Articles: pain-threshold.
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Recent literature suggests that the withdrawal of remifentanil (RF) infusion can be associated with hyperalgesia in clinical and nonclinical settings. We performed a systematic review and a meta-analysis of randomized controlled trials with cross-over design, to assess the effect of discontinuing RF infusion on pain intensity and areas of hyperalgesia and allodynia in healthy volunteers. Nine studies were included. ⋯ The area of hyperalgesia was larger after RF withdrawal (SMD: 0.55; 95% CI: 0.27-0.84; P = 0.001; I 2 = 0%). The area of allodynia did not vary between treatments. These findings suggest that the withdrawal of RF induces a mild but nonclinically relevant degree of hyperalgesia in HVs, likely linked to a reduced pain threshold.
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Individuals vary significantly in their pain sensitivity, with contributions from the brain, genes, and psychological factors. However, a multidimensional model integrating these factors is lacking due to their complex interactions. To address this, we measured pain sensitivity (ie, pain threshold and pain tolerance) using the cold pressor test, collected magnetic resonance imaging (MRI) data and genetic data, and evaluated psychological factors (ie, pain catastrophizing, pain-related fear, and pain-related anxiety) from 450 healthy participants with both sexes (160 male, 290 female). ⋯ Notably, pain catastrophizing was negatively correlated with pain tolerance, and this relationship was mediated by the multimodal covarying brain patterns in male participants only. Furthermore, we identified an association between the single-nucleotide polymorphism rs4141964 within the fatty acid amide hydrolase gene and pain threshold, mediated by the identified multimodal covarying brain patterns across all participants. In summary, we suggested a model that integrates the brain, genes, and psychological factors to elucidate their role in shaping interindividual variations in pain sensitivity, highlighting the important contribution of the multimodal covarying brain patterns as important biological mediators in the associations between genes/psychological factors and pain sensitivity.
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The rostral ventromedial medulla (RVM) is a crucial structure in the descending pain modulatory system, playing a key role as a relay for both the facilitation and inhibition of pain. The chronic social defeat stress (CSDS) model has been widely used to study stress-induced behavioral impairments associated with depression in rodents. Several studies suggest that CSDS also causes changes related to chronic pain. ⋯ In addition, RVM inhibition in animals exposed to a subthreshold social defeat stress protocol induces a susceptible phenotype, facilitating all stress outcomes. Finally, chronic RVM inhibition-without any social stress stimulus-induces chronic pain but not depressive-like behaviors. Our findings provide insights into the comorbidity between chronic pain and depression by indicating the involvement of the RVM in establishing social stress-induced behavioral responses associated with both chronic pain and depression.
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The different clinical presentations of fibromyalgia (FMS) may play independent roles in the unclear etiology of cognitive impairments and depressive symptoms seen in this population. Understanding how these clinical presentations are associated with FMS's clinical and neurophysiological aspects is important when developing effective treatments. ⋯ Depression symptoms seem to be associated with TMS-indexed motor threshold and psychosocial variables, while memory complaints are associated with pain intensity and higher theta oscillations. These mechanisms may be catalyzed and/or triggered by some behavioral and clinical features such as older age, sleep disruption, and anxiety. The correlation with clinical variables suggests the increasing of theta oscillations is a compensatory response in patients with FMS, which can be explored in future studies to improve the treatment for FMS.
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Conditioning and expectation are known to be the main mechanisms of placebo analgesia. They may operate together, so that expectations may be enhanced by a conditioning procedure. Although most of the studies have tried to potentiate expectations through conditioning in order to generate good placebo responders, a few studies have tried to mismatch conditioning and expectations in order to investigate the subsequent administration of a placebo. ⋯ They also stress the importance of expectations in the therapeutic outcome, with important implications for clinical trials. PERSPECTIVE: By using mismatch conditioning, in which study participants did not get what they expected, we reduced expectations of analgesia, and this reduction abolished placebo analgesia. This effect extended to other parts of the body and other types of pain, which indicates that placebo nonresponders can be created in the laboratory.