The journal of pain : official journal of the American Pain Society
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Little is known about the mechanisms by which pain catastrophizing may be associated with opioid use outcomes. This study aimed to investigate the potential mediating role of beliefs about the appropriateness of pain medicines for pain treatment on the association between pain catastrophizing and prescription opioid use in a community chronic non-cancer pain (CNCP) sample. Individuals (N = 420) diagnosed with CNCP participated in a cross-sectional online self-report study with validated measures of pain medication beliefs, pain catastrophizing, and current prescription opioid use. ⋯ A similar pattern of findings was found for high-dose opioid use, with pain medication beliefs significantly mediating the pain catastrophizing-high-dose use association (CI = 0.006, 0.050). Pain medication beliefs are a potentially modifiable psychological mechanism by which pain catastrophizing is associated with opioid use, including high-dose use. These findings have important implications for personalizing prevention and treatment programs.
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Pain interventions typically include effortful exercise and long-term treatment - ie, short-term costs (effort) with delayed benefit (improved pain and/or function). Thus, understanding if long-term pain influences decision-making in context of delays and effort is essential given clear relevance to treatment uptake and/or adherence. We evaluated delay and effort attitudes in those experiencing chronic pain (n = 391) and in pain-free controls (n = 263). ⋯ Data availability: Study materials are available here: https://osf.io/zexm7/?view_only=c9848597361c41808c612874da6f33b7. PERSPECTIVE: People with chronic pain make more short-sighted decisions (prefer less reward sooner) and decreased willingness to undertake effort (prefer less reward with little effort) for monetary gains than people without pain. Interventions targeting discounting behavior may help improve both uptake and adherence for evidence-based, effortful treatments, such as exercise.
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Chronic pain frequently develops after limb injuries, and its pathogenesis is poorly understood. We explored the hypothesis that the autonomic nervous system regulates adaptive immune system activation and nociceptive sensitization in a mouse model of chronic post-traumatic pain with features of complex regional pain syndrome (CRPS). In studies sympathetic signaling was reduced using 6-hydroxydopamine (6-OHDA) or lofexidine, while parasympathetic signaling was augmented by nicotine administration. ⋯ PERSPECTIVE: Selective treatments aimed at autonomic nervous system modulation reduce fracture-related nociceptive and functional sequelae. The same treatment strategies limit pain-supporting immune system activation and the production of pro-nociceptive antibodies. Thus, the therapeutic regulation of autonomic activity after limb injury may reduce the incidence of chronic pain.