The journal of pain : official journal of the American Pain Society
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Randomized Controlled Trial
Diclofenac potassium attenuates dysmenorrhea and restores exercise performance in women with primary dysmenorrhea.
We assessed the efficacy of diclofenac potassium, a nonsteroidal anti-inflammatory drug, in alleviating menstrual pain and restoring exercise performance to that measured in the late-follicular phase of the menstrual cycle. Twelve healthy young women with a history of primary dysmenorrhea completed, in a random order, laboratory exercise-testing sessions when they were in the late-follicular (no menstruation, no pain) phase of the menstrual cycle and when they were experiencing dysmenorrhea and receiving, in a double-blinded fashion, either 100 mg of diclofenac potassium or placebo. We assessed the women's leg strength (1-repetition maximum test), aerobic capacity (treadmill walking test), and ability to perform a functional test (task-specific test). Compared with placebo, diclofenac potassium significantly decreased dysmenorrhea on the day of administration (Visual Analog Scale, P < .001 at all times). When receiving placebo for menstrual pain, the women's performance in the tests was decreased significantly, compared with when they were receiving diclofenac potassium for menstrual pain (P < .05) and compared with when they were in the late-follicular phase of the menstrual cycle (P < .05 for treadmill test, P < .01 for task-specific test and 1-repetition maximum test). Administration of diclofenac potassium for menstrual pain restored exercise performance to a level not different from that achieved in the late-follicular phase of the cycle. ⋯ In women with primary dysmenorrhea, menstrual pain, if untreated, decreases laboratory-assessed exercise performance. A recommended daily dose of a readily available nonsteroidal anti-inflammatory drug, diclofenac potassium, is effective in relieving menstrual pain and restoring physical performance to levels achieved when the women were in the late-follicular (no menstruation, no pain) phase of the menstrual cycle.
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Optimal methods to predict risk of aberrant drug-related behaviors before initiation of opioids for chronic noncancer pain and to identify aberrant behaviors after therapy is initiated are uncertain. We systematically reviewed published literature identified through searches of Ovid MEDLINE and the Cochrane databases through July 2008. Diagnostic test characteristics and accompanying confidence intervals were calculated with data extracted from the studies. Four prospective studies evaluated diagnostic accuracy of risk prediction instruments. Two higher-quality derivation studies found that high scores on the Screener and Opioid Assessment for Patients with Pain (SOAPP) Version 1 and the Revised SOAPP (SOAPP-R) instruments weakly increased the likelihood for future aberrant drug-related behaviors (positive likelihood ratios [PLR], 2.90 [95% CI, 1.91 to 4.39] and 2.50 [95% CI, 1.93 to 3.24], respectively). Low scores on the SOAPP Version 1 moderately decreased the likelihood for aberrant drug-related behaviors (negative likelihood ratio [NLR], 0.13 [95% CI, 0.05 to 0.34]) and low scores on the SOAPP-R weakly decreased the likelihood (NLR, 0.29 [95% CI, 0.18 to 0.46]), but estimates are too imprecise to determine if there is a difference between these instruments. One lower-quality study found that categorization as high risk using the Opioid Risk Tool strongly increased the likelihood for future aberrant drug-related behaviors (PLR, 14.3 [95% CI, 5.35 to 38.4]) and classification as low risk strongly decreased the likelihood (PLR, 0.08 [95% CI, 0.01 to 0.62]). Nine studies evaluated monitoring instruments for identification of aberrant drug-related behaviors in patients on opioid therapy. One higher-quality derivation study found higher scores on the Current Opioid Misuse Measure (COMM) weakly increased the likelihood of current aberrant drug-related behaviors (PLR, 2.77 [95% CI, 2.06 to 3.72]) and lower scores weakly decreased the likelihood (NLR, 0.35 [95% CI, 0.24 to 0.52]). In 8 studies of other monitoring instruments, diagnostic accuracy was poor, results were difficult to interpret due to methodological shortcomings, or standard diagnostic test characteristics were not reported. Definitions for aberrant drug-related behaviors were not standardized across studies and did not account for seriousness of identified behaviors. No reliable evidence exists on accuracy of urine drug screening, pill counts, or prescription drug monitoring programs; or clinical outcomes associated with different assessment or monitoring strategies. ⋯ Evidence on prediction and identification of aberrant drug-related behaviors is limited. Although several screening instruments may be useful, evidence is sparse and primarily based on derivation studies, and methodological shortcomings exist in all studies. Research that performs external validation, uses standardized definitions for clinically relevant aberrant drug-related behaviors, and evaluates clinical outcomes associated with different assessment and monitoring strategies is needed.
