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Contributing to the welfare of others has been shown to have positive effects on people's social and psychological well-being (PWB). The current study examined whether social contribution (SC) could alleviate the negative effects of chronic pain on PWB through perceived social support (PSS) among midlife and older adults. The study consisted of 520 participants with chronic pain from the two waves of the Midlife in the United States dataset (MIDUS II and III). Results from the longitudinal moderated mediation analysis indicated that SC at Time 2 (T2) significantly buffered the negative effect of pain interference (PI) at Time 1 (T1) on PSS at T2, which indirectly alleviated the negative effect of PI at T1 on PWB at T2. The study suggested the protective role of SC and prosocial behaviors in mitigating the detrimental effects of chronic pain on social support and PWB.
Learn More >Objectives Fibromyalgia is a chronic widespread pain (CWP) syndrome of unknown etiology with substantial burden of illness and functional impairment. Pain acceptance has emerged as an interesting target of therapy in chronic pain populations, but few studies have yet been done on the effect of pain acceptance on patients with fibromyalgia. The aim of the present study was to examine the relationship between pain acceptance and its impact on function and symptoms in fibromyalgia with both a cross-sectional and longitudinal design. Methods Three hundred and sixty five participants aged 22-70 with fibromyalgia were recruited from the Norwegian Fibromyalgia Association (NFA). They filled out a questionnaire containing the Fibromyalgia Impact Questionnaire (FIQ), measurement of function and symptoms, and Chronic Pain Acceptance Questionnaire (CPAQ), measurement of pain acceptance, in addition to sociodemographic and clinical variables such as degree of fibromyalgia, depression and pain duration (T1 measures). One year after, 87 of the participants filled out the FIQ and clinical measures once again (T2 measures). Unadjusted and adjusted linear regression analyses were performed both for cross-sectional measures at T1 and for longitudinal measures from T1 to T2, with FIQ score as the outcome variable and CPAQ score at T1 as one of the main independent variables. Results Higher CPAQ score was significantly associated with a lower FIQ score at T1, also when adjusting for age, education, work, depression and Fibromyalgianess Score (p<0.01). Lower FIQ score indicate less impact of fibromyalgia on functioning. In addition, two adjusted linear regression models found higher pain acceptance (CPAQ score) at T1 to be associated with lower negative impact of fibromyalgia on function and symptoms (FIQ score) at T2 (p<0.01). Conclusions Higher pain acceptance is associated with better functional level and less symptoms in fibromyalgia, both cross-sectionally and when measurements are separated in time. Further research should include experimental studies with acceptance-based interventions for this patient group.
Learn More >Women of childbearing age experience the highest prevalence of irritable bowel syndrome (IBS), yet little is known about their psychosocial and parenting needs, which may influence their children's experience of future gastrointestinal or pain-related conditions. The aims of this study were to conduct qualitative interviews to understand the psychosocial and parenting needs of mothers with IBS who have young school-age children, and to assess mothers' potential interest in and acceptability of a preventive parenting intervention program. Ten mothers with IBS who have young (age 5-10), healthy children were interviewed. Interviews were coded with thematic analysis and three themes were identified: (1) Guilt about how IBS impacts children, (2) Worry that children will develop IBS, and (3) Already on high alert for children's health. All mothers expressed interest in an Internet-based preventive intervention and identified tools and strategies they would want included. Results demonstrate that mothers experience guilt about how IBS has impacted their children in their daily lives, concern that they need to pay attention to children's early signs and symptoms that could indicate gastrointestinal problems, and worry about children developing IBS in the future-suggesting that a preventive intervention may address important concerns for this population.
