Pain
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Both neuroticism, a higher-order, stable personality trait, and anxiety sensitivity (AS), a lower-order pain-related construct, have been associated with pain, although no research exists examining the relationship of both these constructs to acute pain in children. In the current study, 99 healthy children (53 girls) completed self-report measures of neuroticism and AS before undergoing pain tasks involving cold and pressure pain. ⋯ Mediational models revealed that AS partially mediated relationships between neuroticism and pain intensity/bother, and fully mediated relationships between neuroticism and anticipatory anxiety. These data suggest that, at least in children, neuroticism may be best understood as a vulnerability factor for elevated pain responses, especially when coupled with a fear of bodily sensations.
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Comparative Study
Variability of "optimal" cut points for mild, moderate, and severe pain: neglected problems when comparing groups.
Defining cut points for mild, moderate, and severe pain intensity on the basis of differences in functional interference has an intuitive appeal. The statistical procedure to derive them proposed in 1995 by Serlin et al. has been widely used. Contrasting cut points between populations have been interpreted as meaningful differences between different chronic pain populations. ⋯ Optimal cut points are strongly influenced by random fluctuations within a sample. Differences in optimal cut points between study groups may be explained by chance variation; no other substantial explanation is required. Future studies that aim to interpret differences between groups need to include measures of variability for optimal cut points.
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Joint pain is a common clinical problem for which both inflammatory and degenerative joint diseases are major causes. The purpose of this study was to investigate the role of CB1 and CB2 cannabinoid receptors in the behavioral, histological, and neurochemical alterations associated with joint pain. The murine model of monosodium iodoacetate (MIA) was used to induce joint pain in knockout mice for CB1 (CB1KO) and CB2 cannabinoid receptors (CB2KO) and transgenic mice overexpressing CB2 receptors (CB2xP). ⋯ All mouse lines developed similar histological changes after MIA intra-articular injection. Nevertheless, MIA intra-articular injection produced specific changes in the expression of cannabinoid and opioid receptor genes in lumbar spinal cord sections that were further modulated by the genetic alteration of the cannabinoid receptor system. These results revealed that CB2 receptor plays a predominant role in the control of joint pain manifestations and is involved in the adaptive changes induced in the opioid system under this pain state.