Pain
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Pain-related social support has been shown to be directly associated with pain-related disability, depending on whether it promotes functional autonomy or dependence. However, previous studies mostly relied on cross-sectional methods, precluding conclusions on the temporal relationship between pain-related social support and disability. Also, research on the behavioral and psychological processes that account for such a relationship is scarce. ⋯ Moderated mediation analyses showed that formal social support for functional dependence (T1) predicted an increase in pain-related disability (T3), that was mediated by self-reported physical functioning (T2) and by pain-related self-efficacy (T2) at short to moderate pain duration and at low to moderate pain intensity, but not at higher levels. Findings emphasized that social support for functional dependence is a risk factor for pain-related disability and uncovered the "why" and "when" of this relationship. Implications for the design of social support interventions aiming at promoting older adults' healthy aging despite chronic pain are drawn.
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Fibromyalgia (FM) tends to coexist with gastroesophageal reflux disease (GERD). This retrospective cohort study was conducted to determine the bidirectional association between FM and GERD, using a nationwide database, the National Health Insurance of Taiwan. We established 2 study arms, including 35,117 patients with FM in arm 1 and 34,630 patients with GERD in arm 2, newly diagnosed between 2000 and 2010. ⋯ The GERD cohort ultimately had a 1.5-fold higher incidence of FM than the non-GERD cohort (5.76 vs 3.96 per 1000 person-years), with an aHR of 1.44 (95% CI = 1.29-1.60). The present study suggests a bidirectional relationship between FM and GERD. There is a greater risk of developing GERD for patients with FM than developing FM for patients with GERD.
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Pain is known to interrupt attentional performance. Such interference effects seem to occur preferentially for tasks that are complex and/or difficult. However, few studies have directly manipulated memory load in the context of pain interference to test this view. ⋯ These results suggest that while cognitive load may influence the interruptive effect of pain on attention, this effect may be selective. Because pain affected the high-load version of the n-back task but did not interrupt performance on attentional switching or dual-task paradigms, this means that our findings did not completely support our hypotheses. Future research should explore further the parameters and conditions under which pain-related interference occurs.
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The dynamics of noxious sensation shapes pain perception, yet the memory of the temporal dimension of pain remains almost completely unexplored. Here, brain activity during the memory of pain duration was contrasted with that associated with the memory of pain intensity using functional magnetic resonance imaging and a delayed reproduction task. Participants encoded, maintained during a short delay, and reproduced (1) the "duration" of pain (ie, onset-to-offset), (2) the "dynamics" of pain (ie, evolution of pain over time), or (3) the intensity of pain (ie, control with no explicit temporal processing required). ⋯ In contrast, the memory delay of the dynamic task involved the bilateral supplementary motor area and the frontoparietal attentional network. Although SI, SII, and insula may contribute to the memory trace of pain sensation, other areas less commonly reported in pain studies are associated with time processing and may therefore contribute to the processing of temporal aspects of pain. Results further suggest a differential role of core timing regions of the brain depending on specific task instructions and attentional allocations to the single dimension of time, as compared to the joint processing of both time and intensity.
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The magnitude of antinociception elicited by intrathecal endomorphin 2 (EM2), an endogenous mu-opioid receptor (MOR) ligand, varies across the rat estrous cycle. We now report that phasic changes in analgesic responsiveness to spinal EM2 result from plastic interactions within a novel membrane-bound oligomer containing estrogen receptors (mERs), aromatase (aka estrogen synthase), metabotropic glutamate receptor 1 (mGluR1), and MOR. During diestrus, spinal mERs, activated by locally synthesized estrogens, act with mGluR1 to suppress spinal EM2/MOR antinociception. ⋯ Finally, spinal neurons were observed not only to coexpress MOR, mERα, aromatase, and mGluR1 but also be apposed by EM2 varicosities. This suggests that modulation of spinal analgesic responsiveness to exogenous EM2 likely reflects changes in its endogenous analgesic activity. Analogous suppression of spinal EM2 antinociception in women (eg, around menses, comparable with diestrus in rats) as well as the (pathological) inability to transition out of that suppressed state at other menstrual cycle stages could underlie, at least in part, the much greater prevalence and severity of chronic pain in women than men.