Pain
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This study investigated whether one becomes more quickly aware of innocuous somatosensory signals at locations of the body where pain is anticipated. Undergraduate students (N=20) indicated which of 2 stimuli that were administered to each hand using a range of stimulus onset asynchronies (SOAs), was presented first. Participants were instructed that the color of a cue (1 of 2 colors) signaled the possible occurrence of pain on 1 hand (threat trials). ⋯ Results showed that during threat trials tactile stimuli on the hand where pain was expected, were perceived earlier in time than stimuli on the "neutral" hand. These findings demonstrate that the anticipation of pain at a particular location of the body resulted in the prioritization in time of somatosensory sensations at that location, indicating biased attention towards the threatened body part. The value of this study for investigating hypervigilance for somatosensory signals in clinical populations such as patients with chronic lower back pain is discussed.
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Inflammatory processes in the sensory ganglia contribute to many forms of chronic pain. We previously showed that local inflammation of the lumbar sensory ganglia rapidly leads to prolonged mechanical pain behaviors and high levels of spontaneous bursting activity in myelinated cells. Abnormal spontaneous activity of sensory neurons occurs early in many preclinical pain models and initiates many other pathological changes, but its molecular basis is not well understood. ⋯ In vivo knockdown of NaV1.6 locally in the lumbar DRG at the time of DRG inflammation completely blocked development of pain behaviors and abnormal spontaneous activity, while having only minor effects on unmyelinated C cells. Current research on isoform-specific sodium channel blockers for chronic pain is largely focused on NaV1.8 because it is present primarily in unmyelinated C fiber nociceptors, or on NaV1.7 because lack of this channel causes congenital indifference to pain. However, the results suggest that NaV1.6 may be a useful therapeutic target for chronic pain and that some pain conditions may be mediated primarily by myelinated A fiber sensory neurons.
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An accurate means of identifying patients at high risk for chronic disabling pain could lead to more cost-effective care, with more intensive interventions targeted to those likely to benefit most. The Chronic Pain Risk Score is a tool developed to predict risk for chronic pain. The aim of this study was to examine whether its predictive ability could be enhanced by: (1) improved measures of the constructs it assesses (Improved Chronic Pain Risk Model); and (2) adding other predictors (Expanded Chronic Pain Risk Model). ⋯ The Expanded Model improved significantly on the prediction of the Improved Model (NRI=0.56, P<0.001) and demonstrated excellent discriminative ability (AUC=0.84, 95% CI=0.79-0.88). The Improved Model (AUC=0.79, 95% CI=0.75-0.84) and the Chronic Pain Risk Score (AUC=0.76, 95% CI=0.71-0.81) showed acceptable discriminative ability. A limited set of measures may be used to predict risk for future clinically significant pain in patients initiating primary care for back pain, but further evaluation of prognostic models is needed.
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The perception of pain is determined by a combination of genetic, neurobiological, cultural, and emotional factors. Recent studies have demonstrated an association between specific genotypes and pain perception. Particular focus has been given to the triallelic polymorphism in the promoter region of the serotonin transporter gene in relation to pain perception. ⋯ However, in participants with a high expression of the serotonin transporter protein, conditioning with negative pictures increased pain intensity and positive pictures decreased pain intensity when compared with neutral pictures. In contrast, there were no significant effects of the pictures on pain perception in participants with either intermediate or low expression of the protein. These results suggest that polymorphisms in the serotonin transporter gene play an important role in emotions modulation of muscle pain.
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Randomized Controlled Trial
Oxycodone alters temporal summation but not conditioned pain modulation: preclinical findings and possible relations to mechanisms of opioid analgesia.
Opioid analgesia is mediated primarily by modulating (inhibiting and enhancing) pain mechanisms at the spinal and supraspinal levels. Advanced psychophysical paradigms of temporal summation (TS) and conditioned pain modulation (CPM) likely represent pain mechanisms at both levels. Therefore, the study of opioid effects on TS and CPM can shed light on their analgesic mechanisms in humans. ⋯ In contrast, no significant effects of either oxycodone (F=0.871, P=.458) or placebo (F=2.086, P=.106) on the magnitude of CPM were found. These results suggest that under the current experimental conditions, oxycodone exerted spinal, rather than supraspinal, analgesic effects. Furthermore, compared with CPM, TS seems more suitable for studying the mechanisms of opioid analgesia in humans.