Pain
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The present study investigated the role of observer pain catastrophizing and personal pain experience as possible moderators of attention to varying levels of facial pain expression in others. Eye movements were recorded as a direct and continuous index of attention allocation in a sample of 35 undergraduate students while viewing slides presenting picture pairs consisting of a neutral face combined with either a low, moderate, or high expressive pain face. Initial orienting of attention was measured as latency and duration of first fixation to 1 of 2 target images (i.e., neutral face vs pain face). ⋯ With respect to attentional maintenance, participants reporting high catastrophizing and pain intensity demonstrated significantly longer gaze duration for all face types (neutral and pain expression), relative to low catastrophizing counterparts. Finally, independent of catastrophizing, higher reported pain intensity contributed to decreased attentional maintenance to pain faces vs neutral faces. Theoretical implications and further research directions are discussed.
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The biopsychosocial model is increasingly accepted in low back pain (LBP) research and clinical practice. In order to assess the role of psychological factors in the development and persistence of pain, a wide array of measures has been developed. Yet there is likely to be considerable conceptual overlap between such measures, and consequently, a lack of clarity about the importance of psychological factors. ⋯ Results confirmed that considerable overlap exists in psychological measures commonly used in LBP research. Most measures tap into patients' emotional distress. These findings help us to understand how psychological constructs relate together; implications for future research and clinical practice are discussed.
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Treating bone cancer pain poses a major clinical challenge, and the mechanisms underlying bone cancer pain remain elusive. EphrinB-EphB receptor signaling may contribute to bone cancer pain through N-methyl-d-aspartate receptor neuronal mechanisms. Here, we report that ephrinB-EphB signaling may also act through a Toll-like receptor 4 (TLR4)-glial cell mechanism in the spinal cord. ⋯ Intrathecal administration of an exogenous EphB1 receptor activator, ephrinB2-Fc, increased the expression of TLR4 and the levels of IL-1β and TNF-α, activated astrocytes and microglial cells, and induced thermal hypersensitivity. These ephrinB2-Fc-induced alterations were suppressed by spinal knockdown of TLR4. This study suggests that TLR4 may be a potential target for preventing or reversing bone cancer pain and other similar painful processes mediated by ephrinB-EphB receptor signaling.