Pain
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Observational Study
Development and Validation of a New Self-Report Measure of Pain Behaviors.
Pain behaviors that are maintained beyond the acute stage after injury can contribute to subsequent psychosocial and physical disability. Critical to the study of pain behaviors is the availability of psychometrically sound pain behavior measures. In this study we developed a self-report measure of pain behaviors, the Pain Behaviors Self Report (PaB-SR). ⋯ Scores on the PaB-SR were found to be measurement invariant with respect to clinical condition. PaB-SR scores, observer reports, and the videotaped protocol yielded distinct, but convergent views of pain behavior, supporting the validity of the new measure. The PaB-SR is expected to be of substantial utility to researchers wishing to explore the relationship between pain behaviors and constructs such as pain intensity, pain interference, and disability.
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Randomized Controlled Trial
A population-based study of the use of chronic pain and opioids in Portugal.
Although increasing doubts exist regarding the long-term effectiveness and safety of opioids in patients with chronic pain (CP), most guidelines still recognize opioids as an option in effective management of CP. We aimed to describe the prevalence and factors associated with opioid use in subjects with CP in Portugal and to evaluate satisfaction and self-assessed treatment effectiveness. A nationwide study was conducted in a representative sample of the adult Portuguese population. ⋯ Indeed, we showed that in Portugal, as in many other regions in the world, opioids are used much less frequently than in those few countries. Moreover, we did not find significant differences among users and nonusers of opioids regarding satisfaction and self-assessed effectiveness, eventually showing the results to be in line with reports that show doubt about opioids' effectiveness. Further research and particular attention to and continuous monitoring of the trends of use and abuse of opioids worldwide are recommended.
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Anti-nerve growth factor (anti-NGF) treatment is analgesic in chronic inflammatory pain conditions without reducing inflammation. Hypothesizing that ongoing pain induced by inflammatory mediators is increased by long term sensitization of nociceptors, we combined the non-inflammatory NGF-sensitization model with an inflammatory ultraviolet-B (UV-B) model in human volunteers. UV-B irradiation of the skin presensitized with NGF 3 weeks before intensified the pre-existing NGF hyperalgesia during the inflammatory phase of UV-B and caused spontaneous pain in about 70% of the subjects. ⋯ Hyperalgesia and spontaneous pain coexisted in NGF/UV-B treated skin but did not significantly correlate (r < -0.1 at day 1 and r < 0.2 at day 3). We conclude that NGF can sensitize nociceptive endings such that inflammatory mediators may cause sufficient excitation to provoke spontaneous pain. Our results suggest that neuronal sensitization and level of inflammation represent independent therapeutic targets in chronic inflammatory pain conditions.
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G-protein coupled inwardly rectifying potassium (GIRK) channels are effectors determining degree of analgesia experienced upon opioid receptor activation by endogenous and exogenous opioids. The impact of GIRK-related genetic variation on human pain responses has received little research attention. We used a tag single nucleotide polymorphism (SNP) approach to comprehensively examine pain-related effects of KCNJ3 (GIRK1) and KCNJ6 (GIRK2) gene variation. ⋯ A continuous GIRK Related Risk Score (GRRS) was derived in the primary sample to summarize each individual's number of KCNJ6 "pain risk" alleles. This GRRS was applied to the replication sample, which revealed significant associations (P < .05) between higher GRRS values and lower acute pain tolerance and higher CLBP intensity and unpleasantness. Results suggest further exploration of the impact of KCNJ6 genetic variation on pain outcomes is warranted.
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Subsequent to peripheral nerve compression and irritation, pathophysiological processes take place within nervous and immune systems. Here, we utilized a multimodal approach to comprehend peripheral and central soft tissue changes as well as alterations occurring in systemic analytes following unilateral chronic constriction injury (CCI) of the sciatic nerve in rodents. Using magnetic resonance imaging and [18F]-2-fluoro-2-deoxy-d-glucose (FDG) positron emission tomography, we demonstrated robust structural abnormalities and enhanced FDG uptake within the injured nerve and surrounding muscle, respectively. ⋯ Area under the receiver operating curve (ROC) calculations of analyte levels, imaging, and behavioral end points ranged from 0.786 to 1, where behavioral and peripheral imaging end points (eg, FDG uptake in muscle) were observed to have the highest discriminatory capabilities (maximum area under ROC = 1) between nerve injury and sham conditions. Lastly, performance of correlation analysis involving all analyte, behavioral, and imaging data provided an understanding of the overall association amongst these end points, and importantly, a distinction in correlation patterns was observed between CCI and sham conditions. These findings demonstrate the multidimensional pathophysiology of sciatic nerve injury and how a combined analyte, behavioral, and imaging assessment can be implemented to probe this complexity.