Browse by Audience
Pain is common in long-term care residents. We examined the effectiveness of interventions involving healthcare aides that aim to manage pain for these residents.
Learn More >Physical therapy practice has greatly improved in providing a biopsychosocial approach when considering persistent pain. However, the spinal cord is often overlooked as a structure with an important role in modulating nociceptive information.
Learn More >Despite the popularity and affordances of social media groups for people with chronic conditions, there have been few controlled tests of the effects of these groups. This randomized controlled superiority trial examined the effects of Facebook groups on pain-related outcomes and tested whether a professional-led group leads to greater effects than a support group alone. We randomly assigned 119 adults with chronic pain to one of two Facebook group conditions: a standard condition (n = 60) in which participants were instructed to offer mutual support, or a professional-led condition (n = 59) in which the investigators disseminated empirically-supported, socially-oriented psychological interventions. Four groups were run (2 standard, 2 professional-led), each lasting 4 weeks and containing approximately 30 participants. Measures were administered at baseline, post-intervention, and 1-month follow-up. Across conditions, participants improved significantly in primary outcomes (pain severity and interference; medium-large effects) and a secondary outcome (depressive symptoms; small-medium effect), and they retained their outcomes 1 month after the groups ended. The two conditions did not differ on improvements. Overall, this study supports the use of social media groups as an additional tool to improve chronic pain-related outcomes. Our findings suggest that professional intervention may not have added value in these groups and that peer support alone may be driving improvements. Alternatively, the psychosocial intervention components used in the current study might have been ineffective, or more therapist direction may be warranted. Future research should examine when and how such guidance could enhance outcomes.
Learn More >We evaluated the association between chronic severe back pain with disability and participation, in U.S. Adults using data from the US 2019 National Health Interview Survey. In our sample of 2,925 adults (weighted n: 20,468,134) who reported having chronic severe back pain, 60% reported mobility disability, 60% had work limitations, 34% were limited for social participation and 16% had self-care limitations. Older age (65+) was associated with mobility difficulties (OR 1.99, 95% CI 1.28,6.09) and work limitation (OR 2.21, 95% CI 1.61,3.05). Lower socioeconomic status was associated with increasing odds of disability across the four categories. Being obese was only associated with mobility difficulties (OR 1.95, 95% CI 1.41,2.71), while not working in the past week was associated with difficulties in mobility (OR 3.55, 95% CI 2.64,4.75), self-care (OR 3.34, 95% CI 2.20,5.08), and social participation (OR 3.20, 95% CI 2.13,4.80). Comorbidities were highly associated with limitations in all four categories. Those deeming their ability to manage their pain ineffective were twice as likely to have limitations in self-care, social and work participation but not mobility. Identifying factors associated with disability and limitation may help target appropriate management for persons with chronic pain at high risk for disability.
Learn More >The inflammatoryresponse of centralnervoussystem (CNS) and microglial activation is important in the development of pain behaviors induced by sleep deprivation. We found that chronic sleep deprivation (CSD) aggravated pain behaviors in rats with chronic pain by upregulating expression of Toll-like receptor 4 (TLR4), NOD-like receptor pyrin domain containing 3 (NLRP3), and interleukin 1β (IL-1β), which promoted microglial activation in the brain. We also found that CSD increased numbers of Iba1 and TLR4 cells, as well as neuronal apoptosis. Inhibitors of TLR4 and NLRP3 (TAK-242 and MCC950, respectively) reduced expression levels of inflammatory factor proteins and M1-related factor mRNA, decreased microglial activation, and relieved the hyperalgesia caused by CSD. These results suggest that CSD aggravated pain behavior in rats with chronic pain through the TLR4/NLRP3/IL-1β signaling pathway, which mediates microglial activation and promotes CNS inflammation and neuronal apoptosis.
