Articles: pain-threshold.
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To determine the absolute and relative within-session test-retest reliability of pressure pain threshold (PPT) and temporal summation of pain (TSP) at the low back and the forearm in individuals with chronic low back pain (CLBP) and to test the impact of different sequences of measurements on reliability metrics. ⋯ Within-session reliability was generally excellent for PPT and TSP at the low back and hand sites among individuals with CLBP. We recommend using 3 measurements for PPT and 2 for TSP to optimize reliability. Caution is recommended when testing PPT of the painful lower back area since a systematic difference was present between the test and retest.
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Obesity is frequently associated with obstructive sleep apnoea syndrome (OSA) and chronic pain. OSA as well as continuous positive airway pressure (CPAP) treatment may modulate the pain perception threshold (PT) in patients with obesity. ⋯ In patients with obesity, this exploratory study showed that the presence of an OSA is associated with a decreased PT, whereas implantation of a CPAP device tends to normalize pain perception.
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Randomized Controlled Trial
Sleep Disruption and Activation of Cellular Inflammation Mediate Heightened Pain Sensitivity: A Randomized Clinical Trial.
Sleep loss heightens pain sensitivity, but the pathways underlying this association are not known. Given that experimental sleep disruption induces increases in cellular inflammation as well as selective loss of slow wave, N3 sleep, this study examined whether these mechanisms contribute to pain sensitivity following sleep loss in healthy adults. This assessor-blinded, cross-over sleep condition, single-site, randomized clinical trial enrolled 95 healthy adults (mean [SD] age, 27.8 [6.4]; female, 44 [53.7%]). ⋯ A comprehensive causal mediation analysis found that FA had an indirect effect on hPTH by decreases in N3 sleep and subsequent increases in inflammation (estimate=-0.15; 95% confidence interval, -0.30 to -0.03; P < 0.05) with the proportion mediated 34.9%. Differential loss of slow wave, N3 sleep, and increases in cellular inflammation are important drivers of pain sensitivity after sleep disruption. Clinical Trials Registration: NCT01794689.
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In neonates, a noxious stimulus elicits pain-related facial expression changes and distinct brain activity as measured by electroencephalography, but past research has revealed an inconsistent relationship between these responses. Facial activity is the most commonly used index of neonatal pain in clinical settings, with clinical thresholds determining if analgesia should be provided; however, we do not know if these thresholds are associated with differences in how the neonatal brain processes a noxious stimulus. The objective of this study was to examine whether subclinical vs clinically significant levels of pain-related facial activity are related to differences in the pattern of nociceptive brain activity in preterm and term neonates. ⋯ Results revealed a sequence of nociceptive cortical network activation that was independent of pain-related behavior; however, a separate but interleaved sequence of early activity was related to the magnitude of the immediate behavioural response. Importantly, the degree of pain-related behavior is related to how the brain processes a stimulus and not simply the degree of cortical activation. This suggests that neonates who exhibit clinically significant pain behaviours process the stimulus differently and that neonatal pain-related behaviours reflect just a portion of the overall cortical pain response.
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The bladder wall is innervated by a complex network of afferent nerves that detect bladder stretch during filling. Sensory signals, generated in response to distension, are relayed to the spinal cord and brain to evoke physiological and painful sensations and regulate urine storage and voiding. Hyperexcitability of these sensory pathways is a key component in the development of chronic bladder hypersensitivity disorders including interstitial cystitis/bladder pain syndrome and overactive bladder syndrome. ⋯ Further evaluation revealed that Ca V 3.2 blockers significantly inhibited both low- and high-threshold afferents, decreasing peak responses to distension, and delayed activation thresholds, thereby attenuating bladder afferent responses to both physiological and noxious distension. Nocifensive visceromotor responses to noxious bladder distension in vivo were also significantly reduced by inhibition of Ca V 3 with TTA-A2. Together, these data provide evidence of a major role for Ca V 3.2 in regulating bladder afferent responses to bladder distension and nociceptive signalling to the spinal cord.