Pain
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Sex differences in pain become apparent during puberty. However, the influence of key pubertal characteristics and pubertal hormones on pain is largely unknown. We examined the prospective associations between self-reported and hormone-indicated pubertal characteristics and pain incidence and severity in 10- to 11-year-old pain-free youth in the Adolescent Brain Cognitive Development (ABCD) Study over 1 year. ⋯ In boys, higher PDS item variance was associated with greater pain incidence (RR = 1.11, 95% CI, 1.03-1.20) and interference (beta = 0.40, 95% CI, 0.03-0.76); higher PDS overall and gonadal scores were associated with higher pain intensity ( P s < 0.05). Associations with hormones were seen in boys only, with each 10-fold higher testosterone levels associated with a 40% lower risk of pain incidence (95% CI, -55% to -22%) and 1.30-point lower (95% CI, -2.12 to -0.48) pain intensity, and higher DHEA levels were associated with lower pain intensity ( P = 0.020). Relationships between pubertal development and pain in peripubertal adolescents are sex specific and puberty measurement specific and warrant further investigation.
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Social support has been shown to reduce pain ratings and physiological responses to acute pain stimuli. Furthermore, this relationship is moderated by adult attachment styles. However, these effects have not been characterized in experimentally induced symptoms of chronic pain, such as secondary hyperalgesia (SH) which is characterized by an increased sensitivity of the skin surrounding an injury. ⋯ Attachment styles did not moderate this effect of social support on the area width. Increasing attachment avoidance was associated with both a smaller width of hyperalgesia and a smaller increase in the sensitivity on the stimulated arm. For the first time, we show that social support can attenuate the development of secondary hyperalgesia and that attachment avoidance may be associated with an attenuated development of secondary hyperalgesia.
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Pain associated with bone cancer remains poorly managed, and chemotherapeutic drugs used to treat cancer usually increase pain. The discovery of dual-acting drugs that reduce cancer and produce analgesia is an optimal approach. The mechanisms underlying bone cancer pain involve interactions between cancer cells and nociceptive neurons. ⋯ Inhibition of ATX or blockade of LPAR attenuated cancer exosome-evoked hypersensitivity in an ATX-LPA-LPAR-dependent manner. Parallel in vitro studies revealed the involvement of ATX-LPA-LPAR signaling in direct sensitization of dorsal root ganglion neurons by cancer exosomes. Thus, our study identified a cancer exosome-mediated pathway, which may represent a therapeutic target for treating tumor growth and pain in patients with bone cancer.
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Uncertainty pervades low back pain (LBP). This study aimed to explore individuals' experiences of navigating uncertainty when seeking care for their LBP, with a view to better understanding the contexts in which they experience uncertainty and gaining insight into how uncertainty may be better navigated during clinical encounters. We conducted 15 semistructured interviews with people who have experienced LBP. ⋯ Suggestions included making time to (actively) listen to, and acknowledge, patients' concerns; asking open-ended questions; being honest about uncertainty; creating management plans and returning to them; challenging assumptions; remaining curious about patients' context; and providing guidance on how to manage LBP rather than simply giving certainty that symptoms will worsen, lessen, or continue. These findings indicate that many of the uncertainties individuals with LBP experience are intertwined with relational aspects of their interactions with clinicians. Clinicians therefore may need to consider these broader and relational aspects of care when navigating uncertainty with people who experience LBP, bringing attention to the importance of drawing from knowledge produced outside of the usual hierarchy of evidence (eg, systematic reviews and randomised controlled trials).