The journal of pain : official journal of the American Pain Society
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Comparative Study
Sex and pain-related psychological variables are associated with thermal pain sensitivity for patients with chronic low back pain.
Biologic and psychological associations with evoked pain sensitivity have been extensively studied in healthy subjects but not among subjects with clinical pain syndromes. This study involved patients with chronic low back pain and investigated whether: 1) sex differences existed for thermal pain sensitivity; and 2) sex, fear-avoidance beliefs, and/or pain catastrophizing influenced thermal pain sensitivity. Thirty-three consecutive patients enrolled in a pain rehabilitation program completed self-report questionnaires and underwent quantitative sensory testing with an established protocol for thermal stimuli. Women had elevated pain sensitivity for measures of tolerance and temporal summation but not for first pulse response. In the multivariate models predicting thermal pain sensitivity, sex was associated with tolerance, and fear-avoidance beliefs were associated with first pulse response. Sex and pain catastrophizing were associated with temporal summation of thermal pain. Future studies involving clinical samples are necessary to replicate these findings and to explore the involvement of cortical structures. ⋯ This study suggests that sex, fear-avoidance beliefs, and pain catastrophizing were associated with thermal pain sensitivity for patients with chronic low back pain. These results corroborated sex differences in tolerance and temporal summation observed in the experimental pain literature for healthy subjects. These results also suggest the potential for these specific pain-related beliefs to be associated with a sensitized state because previous studies have demonstrated their association to clinical pain reports, and this study demonstrated associations with thermal pain sensitivity.
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Randomized Controlled Trial Comparative Study
Placebo-controlled comparison of a morphine/dextromethorphan combination with morphine on experimental pain and hyperalgesia in healthy volunteers.
In this double-blind, placebo-controlled, crossover study we compared the analgesic effect of a single oral dose of 30-mg dextromethorphan and 30-mg morphine combination (MS/DM) to 30 mg morphine (MS) alone and either placebo or 30 mg dextromethorphan (DM) on cutaneous sensitization induced by heat/capsaicin (topical) sensitization on the forearm and the brief thermal sensitization model on the thigh in 22 healthy volunteers. Outcome measures were areas of secondary hyperalgesia to brush and von Frey hair stimulation in both sensitization models and the painfulness of acute thermal noxious stimulation on the upper arm. Compared with placebo, both MS/DM and morphine had some effect on the secondary hyperalgesia and reduced the painfulness of a noxious thermal stimulus. The analgesic effect of MS/DM was not superior to that of morphine on any outcome measure. These results differ from preclinical studies with animal experimental pain models in which DM markedly potentiated the analgesic effects of opioids, but they are in accordance with recent clinical trials for chronic pain. ⋯ Adding dextromethorphan to morphine (1:1 ratio) did not enhance analgesia on measures of experimental cutaneous sensitization and acute noxious thermal stimulation in healthy volunteers. The results differ from preclinical studies but agree with clinical trials. Human experimental models of pain and neuronal sensitization, which are responsive to oral opioids, allow efficient study of opioid combination analgesics and simplify the process for determining the optimal dose and/or dose ratio.
