European journal of pain : EJP
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Investigating possible psychosocial predictors of unexplained chronic pain in adolescents is crucial in understanding its development and prevention. A general population sample of adolescents (n = 2230) from the TRAILS cohort study was investigated longitudinally to assess the influence of maternal vulnerability, in terms of anxiety, depression and stress, and parenting stress at age 10-12 years, on the presence of chronic pain at age 12-15 years. Of these adolescents, 269 (12.9%) reported experiencing chronic pain, of which 77% reported severe chronic pain and 22% reported multiple chronic pain. ⋯ Subgroup analyses showed similar results for adolescents with severe chronic pain. Mediation analyses indicated that parenting stress mediates the effect between maternal anxiety, or stress, and chronic pain. The findings suggest that interventions to diminish maternal feelings of anxiety and stress, while in turn adjusting maternal behaviour, may prevent the development of chronic pain in adolescence.
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Pain and factors related to it constitute serious health problems in the older population. This populationbased cross-sectional study aimed to investigate whether musculoskeletal pain is associated with mobility limitation and whether the relationship between pain and mobility limitation varies according to the use of analgesics among community-dwelling older people. A total of 622 community-dwelling participants aged 75 years and older (mean age 80.4, 74% women) were interviewed about presence and severity of musculoskeletal pain. ⋯ The risk of mobility limitation was highest among those who reported severe or moderate pain (1.84; 1.13, 3.13) and among those who used analgesics (2.37; 1.37, 4.11). In conclusion, musculoskeletal pain increases the risk for mobility limitation. The present findings underline the importance of the careful assessment and pharmacological and nonpharmacological management of pain in promoting mobility in older age.
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Recent studies suggest that CNS phospholipase A(2) (PLA(2) ) isoforms play a role in nociception, but until now, direct evidence of increased brain PLA(2) activity during allodynia or hyperalgesia is lacking. The present study was carried out, using lipidomics or systems wide analyses of lipids using tandem mass spectrometry, to elucidate possible changes in rat brain lipids after inflammatory pain induced by facial carrageenan injection. The caudal medulla oblongata showed decreases in phospholipids including phosphatidylethanolamine and phosphatidylinositol species, but increases in lysophospholipids, including lysophosphatidylethanolamine, lysophosphatidylinositol and lysophosphatidylserine, indicating increased PLA(2) activity and release of arachidonic acid after facial carrageenan injection. ⋯ Increase in sPLA(2) -III mRNA expression was found in the caudal medulla of carrageenan-injected rats, although no difference in sPLA(2) -III protein expression was detected. The changes in lipids as determined by lipidomics were therefore consistent with an increase in PLA(2) enzyme activity, but no change in enzyme protein expression. Together, these findings indicate enhanced PLA(2) activity in the caudal medulla oblongata after inflammatory orofacial pain.
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Several studies have suggested that 5-HT(7) receptors are involved in nociceptive processing but the exact contribution of peripheral versus central 5-HT(7) receptors still needs to be elucidated. In the present study, the respective roles of peripheral and spinal 5-HT(7) receptors in the modulation of mechanical hypersensitivity were investigated under two different experimental pain conditions. In a first set of experiments, the selective 5-HT(7) receptor agonist, E-57431, was systemically, intrathecally or peripherally (intraplantarly) administered to rats sensitized by intraplantar injection of capsaicin. ⋯ Significant inhibition of nerve injury-induced mechanical hypersensitivity was found after intraperitoneal (10 mg/kg) as well as intrathecal (100 μg) administration of E-57431 in this chronic pain model. These studies provide evidence that, under sensitizing neurogenic/neuropathic conditions, activation of 5-HT(7) receptors exerts antinociceptive effects at the level of the spinal cord and pronociceptive effects at the periphery. The antinociceptive effect mediated by central 5-HT(7) receptors seems to predominate over the pronociceptive effect at the periphery when a selective 5-HT(7) receptor agonist is systemically administered.
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Neuropathic pain is often accompanied by stress, anxiety and depression. Although there is evidence for involvement of corticotropin-releasing factor (CRF), the detailed neuronal basis of these pain-related mood alterations is unknown. This study shows that peripheral mononeuropathy was accompanied by changes in limbic forebrain CRF, but did not lead to changes in the functioning of the hypothalamo-pituitary-adrenal axis and the midbrain Edinger-Westphal centrally projecting (EWcp) neuron population, which play main roles in the organism's response to acute pain. ⋯ Similarly, EWcp neurons, producing the CRF family member urocortin 1 (Ucn1) and constitutively activated by various stressors including acute pain, did not show an effect of CCI on Ucn1 mRNA or Ucn1. Also, the immediate early gene products cFos and deltaFosB in the EWcp were unaffected by CCI. These results indicate that neuropathic pain does not act via the HPA-axis or the EWcp, but includes a main role of Crf in the limbic system, which is in clear contrast to stressors like acute and chronic pain, which primarily act on the PVN and the EWcp.