Pain
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Randomized Controlled Trial
Social learning pathways in the relation between parental chronic pain and daily pain severity and functional impairment in adolescents with functional abdominal pain.
Having a parent with chronic pain (CP) may confer greater risk of persistence of CP from childhood into young adulthood. Social learning, such as parental modeling and reinforcement, represents one plausible mechanism for the transmission of risk of CP from parents to offspring. Based on a 7-day pain diary in 154 pediatric patients with functional abdominal CP, we tested a model in which parental CP predicted adolescents' daily average CP severity and functional impairment (distal outcomes) via parental modeling of pain behaviors and parental reinforcement of adolescent's pain behaviors (mediators) and adolescents' cognitive appraisals of pain threat (proximal outcome representing adolescents' encoding of parents' behaviors). ⋯ The indirect pathway through parental reinforcing responses to adolescents' pain did not reach significance for either adolescent pain severity or functional impairment. Identifying mechanisms of increased risk of pain and functional impairment in children of parents with CP ultimately could lead to targeted interventions aimed at improving functioning and quality of life in families with CP. Parental modeling of pain behaviors represents a potentially promising target for family-based interventions to ameliorate pediatric CP.
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Placebo effects have been reported in patients with chronic neuropathic pain. Expected pain levels and positive emotions are involved in the observed pain relief, but the underlying neurobiology is largely unknown. Patients with neuropathic pain are highly motivated for pain relief, and as motivational factors such as expectations of reward, as well as pain processing in itself, are related to the dopaminergic system, it can be speculated that dopamine release contributes to placebo effects in neuropathic pain. ⋯ We found no evidence for an effect of haloperidol and levodopa/carbidopa on neuropathic pain levels (P = 0.071-0.963). Dopamine seemed to influence the levels of expectancy and desire, yet there was no evidence for indirect or interaction effects on the placebo effect. This is the first study to suggest that dopamine does not contribute to placebo effects in chronic neuropathic pain.
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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.
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T lymphocytes play a pivotal role in endogenous regulation of inflammatory visceral pain. The analgesic activity of T lymphocytes is dependent on their production of opioids, a property acquired on antigen activation. Accordingly, we investigated whether an active recruitment of T lymphocytes within inflamed colon mucosa via a local vaccinal strategy may counteract inflammation-induced visceral pain in mice. ⋯ The experiments were reproduced with the bacillus Calmette-Guerin vaccine as antigen. Similarly, inflammatory visceral pain was dramatically alleviated in mice vaccinated against bacillus Calmette-Guerin and then locally administered with live Mycobacterium bovis. Together, these results show that the induction of a secondary adaptive immune response against vaccine antigens in inflamed mucosa may constitute a safe noninvasive strategy to relieve from visceral inflammatory pain.