Pain Reports最新文献

Introduction: More than three-fourths of people with fibromyalgia complain of cognitive difficulties, including memory and attention problems, which result in impaired job performance and disability. Cognitive behavioral therapy (CBT) is efficacious in treating people with attention deficits, depression, anxiety, and chronic pain (eg, fibromyalgia).

Objectives: In this study, we examined the efficacy of CBT for improving attention in patients with fibromyalgia.

Methods: Sixty-nine women with fibromyalgia (M = 42; SD = 13) were randomly assigned to receive CBT or an education control, and completed computer-based attention tasks and surveys at baseline (before receiving treatment) and at the follow-up (after receiving 8 treatment sessions). We hypothesized that CBT would lead to greater improvement in attention compared with fibromyalgia education. We conducted repeated-measures analyses of variance to examine the effects of time (pre- vs postintervention) and whether CBT resulted in greater improvement (time × condition effects) for attention span, attentional switching, and divided attention.

Results: Results indicated an effect of time such that patients in both groups improved from baseline to follow-up for attention span (F = 8.26, P = 0.01) and switch cost response time (F = 4.45, P = 0.04). However, the time by condition interaction was not significant (Ps > 0.05), indicating that improvement in attentional performance did not differ across intervention groups.

Conclusion: Our results support the possibility of practice effects such that completing tasks that engage attentional processes could serve as potential interventions for attentional deficits observed in fibromyalgia.

[This corrects the article DOI: 10.1097/PR9.0000000000001181.].

Objective: Depressive symptoms and chronic pain commonly co-occur among adolescents and share similar proposed underlying processes, including elevation of proinflammatory cytokines. In this study, we investigate how profiles of 4 commonly measured proinflammatory cytokines (IL-1β, IL-6, IL-8, and TNF-α) differ between adolescents with primary chronic pain disorders and pain-free peers. We explored relationships between these cytokines and depressive symptoms, perceived distress (PD), pain severity, functional disability (FD), pain catastrophizing (Pcat), and fear of pain (FOP). Potential mediating effects of cytokines on the relationship between depressive symptoms and FD were also examined.

Methods: Differences in cytokine profiles between groups were compared through t-tests. Relationships between cytokine profiles and outcomes were assessed through partial correlations. Bootstrapping mediation analysis assessed whether cytokines mediated the relationship between depressive symptoms and functional disability. Our sample included 78 youth (chronic pain n = 54, Mage = 14 years; pain-free n = 24; Mage = 16 years).

Results: We found that (1) IL-6 levels were higher among adolescents with chronic pain than pain-free peers; (2) higher IL-1β and IL-6 levels were associated with greater PD among adolescents with and without pain; (3) among the pain group, higher IL-6 levels were associated with greater PD, pain severity, and FD; (4) among the pain group, higher IL-1β levels were associated with greater depressive symptoms, PD, Pcat, and FOP. Mediation effects were not significant.

Conclusion: Our findings suggest that IL-1β and IL-6 play critical roles in the pain experience. Interleukin-6 is more strongly associated with physical symptoms, and IL-1β is more related to fear-avoidance.

Introduction: Pathological levels of methylglyoxal (MG), a reactive dicarbonyl product of glucose, contribute to major neurological complications associated with type II diabetes, including chronic neuropathic pain. Strategies to target elevated MG have included small molecule MG scavengers, but scavenger deficiencies in proteolytic stability and onset of scavenging activity have precluded clinical translation. To address this gap, we developed a long-lasting and highly reactive cyclic peptide CycK(Myr)R₄E, and here evaluated its antihyperalgesic efficacy in the db/db mouse model of type II diabetes painful diabetic neuropathy.

Objectives: To test the hypothesis that CycK(Myr)R₄E can reduce behavioral and molecular signs of painful diabetic neuropathy.

Methods: We assessed heat hypersensitivity as an index of hyperalgesia, and touch-evoked expression of phosphorylated extracellular signal-regulated kinase as a measure of neuronal activity in spinal cord dorsal horn.

Results: We report that a single systemic injection of CycK(Myr)R₄E (3 mg/kg) reversed heat hypersensitivity. Repeated systemic injection of CycK(Myr)R₄E (0.125 mg/kg, 3 times per week, 6-12 weeks of age) prevented heat hypersensitivity and reduced stimulus-evoked phosphorylated extracellular signal-regulated kinase.

Conclusion: These studies promote CycK(Myr)R₄E as the most promising MG scavenger for the prevention and treatment of hyperalgesia in type 2 diabetic neuropathic pain.

Introduction: The central nervous system (CNS) contributes to pain perception across musculoskeletal conditions. The central aspects of pain (CAP) questionnaire captures a single score associated with quantitative sensory testing (QST) evidence of CNS dysfunction validated in knee osteoarthritis.

Objectives: Given the different pathophysiology of rheumatoid arthritis (RA), an inflammatory polyarthritis, this cross-sectional study assessed CAP's psychometric properties and its association with pain in RA.

