Pain
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Low back pain (LBP) is a major health challenge globally. Research has identified common trajectories of pain over time. We aimed to investigate whether trajectories described in 1 primary care cohort can be confirmed in another, and to determine the prognostic value of factors collected 5 years prior to the identification of the trajectory. ⋯ Lower social class and higher pain intensity were significantly associated with a more severe trajectory 5 years later, as were patients' perceptions of the greater consequences and longer duration of pain, and greater passive behavioural coping. Low back pain trajectories identified previously appear generalizable. These allow better understanding of the long-term course of LBP, and effective management tailored to individual trajectories needs to be identified.
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Interrupting ongoing activities whilst intending to resume them later is a natural response to pain. Whereas this response facilitates pain management, at the same time it may also disrupt task performance. Previous research has shown that activity interruptions by pain impair subsequent resumption of the activity, but not more than pain-irrelevant interruptions. ⋯ Pain catastrophizing did not influence the results. As in previous studies, activity interruptions by pain were shown to impair the resumption of a task that requires keeping to a step sequence, but not more than interruptions by nonpainful stimuli. Potential explanations are discussed.
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Humans require the ability to discriminate intensities of noxious stimuli to avoid future harm. This discrimination process seems to be biased by an individual's attention to pain and involves modulation of the relative intensity differences between stimuli (ie, Weber fraction). Here, we ask whether attention networks in the brain modulate the discrimination process and investigate the neural correlates reflecting the Weber fraction for pain intensity. ⋯ Of note, this vigilance-related functional coupling specifically predicted participants' behavioral ability to differentiate pain intensities. Moreover, unique to pain discrimination tasks, the response in the right superior frontal gyrus linearly represented the Weber fraction for pain intensity, which significantly biased participants' pain discriminability. These findings suggest that pain intensity discrimination in humans relies on vigilance-related enhancement in the parieto-thalamic attention network, thereby allowing the prefrontal cortex to estimate the relative intensity differences between noxious stimuli.
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Issues of peripheral circulation have been increasingly suggested as an underlying cause of musculoskeletal pain in many conditions, including sickle cell anemia and peripheral vascular disease. We have previously shown in our model of transient ischemia and reperfusion (I/R) injury of the forelimb that individual group III and IV muscle afferents display altered chemosensitivity and mechanical thresholds 1 day after injury. Functional alterations corresponded to increased evoked and spontaneous pain-related behaviors and decreased muscle strength and voluntary activity-all actions that echo clinical symptoms of ischemic myalgia. ⋯ Interleukin 1 receptor antagonist treatment additionally prevented the I/R-induced changes in mechanical and chemical sensitivity of individual primary muscle afferents. Altogether, these data strengthen the evidence that transient I/R injury sensitizes group III and IV muscle afferents via increased IL1β in the muscles to stimulate ischemic myalgia development. Targeting IL1β may, therefore, be an effective treatment strategy for this insidious type of muscle pain.