Pain Reports最新文献

Introduction: The pathophysiology of pediatric musculoskeletal (MSK) pain is unclear, contributing to persistent challenges to its management.

Objectives: This study hypothesizes that children and adolescents with chronic MSK pain (CPs) will show differences in electroencephalography (EEG) features at rest and during thermal pain modalities when compared with age-matched controls.

Methods: One hundred forty-two CP patients and 45 age-matched healthy controls (HCs) underwent a standardized thermal tonic heat and cold stimulations, while a 21-electrode headset collected EEG data. Cohorts were compared with respect to their EEG features of spectral power, peak frequency, permutation entropy, weight phase-lag index, directed phase-lag index, and node degree at 4 frequency bands, namely, delta (1-4 Hz), theta (4-8 Hz), alpha (8-13 Hz), and beta (13-30 Hz), at rest and during the thermal conditions.

Results: At rest, CPs showed increased global delta (P = 0.0493) and beta (P = 0.0002) power in comparison with HCs. These findings provide further impetus for the investigation and prevention of long-lasting developmental sequalae of early life chronic pain processes. Although no cohort differences in pain intensity scores were found during the thermal pain modalities, CPs and HCs showed significant difference in changes in EEG spectral power, peak frequency, permutation entropy, and network functional connectivity at specific frequency bands (P < 0.05) during the tonic heat and cold stimulations.

Conclusion: This suggests that EEG can characterize subtle differences in heat and cold pain sensitivity in CPs. The complementation of EEG and evoked pain in the clinical assessment of pediatric chronic MSK pain can better detect underlying pain mechanisms and changes in pain sensitivity.

Publications related to pain research have increased significantly in recent years. The abundance of new evidence creates challenges staying up to date with the latest information. A comprehensive understanding of the literature is important for both clinicians and investigators involved in pain research. One commonly used method to combine and analyse data in health care research is meta-analysis. The primary aim of a meta-analysis is to quantitatively synthesise the results of multiple studies focused on the same research question. Meta-analysis is a powerful tool that can be used to advance pain research. However, there are inherent challenges when combining data from multiple sources. There are also numerous models and statistical considerations when undertaking a meta-analysis. This review aims to discuss the planning and preparation for completing a meta-analysis, review commonly used meta-analysis models, and evaluate the clinical implications of meta-analysis in pain research.

Introduction: Back pain is the leading cause of disability worldwide. Although most back pain cases are acute, 20% of acute pain patients experience chronic back pain symptoms. It is unclear whether acute pain and chronic pain have similar or distinct underlying genetic mechanisms.

Objectives: To characterize the molecular and cellular pathways contributing to acute and chronic pain states.

Methods: Cross-sectional observational genome-wide association study.

Results: A total of 375,158 individuals from the UK Biobank cohort were included in the discovery of genome-wide association study. Of those, 70,633 (19%) and 32,209 (9%) individuals met the definition of chronic and acute back pain, respectively. A total of 355 single nucleotide polymorphism grouped into 13 loci reached the genome-wide significance threshold (5x10^-8) for chronic back pain, but none for acute. Of these, 7 loci were replicated in the Nord-Trøndelag Health Study (HUNT) cohort (19,760 chronic low back pain cases and 28,674 pain-free controls). Single nucleotide polymorphism heritability was 4.6% (P=1.4x10^-78) for chronic back pain and 0.81% (P=1.4x10-8) for acute back pain. Similar differences in heritability estimates between acute and chronic back pain were found in the HUNT cohort: 3.4% (P=0.0011) and 0.6% (P=0.851), respectively. Pathway analyses, tissue-specific heritability enrichment analyses, and epigenetic characterization suggest a substantial genetic contribution to chronic but not acute back pain from the loci predominantly expressed in the central nervous system.

Conclusion: Chronic back pain is substantially more heritable than acute back pain. This heritability is mostly attributed to genes expressed in the brain.

Introduction: Despite well-documented pain disparities among adults from non-White and Hispanic groups, less is known about pain disparities in non-White and Hispanic pediatric populations.

Objectives: We compare pain and related psychosocial factors at the individual (pain intensity, pain interference, pain catastrophizing, co-occurring symptoms), social (peer relations), and systemic (health insurance) levels among Hispanic and Non-Hispanic White (NHW) youth with chronic pain.

Methods: Eight hundred thirty-seven (71.4% female) Hispanic (n = 268, 32%) and NHW (n = 569, 68%) youth ages 8 to 17 years (M = 14.00; SD = 2.54) completed a survey at their initial visit to a pain clinic. Independent sample t tests investigated mean differences in psychosocial factors at the individual and social levels. Chi-squared tests investigated differences at the systemic level. Bivariate correlations for each group were compared using Fisher r-to-z transformations.

