Pain
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Although regulation of nociceptive processes in the dorsal horn by deep brain structures has long been established, the role of cortical networks in pain regulation is minimally explored. The medial prefrontal cortex (mPFC) is a key brain area in pain processing that receives ascending nociceptive input and exerts top-down control of pain sensation. We have shown critical changes in mPFC synaptic function during neuropathic pain, controlled by endocannabinoid (eCB) signaling. ⋯ Spared nerve injury reduced the mechanical threshold to induce action potential firing of dorsal horn wide-dynamic-range neurons, but this was reversed in rats by WIN in the chronic phase of SNI and by mPFC injection of AM4113 in the early phase of SNI. Elevated dorsal root ganglion neuronal activity after injury was also diminished in rats by mPFC injection of AM4113, potentially by reducing antidromic activity and subsequent neuronal inflammation. These findings suggest that depending on the phase of the pain condition, both blocking and activating CB1 receptors in the mPFC can regulate descending control of pain and affect both dorsal horn neurons and peripheral sensory neurons, contributing to changes in pain sensitivity.
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Randomized Controlled Trial
Mechanisms of education and graded sensorimotor retraining in people with chronic low back pain: a mediation analysis.
An improved understanding of the biopsychosocial influences that contribute to and maintain pain has promoted the development of new efficacious treatments for chronic low back pain (CLBP). This study aimed to investigate the mechanisms of a new treatment-education and graded sensorimotor retraining-on pain and disability. We conducted a preplanned causal mediation analysis of a randomized clinical trial which allocated 276 participants with CLBP to 12 weekly clinical sessions of education and graded sensorimotor retraining (n = 138) or a sham and attention control (n = 138). ⋯ Five of 7 mechanisms (71%) mediated the intervention effect on disability; the largest mediated effects were for beliefs about back pain consequences (-1.66 [-2.62 to -0.87]), pain catastrophizing (-1.06 [-1.79 to -0.53]), and pain self-efficacy (-0.84 [-1.89 to -0.45]). When all 7 mechanisms were considered simultaneously, the joint mediation effect explained most of the intervention effect for both pain and disability. Optimizing interventions to target beliefs about the consequences of back pain, pain catastrophizing, and pain self-efficacy is likely to lead to improved outcomes for people with CLBP.
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Longitudinal total knee arthroplasty (TKA) studies indicate that a substantial percentage of patients continue to experience clinically significant pain and functional impairment after surgery. Insomnia has been associated with poorer surgical outcomes; however, previous work has largely focused on long-term postsurgical insomnia. This study builds on previous work by examining sleep and pain outcomes about perioperative insomnia trajectories. ⋯ The New Insomnia trajectory had notable long-term insomnia (6 weeks to 6 months) and acute (6 weeks) postoperative pain and physical functioning ( P' s < 0.05). Findings indicated a significant relationship between perioperative insomnia trajectory and postoperative outcomes. Results of this study suggest that targeting presurgical insomnia and preventing the development of acute postoperative insomnia may improve long-term postoperative outcomes, with an emphasis on persistent perioperative insomnia due to poorer associated outcomes.