Articles: hyperalgesia.
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Scand J Med Sci Sports · Jan 2018
Blood flow after contraction and cuff occlusion is reduced in subjects with muscle soreness after eccentric exercise.
Delayed onset muscle soreness (DOMS) occurs within 1-2 days after eccentric exercise, but the mechanism mediating hypersensitivity is unclear. This study hypothesized that eccentric exercise reduces the blood flow response following muscle contractions and cuff occlusion, which may result in accumulated algesic substances being a part of the sensitization in DOMS. Twelve healthy subjects (five women) performed dorsiflexion exercise (five sets of 10 repeated eccentric contractions) in one leg, while the contralateral leg was the control. ⋯ Compared with pre-exercise (day 0), reduced PPT (~25%, P<.002), MVC (~22%, P<.002), ATA diameter (~8%, P<.002), ATA post-contraction/occlusion blood flow (~16%, P<.04), and intramuscular peak blood flow (~23%, P<.03) were found in the DOMS leg on day 2 but not in the control leg. These results showed that eccentric contractions decreased vessel diameter, impaired the blood flow response, and promoted hyperalgesia. Thus, the results suggest that the blood flow reduction may be involved in the increased pain response after eccentric exercise.
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Review
The Underestimated Significance of Conditioning in Placebo Hypoalgesia and Nocebo Hyperalgesia.
Placebo and nocebo effects are intriguing phenomena in pain perception with important implications for clinical research and practice because they can alleviate or increase pain. According to current theoretical accounts, these effects can be shaped by verbal suggestions, social observational learning, and classical conditioning and are necessarily mediated by explicit expectation. In this review, we focus on the contribution of conditioning in the induction of placebo hypoalgesia and nocebo hyperalgesia and present accumulating evidence that conditioning independent from explicit expectation can cause these effects. ⋯ Because only few studies have investigated clinical samples, the picture seems less clear when it comes to patient populations with chronic pain. However, conditioning appears to be a promising means to optimize treatment. In order to get a better insight into the mechanisms of placebo and nocebo effects in pain and the possible benefits of conditioning compared to explicit expectation, future studies should carefully distinguish both methods of induction.
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Journal of pain research · Jan 2018
Peripheral and spinal TRPA1 channels contribute to formalin-induced long-lasting mechanical hypersensitivity.
Transient receptor potential ankyrin 1 (TRPA1) is a non-selective cation channel expressed by a subset of nociceptive neurons that acts as a multimodal receptor. Its activity contributes to modulate nociceptive transmission in acute inflammatory pain. However, the role of this channel in chronic pain has been less studied. The purpose of this study was to investigate the local peripheral and spinal participation of TRPA1 channels in formalin-induced long-lasting hypersensitivity. ⋯ Results indicate that TRPA1 expressed in the DRG and spinal cord plays a relevant role in formalin-induced long-lasting secondary nociceptive hypersensitivity.
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Learning is a key mechanism underpinning the development of the nocebo effect. The learning literature has cataloged and explored numerous ways in which the environment can be manipulated to prevent, reduce, or eradicate learning. ⋯ These learning strategies include overshadowing, latent inhibition, extinction, and contingency degradation. These strategies represent important new avenues for investigation and should be used by researchers to design and test interventions to reduce nocebo effects.
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Frontiers in pharmacology · Jan 2018
Effects of Transcranial Direct Current Stimulation Block Remifentanil-Induced Hyperalgesia: A Randomized, Double-Blind Clinical Trial.
Background: Remifentanil-induced hyperalgesia (r-IH) involves an imbalance in the inhibitory and excitatory systems. As the transcranial Direct Current Stimulation (tDCS) modulates the thalamocortical synapses in a top-down manner, we hypothesized that the active (a)-t-DCS would be more effective than sham(s)-tDCS to prevent r-IH. We used an experimental paradigm to induce temporal summation of pain utilizing a repetitive cold test (rCOLDT) assessed by the Numerical Pain Score (NPS 0-10) and we evaluated the function of the descending pain modulatory system (DPMS) by the change on the NPS (0-10) during the conditioned pain modulation (CPM)-task (primary outcomes). ⋯ Thereby, tDCS could be considered as a new approach to contra-regulate paradoxical mechanisms involved in the r-IH. Clinical trials identification: NCT02432677. URL:https://clinicaltrials.gov/.