Learn More >It is well-established that a single bout of exercise can reduce pain sensitivity (i.e., exercise-induced hypoalgesia) in healthy individuals. However, exercise-induced hypoalgesia is often impaired in individuals with chronic pain. This might suggest that repeated bouts of exercise (i.e., exercise training) are needed in order to induce a reduction in pain sensitivity (i.e., training-induced hypoalgesia) among individuals with chronic pain, given that a single bout of exercise seems to be insufficient to alter pain. However, the effect of repeated bouts of exercise on pain sensitivity and its underlying mechanisms remain poorly understood. Therefore, the purpose of this review was to provide an overview of the existing literature on training-induced hypoalgesia, as well as discuss potential mechanisms of training-induced hypoalgesia and offer considerations for future research. Existing literature suggests that training interventions may induce hypoalgesic adaptations potentially driven by central nervous system and immune system factors. However, the limited number of randomized controlled trials available, along with the lack of understanding of underlying mechanisms, provides a rationale for future research.
Learn More >HIV-associated sensory neuropathies (HIV-SN) are prevalent in >50% of patients aged over 45 years many of which report moderate to severe chronic pain. Previous preclinical studies have investigated the mechanisms by which HIV-1 causes sensory neuropathies and pain-like behaviors. The aim of the present study is to delineate the role of chronic HIV-1 trans-activator of transcription protein (Tat) exposure in the development of neuropathy in mice. The temporal effects of conditional Tat expression on the development of hypersensitivity to mechanical (von Frey filaments) and thermal (heat or cold) stimuli were tested in male and female mice that transgenically expressed HIV-1 Tat in a doxycycline-inducible manner. Inducing Tat expression produced an allodynic response to mechanical or cold (but not heat) stimuli that respectively persisted for at least 23-weeks (mechanical hypersensitivity) or at least 8-weeks (cold hypersensitivity). Both allodynic states were greater in magnitude among females, compared to males, and mechanical increased hypersensitivity progressively in females over time. Acute morphine or gabapentin treatment partly attenuated allodynia in males, but not females. Irrespective of sex, Tat reduced intraepidermal nerve fiber density, the mean amplitude of sensory nerve action potentials (but not conductance), engagement in some pain-related ethological behaviors (cage-hanging and rearing), and down-regulated PPAR-α gene expression in lumbar spinal cord while upregulating TNF-α expression in dorsal root ganglion. Taken together, these data reveal fundamental sex differences in mechanical and cold hypersensitivity in response to Tat and demonstrate the intractable nature in female mice to current therapeutics. Understanding the role of Tat in these pathologies may aid the design of future therapies aimed at mitigating the peripheral sensory neuropathies that accompany neuroHIV.
Learn More >Osteoarthritis (OA) often affects the hands, knees, and hip joints, causing considerable pain and disability, and often affecting the patient's quality of life. Non-steroidal anti-inflammatory drugs (NSAIDs) are common pain relievers often applied as first line therapies for OA. However, prolonged NSAIDs application can have unwanted side effects. Given this, this study was designed to systematically evaluate the efficacy and safety of topical and oral NSAIDs for the treatment of OA.
Learn More >Cytotoxic agents synergize with immune checkpoint inhibitors and improve outcomes for patients with several cancer types. Nonetheless, a parallel increase in the incidence of dose-limiting side effects, such as peripheral neuropathy, is often observed. Here, we investigated the role of the PD-1/PD-L1 axis in the modulation of paclitaxel-induced neuropathic pain. We found that human and mouse neural tissues, including the dorsal root ganglion (DRG), expressed basal levels of PD-1 and PD-L1. During the development of paclitaxel-induced neuropathy, an increase in PD-L1 expression was observed in macrophages from the DRG. This effect depended on Toll-like receptor 4 (TLR4) activation by paclitaxel. Furthermore, PD-L1 inhibited pain behavior triggered by paclitaxel or formalin in mice, suggesting that PD-1/PD-L1 signaling attenuates peripheral neuropathy development. Consistent with this, we observed that the combined use of anti-PD-L1 plus paclitaxel increased mechanical allodynia and chronic neuropathy development induced by single agents. This effect was associated with higher expression of inflammatory markers (Tnf, Il6, and Cx3cr1) in peripheral nervous tissue. Together, these results suggest that PD-1/PD-L1 inhibitors enhance paclitaxel-induced neuropathic pain by suppressing PD-1/PD-L1 antinociceptive signaling.
Learn More >To compare the influence of age on inflammatory (bone marrow oedema. BME) and structural (fat lesions (FL), erosions and ankylosis) MRI lesions in the SIJ of patients with and without axial spondyloarthritis (axSpA).
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