Scandinavian journal of pain
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Pain catastrophizing is linked to heightened pain and poorer coping among individuals with chronic pain, yet little is known about how pain catastrophizing associates with sleep and pain over the course of treatment for chronic pain. Previous research employing a cross-sectional design suggests that sleep mediates the association between pain catstrophizing and pain, but there have been no longitudinal studies examining the directionality of these associations. Thus, the aim of this study was to test two competing theoretical models. The first model specified that pain catastrophizing leads to increased pain via poor sleep. The second model specified that poor sleep leads to increased pain catastrophizing via increased pain. ⋯ These results call into question previous evidence that pain catastrophizing indirectly affects pain by way of its impact on sleep. Rather, our findings suggest that pain mediates the relationship between sleep and levels of pain catastrophizing. These results therefore underscore importance and value in collecting longitudinal data and potential influence on the conclusions gained with regards to sleep, pain and psychological variables. These findings may be of clinical importance when tailoring interventions for individuals with chronic pain and perhaps even more so for those with comorbid pain and sleep disturbance; prioritizing the treatment of sleep difficulties could result in improvements to pain-related outcomes.
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Mirror visual feedback may be a useful clinical tool for reducing pain. Research suggests that reducing the size of a non-painful reflected hand can alleviate complex regional pain syndrome in the affected hand that is out of view. In contrast, research on healthy humans exposed to experimentally induced pain suggests that reducing the appearance of the size of a reflected body part can increase pain. The aim of this study was to investigate the effect of enlarging and reducing the visual appearance of the size of a hand using mirror visual feedback on pain threshold, intensity and tolerance in healthy human participants exposed to cold-pressor pain. ⋯ In future, investigators and clinicians using mirror visual feedback may consider including an adaptive phase to ensure the reflection has been perceptually embodied. Reasons for the lack of effects are explored to inspire further research in the field.
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Although neuropathic pain is known to negatively affect cognition, the neural mechanisms involved are poorly understood. Chronic pain is associated with changes in synaptic plasticity in the brain which may impact on cognitive functioning. The aim of this study was to model neuropathic pain in mid-aged rats using spinal nerve ligation (SNL). Following establishment of allodynia and hyperalgesia, behaviour was assessed in a battery of cognitive tests. Expression of the presynaptic protein, synaptophysin, and its colocalisation with the vesicular GABA and glutamate transporters (vGAT and vGLUT, respectively), was investigated in the medial prefrontal cortex (mPFC) and hippocampus. ⋯ Cognitive complaints are common amongst chronic pain patients. Here we modelled cognitive impairment in a well-established animal model of neuropathic pain and investigated the neural mechanisms involved. A better understanding of this phenomenon is an important prerequisite for the development of improved treatment of patients affected.
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Objective Insomnia is the most commonly diagnosed comorbidity disorder among patients with chronic pain. This circumstance requests brief and valid instruments for screening insomnia in epidemiological studies. The main object of this study was to assess the psychometric properties and factor structure of the Swedish version of the Insomnia Severity Index (ISI). ⋯ An important clinical implication is that the four-item Swedish Insomnia Severity Index can be used in chronic pain cohorts when screening for insomnia problems. Its measurement and structural invariance property across the two sexes shows that the ISI-4 is a valid measure of the insomnia across groups of chronic patients. Our results also suggest its utility both in pain clinical practice and research purposes.
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Background and aims The clinical management of chronic neuropathic pain remains a global health challenge. Current treatments are either ineffective, or associated with unwanted side-effects. The development of effective, safe therapies requires the identification of novel therapeutic targets using clinically relevant animal models of neuropathic pain. ⋯ Conclusion The observation that levels of PPARα protein were increased in ipsilateral spinal cord of neuropathic rats supports a contribution of spinal sites of action mediating the effects of systemic WY-14643. Our data suggests that the inhibitory effects of a PPARα agonist on spinal neuronal responses may account, at least in part, for their analgesic effects of in neuropathic pain. Implication Selective activation of PPARα in the spinal cord may be therapeutically relevant for the treatment of neuropathic pain.