Learn More >Neuropathic pain, which results from impairment of the somatosensory system, has affected about 8% population around the world and leads to considerable burdens for patients and world health care system. However, its underlying mechanisms remain poorly understood. In this study, we hypothesized that miR-24-3p was involved in the progression of neuropathic pain in CCI rat models. By measuring miR-24-3p expression in CCI rats, we found that miR-24-3p expression was increased in CCI rats, suggesting miR-24-3p might participate in neuropathic pain progression. Next, by conducting a serial in vitro and vivo experiments, we found that miR-24-3p regulated the Wnt5a/β-Catenin Signaling levels to promote neuropathic pain progression via targeting LPAR3 in CCI rats. Furthermore, we explored the upstream regulator of miR-24-3p by conducting bioinformatics analysis, we found that circular RNA cZRANB1 might sponge to miR-24-3p. Then we applied biotinylated RNA pull-down and luciferase reporter assays to assess the association between cZRANB1 and miR-24-3p. It was found that cZRANB1 mediated LPAR3 expression via sponging miR-24-3p. Collectively, our study suggests that cZRNAB1 regulated Wnt5a/β-Catenin Signaling expression via miR-24-3p/LPAR3 axis in CCI rat models.
Learn More >An accelerating basic science literature is providing key insights into the mechanisms by which spinal neuropeptide Y (NPY) inhibits chronic pain. A key target of pain inhibition is the G-coupled neuropeptide Y1 receptor (Y1). Y1 is located in key sites of pain transmission, including the peptidergic subpopulation of primary afferent neurons and a dense subpopulation of small, excitatory, glutamatergic/somatostatinergic interneurons (Y1-INs) that are densely expressed in the dorsal horn, particularly in superficial lamina I-II. Selective ablation of spinal Y1-INs with an NPY-conjugated saporin neurotoxin attenuates the development of peripheral nerve injury-induced mechanical and cold hypersensitivity. Conversely, conditional knockdown of NPY expression or intrathecal administration of Y1 antagonists reinstates hypersensitivity in models of chronic latent pain sensitization. These and other results indicate that spinal NPY release and the consequent inhibition of pain facilitatory Y1-INs represent an important mechanism of endogenous analgesia. This mechanism can be mimicked with exogenous pharmacological approaches (e.g. intrathecal administration of Y1 agonists) to inhibit mechanical and thermal hypersensitivity and spinal neuron activity in rodent models of neuropathic, inflammatory, and postoperative pain. Pharmacological activation of Y1 also inhibits mechanical- and histamine-induced itch. These immunohistochemical, pharmacological, and cell type-directed lesioning data, in combination with recent transcriptomic findings, point to Y1-INs as a promising therapeutic target for the development of spinally directed NPY-Y1 agonists to treat both chronic pain and itch.
Learn More >There is increasing evidence that the toll-like receptor 4 (TLR4) signaling pathway contribute to development of hyperalgesia in the trigeminal system. The aim of the present study was to investigate the role of TLR4 in the trigeminal ganglion (TG) in facial hyperalgesia induced by injection of Lipopolysaccharide (LPS) or intraoral mucosal incision, which is an orofacial postoperative pain model, in male Wistar rats. The TLR4 antagonist (LPS-RS, 20 µg/10 µL) was administrated 30 min before LPS injection into the TG (10 µg/10 µL) or oral mucosa (10 µg/50 µL). In the postoperative pain model, rats were treated with LPS-RS (20 µg/10 µL) into the TG for three consecutive days after the incision. Facial heat and mechanical hyperalgesia were assessed hourly after LPS injection or intraoral incision. In addition, expression of NFκB was assessed in the TG on day 3 after intraoral incision. Our results showed that blockade of TLR4 in the TG attenuated facial heat and mechanical hyperalgesia induced by LPS or by mucosal incision, and that both conditions are associated to increase of phosphorylated NFκB in the TG. In conclusion, the present study suggests that activation of TLR4-NFκB signaling pathway in the TG contributes to the development of facial heat and mechanical hyperalgesia and may contribute to pain in inflammatory oral conditions.
Learn More >This systematic review and meta-analysis examined the effectiveness of multidisciplinary based rehabilitation (MBR) in comparison to active physical interventions for adults with chronic pain.
