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Intervertebral disc degeneration (IVDD), for which obesity and genetics are known risk factors, is a chronic process that alters the structure and function of the intervertebral discs (IVD). Circulating leptin is positively correlated with body weight and is often measured to elucidate the pathogenesis of IVD degeneration. In this study, we examined the associations of single nucleotide polymorphisms (SNPs) genetic and environmental effects with IVDD. A total of 303 Taiwanese patients with IVDD (mean age, 58.6 ± 12.7 years) undergoing cervical discectomy for neck pain or lumbar discectomy for back pain were enrolled. Commercially available enzyme-linked immunosorbent assay (ELISA) kits measured the circulating plasma leptin levels. TaqMan SNP genotyping assays genotyped the SNPs rs2167270 and rs7799039. Leptin levels were significantly increased in obese individuals ( < 0.001) and non-obese or obese women ( < 0.001). In the dominant model, recoded minor alleles of rs2167270 and rs7799039 were associated with higher leptin levels in all individuals ( = 0.011, = 0.012). Further, the association between these SNPs and leptin levels was significant only in obese women ( = 0.025 and = 0.008, respectively). There was an interaction effect between sex and obesity, particularly among obese women (interaction = 0.04 and 0.02, respectively). Our findings demonstrate that these SNPs have sex-specific associations with BMI in IVDD patients, and that obesity and sex, particularly among obese women, may modify the transcription effect.
Learn More >Total knee arthroplasty (TKA) is among the most performed orthopaedic surgeries in the United States with at least 1,000,000 cases performed per year. Dissatisfaction following TKA has often been reported as 20% or more, with a multitude of causes including sociodemographic, preoperative, and postoperative factors. The purpose of this study was to reexamine the rate and causes of dissatisfaction following TKA.
Learn More >The multiple comorbidities & dimensions of chronic pain present a formidable challenge in disentangling its aetiology. Here, we performed genome-wide association studies of eight chronic pain types using UK Biobank data (N=4,037-79,089 cases; N=239,125 controls), followed by bivariate linkage disequilibrium-score regression and latent causal variable analyses to determine (respectively) their genetic correlations and genetic causal proportion (GCP) parameters with 1,492 other complex traits. We report evidence of a shared genetic signature across chronic pain types as their genetic correlations and GCP directions were broadly consistent across an array of biopsychosocial traits. Across 5,942 significant genetic correlations, 570 trait pairs could be explained by a causal association (|GCP| > 0.6; 5% false discovery rate), including 82 traits affected by pain while 410 contributed to an increased risk of chronic pain (cf. 78 with a decreased risk) such as certain somatic pathologies (e.g., musculoskeletal), psychiatric traits (e.g., depression), socioeconomic factors (e.g., occupation) and medical comorbidities (e.g., cardiovascular disease). This data-driven phenome-wide association analysis has demonstrated a novel and efficient strategy for identifying genetically supported risk & protective traits to enhance the design of interventional trials targeting underlying causal factors and accelerate the development of more effective treatments with broader clinical utility. PERSPECTIVE: Through large-scale phenome-wide association analyses of >1,400 biopsychosocial traits, this article provides evidence for a shared genetic signature across eight common chronic pain types. It lays the foundation for further translational studies focused on identifying causal genetic variants and pathophysiological pathways to develop novel diagnostic & therapeutic technologies and strategies.
Learn More >There have been several recent calls to "re-think chronic pain" in response to the growing awareness of social inequities that impact the prevalence of chronic pain and its management. This in turn has resulted in new explorations of suffering as it relates to pain. While laudable, many of these clinically oriented accounts are abstract and often fail to offer a critical theoretical understanding of social and structural inequities. To truly rethink pain, we must also reconsider suffering, beginning in the everyday expert knowledge of people with chronic pain who can offer insights in relation to their bodies and also the organization of the social circumstances in which they live. Our team undertook a sociological approach known as institutional ethnography (IE) to explicate the work of people in managing lives beset by chronic pain and the inequities that stem from marginalization. In keeping with our critical paradigm, we describe participant accounts as situated, rather than lived, to de-emphasize the individual in favour of the social and relational. Through our analysis, we offer a new concept of "chronic struggle" to capture how pain, illness, economic deprivation, and suffering constitute a knot of experience that people living with chronic pain are obliged to simplify in order to fit existing logics of medicine. Our goal is to identify the social organization of chronic pain care which underpins experience in order to situate the social as political rather than medical or individual. PERSPECTIVE: This article explicates the health work of people living with chronic pain and marginalization, drawing on their situated experience. We offer the concept of chronic struggle as a conceptualization that allows us to bring into clear view the social organization of chronic pain in which the social is visible as political and structural rather than medical or individual.
