European journal of pain : EJP
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Overactivity in the context of chronic pain (i.e. activity engagement that significantly exacerbates pain) is an important clinical issue that has gained empirical attention in the last decade. Current assessment concepts of overactivity tend to focus on frequency to quantify the severity of the pain behaviour. This study aimed to develop and validate a more comprehensive self-assessment, the Overactivity in Persistent Pain Assessment (OPPA). ⋯ This study deconstructs the overactivity concept and develop a corresponding assessment based on five quantifiable severity features: severity of pain exacerbation, maladaptive coping strategies used, impact on occupational performance, recovery time and frequency. Results of the psychometric evaluation indicate that this comprehensive assessment of overactivity severity features may be necessary to understand the impact of overactivity on pain severity and physical functioning from both a clinical and research perspective.
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The aim of this study was to assess clinical pain, pain sensitization and physical performances to profile patients with chronic painful knee osteoarthritis (OA) or pain after total knee arthroplasty (TKA). Examining the interactions between pain mechanisms and physical performances would enable us to investigate the underlying explanatory relationships between these parameters. ⋯ Quantitative pain profiling assessment was used to assess pain intensities and pain mechanisms. We observed associations between physical performances and temporal summation in the OA group underlining the importance of assessing motor functions and pain mechanisms in the same trial. We observed lower levels of physical performances in the TKA group compared with the OA group, suggesting that examination and rehabilitation of physical performances is essential for TKA patients with chronic pain.
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In past years, and mostly due to contextual psychological therapies, it has been argued that particular behavioural patterns may be useful in certain contexts, but not in others. The goal of this study has been to explore whether pain severity is indeed a contextual factor influencing the relationship between two controversial activity patterns, namely pacing and persistence, and functionality in people with fibromyalgia. ⋯ This manuscript shows that some activity patterns (i.e. pacing to conserve energy for valued activities) might be advisable regardless of pain levels. Conversely, some patterns might be especially recommended (i.e. pain-reduction pacing) or inadvisable (i.e. excessive and pain-contingent persistence) depending on pain levels (i.e. severe and mild pain, respectively).
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Increased bone resorption is driven by augmented osteoclast activity in pathological states of the bone, including osteoporosis, fracture and metastatic bone cancer. Pain is a frequent co-morbidity in bone pathologies and adequate pain management is necessary for symptomatic relief. Bone cancer is associated with severe skeletal pain and dysregulated bone remodelling, while increased osteoclast activity and bone pain are also observed in osteoporosis and during fracture repair. However, the effects of altered osteoclast activity and bone resorption on nociceptive processing of bone afferents remain unclear. ⋯ The role of osteoclasts in peripheral sensitization of sensory neurones is not fully understood. This study reports on the direct link between oestrogen-independent osteoclast activation and skeletal pain. Administration of exogenous receptor activator of nuclear factor kappa-B ligand (RANKL) increases bone resorption, but does not produce pro-nociceptive changes in behavioural pain thresholds. Our data demonstrates that physiologic osteoclasts are not essential for skeletal pain behaviours.
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Paclitaxel (PCX) is the first-line choice for the treatment of several types of cancer, including breast, ovarian, and lung cancers. However, patients who receive even a single dose with PCX commonly develop mechanical and cold allodynia, a symptom known as PCX-associated acute pain syndrome (P-APS). Here, we assessed possible involvement of kinin-kallikrein and renin-angiotensin systems in P-APS in mice. ⋯ Kinin-kallikrein and renin-angiotensin systems, through B1, B2 and AT2 receptors, potentiates paclitaxel-associated acute pain syndrome (P-APS) in mice. Antagonists for AT2R are potential alternatives to prevent P-APS.