Pain
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Perception of emotional stimuli alters the perception of pain. Although facial expressions are powerful emotional cues - the expression of pain especially plays a crucial role for the experience and communication of pain - research on their influence on pain perception is scarce. In addition, the opposite effect of pain on the processing of emotion has been elucidated even less. ⋯ Most important, painful thermal stimuli increased the arousal of simultaneously presented pain expressions, and in turn, pain expressions resulted in higher pain ratings compared to all other facial expressions. These findings demonstrate that the modulation of pain and emotion is bidirectional with pain faces being mostly prone to having mutual influences, and support the view of interconnections between pain and emotion. Furthermore, the special relevance of pain faces for the processing of pain was demonstrated.
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The aim of this study was to investigate whether diagnostic tests for musculoskeletal pain in the orofacial region [temporomandibular disorder (TMD) pain] are influenced by the presence of comorbid conditions, and to determine whether this influence decreases when the presence of "familiar pain" is used as outcome measure. In total, 117 patients (35 men, 82 women; 75 TMD-pain patients, 42 pain-free patients; mean age ± SD = 42.94 ± 14.17 years) were examined with palpation tests and dynamic/static tests. After each test, they were asked whether any pain was provoked and whether this pain response was familiar or not. ⋯ Pain on dynamic/static tests was associated with the primary predictor (P < 0.001, OR = 11.08), but also with somatization (P = 0.037, OR = 4.5), whereas familiar pain on dynamic/static tests was only associated with the primary predictor (P < 0.001, OR = 32.37). In conclusion, diagnostic tests are negatively influenced by the presence of comorbidity. This influence decreases when the presence of familiar pain is used as outcome measure.
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Although previous research has examined the relationships between caregiver proximal soothing and infant pain, there is a paucity of work taking infant age into account, despite the steep developmental trajectory that occurs across the infancy period. Moreover, no studies have differentially examined the relationships between caregiver proximal soothing and initial infant pain reactivity and pain regulation. This study examined how much variance in pain reactivity and pain regulation was accounted for by caregiver proximal soothing at 4 routine immunizations (2, 4, 6, and 12 months) across the first year of life, controlling for preneedle distress. ⋯ Preneedle distress and pain reactivity accounted for the largest amount of variance in pain regulation, with this increasing after 2 months. It was concluded that within each immunization appointment across the first year of life, earlier infant pain behaviour is a stronger predictor of subsequent infant pain behaviour than caregiver proximal soothing. Given the longer-term benefits that have been demonstrated for proximal soothing during distressing contexts, caregivers are still encouraged to use proximal soothing during infant immunizations.
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Peripheral neuropathy is a common adverse effect of paclitaxel treatment. To analyze the contribution of transient receptor potential vanilloid 1 (TRPV1) in the development of paclitaxel-induced thermal hyperalgesia, TRPV1 expression in the rat dorsal root ganglion (DRG) was analyzed after paclitaxel treatment. Behavioral assessment using the tail-flick test showed that intraperitoneal administration of 2 and 4 mg/kg paclitaxel induced thermal hyperalgesia after days 7, 14, and 21. ⋯ TRPV1 immunostaining was up-regulated in paw skin day 14 after paclitaxel treatment. Moreover, in situ hybridization histochemistry revealed that most of the TRPV1 mRNA-labeled neurons in the DRG were small or medium in size. These results suggest that paclitaxel treatment increases TRPV1 expression in DRG neurons and may contribute to functional peripheral neuropathic pain.
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Bradykinin (BK) is an inflammatory mediator that can evoke oedema and vasodilatation, and is a potent algogen signalling via the B1 and B2 G-protein coupled receptors. In naïve skin, BK is effective via constitutively expressed B2 receptors (B2R), while B1 receptors (B1R) are purported to be upregulated by inflammation. The aim of this investigation was to optimise BK delivery to investigate the algesic effects of BK and how these are modulated by inflammation. ⋯ We have optimised a versatile experimental model by which BK and its analogues can be administered to human skin. We have found that there is an early phase of BK-induced pain which partly depends on the release of inflammatory mediators by MCs; however, subsequent hyperalgesia is not dependent on MC degranulation. In naïve skin, B2R signaling predominates, however, cutaneous inflammation results in enhanced B1R responses.