Pain
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Chronic widespread musculoskeletal pain (CWP) is common, having a population prevalence of 10%. This study aimed to define the biological basis of the CWP/body mass association by using a systems biology approach. Adult female twins (n = 2444) from the TwinsUK registry who had extensive clinical, anthropometric, and "omic" data were included. ⋯ Mendelian randomization by rs1581492 genotype showed that EAS is unlikely to be causally related to CWP. Using an agnostic omics approach to focus on the association of CWP with body mass index, we have confirmed a steroid hormone association and identified a genetic variant upstream of the CYP genes, which likely controls this response. This study suggests that steroid hormone abnormalities result from pain rather than causing it, and EAS may provide a biomarker that identifies subgroups at risk of CWP.
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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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The aim of this case-crossover study was to investigate the extent to which patients can accurately nominate what triggered their new episode of sudden-onset acute low back pain (LBP). We interviewed 999 primary care patients to record exposure to 12 standard triggers and also asked the patients to nominate what they believed triggered their LBP. Exposure to the patient-nominated trigger during the case window was compared with exposure in the control window. ⋯ The odds ratios for exposure to patient-nominated triggers ranged from 8.60 to 30.00, suggesting that exposure increases the risk of LBP. Patients' understanding of triggers however seems incomplete, as we found evidence that while some of the standard triggers were well recognised (such as lifting heavy loads), others (such as being distracted during manual tasks) were under-recognised as possible triggers of an episode of LBP. This study provides some evidence that patients can accurately nominate the activity that triggered their new episode of sudden-onset acute LBP.
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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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Referred pain is a phenomenon of feeling pain at a site other than the site of the painful stimulus origin. It arises from a pathological mixing of nociceptive processing pathways for visceral and somatic inputs. Despite numerous studies based on unit recordings from spinal and supraspinal neurons, the exact mechanism and site of this mixing within the central nervous system are not known. ⋯ First, lamina I of the spinal cord is the first site in the central nervous system where somatic and visceral pathways directly converge onto individual projection and local circuit neurons. Second, the mechanism of somatovisceral convergence is complex and based on functional integration of monosynaptic and polysynaptic excitatory as well as inhibitory inputs in specific groups of neurons. This complex pattern of convergence provides a substrate for alterations in the balance between visceral and somatic inputs causing referred pain.