Learn More >Decreased dopaminergic activity and increased kappa opioid activity in the mesolimbic system underlie the negative emotional states related to chronic pain. However, it is not known whether these changes are just consequence of chronic pain or contribute to the sensorial changes associated with chronic pain. In this study, we asked whether the mesolimbic dopamine and kappa opioid systems contribute to the development and maintenance of chronic hyperalgesia, one of the most common sensorial changes related to chronic pain. The lesion of the dopaminergic cells of the ventral tegmental area prevented the transition from acute to chronic hyperalgesia when performed in pain-free rats, but did not affect the maintenance of chronic hyperalgesia, when performed in chronic pain in rats. As hyperalgesia becomes chronic, the dopamine levels in the nucleus accumbens decrease. The blockade of the kappa opioid receptors in the nucleus accumbens both prevented and reversed the development of chronic hyperalgesia, but did not affect its maintenance. Complementarily, the pharmacological activation of the kappa opioid receptors in the nucleus accumbens facilitated the transition from acute to chronic hyperalgesia. None of these interventions affected acute hyperalgesia. These findings suggest that the mesolimbic dopamine and kappa opioid systems specifically drive the pain chronification process, without affecting acute pain or the maintenance of chronic pain.
Learn More >Neuroscientific research on pleasant touch has focused on the C-tactile pathway for gentle stroking and has successfully explained how these sensory fibers transmit information about affective social touch to the brain and induce sensations of pleasantness. The C-tactile social/affective touch hypothesis even proposes that C-tactile fibers form a privileged pathway underlying social touch. However, deep pressure is a type of touch commonly considered pleasant and calming, occurring in hugs, cuddling, and massage. In this paper we introduce a paradigm for studying pleasant deep pressure and propose that it constitutes another important form of social touch. We describe development of the oscillating compression sleeve (OCS) as one approach to administering deep pressure and demonstrate that this touch is perceived as pleasant and calming. Further, we show that deep pressure can be imaged with functional magnetic resonance imaging (MRI) using the air-pressure-driven OCS and that deep pressure activates brain regions highly similar to those that respond to C-tactile stroking, as well as regions not activated by stroking. We propose that deep pressure constitutes another social touch pathway of evolutionary importance signaling the close proximity of conspecifics.
Learn More >This study aimed to evaluate whether the development and/or maintenance of chronic-latent muscle hyperalgesia is modulated by P2X3 receptors. We also evaluate the expression of P2X3 receptors and PKCε of dorsal root ganglions during these processes. A mouse model of chronic-latent muscle hyperalgesia, induced by carrageenan and evidenced by PGE, was used. Mechanical muscle hyperalgesia was measured by Randall-Selitto analgesimeter. The involvement of P2X3 receptors was analyzed by using the selective P2X3 receptors antagonist A-317491 by intramuscular or intrathecal injections. Expression of P2X3 and PKCε in dorsal root ganglion (L4-S1) were evaluated by Western blotting. Intrathecal blockade of P2X3 receptors previously to carrageenan prevented the development and maintenance of acute and chronic-latent muscle hyperalgesia, while intramuscular blockade of P2X3 receptors previously to carrageenan only reduced the acute muscle hyperalgesia and had no effect on chronic-latent muscle hyperalgesia. Intrathecal, but not intramuscular, blockade of P2X3 receptors immediately before PGE, in animals previously sensitized by carrageenan, reversed the chronic-latent muscle hyperalgesia. There was an increase in total and phosphorylated PKCε 48 h after the beginning of acute muscle hyperalgesia, and in P2X3 receptors at the period of chronic muscle hyperalgesia. P2X3 receptors expressed on spinal cord dorsal horn contribute to transition from acute to chronic muscle pain. We also suggest an interaction of PKCε and P2X3 receptors in this process. Therefore, we point out P2X3 receptors of the spinal cord dorsal horn as a pharmacological target to prevent the development or reverse the chronic muscle pain conditions.
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