Pain
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There is wide variation in population-level pain prevalence estimates in studies of survey data around the world. The role of country-level social, economic, and political contextual factors in explaining this variation has not been adequately examined. We estimated the prevalence of unspecified pain in adults aged 25+ years across 52 countries using data from the World Health Survey 2002 to 2004. ⋯ The model including Gender Inequality Index explained the most cross-country variance. However, even when accounting for country-level variables, some variation in pain prevalence remains, suggesting a complex interaction between personal, local, economic, and political impacts, as well as inherent differences in language, interpretations of health, and other difficult to assess cultural idiosyncrasies. The results give new insight into the high prevalence of pain around the world and its demonstrated association with macrofactors, particularly income and gender inequalities, providing justification for regarding pain as a global health priority.
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Sex differences in chronic pain are well established with documented predominance in women. This study assessed relationships between age at menarche and chronic pain, site-specific chronic pain, pain characteristics, and chronic widespread pain (CWP). We used data from the Tromsø Study conducted in 2007 to 2008 and 2015 to 2016 (Tromsø 6 and Tromsø 7 waves) including participants aged 30 to 99 years. ⋯ Age at menarche was significantly associated with chronic pain in the neck, abdomen, and both arms, and CWP. Of the 4 pain characteristics, pain duration was statistically significant. We conclude that early menarche is an independent risk factor for pain across a broad spectrum of pain outcomes.
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Intrathecal application of contulakin-G (CGX), a conotoxin peptide and a neurotensin analogue, has been demonstrated to be safe and potentially analgesic in humans. However, the mechanism of action for CGX analgesia is unknown. We hypothesized that spinal application of CGX produces antinociception through activation of the presynaptic neurotensin receptor (NTSR)2. ⋯ Anatomical studies demonstrated coexpression of NTSR2 and Cav2.3 in dorsal root ganglion neurons. Finally, synaptic fractionation and slice electrophysiology recordings confirmed a predominantly presynaptic effect. Together, these data reveal a nonopioid pathway engaged by a human-tested drug to produce antinociception.
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The experience of pain and pain behaviors is not only determined by physiological but also psychosocial factors. In this context, the learning history of the individual and specifically operant reinforcement related to spouse responses might play an important role. We investigated the effect of a solicitous and habitually pain-reinforcing spouse for the processing of pain in patients with chronic pain. ⋯ This was specific for the painful stimulation at the back and occurred only in the presence but not the absence of the spouse. Pain ratings of intensity and unpleasantness were also higher in the patients with solicitous spouses when the spouse was present during painful stimulation. These data suggest that significant other responses indicative of operant reinforcement may have a direct effect on the cerebral processing of pain and related pain perception.
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High-molecular-weight hyaluronan (HMWH) is an agonist at cluster of differentiation (CD)44, the cognate hyaluronan receptor, on nociceptors, where it acts to induce antihyperalgesia in preclinical models of inflammatory and neuropathic pain. In the present experiments, we studied the CD44 second messengers that mediate HMWH-induced attenuation of pain associated with oxaliplatin and paclitaxel chemotherapy-induced peripheral neuropathy (CIPN). ⋯ Intradermal administration of inhibitors of CD44 second messengers, RhoA (member of the Rho family of GTPases), phospholipase C, and phosphatidylinositol (PI) 3-kinase gamma (PI3Kγ), attenuated HMWH-induced antihyperalgesia as does intrathecal administration of an ODN antisense to PI3Kγ. Our results demonstrated that HMWH induced antihyperalgesia in CIPN, mediated by its action at CD44 and downstream signaling by RhoA, phospholipase C, and PI3Kγ.