Pain
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Recent advances in brain science have shown that the brain function encoding emotion depends on interoceptive signals such as visceral pain. Visceral pain arose early in our evolutionary history. Bottom-up processing from gut-to-brain and top-down autonomic/neuroendocrine mechanisms in brain-to-gut signaling constitute a circuit. ⋯ Serotonin (5-HT) is another likely candidate associated with brain-gut function in IBS, as 5-HT3 antagonists, 5-HT4 agonists, and antidepressants were demonstrated to regulate 5-HT neurotransmission in IBS patients. Autonomic nervous system function, the neuroimmune axis, and the brain-gut-microbiota axis show specific profiles in IBS patients. Further studies on stress and visceral pain neuropathways in IBS patients are warranted.
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Randomized Controlled Trial
Implicit associations between pain and self-schema in patients with chronic pain.
Chronic pain often interferes with daily functioning, and may become a threat to an individual's sense of self. Despite the development of a recent theoretical account focussing upon the relationship between the presence of chronic pain and a person's self, research investigating this idea is limited. In the present study we aimed to (1) compare the strength of association between self- and pain schema in patients with chronic pain and healthy control subjects and (2) research whether the strength of association between self- and pain-schema is related to particular pain-related outcomes and individual differences of patients with chronic pain. ⋯ Results indicated that the pain- and self-schema were more strongly associated in patients with chronic pain than in healthy control subjects. Second, results indicated that, in patients with chronic pain, a stronger association between self- and pain-schema, as measured with the IAT, is related to a heightened level of pain severity, pain suffering, anxiety, and helplessness. Current findings give first support for the use of an IAT to investigate the strength of association between self- and pain-schema in patients with chronic pain and suggest that pain therapies may incorporate techniques that intervene on the level of self-pain enmeshment.
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The molecular/genetic era has seen the discovery of a staggering number of molecules implicated in pain mechanisms [18,35,61,69,96,133,150,202,224]. This has stimulated pharmaceutical and biotechnology companies to invest billions of dollars to develop drugs that enhance or inhibit the function of many these molecules. Unfortunately this effort has provided a remarkably small return on this investment. ⋯ To paraphrase a recent editorial in Science magazine [223], although we live in the Golden age of Genetics, the fundamental unit of biology is still arguably the cell, and the cell is the critical structural and functional setting in which the function of pain-related molecules must be understood. This review summarizes our current understanding of the nociceptor as a cell-biological unit that responds to a variety of extracellular inputs with a complex and highly organized interaction of signaling molecules. We also discuss the insights that this approach is providing into peripheral mechanisms of chronic pain and sex dependence in pain.