Pain
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Sick leave due to low back pain (LBP-SL) is costly and compromises workforce productivity. The fear-avoidance model asserts that maladaptive pain-related cognitions lead to avoidance and disuse, which can perpetuate ongoing pain. Staying home from work is an avoidant behavior, and hence pain-related psychological features may help explain LBP-SL. ⋯ Administrators and managers were less likely to report LBP-SL (OR=0.44, 95% CI 0.27-0.71), and age had a protective effect in individuals in a married or de facto relationship (OR=0.97, 95% CI 0.95-0.98). In summary, fear of movement, passive coping, frequent manual handling, and severe or radiating pain increase the likelihood of LBP-SL. Gender-specific responses to pain radiation and fear of movement are evident.
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Epinephrine (EPI) contributes to hyperalgesia in inflammatory and stress conditions. EPI signals via adrenoceptors, which are regulated by G protein-coupled receptor kinase 2 (GRK2). We previously reported that GRK2 is decreased in nociceptors during chronic inflammation. ⋯ In terms of EPI signalling pathways, the protein kinase A (PKA) inhibitor H-89 inhibited EPI-induced mechanical hyperalgesia in wild-type mice, whereas H-89 had no effect in mice with low GRK2 in sensory neurons (SNS-GRK2(+/-) mice). Conversely, intraplantar injection of the protein kinase Cε PKCε inhibitor TAT-PKC(εv1-2) inhibited hyperalgesia in sensory neuron specific (SNS)-GRK2(+/-) mice and not in wild-type mice. These results indicate that low GRK2 in primary sensory neurons switches EPI-induced signalling from a protein kinase A-dependent toward a PKCε-dependent pathway that ultimately mediates prolonged EPI-induced hyperalgesia.
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Electrical high-frequency stimulation (HFS) of skin afferents elicits long-term potentiation (LTP)-like hyperalgesia in humans. Time courses were evaluated in the facilitating (homotopic) or facilitated (heterotopic) pathways to delineate the relative contributions of early or late LTP-like pain plasticity. HFS in healthy subjects (n=55) elicited highly significant pain increases to electrical stimuli via the conditioning electrode (to 145% of control, homotopic pain LTP) and to pinprick stimuli in adjacent skin (to 190% of control, secondary hyperalgesia). ⋯ Dynamic mechanical allodynia (only present in 16 of 55 subjects) lasted for a shorter time than secondary hyperalgesia. Three different readouts of nociceptive central sensitization suggest that brief intense nociceptive input elicits early LTP1 of pain sensation (based on posttranslational modifications), but susceptible subjects may already develop longer-lasting late LTP2 (based on transcriptional modifications). These findings support the hypothesis that LTP may contribute to the development of persistent pain disorders.
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The shared-representation model of empathy suggests that vicarious pain processes rely partly on the activation of brain systems underlying self-pain in the observer. Here, we tested the hypothesis that self-pain may be facilitated by the vicarious priming of neural systems underlying pain perception. Pictures illustrating painful agents applied to the hand or the foot (sensory information), or painful facial expressions (emotional information) were shown to 43 participants to test the effects of vicarious pain on the nociceptive flexion reflex (NFR) of the lower limb and pain intensity and unpleasantness produced by transcutaneous electrical stimulation applied over the sural nerve. ⋯ In contrast, the change in perceived shock-pain intensity was negatively correlated with empathic traits. This dissociation implies that low-level vicarious priming processes underlying pain facilitation may be downregulated at higher pain-processing stages in individuals reporting higher levels of empathy. We speculate that this process contributes to reducing self-other assimilation and is necessary to adopt higher-order empathic responses and altruistic behaviors.