The journal of pain : official journal of the American Pain Society
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Transcutaneous electrical nerve stimulation (TENS) is an electrophysical modality used for pain management. This study investigated the dose response of different TENS intensities on experimentally induced pressure pain. One hundred and thirty TENS naïve healthy individuals (18-64 years old; 65 males, 65 females) were randomly allocated to 5 groups (n = 26 per group): Strong Non Painful TENS; Sensory Threshold TENS; Below Sensory Threshold TENS; No Current Placebo TENS; and Transient Placebo TENS. Active TENS (80 Hz) was applied to the forearm for 30 minutes. Transient Placebo TENS was applied for 42 seconds after which the current amplitude automatically reset to 0 mA. Pressure pain thresholds (PPT) were recorded from 2 points on the hand and forearm before and after TENS to measure hypoalgesia. There were significant differences between groups at both the hand and forearm (ANOVA; P = .005 and .002). At 30 minutes, there was a significant hypoalgesic effect in the Strong Non Painful TENS group compared to: Below Sensory Threshold TENS, No Current Placebo TENS and Transient Placebo TENS groups (P < .0001) at the forearm; Transient Placebo TENS and No Current Placebo TENS groups at the hand (P = .001). There was no significant difference between Strong Non Painful TENS and Sensory Threshold TENS groups. The area under the curve for the changes in PPT significantly correlated with the current amplitude (r(2) = .33, P = .003). These data therefore show that there is a dose-response effect of TENS with the largest effect occurring with the highest current amplitudes. ⋯ This study shows a dose response for the intensity of TENS for pain relief with the strongest intensities showing the greatest effect; thus, we suggest that TENS intensity should be titrated to achieve the strongest possible intensity to achieve maximum pain relief.
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Case Reports
The contribution of sympathetic mechanisms to postamputation phantom and residual limb pain: a pilot study.
Postamputation pain (PAP) affects over 60% of major limb amputees. One of the main challenges in treating PAP is the difficulty involved in identifying pain mechanism(s), which pertains to both residual limb pain (RLP) and phantom limb pain (PLP). In this study, sympathetic blocks were performed on 17 major limb amputees refractory to treatment, including 2 placebo-controlled blocks done for bilateral amputations. One hour postinjection, mean RLP scores at rest declined from 5.2 (SD 2.8) to 2.8 (SD 2.6) (P = .0002), and PLP decreased from 5.3 (SD 3.1) to 2.3 (SD 2.1) (P = .0009). By 1 week, mean pain scores for RLP and PLP were 4.3 (SD 2.9) and 4.2 (SD 3.0), respectively. Overall, 8 of 16 (50%) patients experienced ≥50% reduction in RLP 1-hour postinjection, with the beneficial effects being maintained at 1 and 8 weeks in 4 and 1 patient(s), respectively. For PLP, 8 of 15 (53%) patients obtained ≥50% decrease in pain 1-hour postblock, with these numbers decreasing to 2 patients at both 1 and 8 weeks. In the 2 bilateral amputees who received controlled injections, mean PLP and RLP at rest scores went from 4.0 and 3.3 to 4.0 and 2.5 1-hour postblock, respectively, on the placebo side. On the treatment side, mean PLP and RLP scores decreased from 7.5 and 6.5, respectively, to 0. ⋯ The results of this study suggest that sympathetic mechanisms play a role in PLP and to a lesser extent, RLP, but that blocks confer long-term benefits in only a small percentage of patients.
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Genetic studies have become indispensable in understanding pain mechanisms, shedding light on the role of monoamine pathways in pain modulation. The present study was aimed to explore the relationship between functional polymorphisms in serotonin and dopamine-related genes and pain modulation. Two paradigms of pain modulation were administered to 191 healthy participants in a random order: Conditioned Pain Modulation in response to painful stimuli (CPM(painful)) tested by the coadministration of repeated short painful heat stimuli and a conditioning tonic cold pain stimulation; and Conditioned Pain Modulation in response to nonpainful stimuli (CPM(nonpainful)) tested similarly, except for using a painless conditioning stimulation. Using the Transmission Disequilibrium Test (TDT), functional variable number of tandem repeat (VNTR) polymorphisms of the following candidate genes were studied: 1) serotonin transporter (5-HTTLPR); 2) dopamine transporter (DAT1); 3) dopamine receptor 4 (DRD4); and 4) monoamine oxidase A (MAOA). DNA samples from both participants and their parents were analyzed. A significant association was found between CPM(nonpainful) and the 5-HTTLPR polymorphism (P = .001). More specifically, carriers of the long allele exhibited a significantly higher magnitude of CPM(nonpainful) than carriers of the short allele. No associations were found between the dopamine-related genes and both types of pain modulation. These results highlight the importance of serotonin in endogenous analgesia. ⋯ This article presents an association between the serotonin transporter gene polymorphism (5-HTTLPR) and pain modulation derived by nonpainful conditioned pain modulation (CPM(nonpainful)), rather than painful conditioned pain modulation (CPM(painful)). These findings emphasize the complex role of serotonin in pain modulation, and highlight the importance of genetic studies in the understanding of interindividual differences in sensitivity to pain.
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The objective of this project was to determine the relationship between cigarette smoking and the reporting of chronic pain syndromes among participants in the Kentucky Women's Health Registry. Data was analyzed on 6,092 women over 18 years of age who responded to survey questions on pain and smoking. The chronic pain syndromes included in the analysis were fibromyalgia, sciatica, chronic neck pain, chronic back pain, joint pain, chronic head pain, nerve problems, and pain all over the body. Analyses controlled for age, body mass index, and Appalachian versus non-Appalachian county of residence. Results showed that women who were daily smokers reported more chronic pain (defined as the presence of any reported chronic pain syndromes) than women who were never smokers (adjusted odds ratio [aOR] = 2.04 and 95% confidence interval [CI] 1.67, 2.49). An increased risk was also seen for "some-day" smokers (aOR 1.68, 95% CI 1.24, 2.27), and former smokers (aOR 1.20, 95% CI 1.06, 1.37), though with less of an association in the latter group. This study provides evidence of an association between chronic pain and cigarette smoking that is reduced in former smokers. ⋯ This paper presents the association between smoking and musculoskeletal pain syndromes among Kentucky women. This finding may provide additional opportunities for intervention in patients with chronic pain.