice versa. Thus, starting by midtreatment and continuing into late treatment, participants may have learned through participation in the treatments that episodes of maladaptive pain-related thoughts and/or spikes in pain need not have detrimental consequences on their subsequent experience.</p>","PeriodicalId":19921,"journal":{"name":"PAIN®","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142120428","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}