Pain
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Randomized Controlled Trial
The role of executive functioning in children's attentional pain control: An experimental analysis.
Directing attention away from pain is often used in children's pain treatment programs to control pain. However, empirical evidence concerning its effectiveness is inconclusive. We therefore sought to understand other influencing factors, including executive function and its role in the pain experience. ⋯ Our findings suggest that distraction as a process for managing pain is complex. While it appears that executive function may play a role in adult distraction, in this study it did not direct attention away from pain. It may instead be involved in the overall pain experience.
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Randomized Controlled Trial
Increasing optimism abolishes pain-induced impairments in executive task performance.
Coping with the demands of pain diminishes self-regulatory capacity and causes self-regulatory fatigue, which then leads to deteriorated executive task performance. It has been suggested that optimism can counteract the depletion of self-regulatory capacity. ⋯ Results indicated that although pain led to significantly worse performance on the executive functioning task in the no optimism condition, this sustained deteriorating effect of pain on task performance was abolished in the optimism condition. This finding is imperative because it suggests that optimism may be an important factor to implement in current psychological treatment approaches to diminish the negative impact of chronic pain on the ability to function in daily life.
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The processes of individual adaptation to chronic pain are complex and occur across multiple domains. We examined the social, cognitive, and affective context of daily pain adaptation in individuals with fibromyalgia and osteoarthritis. By using a sample of 260 women with fibromyalgia or osteoarthritis, we examined the contributions of pain catastrophizing, negative interpersonal events, and positive interpersonal events to daily negative and positive affect across 30days of daily diary data. ⋯ The relationships between pain and negative and positive affect were mediated by stable and day-to-day levels of pain catastrophizing as well as day-to-day positive interpersonal events, but not negative interpersonal events. There were significant and independent contributions of pain catastrophizing and positive interpersonal events to adaptation to pain and pain-related affective dysregulation. These effects occur both between persons and within a person's everyday life.
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Bone cancer pain is a common and disruptive symptom in cancer patients. In cancer pain animal models, massive reactive astrogliosis in the dorsal horn of the spinal cord has been reported. Because astrocytes may behave as driving partners for pathological pain, we investigated the temporal development of pain behavior and reactive astrogliosis in a rat bone cancer pain model induced by injecting MRMT-1 rat mammary gland carcinoma cells into the tibia. ⋯ In contrast, all these parameters were increased in the dorsal horn of rats 2weeks after sciatic nerve ligation. This suggests that in some cases, bone cancer pain may not be correlated with spinal overexpression of reactive glia markers, whereas neuropathic pain is. Glia may thus play different roles in the development and maintenance of chronic pain in these 2 situations.
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The unpredictable efficacy of current therapies for neuropathic pain may reflect diverse etiological mechanisms operating between, and within, diseases. As descriptions of pain rarely establish specific mechanisms, a tool that can identify underlying causes of neuropathic pain would be useful in developing patient-specific treatments. Rate-dependent depression (RDD), a measure of the change in amplitude of the Hoffman reflex over consecutive stimulations, is attenuated in diabetic rats that also exhibit impaired spinal γ-aminobutyric acid (GABA)A receptor function, reduced spinal potassium chloride co-transporter (KCC2) expression, and indices of painful neuropathy. ⋯ Treating diabetic rats with TrkB/Fc restored RDD and alleviated indices of painful neuropathy. In paclitaxel-treated rats, RDD was not impaired and behavioral indices of neuropathic pain were not associated with spinal GABAergic dysfunction or reduced dorsal spinal KCC2 expression. Our data reveal BDNF as part of the mechanism underlying spinal cord disinhibition caused by altered GABAA receptor function in diabetic rats and suggest that RDD deficits may be a useful indicator of neuropathic pain states associated with spinal disinhibition, thereby revealing specific therapeutic targets.