Learn More >This study investigates thoracic hyper kyphosis (THK) rehabilitation using the Denneroll™ thoracic traction orthosis (DTTO). Eighty participants, with chronic non-specific neck pain (CNSNP) and THK were randomly assigned to the control or intervention group (IG). Both groups received the multimodal program; IG received the DTTO. Outcomes included formetric thoracic kyphotic angle ICT-ITL, neck pain and disability (NDI), head repositioning accuracy (HRA), smooth pursuit neck torsion test (SPNT) and overall stability index (OSI). Measures were assessed at baseline, after 30 treatment sessions over the course of 10 weeks, and 1-year after cessation of treatment. After 10 weeks, the IG improved more in neck pain intensity ( < 0.0001) and NDI ( < 0.001). No differences were found for SPNT ( = 0.48) and left-sided HRA ( = 0.3). IG improved greater for OSI ( = 0.047) and right sided HRA ( = 0.02). Only the IG improved in THK ( < 0.001). At 1-year follow-up, a regression back to baseline values for the control group was found for pain and disability such that all outcomes favored improvement in the IG receiving the DTTO; all outcomes ( < 0.001). The addition of the DTTO to a multimodal program positively affected CNSNP outcomes at both the short and 1-year follow-up.
Learn More >The current investigation aimed to compare the sensorimotor integration, sensorimotor control, and cost of cognitive-motor dual task during walking, in persons with chronic WAD as compared to matched chronic idiopathic neck pain and normal healthy controls.
Learn More >Existing data demonstrate reduced delta power during sleep in patients with depression and chronic pain. However, there has been little examination of the relationship between delta power and pain-reports, or pain-catastrophizing. We recruited female participants (n=111) with insomnia and temporomandibular disorder, and measured nocturnal and daytime measures of pain and pain catastrophizing, and calculated relative nocturnal delta (0.5-4 Hz) power during sleep. We fit linear regression models, and further examined the moderating effect of depressive symptom severity. Lower relative delta power across the whole night was significantly associated with greater nocturnal pain (B = -20.276, p = 0.025, R = 0.214). Lower relative delta power during the first-third of the night, was associated with greater nocturnal pain (B = -17.807, p = 0.019, R = 0.217), next-day pain (B = 13.876, p = 0.039, R = 0.195), and next-morning pain (B = -15.751, p = 0.022, R = 0.198). Lower relative delta power during the final-third of the night was significantly associated with greater nocturnal (B = -17.602, p = 0.029, R = 0.207) and next-morning pain (3: B = -14.943, p = 0.042, R = 0.187). Depressive symptom severity did not moderate these relationships. Delta power was not significantly associated with nocturnal or daytime pain catastrophizing. These findings demonstrate that greater relative delta power during sleep is associated with lower nocturnal and next-day pain in patients with temporomandibular disorder. This data may guide the use of sleep interventions in clinical pain populations, with the aim of improving pain outcomes. PERSPECTIVE: This article presents data demonstrating an association between increased nocturnal delta power and reduced next-day pain. These findings may help promote interventions which aim to increase nocturnal delta power in clinical pain populations, with the goal of improving pain outcomes.
Learn More >Although insomnia symptoms and chronic pain are associated, less is known about the temporal nature of the associations between these variables or the impact of internalizing symptoms on the associations. Concurrent and longitudinal associations were examined among insomnia symptoms, internalizing symptoms, and pain in youth with chronic pain in this retrospective analysis of clinical records. We hypothesized the following: (a) pain, insomnia symptoms, and internalizing symptoms would be significantly interrelated at all waves, (b) insomnia symptoms would more strongly predict future pain than the reverse, and (c) internalizing symptoms would mediate the longitudinal association between insomnia symptoms and pain.
Learn More >Tension type headache (TTH) is a prevalent but poorly understood pain disease. Current understanding supports the presence of multiple associations underlying its pathogenesis. Our aim was to compare competing multivariate pathway models that explains the complexity of TTH. Headache features (intensity, frequency, or duration – headache diary), headache-related disability (Headache Disability Inventory-HDI), anxiety/depression (Hospital Anxiety and Depression Scale), sleep quality (Pittsburgh Sleep Quality Index), widespread pressure pain thresholds (PPTs) and trigger points (TrPs) were collected in 208 individuals with TTH. Four latent variables were formed from the observed variables – Distress (anxiety, depression), Disability (HDI subscales), Severity (headache features), and Sensitivity (all PPTs). Structural equation modelling (SEM) and Bayesian network (BN) analyses were used to build and compare a theoretical (model) and a data-driven (model) latent variable model. The model (root mean square error of approximation [RMSEA] = 0.035) provided a better statistical fit than model (RMSEA = 0.094). The only path common between model and model was the influence of years with pain on TrPs. The model revealed that the largest coefficient magnitudes were between the latent variables of Distress and Disability (β=1.524, P=0.006). Our theoretical model proposes a relationship whereby psycho-physical and psychological factors result in clinical features of headache and ultimately affect disability. Our data-driven model proposes a more complex relationship where poor sleep, psychological factors, and the number of years with pain takes more relevance at influencing disability. Our data-driven model could be leveraged in clinical trials investigating treatment approaches in TTH.
Learn More >Screening trials before full implantation of a spinal cord stimulation device are recommended by clinical guidelines and regulators, although there is limited evidence for their use. The TRIAL-STIM study showed that a screening trial strategy does not provide superior patient pain outcome at 6-month follow-up compared with not doing a screening trial and that it was not cost-effective.
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