The journal of pain : official journal of the American Pain Society
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Acupuncture is a widely used symptomatic treatment for carpal tunnel syndrome (CTS). The objective of this systematic review was to evaluate the evidence of the effectiveness of acupuncture and acupuncture-like treatments for CTS. Systematic searches were conducted on 11 electronic databases without language restrictions. All randomized controlled trials (RCTs) of acupuncture as a treatment of CTS were included. Methodological quality was assessed using the Cochrane risk of bias tool. Six RCTs met our inclusion criteria. Their methodological quality was generally low. Two RCTs compared the effectiveness of acupuncture with a sham control. The others used active controls. A meta-analysis of acupuncture versus steroid block therapy favored acupuncture (2 studies, n = 144; risk ratio, 1.28; 95% CI, 1.08 to 1.52; P = .005; heterogeneity, I(2) = 10%) in terms of responder rate. Our systematic review and meta-analysis demonstrate that the evidence for acupuncture as a symptomatic therapy of CTS is encouraging but not convincing. The total number of included RCTs and their methodological quality were low. Further rigorous studies are required to establish whether acupuncture has therapeutic value for this indication. ⋯ This systematic review of RCTs focused on clinical trials testing the effectiveness of acupuncture for CTS. The existing evidence is not convincing enough to suggest that acupuncture is an effective therapy for CTS. Further RCTs should overcome the limitation of previous studies.
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Randomized Controlled Trial
Association between substance use disorder status and pain-related function following 12 months of treatment in primary care patients with musculoskeletal pain.
The goal of this study was to examine relationships between substance use disorder (SUD) history and 12-month outcomes among primary care patients with chronic noncancer pain (CNCP). Patients were enrolled in a randomized trial of collaborative care intervention (CCI) versus treatment as usual (TAU) to improve pain-related physical and emotional function. At baseline, 72 of 362 patients (20.0%) had a history of SUD. Compared to CNCP patients without SUD, those with comorbid SUD had poorer pain-related function and were more likely to meet criteria for current major depression and posttraumatic stress disorder (all P values <.05). Logistic regression analyses were conducted to examine whether SUD status was associated with clinically significant change over 12 months in pain-related function (30% reduction in Roland Morris Disability Questionnaire Score). The overall model was not significant in the CCI group. However, within the TAU group, participants with a SUD history were significantly less likely to show improvements in pain-related function (OR = .30, 95% CI = .11-.82). CNCP patients with comorbid SUD reported greater functional impairment at baseline. Patients with SUD who received usual care were 70% less likely to have clinically significant improvements in pain-related function 12 months postbaseline, and SUD status did not impede improvement for the CCI group. ⋯ Chronic noncancer pain patients with a history of a substance use disorder (SUD) report poorer pain-related functioning and are less likely to experience clinically significant improvements from usual pain treatment. Providers should assess for SUD status and provide more intensive interventions for these patients.
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Randomized Controlled Trial Clinical Trial
Effects of lidocaine patch on intradermal capsaicin-induced pain: a double-blind, controlled trial.
This study evaluated the effects of topical lidocaine on skin sensation and on intradermal capsaicin-induced pain and hyperalgesia. A randomized, double-blinded, placebo controlled methodology was used. After baseline sensory testing, a placebo patch and a lidocaine patch were randomized to the volar aspect of the left or right forearm for 4 hours. The right forearm patch was removed, the sensory testing was repeated, and capsaicin was injected intradermally at the site. Pain scores were measured at the time of injection and every 2.5 minutes for 10 minutes followed by measurement of the hyperalgesic area to von Frey hair and stroking, flare response, and repeat sensory testing. At the completion of the testing on the right forearm, the left forearm patch was removed and the procedures described for the right forearm were repeated for the left forearm. There was a significant reduction in cool sensation, warm sensation, and touch thresholds in the lidocaine but not placebo patch arm. The lidocaine patch had no significant effect on hot pain or mechanical pain thresholds. Intradermal capsaicin resulted in a significant decrease in hot pain and mechanical pain thresholds; however, lidocaine was unable to significantly reverse the thermal or mechanical hyperalgesia induced by capsaicin. The lidocaine patch did not reduce flare area, nor areas of hyperalgesia or allodynia. This study suggests that the sodium channels and the capsaicin receptors function independently to control peripheral terminal depolarization. ⋯ The sodium channel and the transient receptor potential vanilloid 1 (TRPV1) receptor coexist on peripheral terminals of unmyelinated fibers. This study showed that activation of the TRPV1 receptor can depolarize the fibers in the presence of sodium channel blockade. This suggests that the sodium channel and TRPV1 receptor function independently in depolarizing the fibers.