Results: Hispanic youth reported higher levels of pain intensity (t[811] = -2.75, P = 0.006). Groups did not differ in reports of other individual or social factors. Non-Hispanic White youth were more likely to have private insurance (OR, 5.66). All examined variables were significantly correlated among NHW youth. Correlations were weaker or nonsignificant among Hispanic youth. Fisher r-to-z transformations revealed these group differences to be significant.

Conclusion: Hispanic youth report higher pain levels than NHW counterparts and lower likelihood of having private insurance. Pain and psychosocial factors correlate differently among the 2 groups highlighting a need to better understand the chronic pain experiences of diverse youth because models derived primarily from NHW populations may not generalize across ethnic and racial groups.

[This corrects the article DOI: 10.1097/PR9.0000000000000878.].

Introduction: Central sensitization (CS) involves dysfunctional central nervous system pain modulation resulting in heightened pain perception. Central sensitization is not commonly assessed among patients with opioid use disorder (OUD), despite the fact that pain has been implicated in the development, maintenance, and relapse of OUD and chronic opioid use may produce opioid-induced hyperalgesia. Central sensitization is a plausibly important mechanism underlying the complex relationship between OUD and chronic pain. However, this premise is largely untested.

Methods: Participants with OUD (n = 141) were recruited from an academic addiction treatment center in Columbus, Ohio. An established surrogate measure of CS, the American College of Rheumatology 2011 Fibromyalgia Survey Criteria, was administered using electronic survey. Participants also responded to questions about pain interference (Brief Pain Inventory), quality of life (RAND-36), and items regarding pain beliefs and expectations of pain and addiction treatment. Descriptive analyses, Spearman rho correlations, and Mann-Whitney U tests were performed.

Results: Hypothesized relationships were confirmed between degree of CS, pain interference, and health-related quality of life. Degree of CS was also positively correlated with greater endorsement of pain as a reason for the onset, maintenance, and escalation of OUD; treatment delay; and OUD relapse. Participants with the American College of Rheumatology 2011 Fibromyalgia Survey Criteria ≥13 had significantly greater endorsement of pain as a reason for delaying OUD treatment, continuing and increasing opioid use, and precipitating OUD relapse.

Conclusions: This study provides early evidence CS may underlie previously observed connections between clinically salient features of chronic pain and OUD, potentially informing future mechanistic research and precision treatment.

Opioid misuse is at a crisis level. In response to this epidemic, the National Institutes of Health has funded $945 million in research through the Helping to End Addiction Long-term (HEAL) Pain Management Initiative, including funding to the Vanderbilt Recruitment Innovation Center (RIC) to strategize methods to catalyze participant recruitment. The RIC, recognizing the challenges presented to clinical researchers in recruiting individuals experiencing pain, conducted a review of evidence in the literature on successful participant recruitment methods for chronic pain trials, in preparation for supporting the HEAL Pain trials. Study design as it affects recruitment was reviewed, with issues such as sufficient sample size, impact of placebo, pain symptom instability, and cohort characterization being identified as problems. Potential solutions found in the literature include targeted electronic health record phenotyping, use of alternative study designs, and greater clinician education and involvement. For retention, the literature reports successful strategies that include maintaining a supportive staff, allowing virtual study visits, and providing treatment flexibility within the trial. Community input on study design to identify potential obstacles to recruitment and retention was found to help investigators avoid pitfalls and enhance trust, especially when recruiting underrepresented minority populations. Our report concludes with a description of generalizable resources the RIC has developed or adapted to enhance recruitment and retention in the HEAL Pain studies. These resources include, among others, a Recruitment and Retention Plan Template, a Competing Trials Tool, and MyCap, a mobile research application that interfaces with Research Electronic Data Capture (REDCap).

Adverse childhood experiences (ACEs) affect over half of the adults in the United States and are known to contribute to the development of a wide variety of negative health and behavioral outcomes. The consequences of ACE exposure have been studied in patient populations that include individuals with gynecologic, orthopedic, metabolic, autoimmune, cardiovascular, and gastrointestinal conditions among others. Findings indicate that ACEs not only increase risks for chronic pain but also influence emotional responses to pain in many of these individuals. A growing body of research suggests that these effects may be the result of long-lasting changes induced by ACEs in neurobiological systems during early development. However, one area that is still largely unexplored concerns the effects of ACEs on burn patients, who account for almost 450,000 hospitalizations in the United States annually. Patients with severe burns frequently suffer from persistent pain that affects their well-being long after the acute injury, but considerable variability has been observed in the experience of pain across individuals. A literature search was conducted in CINAHL and PubMed to evaluate the possibility that previously documented ACE-induced changes in biological, psychological, and social processes might contribute to these differences. Findings suggest that better understanding of the role that ACEs play in burn outcomes could lead to improved treatment strategies, but further empirical research is needed to identify the predictors and mechanisms that dictate individual differences in pain outcomes in patients with ACE exposure and to clarify the role that ACE-related alterations play in early healing and recovery from burn injuries.