European journal of pain : EJP
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Offset analgesia (OA) is a pain-inhibiting mechanism, defined as a disproportionately large decrease in pain perception in response to a discrete decrease in noxious stimulus intensity. Hence, the aims were (1) to investigate whether psychophysics and electroencephalography (EEG) can be assessed simultaneously during OA and (2) to assess whether OA is reproducible within the same day as well as between different days. ⋯ OA is a robust and reproducible model for experimental pain research, making it suitable for future research.
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The aim was to investigate influence from variations in intensity of a painful conditioning stimulation (CS) on early (0-6 min) and prolonged (6-12 min) conditioned pain modulation (CPM) in volunteers during concurrent exposure to test stimuli (TS). CS was applied to either forearm using painful heat with an intensity of 2/10 and 5/10, respectively, rated on a 0-10 numerical pain rating scale. At a second session, CS with an intensity of 7/10 was applied to the arm using a tourniquet. Threshold and suprathreshold painful heat and pressure as well as painful repeated monofilament pricking (RMP) were assessed as TS. ⋯ The CS intensity and the duration of CPM modulated pain sensitivity differentially across TS modalities.
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Up-regulation of transient receptor potential vanilloid subfamily, member 1 (TRPV1) is associated with the development and maintenance of cancer pain. The present study aimed to investigate the electrophysiological function of the up-regulated TRPV1 and the potential regulatory effects of insulin-like growth factor-1 (IGF-1) on TRPV1 expression in peripheral nerves in a rat model of bone cancer pain. ⋯ Our results provide novel evidence for the increase of IGF-1 in tibia bone marrow, which is responsible for the up-regulation of TRPV1 expression and function in the peripheral nerves of bone cancer pain rats.
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Control of trunk movement relies on the integration between central neuronal circuits and peripheral skeletomuscular activities and it can be altered by pain. There is increasing evidence that there are deficits within the central nervous system controlling the trunk muscles in people with low back pain (LBP). However, it is unclear how LBP impacts upon neural drive to back muscles at different levels of voluntary contraction. Therefore, the purpose of this study was to investigate if neural drive is impaired in these patients. ⋯ A decline of central neural drive to the back muscles at high level of voluntary contraction was observed in patients with LBP. These results suggest that it might be pertinent to include neuromuscular facilitation programmes and therapeutic exercise utilizing high voluntary contractions for patients with LBP.