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The purpose of the study was to examine the effect of 3 different application strategies for transcutaneous electrical nerve stimulation (TENS) on neuropathy-induced allodynia and dorsal horn neurotransmitter content. Rats were treated with high-frequency, low-frequency, or a combination of high and low-frequency stimulation. TENS was delivered through self-adhesive electrodes daily for 1 hour to rats with a right-sided chronic constriction injury (CCI). Stimulation was delivered to skin or acupuncture points on the left and mechanical and thermal pain thresholds were assessed in the right hind paw. Neurotransmitter content was assessed bilaterally in the dorsal horn of the spinal cord. Daily, high-frequency or a combination of high- and low-frequency TENS reduced mechanical (P < .001), but not thermal allodynia in the right hind paw when compared with untreated CCI rats. Daily high frequency TENS elevated the dorsal horn synaptosomal content of GABA bilaterally (P < .014) and a combination of high- and low-frequency TENS elevated the dorsal horn content of aspartate (P < .001), glutamate (P < .001) and glycine (P < .001) bilaterally over that seen in untreated CCI rats. The present findings support a contralateral approach to the application of TENS and suggest that distinct strategies for TENS application may differentially alter neurotransmission in the central nervous system. ⋯ Because CCI rats are reminiscent of humans with neuropathy, daily high or a combination of high- and low-frequency TENS may reduce mechanical allodynia in humans with neuropathic pain. Because the 2 intervention strategies produce distinctive alterations in spinal cord neurotransmitter content, each may represent a distinctive option for treatment.
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Clinical Trial
Associations between catastrophizing and endogenous pain-inhibitory processes: sex differences.
Pain catastrophizing is among the most robust predictors of pain outcomes, and a disruption in endogenous pain-inhibitory systems is 1 potential mechanism that may account for increased pain among individuals who report higher pain catastrophizing. Pain catastrophizing may negatively influence diffuse noxious inhibitory controls (DNIC), a measure of endogenous pain inhibition, through complex anatomical circuitry linking cortical responses to pain with processes that modulate pain. The current study examined whether DNIC mediated the relationship between catastrophizing and pain among 35 healthy young adults and examined the moderating effects of sex to determine whether the magnitude or direction of associations differed among men and women. DNIC was assessed using pressure pain thresholds on the forearm before and during a cold pressor task. Using bias-corrected bootstrapped confidence intervals, results showed that diminished DNIC was a significant partial mediator of the relation between greater pain-related catastrophizing and more severe pain ratings. Participant sex moderated these associations; higher catastrophizing predicted lower DNIC for men and women, however, the effect of catastrophizing on pain ratings was partially mediated by DNIC for women only. These findings further support the primary role of pain catastrophizing in modulation of pain outcomes. ⋯ These findings support the hypothesis that the heightened pain reported by individuals higher in pain catastrophizing may be related to a disruption in the endogenous modulation of pain, operationalized by assessing DNIC. Whether interventions that reduce pain catastrophizing affect pain outcomes via effects on DNIC is in need of investigation.
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Chronic noncancer pain is common and use of opioids is increasing. Previously published guidelines on use of opioids for chronic noncancer pain have been based primarily on expert consensus due to lack of strong evidence. We conducted searches on Ovid MEDLINE and the Cochrane databases through July 2008 to identify studies that addressed one or more of 37 Key Questions that a multidisciplinary expert panel identified as important to be answered to generate evidence-based recommendations on the use of opioids for chronic noncancer pain. A total of 14 systematic reviews, 38 randomized trials not included in a previously published systematic review, and 13 other studies met inclusion criteria. Almost all of the randomized trials of opioids for chronic noncancer pain were short-term efficacy studies. Critical research gaps on use of opioids for chronic noncancer pain include: lack of effectiveness studies on long-term benefits and harms of opioids (including drug abuse, addiction, and diversion); insufficient evidence to draw strong conclusions about optimal approaches to risk stratification, monitoring, or initiation and titration of opioid therapy; and lack of evidence on the utility of informed consent and opioid management plans, the utility of opioid rotation, the benefits and harms specific to methadone or higher doses of opioids, and treatment of patients with chronic noncancer pain at higher risk for drug abuse or misuse. ⋯ Currently, clinical decisions regarding the use of opioids for chronic noncancer pain need to be made based on weak evidence. Research funding priorities need to be set to address these critical research needs if the care of patients with chronic noncancer pain is to improve.