Pain
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Placebos are often used by clinicians, usually deceptively and with little rationale or evidence of benefit, making their use ethically problematic. In contrast with their typical current use, a provocative line of research suggests that placebos can be intentionally exploited to extend analgesic therapeutic effects. Is it possible to extend the effects of drug treatments by interspersing placebos? We reviewed a database of placebo studies, searching for studies that indicate that placebos given after repeated administration of active treatments acquire medication-like effects. ⋯ Third, using placebos along with active medication, for part of the course of treatment, should limit dose escalation and lower costs. Provided that nondisclosure is preauthorized in the informed consent process and that robust evidence indicates therapeutic benefit comparable to that of standard full-dose therapeutic regimens, introducing dose-extending placebos into the clinical arsenal should be considered. This novel prospect of placebo use has the potential to change our general thinking about painkiller treatments, the typical regimens of painkiller applications, and the ways in which treatments are evaluated.
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Randomized Controlled Trial
The effect of local versus remote experimental pain on motor learning and sensorimotor integration using a complex typing task.
Recent work demonstrated that capsaicin-induced acute pain improved motor learning performance; however, baseline accuracy was very high, making it impossible to discern the impact of acute pain on motor learning and retention. In addition, the effects of the spatial location of capsaicin application were not explored. Two experiments were conducted to determine the interactive effects of acute pain vs control (experiment 1) and local vs remote acute pain (experiment 2) on motor learning and sensorimotor processing. ⋯ Experiment 2: The P25 SEP peak decreased in the local group after application of capsaicin cream (P < 0.01), whereas the N30 SEP peaks increased after motor learning in both groups (P < 0.05). Accuracy improved in the local group at retention (P < 0.005), and response time improved after motor learning (P < 0.005) and at retention (P < 0.001). This study suggests that acute pain may increase focal attention to the body part used in motor learning, contributing to our understanding of how the location of pain impacts somatosensory processing and the associated motor learning.
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We have recently described a novel form of hyperalgesic priming (type II) induced by agonists at two clinically important Gi-protein-coupled receptors (Gi-GPCRs), mu-opioid and A1-adenosine. Like mu-opioids, the antimigraine triptans, which act at 5-HT1B/D Gi-GPCRs, have been implicated in pain chronification. We determined whether sumatriptan, a prototypical 5-HT1B/D agonist, produces type II priming. ⋯ The prolongation of PGE2 hyperalgesia induced by sumatriptan was partially prevented by coinjection of antagonists for the 5-HT1B and 5-HT1D, but not 5-HT7, serotonin receptors and completely prevented by coadministration of a combination of the 5-HT1B and 5-HT1D antagonists. Moreover, the injection of selective agonists, for 5-HT1B and 5-HT1D receptors, also induced hyperalgesic priming. Our results suggest that sumatriptan, which signals through Gi-GPCRs, induces type I hyperalgesic priming, unlike agonists at other Gi-GPCRs, which induce type II priming.