European journal of pain : EJP
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Randomized Controlled Trial
Catastrophizing moderates the effect of exposure in vivo for back pain patients with pain-related fear.
This investigation was an initial attempt to explore psychological factors that might help or hinder the effect of exposure in vivo for patients with musculoskeletal pain and pain-related fear. The study was based on data from a randomized-controlled trial for patients with non-specific spinal pain (Linton et al., 2008). First, catastrophizing, anxiety, and depression were studied as possible treatment moderators. ⋯ Next, patients were divided into high change participants and low change participants based on their improvement in disability after treatment in order to investigate the change in psychological variables during treatment. Descriptive data indicated that high change participants had large improvements across treatment on depression, anxiety, catastrophizing, and fear-avoidance beliefs whereas low change participants virtually did not change at all on these variables across treatment. These findings denote that catastrophizing is a moderator of treatment outcome in exposure whereas several psychological variables might be important for the treatment process.
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Why traumatic injuries to the peripheral nervous system infrequently result in neuropathic pain is still unknown. The aim of this study was to examine the somatosensory system in patients with traumatic peripheral nerve injury with and without pain to try to unravel possible links to mechanisms underlying development and maintenance of pain. Eighteen patients with spontaneous ongoing pain and 16 patients without pain after unilateral partial peripheral traumatic nerve injury were studied. ⋯ There were no side differences in stimulus-response functions using painful heat stimuli in any of the groups. In addition, no significant difference could be demonstrated in any sensory modality comparing side-to-side differences between the two groups. In conclusion, increased pain sensitivity to cold and pressure was found on the injured side in pain patients, pointing to hyperexcitability in the pain system, a finding not verified by a more challenging analysis of side-to-side differences between patients with and without pain.
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The novel analgesic tapentadol combines mu-opioid receptor agonism and noradrenaline reuptake inhibition in a single molecule and shows potent analgesia in various rodent models of pain. We analyzed the contribution of opioid and monoaminergic mechanisms to the activity of tapentadol in rat models of nociceptive and neuropathic pain. Antinociceptive efficacy was inferred from tail withdrawal latencies of experimentally naive rats using a tail flick test. ⋯ Ritanserin did not affect antinociceptive or antihypersensitive ED(50) values of tapentadol. Activation of both mu-opioid receptors and alpha2-adrenoceptors contribute to the analgesic effects of tapentadol. The relative contribution is, however, dependent on the particular pain indication, as mu-opioid receptor agonism predominantly mediates tapentadol's antinociceptive effects, whereas noradrenaline reuptake inhibition predominantly mediates its antihypersensitive effects.
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The precise mechanism by which gonadal hormones influence pain perception is still obscure. However, no studies have examined experimental pain responses at supra-physiological hormone levels. This study explored the influence of pharmacological estradiol (E2) levels on the stability of pain perception obtained via quantitative sensory testing. ⋯ Mixed model repeated measures ANOVA indicated that participants who over-responded to the ovarian stimulation session (E2 > 10,500 pmol/l) showed significant enhanced pain responses under this condition (p=0.004). No correlations between progesterone, LH and experimental pain perception were found in any of the study sessions. Although pain perceptions at different E2 levels remained constant, the enhancement of pain scoring at supra-physiological E2 levels, underscore the possible role of sex hormones in pain modulation and experience.
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The effects of gentle mechanical skin stimulation on reflex discharges in cardiac sympathetic nerve evoked by somatic afferent stimulation were studied in anesthetized rats. Mass discharges were recorded from cardiac sympathetic efferent nerve while somatocardiac sympathetic A- and C-reflexes were elicited by single electrical stimuli to myelinated A- and unmyelinated C-afferent fibers of the tibial nerve. Continuous touch was applied to inner thigh skin with a force of 0.12 N for 10 min periods by a soft elastomer "brush" (1.1cm in diameter with 417 microcones). ⋯ We recorded unitary afferent activity from thigh branches of the saphenous nerve and found fibers excited by touch were low-threshold mechanoreceptive Abeta, Adelta and C fibers that have rapidly or slowly adapting properties. In all units tested, average discharge rates during touch period were less than 4 Hz. The results suggest that touch-induced excitation of low threshold cutaneous mechanoreceptive fibers inhibits nociceptive transmission conveyed by C-primary-afferents, via the release of both opioid and non-opioid inhibitory mediators.