Pain
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One of the most common forms of chronic pain is back pain. Until now, nothing has been known about the influence of visualizing one's own back on pain perception at this site. We tested 18 patients with chronic back pain and 18 healthy controls, by implementing online video feedback of the back during painful pressure and subcutaneous electrical stimuli over the trapezius muscle. ⋯ Subjects had to rate pain intensity and unpleasantness after each stimulation block on an 11-point numerical rating scale. Visual feedback of the back reduced perceived pain intensity compared to feedback of the hand in both patients and controls. These findings suggest novel intervention modes for chronic back pain based on visualization of body parts by augmented reality applications.
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Bradykinin (BK) is an inflammatory mediator that can evoke oedema and vasodilatation, and is a potent algogen signalling via the B1 and B2 G-protein coupled receptors. In naïve skin, BK is effective via constitutively expressed B2 receptors (B2R), while B1 receptors (B1R) are purported to be upregulated by inflammation. The aim of this investigation was to optimise BK delivery to investigate the algesic effects of BK and how these are modulated by inflammation. ⋯ We have optimised a versatile experimental model by which BK and its analogues can be administered to human skin. We have found that there is an early phase of BK-induced pain which partly depends on the release of inflammatory mediators by MCs; however, subsequent hyperalgesia is not dependent on MC degranulation. In naïve skin, B2R signaling predominates, however, cutaneous inflammation results in enhanced B1R responses.
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When a newly developed experimental method to vibrate vellus hairs on human skin was applied to the face and arm in healthy subjects, intense itch was reproducibly induced on the face, but not on the arm, without any flare reactions. In contrast to histamine-induced itch, mechanically evoked itch was not characterized as burning or stinging by any subjects, and was resistant to histamine H1-receptor antagonists. When the stimulation was continued for 10 min, mechanically evoked itch reached the maximum intensity within 10 s, but gradually attenuated after 60 to 90 s and was rarely perceivable at the end of stimulation. ⋯ Touch-alloknesis was present in the adjacent skin area until mechanically evoked itch completely diminished, supporting the hypothesis that itch sensitization can be caused by a continuous activation of peripheral itch neurons whether or not they are histamine-sensitive C nerves. In conclusion, this study provides direct evidence of mechanosensitive nerves involved in itch in human skin. The purity of mechanically evoked itch without any pain-related sensory components is a major advantage for investigating the differentiation of itch from pain.