Date Published: April 18, 2019
Publisher: Public Library of Science
Author(s): Hee Jun Kim, Joel D. Greenspan, Richard Ohrbach, Roger B. Fillingim, William Maixner, Cynthia L. Renn, Meg Johantgen, Shijun Zhu, Susan G. Dorsey, Julian Koenig.
This study evaluated the contributions of psychological status and cardiovascular responsiveness to racial/ethnic differences in experimental pain sensitivity. The baseline measures of 3,159 healthy individuals—non-Hispanic white (NHW): 1,637, African-American (AA): 1,012, Asian: 299, and Hispanic: 211—from the OPPERA prospective cohort study were used. Cardiovascular responsiveness measures and psychological status were included in structural equation modeling based mediation analyses. Pain catastrophizing was a significant mediator for the associations between race/ethnicity and heat pain tolerance, heat pain ratings, heat pain aftersensations, mechanical cutaneous pain ratings and aftersensations, and mechanical cutaneous pain temporal summation for both Asians and AAs compared to NHWs. HR/MAP index showed a significant inconsistent (mitigating) mediating effect on the association between race/ethnicity (AAs vs. NHWs) and heat pain tolerance. Similarly, coping inconsistently mediated the association between race/ethnicity and mechanical cutaneous pain temporal summation in both AAs and Asians, compared to NHWs. The factor encompassing depression, anxiety, and stress was a significant mediator for the associations between race/ethnicity (Asians vs. NHWs) and heat pain aftersensations. Thus, while pain catastrophizing mediated racial/ethnic differences in many of the QST measures, the psychological and cardiovascular mediators were distinctly restrictive, signifying multiple independent mechanisms in racial/ethnic differences in pain.
Pain is a major health problem in the US, with an estimated 120 million (55.7%) adults reporting some level of pain in the previous three months, including chronic pain . Racial/ethnic disparities related to pain in the US have been studied widely, with racial/ethnic minorities reporting greater severity of chronic pain than non-Hispanic white (NHWs) [2–4]. The problem is compounded by lower quality of care provided to patients who are racial/ethnic minorities, including African Americans (AAs) and Hispanics compared to NHWs, whether the treatment is for acute pain, chronic pain, cancer pain, and or palliative pain care , . Furthermore, among AAs compared to NHWs, disability due to chronic pain is greater [7–9], quality of life among AAs with chronic knee and hip pain is poorer , and comorbid health conditions, including pain related anxiety, depression, and decreased physical function, are more common , , .
This secondary analysis used data from the Orofacial Pain Prospective Evaluation and Risk Assessment Study (OPPERA). The OPPERA study was originally reviewed and approved by the Institutional Review Boards at the data coordinating center and at each of the four study sites. Exemption review with minimal risk was approved from the University of Maryland IRB for the present study.
Demographic characteristics of the four racial/ethnic groups are shown in Table 1.
Racial/ethnic differences in experimental pain sensitivity were found for many of our measures, and largely replicated studies that evaluated such measures individually. Pain catastrophizing was the most robust mediator of racial/ethnic differences in pain sensitivity, as it was found relevant to most pain measures for both AAs and Asians compared to NHWs. Two other psychological measures (DAS and Coping) and one cardiovascular response measure (HR/MAP) were found to be significant mediators for individual pain measures. Two of these mediators–Coping and HR/MAP–were inconsistent mediators, suggesting that they mitigated the total racial/ethnic differences in experimental pain sensitivity. Inconsistent mediation means that the mediator’s effects are in the opposite direction of the direct effects of the racial/ethnic differences in pain sensitivity, thus the total racial/ethnic differences combining the mediator’s effects and direct effects mitigated .
The current study provides several novel findings regarding factors significantly contributing to racial/ethnic differences in experimental pain sensitivity. The identified mediators, most notably pain catastrophizing, should be considered in pain management programs to implement better strategies to reduce clinical pain. Such better strategies may be particularly beneficial for AAs and Asians in the US. Other psychological and cardiovascular response factors appear to have very selective mediating effects, suggesting different mechanisms are relevant for racial/ethnic differences in specific types of pain. Further clinical and experimental research is required to increase our understanding of the suggested mechanisms explaining racial/ethnic differences in pain sensitivity and to extend our findings to clinical pain populations.