European journal of pain : EJP
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Children of chronic pain patients run greater risk for developing chronic pain themselves. Exposure to chronic pain of the parent might install cognitive (e.g., pain catastrophizing, interpretation and attentional bias) and affective (e.g., pain anxiety) vulnerability which increase the risk for the development of chronic pain complaints in offspring. This study examines whether pain-free offspring of parents with chronic pain complaints make more health-threatening interpretations and display a stronger pain-related attentional bias compared to the offspring of pain-free parents. We furthermore examined differences between both groups on pain catastrophizing, pain anxiety and somatic symptoms and explored the relations between parental pain catastrophizing and aforementioned pain vulnerability measures in offspring. ⋯ Parental chronic pain may install psychological vulnerability for developing chronic pain and associated complaints in offspring. This study did not show differences in pain-directed attentional and interpretation bias between offspring of parents with chronic pain complaints and offspring of pain-free parents. Further (longitudinal) research is needed to elucidate the precise role of parental pain factors in the development of pain-related vulnerability in offspring of chronic pain parents, thereby identifying important targets for the prevention and early intervention of chronic pain.
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Observational Study
Exercise-induced hypoalgesia is present in people with Parkinson's disease: Two observational cross-sectional studies.
Exercise is prescribed for people with Parkinson's disease to address motor and non-motor impairments, including pain. Exercise-induced hypoalgesia (i.e., an immediate reduction in pain sensitivity following exercise) is reported in the general population; however, the immediate response of pain sensitivity to exercise in people with Parkinson's disease is unknown. The purpose of this study was to investigate if exercise-induced hypoalgesia is present following isometric and aerobic exercise in people with Parkinson's disease, and if so, if it varies with the dose of aerobic exercise. ⋯ Isometric and aerobic exercise reduces pain sensitivity in people with Parkinson's disease. As exercise is important for people with Parkinson's disease, these results provide assurance that people with Parkinson's disease and pain can exercise without an immediate increase in pain sensitivity. The reduction in pain sensitivity with both modes and with low and moderate intensities of aerobic exercise suggests that people with Parkinson's disease can safely choose the mode and intensity of exercise that best suits their needs.
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This study presents an adaptation of the Brief Pain Inventory (BPI) extending its use in clinical/epidemiological contexts and the evaluation of the properties of BPI (short form) in a sample of Brazilian adults. ⋯ This study presents evidence related to the validity of applying the Brief Pain Inventory (BPI) in adults with and without pain considering the present pain or memory of pain, enabling the clinician to collect additional information that may be relevant to the clinical management of pain.
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Experimental models of pain in humans are crucial for understanding pain mechanisms. The most often used muscle pain models involve the injection of algesic substances, such as hypertonic saline solution or nerve growth factor or the induction of delayed onset muscle soreness (DOMS) by an unaccustomed exercise routine. However, these models are either invasive or take substantial time to develop, and the elicited level of pain/soreness is difficult to control. To overcome these shortcomings, we propose to elicit muscle pain by a localized application of short-wave diathermy (SWD). ⋯ This study presents an experimental model to elicit sustained muscle pain based on short-wave diathermy. The main advantages of the model are its noninvasiveness, the possibility to control stimulation parameters in a reliable way and the convenience of the time frame in which pain and hyperalgesia are developed.
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Morphine is an effective analgesic for the treatment of severe pain, but it can cause itching in patients. In the present study, we examined the possible involvement of interleukin-31 (IL-31) receptor A (IL-31RA) on the morphine-induced itching and antinociception in mice. ⋯ Here, we demonstrate a possible common mediator of itching and antinociception of morphine, interleukin-31 (IL-31) receptor A (IL-31RA). IL-31RA may be a noteworthy target for considering the novel mechanism of itch and pain signalling affected by morphine.