Pain
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Overactivity is a frequently used term in chronic pain literature. It refers to the phenomenon whereby individuals engage in activity in a way that significantly exacerbates pain, resulting in periods of incapacity. Overactivity, as a construct, has been derived solely from patients' self-reports, raising concerns about the legitimacy of the construct. ⋯ Over the 5-day period, participants wore an activity monitor and recorded their pain intensity 6 times a day using a handheld computer. Associations were found between (1) high levels of pain and both high overactivity and high avoidance, (2) high levels of overactivity and more variation in pain and objective activity across days, and (3) high levels of overactivity and the reoccurrence of prolonged activity engagement followed by significant pain increases observed in data sets. These results offer some preliminary support for the validity of overactivity as a legitimate construct in chronic pain.
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Pain captures attention, displaces current concerns, and prioritises escape and repair. This attentional capture can be measured by its effects on general cognition. Studies on induced pain, naturally occurring acute pain, and chronic pain all demonstrate a detrimental effect on specific tasks of attention, especially those that involve working memory. ⋯ Furthermore, we also found an effect of pain intensity; performance was poorer in participants with higher intensity compared with that in those with lower intensity pain. We suggest that the effects of pain on attention found in the laboratory occur in more naturalistic settings. Pain is common in the general population, and such interruption may have important, as yet uninvestigated, consequences for tasks of everyday cognition that involve working memory, such as concentration, reasoning, motor planning, and prospective memory.
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This study examines the effect of normal aging on temporal summation (TS) of pain and the nociceptive flexion reflex (RIII). Two groups of healthy volunteers, young and elderly, received transcutaneous electrical stimulation applied to the right sural nerve to assess pain and the nociceptive flexion reflex (RIII-reflex). ⋯ This study shows that robust TS of pain and RIII-reflex is observable in individuals aged between 18 and 75 years and indicates that these effects are comparable between young and older individuals. These results contrast with some previous findings and imply that at least some pain regulatory processes, including TS, may not be affected by normal aging, although this may vary depending on the method.
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Cancer-induced bone pain is described as dull, aching ongoing pain. Ongoing bone cancer pain was characterized after intratibial injection of breast cancer cells in rats. Cancer produced time-dependent bone remodeling and tactile hypersensitivity but no spontaneous flinching. ⋯ Consistent with clinical experience, ongoing cancer pain was controlled by morphine but not by a dose of diclofenac that reversed evoked hypersensitivity. Additionally, the intrinsic reward of morphine can be dissociated from the reward of relief of cancer pain by blockade of rACC MOR. This approach allows mechanistic and therapeutic assessment of ongoing cancer pain with likely translation relevance.
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Activation of neuronal nitric oxide synthase, and consequent production of nitric oxide (NO), contributes to spinal hyperexcitability and enhanced pain sensation. All NOS isoforms are inhibited endogenously by asymmetric dimethylarginine, which itself is metabolised by dimethylarginine dimethylaminohydrolase (DDAH). Inhibition of DDAH can indirectly attenuate NO production by elevating asymmetric dimethylarginine concentrations. ⋯ Spinal application of L-291 decreased N-methyl-D-aspartate-dependent postdischarge and windup of dorsal horn sensory neurons--2 measures of spinal hyperexcitability. Finally, spinal application of L-291 reduced both neuronal and behavioral measures of formalin-induced central sensitization. Thus, DDAH-1 may be a potential therapeutic target in neuronal disorders, such as chronic pain, where elevated NO is a contributing factor.