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Randomized Controlled Trial
Drug response profiles to experimental pain are opioid and pain modality specific.
Given our limited ability to predict analgesic efficacy, further research is needed to understand factors influencing analgesic response patterns. The aim of this study was to better understand the relationship between morphine and butorphanol analgesic efficacy tested against multiple pain modalities within the same individuals. Participants included healthy men (n = 72) and women (n = 67) who underwent thermal, pressure, and ischemic experimental pain testing before and after the double-blind administration of morphine and butorphanol during separate testing sessions. Factor analysis revealed 6 factors with analgesic effects grouped primarily by pain modality and specific to either morphine or butorphanol. Hierarchical cluster analysis of individual factor scores led to 4 distinct drug response profiles. Three groups displayed exceptional analgesic efficacy produced by 1 type of opioid on 1 pain stimulus modality, whereas the fourth drug response profile was characterized by average analgesic efficacy across all pain modalities for both opioids. These findings suggest that opioids with varying efficacy at the μ and κ receptors produce independent effects on unique pain mechanisms and that individual responsiveness for some is dependent on pain mechanism and opioid type, although a subset of the population is moderately responsive to opioids regardless of efficacy of receptor binding or predominant pain mechanism being activated. ⋯ This investigation provides a foundation for understanding patterns of opioid efficacy in varying types of pain. Our findings suggest that opioid response patterns are more complex than originally thought with about half of individuals exhibiting opioid and pain modality specific analgesic response profiles.
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Randomized Controlled Trial
Association of nociceptive responsivity with clinical pain and the moderating effect of depression.
The role of central sensitization (CS) in clinical pain reported by FMS patients is unclear. In this report, we sought to establish evidence of a prospective association between clinical pain and an objective measure of spinal nociception (nociceptive flexion reflex [NFR] threshold) and explore whether depression moderates this relationship. We collected measures that included the NFR threshold (in the range of 0-60 milliamperes (mA); a lower threshold represents greater nociceptive responsivity) and clinical variables (ie, Fibromyalgia Impact Questionnaire (FIQ)-total, FIQ-pain, depression and current pain intensity) at 3 time points (baseline, weeks 6 and 12). Using linear mixed effects models, clinical variables were treated as time-varying covariates. Across time, current pain intensity [estimate -1.79 mA (.8), P = .03] and the presence of depression [estimate -6.30 mA (3.2), P = .059] were significantly associated with NFR threshold. The interaction of current pain intensity and depression was also significantly associated with NFR threshold. Specifically, the relationship between current pain intensity and NFR threshold was present in the nondepressed group but not in the depressed group (estimate -3.9 versus .07, P = .01). Both FIQ-total and FIQ-pain were not associated with NFR threshold. In conclusion, higher level of clinical pain intensity correlated with greater nociceptive responsivity, and that depression moderated this association. ⋯ Given that clinical pain correlated with nociceptive responsiveness, our findings support the mechanistic role of CS in fibromyalgia. If replicated in larger studies, NFR threshold may serve as a biomarker of clinical pain in nondepressed fibromyalgia patients. Also, our results may have future implication for treatment of FMS with and without comorbid depression.