The Declaration of Lima on Pain in Childhood is a call into action to improve the care provided to children and adolescents with pain.
The Declaration of Lima on Pain in Childhood is a call into action to improve the care provided to children and adolescents with pain.
Introduction: Inadequate pain management remains a problem in the emergency department (ED) and might increase the risk of chronic pain. Previous studies suggested that pain intensity is associated with pain chronification in specific patient groups. This study aims to study the association between pain intensity {[verbal] numeric rating scale ([V]NRS) ≥ 7} at discharge from the ED and pain chronification in the general population.
Objective: To assess whether a high pain score at discharge from the ED increases the risk of chronic pain development.
Methods: Adults who visited the ED with pain as their main complaint, and who were not hospitalized, were eligible for inclusion. Chronic pain was defined as pain with an (V)NRS score ≥1 90 days after the ED visit and with a similar location to the acute pain.
Results: We included 1906 patients, of whom 825 participants completed 90 days of follow-up. Approximately 34.1% left the ED with an (V)NRS score ≥7, and 67.8% reported an (V)NRS score of ≥1 90 at days. Of all patients leaving the ED with an (V)NRS score ≥7, 76.5% developed chronic pain vs 63.2% of patients with (V)NRS score <7 (P < 0.01). After correction, this difference was borderline statistically significant with an odds ratio of 1.45 (95% confidence interval: 0.99-2.13, P = 0.054). Various sensitivity analyses using a different (V)NRS at discharge and different definitions of chronic pain at 90 days showed a significant difference in the chronification of pain.
Conclusion: This study suggests that pain intensity at discharge from the ED, regardless of the localization or cause of pain, increased the risk of developing chronic pain. By distinguishing patients at risk and providing an effective treatment, chronic pain and the associated burden of disease might be preventable.
The ability of clinical trials to inform the care of chronic pain may be limited if only an unrepresentative subset of patients are allowed to enroll. We summarize and report new insights on published studies that report on how trial exclusions affect the generalizability of their results. We conducted a PubMed search on the following terms: (("eligibility criteria" AND generalizability) OR ("exclusion criteria" AND generalizability) OR "exclusion criteria"[ti] OR "eligibility criteria"[ti]) AND pain. We only considered studies relevant if they analyzed data on (1) the prevalence and nature of exclusion criteria or (2) the impact of exclusion criteria on sample representativeness or study results. The 4 articles that were identified reported differences in patients who were included and excluded in different clinical trials: excluded patients were older, less likely to have a paid job, had more functional limitations at baseline, and used strong opioids more often. The clinical significance of these differences remains unclear. The pain medicine literature has very few published studies on the prevalence and impact of exclusion criteria, and the outcomes of excluded patients are rarely tracked. The frequent use of psychosocial exclusions is especially compromising to generalizability because chronic pain commonly co-occurs with psychiatric comorbidities. Inclusion of more representative patients in research samples can reduce recruitment barriers and broaden the generalizability of findings in patients with chronic pain. We also call for more studies that examine the use of exclusion criteria in chronic pain trials to better understand their implications.
Introduction: Many patients with chronic pain use prescription opioids. Epigenetic modification of the μ-opioid receptor 1 (OPRM1) gene, which codes for the target protein of opioids, may influence vulnerability to opioid abuse and response to opioid pharmacotherapy, potentially affecting pain outcomes.
Objective: Our objective was to investigate associations of clinical and sociodemographic factors with OPRM1 DNA methylation in patients with chronic musculoskeletal pain on long-term prescription opioids.
Methods: Sociodemographic variables, survey data (Rapid Estimate of Adult Health Literacy in Medicine-Short Form, Functional Comorbidity Index [FCI], PROMIS 43v2.1 Profile, Opioid Risk Tool, and PROMIS Prescription Pain Medication Misuse), and saliva samples were collected. The genomic DNA extracted from saliva samples were bisulfite converted, amplified by polymerase chain reaction, and processed for OPRM1-targeted DNA methylation analysis on a Pyrosequencing instrument (Qiagen Inc, Valencia, CA). General linear models were used to examine the relationships between the predictors and OPRM1 DNA methylation.
Results: Data from 112 patients were analyzed. The best-fitted multivariable model indicated, compared with their counterparts, patients with > eighth grade reading level, degenerative disk disease, substance abuse comorbidity, and opioid use < 1 year (compared with >5 years), had average methylation levels that were 7.7% (95% confidence interval [CI] 0.95%, 14.4%), 11.7% (95% CI 2.7%, 21.1%), 21.7% (95% CI 10.7%, 32.5%), and 16.1% (95% CI 3.3%, 28.8%) higher than the reference groups, respectively. Methylation levels were 2.2% (95% CI 0.64%, 3.7%) lower for every 1 unit increase in FCI and greater by 0.45% (95% CI 0.08%, 0.82%) for every fatigue T score unit increase.
Conclusions: OPRM1 methylation levels varied by several patient factors. Further studies are warranted to replicate these findings and determine potential clinical utility.
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.