Previous research has demonstrated that older adults are not as accurate as younger adults at perceiving negative emotions in facial expressions. These studies rely on emotion recognition tasks that involve choosing between many alternatives, creating the possibility that age differences emerge for cognitive rather than perceptual reasons. In the present study, an emotion discrimination task was used to investigate younger and older adults' ability to visually discriminate between negative emotional facial expressions (anger, sadness, fear, and disgust) at low (40%) and high (80%) expressive intensity. Participants completed trials blocked by pairs of emotions. Discrimination ability was quantified from the participants' responses using signal detection measures. In general, the results indicated that older adults had more difficulty discriminating between low intensity expressions of negative emotions than did younger adults. However, younger and older adults did not differ when discriminating between anger and sadness. These findings demonstrate that age differences in visual emotion discrimination emerge when signal detection measures are used but that these differences are not uniform and occur only in specific contexts.
Native Americans (NAs) have a higher prevalence of chronic pain than other U.S. racial/ethnic groups, but there have been few attempts to understand the mechanisms of this pain disparity. This study used a comprehensive battery of laboratory tasks to assess peripheral fiber function (cool/ warm detection thresholds), pain sensitivity (eg, thresholds/tolerances), central sensitization (eg, temporal summation), and pain inhibition (conditioned pain modulation) in healthy, pain-free adults (N=155 NAs, N=150 non-Hispanic Whites, NHW). Multiple pain stimulus modalities were used (eg, cold, heat, pressure, ischemic, electric), and subjective (eg, pain ratings, pain tolerance) and physiological (eg, nociceptive flexion reflex) outcomes were measured. There were no group differences on any measure, except that NAs had lower cold pressor pain thresholds and tolerances, indicating greater pain sensitivity than NHWs. These findings suggest that there are no group differences between healthy NAs and NHWs on peripheral fiber function, central sensitization, or central pain inhibition, but NAs may have greater sensitivity to cold pain. Future studies are needed to examine potential within-group factors that might contribute to NA pain risk.
Introduction: Native Americans (NAs) have a higher prevalence of chronic pain than other US racial/ethnic groups, but the mechanisms contributing to this pain disparity are under-researched. Pain catastrophizing is one of the most important psychosocial predictors of negative pain outcomes, and the Pain Catastrophizing Scale (PCS) has been established as a reliable and valid measure of the pain catastrophizing construct. However, before the PCS can be used to study pain risk in NAs, it is prudent to first determine whether the established 3-factor structure of the PCS also holds true for NAs. Methods: The current study examined the measurement (configural, metric, and scalar) invariance of the PCS in a healthy, pain-free sample of 138 NA and 144 non-Hispanic white (NHW) participants. Results: Results suggest that the previously established 3-factor solution fits for both groups (configural invariance) and that the factor loadings were equivalent across groups (metric invariance). Scalar invariance was also established, except for 1 minor scalar difference in a single threshold for item 3 (suggesting NHWs were more likely to respond with a 4 on that item than NAs). Discussion: Results provide additional evidence for the psychometric properties of the PCS and suggest it can be used to study pain catastrophizing in healthy, pain-free NA samples.
Introduction:
Evidence suggests Native Americans (NAs) experience higher rates of chronic pain than the general US population, but the mechanisms contributing to this disparity are poorly understood. Recently, we conducted a study of healthy, pain-free NAs (n = 155), and non-Hispanic whites (NHWs, n = 150) to address this issue and found little evidence that NAs and NHWs differ in pain processing (assessed from multiple quantitative sensory tests). However, NAs reported higher levels of pain-related anxiety during many of the tasks.
Objective:
The current study is a secondary analysis of those data to examine whether pain-related anxiety could promote pronociceptive processes in NAs to put them at chronic pain risk.
Methods:
Bootstrapped indirect effect tests were conducted to examine whether pain-related anxiety mediated the relationships between race (NHW vs NA) and measures of pain tolerance (electric, heat, ischemia, and cold pressor), temporal summation of pain and the nociceptive flexion reflex (NFR), and conditioned pain modulation of pain/NFR.
Results:
Pain-related anxiety mediated the relationships between NA race and pain tolerance and conditioned pain modulation of NFR. Exploratory analyses failed to show that race moderated relationships between pain-related anxiety and pain outcomes.
Conclusion:
These findings imply that pain-related anxiety is not a unique mechanism of pain risk for NAs, but that the greater tendency to experience pain-related anxiety by NAs impairs their ability to engage descending inhibition of spinal nociception and decreases their pain tolerance (more so than NHWs). Thus, pain-related anxiety may promote pronociceptive processes in NAs to place them at risk for future chronic pain.
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