Pain
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P2X7 is a nonselective cation channel activated by extracellular ATP. P2X7 activation contributes to the proinflammatory response to injury or bacterial invasion and mediates apoptosis. Recently, P2X7 function has been linked to chronic inflammatory and neuropathic pain. ⋯ Rs7958311 was associated with experimental pain intensity in the meta-analysis of both cohorts. Significant associations were also found for multisite pain and postoperative pain. Our results strengthen the existing evidence and suggest that P2X7 and genetic variation in the P2RX7-gene may be involved in the modulation of human pain sensitivity.
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Moderate to severe chronic pain affects 1 in 5 adults and its impact increases with age. People with chronic pain that interferes with their lives have an increased risk of mortality. Identifying how interfering chronic pain can lead to mortality may highlight potential intervention strategies. ⋯ The strongest mediating factors for the relationship between troubling pain and mortality were functional limitation (hazard ratio 1.31; 95% confidence interval 1.20-1.39), symptoms preventing walking quarter of a mile (1.45 [1.35-1.58]), physical inactivity (1.14 [1.10-1.20]), and poor self-rated health (1.32 [1.23-1.41]). Mediators of the relationship between troubling pain and mortality provide targets for preventive health programmes. Interventions to improve general health, activity, and function could improve long-term survival in patients with this clinical problem.
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Pain has the capacity to interfere with daily tasks. Although task interference by pain is largely unintentional, it can be controlled to a certain extent. Such top-down control over pain has been believed to be reduced in patients with fibromyalgia (FM). ⋯ In conclusion, current study provides support for contemporary theories claiming that attention modulates the experience of pain and vice versa. However, no evidence was found for an altered attentional processing of pain in patients with FM. Furthermore, results indicate that task interference and distraction efficacy are not just 2 sides of the same coin.
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Human studies have demonstrated a correlation between noncoding polymorphisms of "the pain protective" haplotype in the GCH1 gene that encodes for GTP cyclohydrolase I (GTPCH1)-which leads to reduced tetrahydrobiopterin (BH4) production in cell systems-and a diminished perception of experimental and clinical pain. Here, we investigate whether heterozygous mutations in the GCH1 gene which lead to a profound BH4 reduction in patients with dopa-responsive dystonia (DRD) have any effect on pain sensitivity. The study includes an investigation of GCH1-associated biomarkers and pain sensitivity in a cohort of 22 patients with DRD and 36 controls. ⋯ The patients with DRD were heterozygous for the pain protective haplotype in cis with the GCH1 disease-causing mutation, c.899T>C. No effect on pain perception was observed for this combined haplotype. In conclusion, a reduced concentration of BH4 is not sufficient to alter ongoing pain sensitivity or evoked pain responses.
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Pain is a major complication for patients with cancer significantly compromising their quality of life. Current treatment is far from optimal and particularly bone-related cancer pain poses an increasing clinical and socioeconomical problem. Connexins, key proteins in cell-cell communication, have the potential to affect cancer-induced bone pain at multiple levels, including nociceptive signaling and bone degradation. ⋯ Carbenoxolone treatment had a minor effect on the bone degradation in the early phase of disease progression, whereas no effect was observed in the late phase. Surprisingly, connexin43 was downregulated in the cancer-bearing animals compared with shams. The results suggest that connexins are involved in cancer-induced bone pain, and that carbenoxolone could be a novel analgesic treatment for the pain state.