Pain
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The use of unidimensional scales to measure pain intensity has been criticised because of the multidimensional nature of pain. We conducted multiple linear regression analyses to determine which dimensions of pain--sensory versus affective--predicted scores on unidimensional scales measuring pain intensity and emotions in 109 Italian women suffering from chronic, non-malignant musculoskeletal pain. We then compared the results with earlier findings in two groups of cancer patients suffering from acute post-operative pain and chronic cancer-related pain, respectively. ⋯ Therefore, in contrast to earlier findings in two different types of cancer patients, in subjects affected by chronic non-malignant musculoskeletal pain, the scores on unidimensional pain intensity scales mainly reflect sensory pain dimensions, supporting the discriminant validity of the NRS and VAS used. However, the patients had some difficulty in distinguishing between sensory and emotional information. For this reason, several unidimensional scales to rate pain intensity and emotions separately should be used to obtain a complete picture of the status and needs of any given patient.
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Using a gene expression analysis approach we found that the mRNA encoding the lysosomal cysteine protease cathepsin S (CatS) was up-regulated in rat dorsal root ganglia (DRG) following peripheral nerve injury. CatS protein was expressed in infiltrating macrophages in DRG and near the site of injury. At both sites CatS expression progressively increased from day 3 to day 14 after injury. ⋯ In nerve-injured rats, mechanical hyperalgesia, but not allodynia, was significantly reversed for up to 3h by systemic administration of a non-brain penetrant, irreversible CatS inhibitor (LHVS, 3-30 mg/kg s.c.). Depletion of peripheral macrophages by intravenous injection of liposome encapsulate clodronate (1ml, 5 mg/ml) partially reduced established mechanical hyperalgesia but not allodynia, and abolished the anti-hyperalgesic effect of LHVS. Our results demonstrate a pro-nociceptive effect of CatS and indicate that endogenous CatS released by peripheral macrophages contributes to the maintenance of neuropathic hyperalgesia following nerve injury.
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Randomized Controlled Trial
Trait anger expressiveness and pain-induced beta-endorphin release: support for the opioid dysfunction hypothesis.
The anger management styles of anger-in (inhibition) and anger-out (direct expression) are positively associated with pain responsiveness. Opioid blockade studies suggest that hyperalgesic effects of trait anger-out, but not those of trait anger-in, are mediated in part by opioid analgesic system dysfunction. The current study tested the opioid dysfunction hypothesis of anger-out using an alternative index of opioid function: pain-induced changes in plasma endogenous opioids. ⋯ This suggests unique associations with expressive anger regulation. Elevated trait anger-out therefore appears to be associated with opioid analgesic system dysfunction, whether it is indexed by responses to opioid blockade or by examining circulating endogenous opioid levels. Possible "statextrait" interactions on these anger-related opioid system differences are discussed.
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Neuromedin U (NMU) has recently been reported to have a role in nociception and inflammation. To clarify the function of the two known NMU receptors, NMU receptor 1 (NMUR1) and NMU receptor 2 (NMUR2), during nociception and inflammation in vivo, we generated mice in which the genes for each receptor were independently deleted. Compared to wild type littermates, mice deficient in NMUR2 showed a reduced thermal nociceptive response in the hot plate, but not in the tail flick, test. ⋯ In contrast, NMUR1-deficient mice did not show any nociceptive differences compared to their wild type littermates in any of the behavioral tests used. We observed the same magnitude of inflammation in both lines of NMU receptor mutant mice compared to their wild type littermates after injection with complete Freund's adjuvant (CFA), suggesting no requirement for either receptor in this response. Thus, the pro-nociceptive effects of NMU in mice appear to be mediated through NMUR2, not NMUR1.
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For years, physical deconditioning has been thought to be both a cause and a result of back pain. As a consequence physical reconditioning has been proposed as treatment-goal in patients with chronic low back pain (LBP). However, it is still unclear whether a patient's physical fitness level really decreases after pain-onset. ⋯ Results showed that only in a subgroup of patients a PAL-decrease had occurred after the onset of pain, whereas no signs of physical deconditioning were found. Negative affect and the patients' perceived physical activity decline in the subacute phase predicted a decreased level of PAL over one year. Based on these results, we conclude that as to the assumption that patients with CLBP suffer from disuse and physical deconditioning empirical evidence is still lacking.