The journal of pain : official journal of the American Pain Society
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The effect of cognition on the plasticity of the nociceptive system remains controversial. In this study, we examined whether working memory can buffer against the development of secondary hypersensitivity. Thirty-five healthy women participated in 3 experimental conditions. ⋯ In conclusion, we found no evidence that working memory affects the plasticity of the nociceptive system, yet pain-related fear plays a role. PERSPECTIVE: This study shows that the execution of a cognitive task, irrespective of cognitive load or working memory, does not significantly modulate the development of secondary hypersensitivity, heart rate variability, or steady-state evoked potentials. However, higher pain-related fear seems to contribute to greater hypersensitivity.
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Social context has been shown to influence pain perception. This study aimed to broaden this literature by investigating whether relevant social stimuli, such as faces with different levels of intrinsic (based on physical resemblance to known individuals) and episodic (acquired through a previous experience) familiarity, may lead to hypoalgesia. We hypothesized that familiarity, whether intrinsic or acquired through experience, would increase pain threshold and decrease pain intensity. ⋯ This study provides further evidence on the social modulation of pain and contributes to the literature on first impressions' influence on social behavior. PERSPECTIVE: Consistent with the idea that familiar others signal safety and reduce the sense of threat, facial features conveying familiarity induce a top-down hypoalgesic modulation. This knowledge may contribute to understanding differences in pain perception in experimental and clinical contexts.
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Chemotherapy-induced peripheral neuropathy (CIPN) is a common, dose-limiting side effect of cancer therapy. Protease-activated receptor 2 (PAR2) is implicated in a variety of pathologies, including CIPN. In this study, we demonstrate the role of PAR2 expressed in sensory neurons in a paclitaxel (PTX)-induced model of CIPN in mice. ⋯ Similar results were seen with satellite cell gliosis in the DRG, where gliosis induced by PTX was absent in PAR cKO mice. Finally, C781 was able to transiently reverse established PTX-evoked mechanical allodynia. PERSPECTIVE: Our work demonstrates that PAR2 expressed in sensory neurons plays a key role in PTX-induced mechanical allodynia, spontaneous pain, and signs of neuropathy, suggesting PAR2 as a possible therapeutic target in multiple aspects of PTX CIPN.
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Linguistic stimuli are commonly used in research to investigate the processing of pain. To provide researchers with a dataset of pain-related and non-pain-related linguistic stimuli, this research investigated 1) the associative strength between pain-related words and the pain construct; 2) the pain-relatedness ratings of pain words; and 3) the variability in the relatedness of pain words within pain word classifications (eg, sensory pain words). In Study 1, 194 pain-related and matched non-pain-related words were retrieved by reviewing the pain-related attentional bias literature. ⋯ The resulting dataset is openly accessible and new published sets can be added to the Linguistic Materials for Pain (LMaP) Repository. PERSPECTIVE: This article presents the development and preliminary evaluation of a large pool of pain-related and non-pain-related words in adults with and without self-reported chronic pain. Findings are discussed and guidelines are offered to select the most suitable stimuli for future research.
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We conducted a bidirectional Mendelian randomization study to examine the causal effects of six personality traits (anxiety, neuroticism, extraversion, openness to experience, agreeableness, and conscientiousness) on back pain associated with health care use and the causal effect of back pain on the same risk factors. Genetic instruments for the personality traits and back pain were obtained from the largest published genome-wide association studies conducted in individuals of European ancestry. We used inverse weighted variance meta-analysis and Causal Analysis Using Summary Effect for primary analyses and sensitivity analyses to examine evidence for causal associations. ⋯ We found evidence for statistically significant bidirectional causal associations between neuroticism and back pain, with odds ratio 1.51 (95% confidence interval 1.37; 1.67) of back pain per neuroticism sum score standard deviation, P-value = 7.80e-16; and beta = .12, se = .04 of neuroticism sum score standard deviation per log odds of back pain, P-value = 2.48e-03. Other relationships did not meet our predefined criteria for causal association. PERSPECTIVE: The significant positive feedback loop between neuroticism and back pain highlights the importance of considering neuroticism in the management of patients with back pain.