The journal of pain : official journal of the American Pain Society
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Acute postoperative pain is a common clinical condition that, when poorly controlled, can result in a number of significant negative consequences. The American Pain Society commissioned an evidence-based guideline on the management of postoperative pain to promote evidence-based, safe, and effective perioperative pain management. An interdisciplinary panel developed 31 key questions and inclusion criteria to guide the evidence review. Investigators reviewed 6556 abstracts from multiple electronic databases up to November 2012, an updated evidence review to October 2014, and key references suggested by expert reviewers. More than 800 primary studies not included in a systematic review and 107 systematic reviews were included. Despite a large body of evidence, a number of critical research gaps were identified where only low-quality or insufficient evidence was found to help guide clinical practice recommendations. This report identifies evidence gaps including optimal methods and timing of perioperative patient education, nonpharmacological modalities, combinations of analgesic techniques, monitoring of patient response to treatment, techniques for neuraxial and regional analgesia, and organizational care delivery models. Recommendations to help guide the design of future perioperative studies are offered. ⋯ Acute postoperative pain is a common clinical condition requiring an evidence-based, planned, and multimodal approach. Despite the plethora of published evidence, much of it is weak and key questions remain unanswered. Researchers are encouraged to work together to produce strong evidence to help guide clinical decisions in perioperative pain management.
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Comparative Study
Reorganized Trunk Muscle Activity During Multi-Directional Floor Perturbations After Experimental Low Back Pain: A Comparison Of Bilateral Versus Unilateral Pain.
Low back pain changes trunk muscle activity after external perturbations but the relationship between pain intensities and distributions and their effect on trunk muscle activity remains unclear. The effects of unilateral and bilateral experimental low back pain on trunk muscle activity were compared during unpredictable multidirectional surface perturbations in 19 healthy participants. Pain intensity and distribution were assessed using a visual analogue scale (VAS) and pain drawings. Root mean square (RMS) of the electromyographic (EMG) signals from 6 trunk muscles bilaterally after each perturbation was extracted and averaged across perturbations. The difference (ΔRMS-EMG) and absolute difference (absolute ΔRMS-EMG) RMS from baseline conditions were extracted for each muscle during pain conditions and averaged bilaterally for back and abdominal muscle groups. Bilateral compared with unilateral pain induced higher VAS scores (P < .005) and larger pain areas (P < .001). Significant correlation was present between VAS scores and muscle activity during unilateral (P < .001) and bilateral pain (P < .001). Compared with control injections ΔRMS-EMG increased in the back (P < .03) and abdominal (P < .05) muscles during bilateral and decreased in the back (P < .01) and abdominal (P < .01) muscles during unilateral pain. Bilateral pain caused greater absolute ΔRMS-EMG changes in the back (P < .01) and abdominal (P < .01) muscle groups than unilateral pain. ⋯ This study provided novel observations of differential trunk muscle activity in response to perturbations dependent on pain intensity and/or pain distribution. Because of complex and variable changes the relevance of clinical examination of muscle activity during postural tasks is challenged.
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Depression, pain catastrophizing, and anxiety commonly co-occur with chronic pain. However, the degree to which improvement in these psychological comorbidities predicts subsequent pain outcomes and, in particular, the relative effects of these 3 psychological factors with respect to each other is only partially known. Longitudinal analysis of 250 primary care patients with chronic musculoskeletal pain enrolled in the Stepped Care to Optimize Pain care Effectiveness (SCOPE) trial was examined, using data gathered at baseline, and at 3 and 12 months. Mixed effects model repeated measures analyses were used to determine if changes in depression, pain catastrophizing, and anxiety predicted a subsequent reduction in pain intensity or interference and pain-related disability. Defining a clinically significant change as twice the standard error of measurement for each predictor, we found that a 2-standard error of measurement improvement in depression, pain catastrophizing, and anxiety resulted in, respectively, an effect size decrease in pain intensity or interference of .45, .33, and .12; a 14%, 12%, and 6% reduction in the number of pain-specific disability days; and a 43%, 30%, and 28% decreased likelihood of high disability (defined as ≥10 pain-specific disability days in the past 4 weeks). In summary, improvements in 3 common psychological comorbidities predicted better pain outcomes. ⋯ Because depression, pain catastrophizing, and anxiety commonly accompany chronic pain and might adversely affect pain outcomes, treatment of these modifiable psychological factors is warranted to optimize the effectiveness of pain-specific therapies.
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Results of clinical studies suggest that descending inhibitory controls from the brainstem are important for speeding recovery from pain after surgery. We examined the effects of destroying spinally projecting noradrenergic neurons via intrathecally administered antibody to dopamine β-hydroxylase conjugated to saporin (DβH-saporin) on recovery in an acute incisional pain model. Mechanical and thermal paw withdrawal thresholds and nonevoked spontaneous guarding scores were tested for several weeks postoperatively and analyzed using mixed effects growth curve modeling. DβH-saporin treatment resulted in a significant prolongation in the duration of mechanical and to a lesser degree thermal hypersensitivity in the ipsilateral paw of incised rats but did not increase the duration of spontaneous guarding. DβH-saporin treatment was also associated with increased microglial and astrocyte activation in the ipsilateral spinal cord 21 days after incision compared with immunoglobulin G-saporin treated controls. Chronic intrathecal administration of the α2 adrenergic receptor antagonist atipamezole (50-200 μg/d) produced similar effects. These data suggest that spinally projecting noradrenergic pathways and spinal α2 adrenergic receptor activation are important for speeding recovery from hypersensitivity after surgical incision possibly by reducing spinal glial activation. Interventions that augment the noradrenergic system might be important to speed recovery from pain after surgery. ⋯ Endogenous descending spinal noradrenergic activation promotes resolution of incision-induced hypersensitivity and inhibits spinal microglial and astrocyte activation in part through α2 adrenergic receptors.
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Expectation and previous experience are both well established key mediators of placebo and nocebo effects. However, the investigation of their respective contribution to placebo and nocebo responses is rather difficult because most placebo and nocebo manipulations are contaminated by pre-existing treatment expectancies resulting from a learning history of previous medical interventions. To circumvent any resemblance to classical treatments, a purely psychological placebo-nocebo manipulation was established, namely, the "visual stripe pattern-induced modulation of pain." To this end, experience and expectation regarding the effects of different visual cues (stripe patterns) on pain were varied across 3 different groups, with either only placebo instruction (expectation), placebo conditioning (experience), or both (expectation + experience) applied. Only the combined manipulation (expectation + experience) revealed significant behavioral and physiological placebo-nocebo effects on pain. Two subsequent experiments, which, in addition to placebo and nocebo cues, included a neutral control condition further showed that especially nocebo responses were more easily induced by this psychological placebo and nocebo manipulation. The results emphasize the great effect of psychological processes on placebo and nocebo effects. Particularly, nocebo effects should be addressed more thoroughly and carefully considered in clinical practice to prevent the accidental induction of side effects. ⋯ Even purely psychological interventions that lack any resemblance to classical pain treatments might alter subjective and physiological pain correlates. A manipulation of treatment expectation and actual treatment experience were mandatory to elicit this effect. Nocebo effects were especially induced, which indicated the necessity for prevention of accidental side effects besides exploitation of placebo responses.