Pain
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Sex differences in chronic pain are reported to emerge during adolescence, although it is unclear if this includes responses to treatment. We conducted a meta-analysis to examine whether sex differences were present on outcome variables at pre-treatment, and whether the efficacy of psychological therapies for pediatric chronic pain differs between boys and girls at post-treatment and follow-up time points. Searches were conducted, extending two existing Cochrane reviews of randomized-controlled trials examining the efficacy of psychological therapies for chronic and recurrent pain in children and adolescents. ⋯ Treatment gains were consistent across the sexes. One exception was for post-treatment disability in children with non-headache pain conditions; girls exhibited a significant effect of treatment relative to control condition (SMD= -0.50[-0.80,-0.20], p < .01), but no such effect was observed for boys (SMD= -0.08[-0.44,0.28], p = .66). Future research should examine whether mechanisms of treatment efficacy differ between boys and girls, and consider the impact of pre-treatment sex differences on response to treatment.
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Pain is one of the most challenging and stressful conditions to patients with sickle cell disease (SCD) and their clinicians. Patients with SCD start experiencing pain as early as 3 months old and continue having it throughout their lives. Although many aspects of the disease are well understood, little progress has been made in understanding and treating pain in SCD. ⋯ We further targeted CaMKIIα by siRNA knockdown. Both evoked pain and ongoing spontaneous pain were effectively attenuated in BERK mice. These findings elucidated, for the first time, an essential role of CaMKIIα as a cellular mechanism in the development and maintenance of spontaneous and evoked pain in SCD, which can potentially offer new targets for pharmacological intervention of pain in SCD.
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Withdrawal pain can be a barrier to opioid cessation. Yet, little is known about old injury site pain in this context. We conducted an exploratory mixed-methods descriptive case series using a web-based survey and in-person interviews with adults recruited from pain and addiction treatment and research settings. ⋯ Fifteen surveyed participants (44%) reported returning to opioid use because of WISP in the past. Participants developed theories about the etiology of WISP, including that the pain is the brain's way of communicating a desire for opioids. This research represents the first known documentation that previously healed, and pain-free injury sites can temporarily become painful again during opioid withdrawal, an experience which may be a barrier to opioid cessation, and a contributor to opioid reinitiation.
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For musculoskeletal complaints (MSCs) among adults, several risk factors are known, but the most important determinant is an earlier episode of MSCs. Research has shifted to younger ages, showing a high prevalence of MSCs among children and adolescents. Our purpose was to evaluate the prevalence of MSCs among those growing up from age 11 to 14 and to explore the role of several sociodemographic, growth and development, psychosocial, and lifestyle factors. ⋯ More MSCs were found among girls, those with sports injuries, those with sleeping problems, and those with daytime tiredness, although complaints at age 11 were by far the most important factor associated with MSCs at age 14 for all pain sites. This study showed that MSC is already common at an early age and that already at age 14 the factor with the strongest association is an earlier episode of MSCs. Sleeping problems and tiredness may also play a role in the early development of MSCs, either as determinant or as a consequence.
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Migraine attacks are often preceded by premonitory symptoms (PS) that may be triggered pharmacologically. We investigated the incidence of PS after administration of calcitonin gene-related peptide (CGRP) or pituitary adenylate cyclase-activating peptide-38 (PACAP38) in patients with migraine without aura (MO) who reported and did not report migraine-like attacks induced by these pharmacological triggers. In addition, we investigated the association between PS and familial predisposition for migraine. ⋯ Additionally, we found no difference in PS between patients with familial predisposition of migraine (75%) and patients with no family predisposition (56%) (P = 0.101). In conclusion, CGRP did not induce PS, whereas PACAP38 induced PS in 48% of patients. However, CGRP and PACAP38 did not induce more PS in patients who developed an attack compared with those who did not develop an attack.