The journal of pain : official journal of the American Pain Society
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Comparative Study
Mild social stress in mice produces opioid-mediated analgesia in visceral but not somatic pain states.
Visceral pain has a greater emotional component than somatic pain. To determine if the stress-induced analgesic response is differentially expressed in visceral versus somatic pain states, we studied the effects of a mild social stressor in either acute visceral or somatic pain states in mice. We show that the presence of an unfamiliar conspecific mouse (stranger) in an adjacent cubicle of a standard transparent observation box produced elevated plasma corticosterone levels compared with mice tested alone, suggesting that the mere presence of a stranger is stressful. ⋯ Compared with mice tested alone, the presence of a stranger produced a dramatic opioid-dependent reduction in pain behavior associated with visceral but not somatic pain. This social stress-induced reduction of visceral pain behavior relied on visual but not auditory/olfactory cues. These findings suggest that visceral pain states may provoke heightened responsiveness to mild stressors, an effect that could interfere with testing outcomes during simultaneous behavioral testing of multiple rodents.
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Aerobic exercise improves outcomes in a variety of chronic health conditions, yet the support for exercise-induced effects on chronic pain in humans is mixed. Although many rodent studies have examined the effects of exercise on persistent hypersensitivity, the most used forced exercise paradigms that are known to be highly stressful. ⋯ Our data indicate that voluntary exercise rapidly and effectively reduces hypersensitivity as well as stress-related outcomes without altering swelling. Moreover, the level of exercise is unrelated to the analgesic and stress-reducing effects, suggesting that even modest amounts of exercise may impart significant benefit in persistent inflammatory pain states.
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Review Meta Analysis
Analgesic effects of alcohol: A systematic review and meta-analysis of controlled experimental studies in healthy participants.
Despite the long-standing belief in the analgesic properties of alcohol, experimental studies have produced mixed results. This meta-analysis aimed to clarify whether alcohol produces a decrease in experimentally-induced pain and to determine the magnitude of any such effect. PubMed, PsycINFO, and Embase databases were searched from inception until April 21, 2016 for controlled studies examining the effect of quantified dosages of alcohol on pain response to noxious stimulation. Eighteen studies involving 404 participants were identified providing alcohol versus no-alcohol comparisons for 13 tests of pain threshold (n = 212) and 9 tests of pain intensity ratings (n = 192). Random effects meta-analysis of standardized mean difference (SMD) provided robust support for analgesic effects of alcohol. A mean blood alcohol content (BAC) of approximately .08% (3-4 standard drinks) produced a small elevation of pain threshold (SMD [95% CI] = .35 [.17-.54], P = .002), and a moderate to large reduction in pain intensity ratings (SMD [95% CI] = .64 [.37-.91], P < .0001), or equivalently, a mean reduction of 1.25 points on a 0- to 10-point pain rating scale. Furthermore, increasing BAC resulted in increasing analgesia, with each .02% BAC increment producing an increase of SMD = .11 for pain threshold and SMD = .20 for reduced pain intensity. Some evidence of publication bias emerged, but statistical correction methods suggested minimal impact on effect size. Taken together, findings suggest that alcohol is an effective analgesic that delivers clinically-relevant reductions in ratings of pain intensity, which could explain alcohol misuse in those with persistent pain despite its potential consequences for long-term health. Further research is needed to corroborate these findings for clinical pain states. ⋯ This meta-analysis provides robust evidence for the analgesic properties of alcohol, which could potentially contribute to alcohol misuse in pain patients. Strongest analgesia occurs for alcohol levels exceeding World Health Organization guidelines for low-risk drinking and suggests raising awareness of alternative, less harmful pain interventions to vulnerable patients may be beneficial.
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Randomized Controlled Trial
TRPA1 and TRPV1 antagonists do not inhibit human acidosis-induced pain.
Acidosis occurs in a variety of pathophysiological and painful conditions where it is thought to excite or contribute to excitation of nociceptive neurons. Despite potential clinical relevance the principal receptor for sensing acidosis is unclear, but several receptors have been proposed. We investigated the contribution of the acid-sensing ion channels, transient receptor potential vanilloid type 1 (TRPV1) and transient receptor potential ankyrin type 1 (TRPA1) to peripheral pain signaling. ⋯ A continuous intraepidermal injection of pH 4.3 was used to counter the buffering capacity of tissue and generate a prolonged painful stimulation. In this model, addition of A-967079, BCTC or amiloride did not reduce the reported pain. In conclusion, target-validated antagonists, applied locally in human skin, have excluded the main hypothesized targets and the mechanism of the human acidosis-induced pain remains unclear.