Methods: Adults with RA were recruited from Nottinghamshire, London, and Cardiff. Participants completed CAP and reported pain using a numerical rating scale. A subgroup underwent additional assessments, including quantitative sensory testing (QST; Pressure Pain detection Threshold, Temporal Summation, Conditioned Pain Modulation), Disease Activity Score-28, C-reactive protein, questionnaires addressing pain and related characteristics, and Central Sensitization Inventory short form (CSI-9). Cronbach alpha, confirmatory factor (CFA), and Rasch measurement theory assessed CAP's reliability and validity. Multivariable linear regression modelled contributions to pain by inflammation indices and CAP or CSI-9.

Results: The 380 participants (73% female, median 63 years) reported average pain over the past 4 weeks of 6/10 and a CAP score of 9/16. Central aspects of pain demonstrated acceptable reliability (ICC_(2,1) = 0.71), CFA fit (comparative fit index = 0.99, Tucker-Lewis index = 0.99, root mean square error of approximation = 0.034, standardized root mean residuals = 0.03), and internal consistency (α = 0.82). Central aspects of pain was significantly associated with pain (0.50 ≤ β ≤ 0.57) but not QST. Central aspects of pain explained 33% of pain variance, rising to 42% with inflammation, age, sex, and body mass index. Central Sensitization Inventory-9 correlated with pain, not QST and explained less pain variance than CAP.

Conclusion: Central aspects of pain is reliable and valid for use with people with RA and explains RA pain variance better than inflammation or CSI-9.

Objective: Multiple voltage-gated sodium channels (Na_Vs) in the peripheral sensory neurons (PSNs) regulate action potentials and their dysfunction contributes to the pain pathogenesis of osteoarthritis (OA). A combined block of multiple Na_V subtypes selectively in the PSNs may, therefore, represent an effective analgesic approach in OA painful neuropathy.

Methods: To test this hypothesis, we generated recombinant adeno-associated virus (AAV) encoding a potent Na_V inhibitory peptide aptamer, termed Na_ViPA1, that has a multipronged feature of inhibiting tetrodotoxin-sensitive Na_V1.7, 1.6, 1.1, and 1.3, characterized in our recent report. Adeno-associated virus-encoded Na_ViPA1 was delivered into the ipsilateral lumbar 4/5 dorsal root ganglia of rats 2 weeks after induction of knee monoiodoacetate-OA (MIA-OA) and evoked and spontaneous sensory behaviors were followed in 6 weeks.

Results: Expression of Na_ViPA1 selective in the PSNs produced significant and comparable mitigations of evoked and spontaneous pain behavior and reversal of weight-bearing asymmetry in both male and female MIA-OA rats. Whole-cell current-clamp recordings showed that AAV-mediated Na_ViPA1 expression normalized action potential firing of the PSNs from MIA animals, suggesting that Na_ViPA1 attenuated pain behavior by, at least in part, reversing neuronal hyperexcitability.

Conclusion: Together, these results support that (1) Na_Vs in peripheral sensory pathways contribute to MIA-OA pain pathogenesis and (2) Na_ViPA1 is a promising analgesic lead that, combined with AAV-targeted delivery to pathological sensory ganglia, may be a viable peripherally selective PSN-targeting strategy in mitigating chronic MIA-OA pain behaviors.

Bridging the gender pain gap requires collaborative efforts that address female-specific biological and psychosocial dimensions of pain through evidence-based, compassionate and empathy-driven approaches.

Introduction: Low back pain (LBP) is a leading global factor in disability among older adults. Movement-evoked pain (MEP) is potentially an important mediator in the disability pathway but is predominantly tested in the laboratory.

Objectives: We aimed to explore MEP in the natural environment ("daily" MEP) and its correlation with laboratory MEP, along with potential psychological and immunological influences.

Method: Thirty-five older adults with persistent LBP attended a single laboratory session. Pain catastrophizing, pain-related fear of movement, and pain self-efficacy were measured by questionnaire. Resting inflammation and inflammatory reactivity to painful movement were evaluated using serum interleukin-6, tissue necrosis factor alpha, and C-reactive protein (CRP). Laboratory MEP was defined by aggregate pain intensity with a movement provocation test. Daily MEP was measured for the next 7 days using ecological momentary assessment.

Results: Laboratory MEP was strongly correlated with daily MEP (ρ = 0.780, P = <0.001). C-reactive protein (Hedges [g] = 0.266) and interleukin-6 (g = 0.433) demonstrated small to moderate reactivity to painful movement. After controlling for age and multimorbidity, pain catastrophizing and pain self-efficacy explained 24% to 37% variance in laboratory and daily MEP. Resting inflammatory markers were not associated with MEP; however, C-reactive protein reactivity to painful movement explained 19% to 25% variance in laboratory and daily MEP.

Conclusion: Preliminary indication is that laboratory and daily MEP may be proxy measures for one another, and that MEP is influenced by psychological and immunological factors. Future studies will aim to (1) validate findings among older adults with persistent LBP and (2) for clinical phenotyping, clarify complex relationships among psychological and immunological factors with disability pathway components like MEP.