Pain
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Controlled Clinical Trial
Psychological determinants of problematic outcomes following Total Knee Arthroplasty.
The primary objective of the present study was to examine the role of pain-related psychological factors in predicting pain and disability following Total Knee Arthroplasty (TKA). The study sample consisted of 75 (46 women, 29 men) individuals with osteoarthritis of the knee who were scheduled for TKA. Measures of pain severity, pain catastrophizing, depression, and pain-related fears of movement were completed prior to surgery. ⋯ The results of this study add to a growing literature highlighting the prognostic value of psychological variables in the prediction of post-surgical health outcomes. The results support the view that the psychological determinants of post-surgical pain severity differ from the psychological determinants of post-surgical disability. The results suggest that interventions designed to specifically target pain-related psychological risk factors might improve post-surgical outcomes.
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Controlled Clinical Trial
Influence of heterotopic noxious conditioning stimulation on spontaneous pain and dynamic mechanical allodynia in central post-stroke pain patients.
In 10 patients with central post-stroke pain (CPSP), the influence of ischemia-induced heterotopic noxious conditioning stimulation (HNCS) on the intensity of spontaneous ongoing- and brush-evoked pain was examined. In addition, the modulating effect of ongoing pain and HNCS on pain sensitivity in a remote pain-free area was explored. A semi-quantitative brushing technique was employed in combination with a computerized visual analogue scale (VAS) to monitor the allodynic percept over time, by calculating the area under the VAS curve as the total brush-evoked pain intensity. ⋯ During HNCS, higher pressure pain thresholds were demonstrated in patients and controls alike (P<0.001), whereas in controls only decreased sensitivity to suprathreshold pressure pain was found (P<0.05). Lack of influence from HNCS on ongoing- and brush-evoked pain on a group level, indicates inability of modulation from endogenous pain controlling systems on nociceptive activity generated in the brain. Increased pressure pain sensitivity at baseline suggests alteration in corticofugal control of nociceptive sensitivity due to the brain lesion, whereas patients during HNCS seemed to activate modulatory systems interacting with nociceptive input from the spinal level equal to controls.
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Pain, among the most common symptoms of cancer, impacts on multiple domains of wellbeing. Significant numbers of patients continue to experience pain despite pharmacological interventions. Although there is evidence to suggest that acceptance of pain is related to better wellbeing among patients with chronic nonmalignant pain, little is known about acceptance of cancer pain. ⋯ These relationships were independent of pain severity and physical functioning. These preliminary results suggest that acceptance of cancer pain is related to better psychological wellbeing and that there may be a relational element, with parents at risk of experiencing difficulty in adapting to ongoing cancer pain. These data lay the groundwork for future research and interventions designed to enhance quality of life for patients with advanced cancer and pain.
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To explore cellular changes in sensory neurons after nerve injury and to identify potential target genes contributing to different stages of neuropathic pain development, we used Affymetrix oligo arrays to profile gene expression patterns in L5/6 dorsal root ganglia (DRG) from the neuropathic pain model of left L5/6 spinal nerve ligation at different stages of neuropathic pain development. Our data indicated that nerve injury induced changes in expression of genes with similar biological functions in a temporal specific manner that correlates with particular stages of neuropathic pain development, indicating dynamic neuroplasticity in the DRG in response to peripheral nerve injury and during neuropathic pain development. ⋯ Intrathecal GFAP antisense oligonucleotide treatment in injured rats with neuropathic pain states reversed injury-induced behavioral hypersensitivity and GFAP upregulation in DRG and spinal cord. Together, these findings indicate that injury-induced GFAP upregulation not only serves as a marker for astrocyte activation, but it may also play a critical, but yet identified, role in the maintenance of neuropathic pain states.