The journal of pain : official journal of the American Pain Society
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Comparative Study
Ibuprofen blocks changes in Na v 1.7 and 1.8 sodium channels associated with complete Freund's adjuvant-induced inflammation in rat.
Although nerve growth factor plays a role in augmenting sodium channel expression in small dorsal root ganglion (DRG) cells, the cytochemical mediators responsible for enhanced expression in large DRG neurons are unknown. To narrow the search for mediators involved in the increased production of sodium channels in large DRG neurons, we examined the effect of cyclooxygenase inhibition on sodium channel production during inflammation. Thirty minutes before the subcutaneous injection of complete Freund's adjuvant (CFA), rats received ibuprofen (nonselective, cyclooxygenase inhibitor), NS-398 (selective, cyclooxygenase inhibitor), or vehicle. Withdrawal thresholds from thermal and mechanical stimulation were measured before and immediately after CFA injection and at selected hourly intervals after injection for the next 24 hours. Sodium channel up-regulation was then examined in DRG by using site-specific, anti-sodium channel antibodies, Na(v) 1.7 and 1.8. Both ibuprofen and NS-398 provided analgesia during the second phase of inflammatory hyperalgesia that begins 3 hours after CFA injection. The up-regulation, predominantly of Na(v) 1.7 and minimally of Na(v) 1.8 channels, seen in vehicle-treated rats was suppressed by both drugs at 24 hours after injection. By 72 hours after injection, no difference in labeling between the drug- and vehicle-treated animals was observed. Sodium channel labeling in large DRG neurons returned to baseline between 1 and 2 weeks after CFA injection, whereas small cell labeling persisted. The cytochemical signal for sodium channel up-regulation in the large DRG cells that most closely correlates with inflammatory hyperalgesia is mediated at least in part through products of the cyclooxygenase pathway. ⋯ Expression of sodium channels in dorsal root ganglia increases dramatically during inflammation. The increase in sodium channels is thought to enhance neuronal excitability and to play a role in hyperalgesia and wound vigilance during healing. We provide evidence that prostaglandins play a role in signaling channel augmentation.
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Comparative Study
Does fear of pain moderate the effects of sensory focusing and distraction on cold pressor pain in pain-free individuals?
The present study investigated the influence of sensory focusing and distraction on pain tolerance and self-reported pain intensity in healthy female university students ranking high or low in pain-related fear. Pain was induced experimentally by means of a cold pressor test. Results showed that individuals high in pain-related fear groups had greater pain intensity ratings than those low in pain-related fear groups. A planned comparison analysis showed that distraction produced reduced pain ratings only in low fearful individuals, whereas sensory focusing led to reduced pain ratings only in high fearful individuals. Self-report measures of anxiety sensitivity, pain vigilance, and pain catastrophizing were positively associated with pain intensity, but, except for pain vigilance, no meaningful association was found between these measures and pain tolerance. Implications of the results and directions for future research are provided. ⋯ In the management of chronic pain, distraction might be especially useful in low fearful individuals. Learning to focus on the sensory aspects (ie, monitoring) of the pain experience might be beneficial for high fearful individuals.
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Comparative Study
Assessment of self-reported physical activity in patients with chronic pain: development of an abbreviated Roland-Morris disability scale.
The Roland-Morris Disability Scale has been shown to be a reliable and valid measure of disability in persons with chronic pain. A short form with psychometric properties similar to the full scale would have numerous benefits, including decreased patient assessment burden and scoring time. On the basis of data obtained from 993 individuals with chronic pain screened for admission to a multidisciplinary pain management program, an 11-item short form of the Roland scale was developed using procedures and models from item response theory. This short form was found to be a good predictor of the 24-item parent scale and a previously published 18-item short form. The 11-item scale also demonstrated concurrent validity with measures of pain intensity and depression. Item content reflected limitations in specific functional behaviors. ⋯ Brief measures of important pain-related variables can be created using item response theory (IRT). In this study, a reliable and valid 11-item version of the Roland-Morris Disability Scale was created using IRT. Clinicians and researchers might consider using this scale when patient or subject assessment burden is an issue.
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Comparative Study
Prior pain experience: influence on the observation of experimental pain in men and women.
Research examining perceptions of subjects participating in an experimental pain task has not been widely studied. The primary purpose of this study was to examine the influence of prior experience with the cold pressor on subsequent perceptions of others experiencing this same pain task. Furthermore, to replicate our previous work, we examined how individuals observe experimentally induced pain in male and female participants. Possible interactions between order of cold pressor experience, sex of the viewer, sex of the individual being observed, and characteristics attributed to the individuals in the videos were also analyzed. The sample was composed of 57 participants. They were each randomized to 1 of 2 conditions: (1) participate in cold pressor task before viewing a presentation of 10 video clips (of subjects in cold pressor task), rate videos, and complete battery of questionnaires or (2) cold pressor participation after completion of the same questionnaires, and viewing/rating videos. Participants viewing the videos provided ratings including observed pain and emotional characteristics they attributed to the individuals. These results replicated and extended our previous work by demonstrating a gender bias (ie, a stereotypical belief about an individual on the basis of their sex) in the observation of pain, such that participants rated female subjects as experiencing greater pain intensity when undergoing a cold pressor task compared to male subjects. Furthermore, experiencing the cold pressor before watching the videos increased a participant's pain ratings of observed pain. There were also several significant interactions between cold pressor condition, sex of video participant, sex of viewer, and emotional/behavioral characteristics attributed to the video participant. ⋯ Results of this study demonstrate that prior experience with pain increases accuracy of estimating others' pain. Gender role expectations also influence observer's ratings of pain, and prior experience of pain influences men and women differently.
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Systemic administration of local anesthetics has been shown to transiently reverse thermal and tactile hypersensitivity induced by peripheral nerve injury, effects that have been taken as suggesting direct actions on the peripheral nerves. The present study sought to determine whether a central site of action could contribute to, or account for, the effects of lidocaine on nerve injury-induced thermal and tactile hypersensitivity. Systemic lidocaine and its peripherally restricted analogues, QX-314 or QX-222, effectively reversed thermal hypersensitivity after spinal nerve ligation injury. Nerve injury-induced tactile hypersensitivity, however, was reversed by systemic lidocaine but not QX-314 or QX-222. Microinjection of either lidocaine or QX-314 into the rostral ventromedial medulla fully reversed spinal nerve ligation-induced thermal and tactile hypersensitivity. The data strongly suggest that nerve injury-induced thermal and tactile hypersensitivity are mediated through different mechanisms. In addition, the present study supports a prominent contribution of the central nervous system in the activity of systemically given lidocaine against nerve injury-induced tactile and thermal hypersensitivity. Thus, lidocaine might reverse tactile hypersensitivity mainly through its actions within the central nervous system, whereas its reversal of thermal hypersensitivity might occur through either central or peripheral sites. ⋯ Nerve injury-induced neuropathic pain has proved remarkably difficult to treat. Systemic administration of ion channel blockers such as lidocaine has been explored for the management of chronic pain. This work indicates that systemic rather than local administration of lidocaine would be more effective in treating tactile allodynia.