Pain
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Being able to detect pain from facial expressions is critical for pain communication. Alongside identifying the specific facial codes used in pain recognition, there are other types of more basic perceptual features, such as spatial frequency (SF), which refers to the amount of detail in a visual display. Low SF carries coarse information, which can be seen from a distance, and high SF carries fine-detailed information that can only be perceived when viewed close up. ⋯ This general low-SF bias would seem an advantageous way of potential threat detection, as facial displays will be degraded if viewed from a distance or in peripheral vision. One exception was found, however, in the "pain-fear" task, where responses were not affected by SF type. Together, this not only indicates a flexible role for SF information that depends on task parameters (goal context) but also suggests that in challenging visual conditions, we perceive an overall affective quality of pain expressions rather than detailed facial features.
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Activity treatments, such as treadmill exercise, are used to improve functional recovery after nerve injury, parallel to an increase in neurotrophin levels. However, despite their role in neuronal survival and regeneration, neurotrophins may cause neuronal hyperexcitability that triggers neuropathic pain. ⋯ Injury also induced Na⁺-K⁺-2Cl⁻ cotransporter 1 (NKCC1) upregulation in DRG, and K⁺-Cl⁻ cotransporter 2 (KCC2) downregulation in lumbar spinal cord dorsal horn. iTR normalized NKCC1 and boosted KCC2 expression, together with a significant reduction of microgliosis in L3-L5 dorsal horn, and a reduction of BDNF expression in microglia at 1 to 2 weeks postinjury. These data demonstrate that specific activity protocols, such as iTR, can modulate neurotrophins expression after peripheral nerve injury and prevent neuropathic pain by blocking early mechanisms of sensitization such as collateral sprouting and NKCC1/KCC2 disregulation.
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The subjective experience of pain is influenced by interactions between experiences, future predictions, and incoming afferent information. Expectations of high pain can exacerbate pain, whereas expectations of low pain during a consistently noxious stimulus can produce significant reductions in pain. However, the brain mechanisms associated with processing mismatches between expected and experienced pain are poorly understood, but are important for imparting salience to a sensory event to override erroneous top-down expectancy-mediated information. ⋯ Thus, violated expectations of pain engage mechanisms supporting salience-driven sensory discrimination, working memory, and associative learning processes. By overriding the influence of expectations on pain, these brain mechanisms are likely engaged in clinical situations in which patients' unrealistic expectations of pain relief diminish the efficacy of pain treatments. Accordingly, these findings underscore the importance of maintaining realistic expectations to augment the effectiveness of pain management.