Pain
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Perceived pain can be viewed because of a competition between nociceptive inputs and other competing goals, such as performing a demanding cognitive task. Task performance, however, suffers when cognitively fatigued. We therefore predicted that cognitive fatigue would weaken the pain-reducing effects of performing a concurrent cognitive task, which would indicate a causal link between fatigue and heightened pain sensitivity. ⋯ In 1 group, we induced cognitive fatigue before performing the tasks. We found that fatigue led to more pain and worse performance when the task was demanding, suggesting that fatigue weakens one's ability to distract from pain. These findings show that cognitive fatigue can impair performance on subsequent tasks and that this impairment can lower a person's ability to distract from and reduce their pain.
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Pain is an unpleasant sensory and emotional experience. Both pain and emotions are warning signals against outside harm. Interoception, bodily sensations of emotions can be assessed with the emBODY tool where participants colour the body parts where they feel different emotions. ⋯ Patients and controls marked different body areas as sensitive to nociceptive and tactile stimulation, but there was no difference in sensitivity to hedonic touch. Our findings suggest that emotional processing changes when pain persists, and this can be assessed with these colouring tasks. BMoEs may offer a new approach to assessing pain.
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Endometriosis is a chronic gynaecological condition, of which pain is both the most common and most debilitating symptom. As with other forms of pain, there is increasing recognition of the role of psychological processes in bridging the gap between pain and pain impact, and yet these processes are not well understood in endometriosis. The aim of this study was to investigate the relevance of fear of progression, imagery, and interpretation bias in endometriosis, and their contribution to pain interference. ⋯ Controlling for age and pain intensity, we found that imagery, interpretation bias, and their interaction were associated with increased fear of progression and that fear of progression was associated with greater pain-related interference. In exploratory analysis, we also found that the frequency and distress of endometriosis-related intrusive imagery were associated with greater fear of progression and pain interference, after controlling for age and pain intensity. These findings provide the first support of the importance of fear of progression in people with endometriosis and suggest possible pathways for causal investigation.
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Insight into nociceptive circuits will ultimately build our understanding of pain processing and aid the development of analgesic strategies. Neural circuit analysis has been advanced greatly by the development of optogenetic and chemogenetic tools, which have allowed function to be ascribed to discrete neuronal populations. Neurons of the dorsal root ganglion, which include nociceptors, have proved challenging targets for chemogenetic manipulation given specific confounds with commonly used DREADD technology. ⋯ We also demonstrated that our strategy can effectively silence inflammatory-like pain in a chemical pain model. Collectively, we have generated a novel tool that can be used to selectively silence defined neuronal circuits in vitro and in vivo. We believe that this addition to the chemogenetic tool box will facilitate further understanding of pain circuits and guide future therapeutic development.
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We have previously shown that intradermal injection of high-molecular-weight hyaluronan (500-1200 kDa) produces localized antihyperalgesia in preclinical models of inflammatory and neuropathic pain. In the present experiments, we studied the therapeutic effect of topical hyaluronan, when combined with each of 3 transdermal drug delivery enhancers (dimethyl sulfoxide [DMSO], protamine or terpene), in preclinical models of inflammatory and neuropathic pain. Topical application of 500 to 1200 kDa hyaluronan (the molecular weight range used in our previous studies employing intradermal administration), dissolved in 75% DMSO in saline, markedly reduced prostaglandin E 2 (PGE 2 ) hyperalgesia, in male and female rats. ⋯ The topical administration of a combination of hyaluronan with 2 other transdermal drug delivery enhancers, protamine and terpene, also attenuated CIPN hyperalgesia, an effect that was more prolonged than with DMSO vehicle. Repeated administration of topical hyaluronan prolonged the duration of antihyperalgesia. Our results support the use of topical hyaluronan, combined with chemically diverse nontoxic skin penetration enhancers, to induce marked antihyperalgesia in preclinical models of inflammatory and neuropathic pain.