Pain
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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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Pain is a common symptom in patients referred to polyneuropathy assessment. Diagnostic evaluation and choice of treatment may depend on whether the pain is likely to be neuropathic or not. This study aimed to investigate the diagnostic accuracy of 3 tools commonly used to differentiate between neuropathic and nonneuropathic pain. ⋯ Only DN4 demonstrated high sensitivity (0.87), whereas all 3 tools had low specificity (≤0.65). Importantly, the tools' predictive ability was unsatisfactory; The probability of getting a correct test result was 3 quarters at best, and at worst, no better than two fifths. Consequently, we show that neither DN4, painDETECT, nor S-LANSS can be confidently used to assess neuropathic pain in a neurological outpatient population with symptoms of polyneuropathy.
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To enhance patient-centred care of people with hip pain, we need a comprehensive understanding of peoples' beliefs about their hip pain. This systematic review explored the beliefs and expectations of middle-aged and older adults about chronic hip pain and its care across different healthcare settings and contexts. This review was a synthesis of qualitative studies using a framework synthesis approach. ⋯ People coped with their hip pain by avoiding or modifying activity. People were not educated about treatments or used treatments that failed to improve their hip pain. People believed that surgery for their hip was inevitable.
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Randomized Controlled Trial
Referred sensation location can be altered by a strong heterotopic nociceptive stimulus: Implications for clinical pain conditions.
Referred sensations (RS) are a common clinical phenomenon in patients with musculoskeletal pain; however, the underlying mechanisms of RS and implications for diagnosis and management are poorly understood. The location of referral seems to have a preferred site, but studies have suggested it can be redirected to a site of previous injury and pain. However, it is not known if the same phenomenon can occur for a much shorter-lasting painful stimulus in the trigeminal system. ⋯ However, the RS location was displaced on average 1.2 cm between the baseline and postinfusion assessments for the hypertonic saline infusion, which was significantly increased when compared with the isotonic saline infusion which was on average 0.4 cm. These novel findings indicate the potential to modify the location of RS in the trigeminal system following a relatively brief noxious input. Clinicians need to be aware of the possible rerouting of RS in patients with complex orofacial pain.
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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.