The journal of pain : official journal of the American Pain Society
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Musculoskeletal pain is associated with multiple adaptions in movement control. This study aimed to determine whether changes in movement control acquired during acute pain are maintained over days of pain exposure. On day 0, the extensor carpi radialis brevis muscle of healthy participants was injected with nerve growth factor (NGF) to induce persistent movement-evoked pain (n = 13) or isotonic saline as a control (n = 13). On day 2, short-lasting pain was induced by injection of hypertonic saline into extensor carpi radialis brevis muscles of all participants. Three-dimensional force components were recorded during submaximal isometric wrist extensions on day 0, day 4, and before, during, and after saline-induced pain on day 2. Standard deviation (variation of task-related force) and total excursion of center of pressure (variation of force direction) were assessed. Maximal movement-evoked pain was 3.3 ± .4 (0-10 numeric scale) in the NGF-group on day 2 whereas maximum saline-induced pain was 6.8 ± .3 cm (10-cm visual analog scale). The difference in centroid position of force direction relative to day 0 was greater in the NGF group than in the control group (P < .05) on day 2 (before saline-induced pain) and day 4, reflecting changes in tangential force direction used to achieve the task. During saline-induced pain in both groups, tangential and task-related force variation was greater than before and after saline-induced pain (P < .05). ⋯ Persistent movement-evoked pain changes force direction from the pain-free direction. Acute pain leads to increased variation in force direction irrespective of persistent movement-evoked pain preceding the acutely painful event. These differences provide novel insight into the search for and consolidation of new motor strategies in the presence of pain.
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Previous studies have provided evidence for pain-alleviating effects of segmental tactile stimulation, yet the effect of social touch and its underlying mechanism is still unexplored. Considering that the soma affects the way we think, feel, and interact with others, it has been proposed that touch may communicate emotions, including empathy, interacting with the identity of the toucher. Thus, the goal of the current study was to examine the analgesic effects of social touch, and to test the moderating role of the toucher's empathy in analgesia using an ecological paradigm. Tonic heat stimuli were administered to women. Concurrently, their partners either watched or touched their hands, a stranger touched their hands, or no one interacted with them. The results revealed diminished levels of pain during partners' touch compared with all other control conditions. Furthermore, taking into account the dyadic interaction, only during the touch condition we found 1) a significant relationship between the partners' pain ratings, and 2) a significant negative relationship between the male touchers' empathy and the pain experience of their female partners. The findings highlight the powerful analgesic effect of social touch and suggest that empathy between romantic partners may explain the pain-alleviating effects of social touch. ⋯ Pain research mostly concentrates on different factors around a single pain target, without taking into account various social interactions with the observers. Our findings support the idea that pain perception models should be extended, taking into account some psychological characteristics of observers. Our conclusions are on the basis of advanced statistical methods.
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Macrophages play a role in innate immunity within the body, are located in muscle tissue, and can release inflammatory cytokines that sensitize local nociceptors. In this study we investigate the role of resident macrophages in the noninflammatory muscle pain model induced by 2 pH 4.0 preservative-free sterile saline (pH 4.0) injections 5 days apart in the gastrocnemius muscle. We showed that injecting 2 pH 4.0 injections into the gastrocnemius muscle increased the number of local muscle macrophages, and depleting muscle macrophages with clodronate liposomes before acid injections attenuated the hyperalgesia produced by this model. To further examine the contribution of local macrophages to this hyperalgesia, we injected mice intramuscularly with C34, a toll-like receptor 4 (TLR4) antagonist. When given before the first pH 4.0 injection, C34 attenuated the muscle and tactile hyperalgesia produced by the model. However, when given before the second injection C34 had no effect on the development of hyperalgesia. Then to test whether activation of local macrophages sensitizes nociceptors to normally non-nociceptive stimuli we replaced either the first or second acid injection with the immune cell activator lipopolysaccharide, or the inflammatory cytokine interleukin (IL)-6. Injecting LPS or IL-6 instead of the either the first or second pH 4.0 injection resulted in a dose-dependent increase in paw withdrawal responses and decrease in muscle withdrawal thresholds. The highest doses of LPS and IL-6 resulted in development of hyperalgesia bilaterally. The present study showed that resident macrophages in muscle are key to development of chronic muscle pain. ⋯ This article presents evidence for the role of macrophages in the development of chronic muscle pain using a mouse model. These data suggest that macrophages could be a potential therapeutic target to prevent transition of acute to chronic muscle pain particularly in tissue acidosis conditions.