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The relief of neuropathic pain after spinal cord injury (SCI) remains daunting, because pharmacologic intervention works incompletely and is accompanied by multiple side effects. Transplantation of human cells that make specific biologic agents that can potentially modulate the sensory responses that are painful would be very useful to treat problems such as pain. To address this need for clinically useful human cells, the human neuronal NT2 cell line was used as a source to isolate a unique human neuronal cell line that synthesizes and secretes/releases the inhibitory neurotransmitters gamma-aminobutyric acid (GABA) and glycine. This new cell line, hNT2.17, expresses an exclusively neuronal phenotype, does not incorporate bromodeoxyuridine during differentiation, and does not express the tumor-related proteins fibroblast growth factor 4 and transforming growth factor-alpha during differentiation after 2 weeks of treatment with retinoic acid and mitotic inhibitors. The transplant of predifferentiated hNT2.17 cells was used in the excitotoxic SCI pain model, after intraspinal injection of the mixed AMPA/metabotropic receptor agonist quisqualic acid (QUIS). When hNT2.17 cells were transplanted into the lumbar subarachnoid space, tactile allodynia and thermal hyperalgesia induced by the injury were quickly and potently reversed. Control cell transplants of nonviable hNT2.17 cells had no effect on the hypersensitivity induced by QUIS. The effects of hNT2.17 cell grafts appeared 1 week after transplants and did not diminish during the 8-week course of the experiment when grafts were placed 2 weeks after SCI. Immunohistochemistry and quantification of the human grafts were used to ensure that many grafted cells were still present and synthesizing GABA at the end of the study. These data suggest that the human neuronal hNT2.17 cells can be used as a "biologic minipump" for antinociception in models of SCI and neuropathic pain. ⋯ This study describes the initial characterization and use of a human-derived cell line to treat neuropathic pain that would be suitable for clinical application, once further tested for safety and approved by the Food and Drug Administration. A dose of these human cells could be delivered with a spinal tap and affect the intrathecal spinal environment for sensory system modulation.
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Racial and ethnic disparities in healthcare persist in the U.S. Although pain is one of the most prevalent and disabling symptoms of disease, only a few studies have assessed disparities in pain in large racially and ethnically diverse, middle- to late aged community samples, thus limiting the generalizability of study findings in broader populations. With data from the 2000 Health and Retirement Study, we assessed the prevalence and impact of pain in a community sample of aging (> or =51 years old) non-Hispanic whites (n = 11,021), non-Hispanic blacks (n = 1,804), and Hispanics (n = 952) in the U.S. Pain, pain severity, activity limitation as a result of pain, comorbid conditions, and sociodemographic variables were assessed. Results showed that pain prevalence was 28%, and 17% of the sample reported activity limitation as a result of pain. Non-Hispanic blacks (odds ratio [OR], 1.78; 99% confidence interval [CI], 1.33-2.37) and Hispanics (OR, 1.80; 99% CI, 1.26-2.56) had higher risk for severe pain compared with non-Hispanic whites. Analyses of respondents with pain (n = 3,811) showed that having chronic diseases (2 comorbid conditions, OR, 1.5; 99% CI, 1.09-2.17), psychological distress (OR, 1.99; 99% CI, 1.54-2.43), being a Medicaid recipient (OR, 1.63; 99% CI, 1.17-2.25), and lower educational level (OR, 1.45; 99% CI, 1.14-1.85) were significant predictors for severe pain and helped to explain racial/ethnic differences in pain severity. ⋯ This study, which used a large racially and ethnically diverse community sample, provided empirical evidence that racial/ethnic difference in pain severity in aging community adults in the U.S. can be accounted for by differential vulnerability in terms of chronic disease, socioeconomic conditions, and access to care.
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The purpose of this study was to document analgesic use for limb and clavicle injuries in the pediatric emergency department (ED) and to determine whether a physician-oriented pain scale form on the patient's chart would enhance the administration of analgesia. Patients 3 to 18 years old were recruited prospectively in our tertiary pediatric ED in Toronto. The study included 4 crossover periods, 2 with the pain scale form on the patient's chart and 2 without. A total of 310 patients were recruited, mean age was 10 years, 64% were boys, and 62% had sustained fractures. The mean pain score was 4.4. Only 90 (29%) patients received an analgesic in the ED, and 65 (72%) of them were ordered by a physician. Only 24 (20%) in the study group and 22 (14%) in the control group received sufficient analgesia (P = .13). The median time to physician-initiated analgesia after arrival was 2.0 hours (1.0 to 3.3 hours), without a significant difference between groups. Pain control was 4-fold more appropriate in children receiving opioids versus nonopioids. Physician pain reminders did not enhance, and other measures should be taken to increase the dispensing of analgesia. ⋯ This is the first study to evaluate whether the addition of a physician-oriented pain-scale form on the chart of patients with injuries improves administration of analgesia in the ED. We found that physicians do not give sufficient analgesia even with this reminder form.