Pain
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An accurate means of identifying patients at high risk for chronic disabling pain could lead to more cost-effective care, with more intensive interventions targeted to those likely to benefit most. The Chronic Pain Risk Score is a tool developed to predict risk for chronic pain. The aim of this study was to examine whether its predictive ability could be enhanced by: (1) improved measures of the constructs it assesses (Improved Chronic Pain Risk Model); and (2) adding other predictors (Expanded Chronic Pain Risk Model). ⋯ The Expanded Model improved significantly on the prediction of the Improved Model (NRI=0.56, P<0.001) and demonstrated excellent discriminative ability (AUC=0.84, 95% CI=0.79-0.88). The Improved Model (AUC=0.79, 95% CI=0.75-0.84) and the Chronic Pain Risk Score (AUC=0.76, 95% CI=0.71-0.81) showed acceptable discriminative ability. A limited set of measures may be used to predict risk for future clinically significant pain in patients initiating primary care for back pain, but further evaluation of prognostic models is needed.
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Review Meta Analysis
Evidence for working memory deficits in chronic pain: a systematic review and meta-analysis.
People with chronic pain commonly report impaired cognitive function. However, to date, there has been no systematic evaluation of the body of literature concerning cognitive impairment and pain. Nor have modern meta-analytical methods been used to verify and clarify the extent to which cognition may be impaired. ⋯ High heterogeneity within the field was found with the inclusion of 24 papers using 21 different working memory tests encompassing 9 different working memory constructs and 9 different chronic pain populations. Notwithstanding high heterogeneity, pooled results from behavioural outcomes reflected a consistent, significant moderate effect in favour of better performance by healthy controls and, with the exception of one study, pooled results from physiological outcomes reflected no evidence for an effect. Future research would benefit from the use of clearly defined constructs of working memory, as well as standardised methods of testing.
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A link between fibromyalgia syndrome (FMS) and posttraumatic stress disorder (PTSD) has been suggested because both conditions share some similar symptoms. The temporal relationships between traumatic experiences and the onset of PTSD and FMS symptoms have not been studied until now. All consecutive FMS patients in 8 study centres of different specialties were assessed from February 1 to July 31, 2012. ⋯ In 4.0% of patients' most burdensome traumatic experience, PTSD and FMS symptoms occurred in the same year. FMS and PTSD are linked in several ways: PTSD is a potential risk factor of FMS and vice versa. FMS and PTSD are comorbid conditions because they are associated with common antecedent traumatic experiences.
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Translational studies are key to furthering our understanding of nociceptive signalling and bridging the gaps between molecules and pathways to the patients. This requires use of appropriate preclinical models that accurately depict outcome measures used in humans. Whereas behavioural animal studies classically involve reports related to nociceptive thresholds of, for example, withdrawal, electrophysiological recordings of spinal neurones that receive convergent input from primary afferents permits investigation of suprathreshold events and exploration of the full-range coding of different stimuli. ⋯ Thirdly, there was a significant degree of spatial summation of laser nociceptive input. The remarkable similarity in rodent and human coding indicates that responses of rat dorsal horn neurones can translate to human nociceptive processing. These findings suggest that recordings of spinal neuronal activity elicited by laser stimuli could be a valuable predictive measure of human pain perception.
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Individual vulnerability factors influencing the function of the hypothalamic-pituitary-adrenal axis may contribute to the risk of the development of persistent musculoskeletal pain after traumatic stress exposure. The objective of the study was to evaluate the association between polymorphisms in the gene encoding FK506 binding protein 51, FKBP5, a glucocorticoid receptor co-chaperone, and musculoskeletal pain severity 6 weeks after 2 common trauma exposures. The study included data from 2 prospective emergency department-based cohorts: a discovery cohort (n=949) of European Americans experiencing motor vehicle collision and a replication cohort of adult European American women experiencing sexual assault (n=53). ⋯ The association of rs3800373, rs9380526, rs9394314, rs2817032, and rs2817040 with neck pain and/or overall pain 6 weeks after trauma was replicated in the sexual assault cohort, showing the same direction of the effect in each case. The results of this study indicate that genetic variants in FKBP5 influence the severity of musculoskeletal pain symptoms experienced during the weeks after motor vehicle collision and sexual assault. These results suggest that glucocorticoid pathways influence the development of persistent posttraumatic pain, and that such pathways may be a target of pharmacologic interventions aimed at improving recovery after trauma.