Pain
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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.
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Traumatic musculoskeletal injury results in a high incidence of chronic pain; however, there is little evidence about the nature, quality, and severity of the pain. This study uses a prospective, observational, longitudinal design to (1) examine neuropathic pain symptoms, pain severity, pain interference, and pain management at hospital admission and 4 months after traumatic musculoskeletal injury (n = 205), and (2) to identify predictors of group membership for patients with differing moderate-to-severe putative neuropathic pain trajectories. Data were collected on mechanism of injury, injury severity, pain (intensity, interference, neuropathic quality), anxiety (anxiety sensitivity, general anxiety, pain catastrophizing, pain anxiety), depression, and posttraumatic stress while patients were in-hospital and 4 months after injury. ⋯ Significant predictors of the development and maintenance of moderate-to-severe neuropathic pain included high levels of general anxiety while in-hospital immediately after injury (P < 0.001) and symptoms of posttraumatic stress 4 months after injury (P < 0.001). Few patients had adequate pharmacological, physical, or psychological pain management in-hospital and at 4 months. Future research is needed among trauma patients to better understand the development of chronic pain and to determine the best treatment approaches.
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Affective instability, conceptualized as fluctuations in mood over time, has been related to ill-health and psychopathology. In this study, we examined the role of affective instability on daily pain outcomes in 70 patients with chronic pain (Mage = 49.7 years; 46 females) using an end-of-day diary. During a baseline phase, patients completed self-reported questionnaires of pain severity, pain duration, disability, depression, and anxiety. ⋯ Positive affect instability, however, showed to be unrelated to all outcomes. Current findings extend previous results and reveal the putative role of affective instability on pain-related outcomes and may yield important clinical implications. Indeed, they suggest that targeting NA instability by improving emotion regulation skills may be a strategy to diminish disability and cognitive complaints in patients with chronic pain.
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The painDETECT Questionnaire (PDQ) is commonly used as a screening tool to discriminate between neuropathic pain (NP) and nociceptive pain, based on the self-report of symptoms, including pain qualities, numbness, and pain to touch, cold, or heat. However, there are minimal data about whether the PDQ is differentially sensitive to different sensory phenotypes in NP. The aim of the study was to analyze whether the overall PDQ score or its items reflect phenotypes of sensory loss in NP as determined by quantitative sensory testing. ⋯ Patients with loss of thermal sensation (2 and 4) significantly more often reported pain evoked by light touch, and patients with loss of mechanical sensation (3 and 4) significantly more often reported numbness and significantly less often burning sensations and pain evoked by light touch. Although the PDQ was not designed to assess sensory loss, single items reflect thermal and/or mechanical sensory loss at group level, but because of substantial variability, the PDQ does not allow for individual allocation of patients into sensory profiles. It will be useful to develop screening tools according to the current definition of NP.