The journal of pain : official journal of the American Pain Society
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A number of adolescents with chronic pain have clinically significant disability across physical, social, and academic activities, and pain severity only explains a portion of the variance in functioning. Thus, it is important to identify therapeutic options to improve adolescents' functioning. In contrast to studies with adults with chronic pain, research in pediatric pain has not consistently found anxiety to be a good predictor of pain-related disability. The present study evaluated pain, anxiety, and functioning in 222 adolescents with chronic pain. Results indicated that pain was consistently and linearly related to disability across measures of physical and social functioning, school attendance, and physician visits. The relation between anxiety and functioning was complex; increased anxiety was related to poorer physical and social functioning and was related to fewer physician visits, although it was not associated with school attendance. Additional analyses revealed that anxiety serves to moderate the relation between pain and functioning. Specifically, at high anxiety, pain was not related to functioning, but at low anxiety, pain consistently predicted disability. In other words, highly anxious adolescents were functioning poorly regardless of the level of pain. The moderating role of anxiety highlights a number of research and clinical possibilities to explore with adolescents with chronic pain-related disability. ⋯ Data suggest that high anxiety is associated with poor functioning irrespective of pain intensity. At low anxiety, higher pain predicted greater disability. Anxiety is important to assess when investigating potential reasons for pain-related disability.
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Burn injury induces severe pain that can be refractory to existing pharmacotherapies. The underlying mechanism of burn pain remains unclear. We previously established an animal model and reported that unilateral burn injury induces chronic and bilateral mechanical allodynia, which is associated with central sensitization and microglial activation in the spinal cord dorsal horn. Modulation of the activity of microglia and p38 mitogen-activated protein kinase (MAPK) has been shown to ameliorate neuropathic pain in several nerve-injury pain models. In the present study, we show in this rat model that daily treatment with the microglial inhibitor minocycline (10 mg/kg), administered at the time of burn injury and for 7 days thereafter, significantly attenuates ipsilateral and contralateral allodynia as assessed up to 1 month following burn injury. These sensory changes are paralleled by significant suppression of evoked hyperexcitability of dorsal-horn neurons and of the expression of phosphorylated p38 (phospho-p38) in OX42+ microglial cells within the dorsal horn. Our results suggest that modulation of inflammation at early times after burn injury may have long-lasting effects, attenuating central neuropathic mechanisms which contribute to pain after burn injury. ⋯ We demonstrate, in a rodent model of burn-associated pain, that the microglial inhibitor minocycline, delivered at the time of burn injury and for 1 week thereafter, has long-lasting effects, attenuating microglial activation and neuronal hyperresponsiveness in the dorsal horns, and ameliorating allodynia for at least 1 month.
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We used multiple pain models to investigate the effects of (-)-linalool, a monoterpene alcohol present in the essential oil of plants, on chronic inflammatory and neuropathic hypersensitivity in adult Swiss mice. Inflammatory or neuropathic hypersensitivity was induced by intraplantar (i.pl.) injection of complete Freund's adjuvant (CFA) or partial sciatic nerve ligation (PSNL), respectively. Twenty-four hours after CFA injection, we used Von Frey filaments and acetone-evoked cooling to evaluate tactile and thermal hypersensitivity, respectively. A single i.p. injection of (-)-linalool (50 or 200 mg/kg) administered 30 minutes before testing reduced CFA-induced mechanical hypersensitivity. Similarly, (-)-linalool reduced acetone-evoked hypersensitivity up to 4 hours after treatment. Compared with vehicle, (-)-linalool produced a marked reduction in CFA-induced paw edema. (-)-Linalool also reduced mechanical hypersensitivity induced by PSNL 7 days after injury. Multiple (-)-linalool treatments given chronically (twice a day for 10 days; 50 mg/kg, i.p.) significantly reduced mechanical hypersensitivity induced by CFA and PSNL. This multidose strategy did not cause tolerance. We also reasoned that (-)-linalool might reduce nociceptive behavior in response to direct administration of inflammatory mediators. Therefore, we injected the cytokines IL-1β (.1 pg/site) and TNF-α (1 pg/site) intrathecally. (-)-Linalool inhibited the biting response induced by IL-1β and TNF-α. ⋯ The article adds information about antinociceptive properties of (-)-linalool in chronic inflammatory and neuropathic hypersensitivity. It also indicates that (-)-linalool might be potentially interesting in the development of new clinically relevant drugs for the management of persistent pain.