Pain
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Randomized Controlled Trial Comparative Study
Supervised walking in comparison with fitness training for chronic back pain in physiotherapy: results of the SWIFT single-blinded randomized controlled trial (ISRCTN17592092).
Effectiveness of brief/minimal contact self-activation interventions that encourage participation in physical activity (PA) for chronic low back pain (CLBP >12 weeks) is unproven. The primary objective of this assessor-blinded randomized controlled trial was to investigate the difference between an individualized walking programme (WP), group exercise class (EC), and usual physiotherapy (UP, control) in mean change in functional disability at 6 months. A sample of 246 participants with CLBP aged 18 to 65 years (79 men and 167 women; mean age ± SD: 45.4 ± 11.4 years) were recruited from 5 outpatient physiotherapy departments in Dublin, Ireland. ⋯ An intention-to-treat analysis using a mixed between-within repeated-measures analysis of covariance found significant improvements over time on the Oswestry Disability Index (Primary Outcome), the Numerical Rating Scale, Fear Avoidance-PA scale, and the EuroQol EQ-5D-3L Weighted Health Index (P < 0.05), but no significant between-group differences and small between-group effect sizes (WP: mean difference at 6 months, 6.89 Oswestry Disability Index points, 95% confidence interval [CI] -3.64 to -10.15; EC: -5.91, CI: -2.68 to -9.15; UP: -5.09, CI: -1.93 to -8.24). The WP had the lowest mean costs and the highest level of adherence. Supervised walking provides an effective alternative to current forms of CLBP management.
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Tailored treatment based on individual risk factors is an area with promise to improve options for pain relief. Musculoskeletal pain has a biopsychosocial nature, and multiple factors should be considered when determining risk for chronic pain. This study investigated whether subgroups comprised genetic and psychological factors predicted outcomes in preclinical and clinical models of shoulder pain. ⋯ Risk subgroups comprised the COMT high pain sensitivity variant and either pain catastrophizing or fear of pain were predictive of heightened shoulder pain responses in the preclinical model. Further analysis in the clinical model identified the COMT high pain sensitivity variant and pain catastrophizing subgroup as the better predictor. Future studies will determine whether these findings can be replicated in other anatomical regions and whether personalized medicine strategies can be developed for this risk subgroup.
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Pain-related depression of behavior and mood is a key therapeutic target in the treatment of pain. Clinical evidence suggests a role for decreased dopamine (DA) signaling in pain-related depression of behavior and mood. Similarly, in rats, intraperitoneal injection of dilute lactic acid (IP acid) serves as a chemical noxious stimulus to produce analgesic-reversible decreases in both (1) extracellular DA levels in nucleus accumbens (NAc) and (2) intracranial self-stimulation (ICSS), an operant behavior reliant on NAc DA. ⋯ In the absence of the noxious stimulus, amitifadine increased NAc levels of both DA and serotonin, and behaviorally, amitifadine produced significant but weak abuse-related ICSS facilitation. Moreover, amitifadine was more potent to block IP acid-induced depression of ICSS than to facilitate control ICSS. These results support consideration of amitifadine and related monoamine uptake inhibitors as candidate analgesics for treatment of pain-related behavioral depression.
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Pain modulation efficiency delays seeking medical help in patients with acute myocardial infarction.
Rapid reperfusion is crucial to reduce mortality in patients with ST elevation myocardial infarction. Prehospital patient delay, defined as time from symptoms onset to the decision to seek medical attention, accounts for a large proportion of cases with delayed reperfusion. However, whether pain modulation processes are involved in this phenomenon is not known. ⋯ Multivariable regression analysis (R = 0.449; P < 0.0001) revealed an inverse independent association between chest pain intensity (P < 0.001) and patient delay, whereas efficient CPM was positively associated with prolonged patient delay (P = 0.034). The electrocardiography-derived myocardial ischemic area was not associated with chest pain intensity or patient delay, indicating that the affected ischemic tissue is not a dominant component that determines pain response. In conclusion, beyond the perceived chest pain intensity, the activation pattern of descending inhibition pathways during coronary occlusion affects pain interpretation and behavior during acute coronary occlusion.
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Comparative Study
Differences in pain-related fear acquisition and generalization: an experimental study comparing patients with fibromyalgia and healthy controls.
Anomalies in fear learning, such as failure to inhibit fear to safe stimuli, lead to sustained anxiety, which in turn may augment pain. In the same vein, stimulus generalization is adaptive as it enables individuals to extrapolate the predictive value of 1 stimulus to similar stimuli. However, when fear spreads in an unbridled way to novel technically safe stimuli, stimulus generalization becomes maladaptive and may lead to dysfunctional avoidance behaviors and culminate in severe pain disability. ⋯ Fear of movement-related pain spreads selectively to novel movements similar to the original painful movement, and not to those resembling the nonpainful movement in the healthy controls, but nondifferential fear generalization was observed in FM. As expected, in the unpredictable context, we also observed nondifferential fear generalization; this effect was more pronounced in FM. Given the status of overgeneralization as a plausible transdiagnostic pathogenic marker, we believe that this research might increase our knowledge about pathogenesis of musculoskeletal widespread pain.