Pain research and treatment
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Background. Many critically ill patients with a traumatic brain injury (TBI) are unable to communicate. While observation of behaviors is recommended for pain assessment in nonverbal populations, they are undetectable in TBI patients who are under the effects of neuroblocking agents. ⋯ Conclusions. Findings from this study support previous ones that vital signs are not specific for pain detection. While RR could be a potential pain indicator in critical care, further research is warranted to support its validity in TBI patients with different LOC.
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Behavioral hypersensitivity is common following spinal cord injury (SCI), producing significant discomfort and often developing into chronic pain syndromes. While the mechanisms underlying the development of behavioral hypersensitivity after SCI are poorly understood, previous studies of SCI contusion have shown an increase in amino acids, namely, aspartate and glutamate, along with a decrease in GABA and glycine, particularly below the injury. The current study sought to identify alterations in key enzymes and receptors involved in mediating central inhibition via GABA and glycine after a clinically-relevant contusion SCI model. ⋯ Combined, these changes result in the disinhibition of excitatory impulses and contribute to behavioral hyperexcitability. This study demonstrates a loss of central inhibition and the development of behavioral hypersensitivity in a contusive SCI paradigm. Future use of this model will permit the evaluation of different antinociceptive strategies and help in the elucidation of new targets for the treatment of neuropathic pain.
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Background. The overall effect of perineural dexamethasone on postoperative analgesia outcomes has yet to be quantified. The main objective of this quantitative review was to evaluate the effect of perineural dexamethasone as a nerve block adjunct on postoperative analgesia outcomes. ⋯ Conclusions. Perineural dexamethasone improves postoperative pain outcomes when given as an adjunct to brachial plexus blocks. There were no reports of persistent nerve injury attributed to perineural administration of the drug.
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This study sought to model and test the role of parental catastrophizing in relationship to parent-reported child pain behavior and parental protective (solicitous) responses to child pain in a sample of children with Inflammatory Bowel Disease and their parents (n = 184 dyads). Parents completed measures designed to assess cognitions about and responses to their child's abdominal pain. They also rated their child's pain behavior. ⋯ Parent-reported child pain behavior predicted parental protective responses and this association was mediated by parental catastrophizing about child pain: indirect effect (SE) = 2.08 (0.56); 95% CI = 1.09, 3.30. The proportion of the total effect mediated was 68%. Findings suggest that interventions designed to modify maladaptive parental responses to children's pain behaviors should assess, as well as target, parental catastrophizing cognitions about their child's pain.
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Background. Pediatric chronic pain is considered to be a multidimensional construct that includes biological, psychological, and social components. Methods. ⋯ Conclusions. These findings provide empirical support of a multidimensional Biobehavioral Model of Pediatric Pain. However, the practical clinical application of the present findings and much of the similar previously published data may be tenuous.