Pain
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Overactivity (activity engagement that significantly exacerbates pain) is a common term in the chronic pain literature. Overactivity is accepted clinically as a behaviour that adversely affects an individual's daily functioning and is the target of one of the most widely endorsed pain management strategies among health professionals (ie, activity pacing). Little research, however, has investigated links between overactivity behaviour and indicators of patient functioning, and activity pacing has not been evaluated as a stand-alone treatment specifically for individuals with chronic pain who are habitually overactive. ⋯ Some participants who were followed up 3 to 6 months after a pain management program were able to learn pacing strategies and enact behaviour change with health professional support; however, the majority reported difficulties changing their behaviour after treatment. It is suggested that provision of pacing education, alone, to chronic pain patients who engage in overactivity behaviour may not be effective in eliciting behavioural change. Key factors that participants believed to contribute to the development and maintenance of their overactive behaviour in this study should be considered in future clinical approaches and empirical investigations.
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Accumulating evidence suggests that opioid analgesics can lead to paradoxical sensitization to pain when delivered in different administration patterns. Although opioid tolerance-induced hyperalgesia is largely studied, little is known about the mechanisms underlying acute ultra-low-dose morphine hyperalgesia. Activation of spinal glial cells is reported to regulate pain hypersensitivity. ⋯ Immunofluorescence experiments indicated the neuronal localization of spinal MOR. However, JNK was not detected in MOR-expressing cells, showing the presence of a neuron-astrocyte signaling pathway. These results illustrate the selective activation of an astrocyte JNK pathway after the stimulation of neuronal MOR, which contributes to ultra-low-dose morphine hyperalgesia.
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This study considered the attentional functioning of adolescents with varying levels of pain catastrophizing. Specifically, we investigated the relationship between pain catastrophizing and attention bias to pain facial expressions. Furthermore, drawing on dual process models in the context of pain, we investigated the moderating role of attention control on this relationship. ⋯ In addition, we found that poorer attention control was related to increased attention bias for pain faces (regardless of pain catastrophizing level) when these faces were presented for relatively longer durations (ie, 1250 milliseconds) but not for short durations (ie, 100 milliseconds). This study supports a dual process model of attentional processes in pain, thus replicating previous findings within the psychopathology literature but extending them to the study of pain. Theoretical and clinical implications of our findings are discussed.
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Pathological pain is one of the most common neurological complications in patients with HIV-1/AIDS. However, the pathogenic process is unclear. Our recent studies show that Wnt5a is upregulated in the spinal cord dorsal horn (SDH) of the patients with HIV who develop pain and that HIV-1 gp120, a potential causal factor of the HIV-associated pain, rapidly upregulates Wnt5a in the mouse SDH. ⋯ Furthermore, while Foxy5 potentiated spike frequency of SDH neurons, either SP600125 or Enbrel blocked the potentiation. The data indicate that Wnt5a potentiates the activity of SDH neurons through the JNK-TNF-α pathway. Collectively, our findings suggest that Wnt5a regulates the pathogenesis of gp120-induced pain, likely by sensitizing pain-processing SDH neurons through JNK/TNF-α signaling.