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Posttraumatic stress (PTS), depressive symptoms (DS), and musculoskeletal pain (MSP) are common sequelae of trauma exposure. Although these adverse posttraumatic neuropsychiatric sequelae (APNS) are often studied separately, clinical comorbidity is high. In a cohort of European American motor vehicle collision (MVC) trauma survivors (n = 781), substantial PTS (≥33, IES-R), DS (≥26, CES-D), and MSP (≥4, 0-10 NRS) were identified via a 6-month survey. Genetic risk was estimated using polygenic risk scores (PRSs) calculated from the largest available GWAS datasets of PTSD, MDD, and back pain. We then assessed comorbidity and genetic risk influence for developing chronic PTS, DS, and MSP after MVC. Secondary analyses explored whether common social determinants of health ameliorate genetic vulnerability. We found that 6 months after MVC, nearly half 357/781 (46%) of the participants had substantial PTS, DS, and/or MSP, and overlap was common (PTS + MSP (23%), DS + MSP (18%), PTS + DS (12%)). Genetic risk predicted post-MVC outcomes. PTSD-PRSs predicted PTS and DS (R = 2.21% and 2.77%, p < 0.01), MDD-PRSs predicted DS and MSP (R = 1.89%, p < 0.01) and 0.79%, p < 0.05), and back pain-PRS predicted MSP (R = 1.49%, p < 0.01). Individuals in the highest quintile of PTSD-PRSs had 2.8 and 3.5 times the odds of developing PTS and DS vs. the lowest quintile (95% CI = 1.39-5.75 and 1.58-7.76). Among these high-risk individuals, those living in non-disadvantaged neighborhoods and with college education had 47% (p = 0.048) and 52% (p = 0.04) less risk of developing PTS, and those with high social support had 60% (p = 0.008) less risk of developing DS. Overall, genetic factors influence the risk of APNS after MVC, genetic risk of distinct APNS are overlapping, and specific social determinants greatly augment genetic risk of APNS development after MVC.
Learn More >Quantitative Sensory Testing (QST) can be useful to identify high-risk patients for the development of chronic postsurgical pain (CPSP). This systematic review aims to assess if presurgical sensory sensitivity measured using QST is associated with acute and CPSP after total joint arthroplasty.A systematic search was performed in Sep/2020 in PubMed, EMBASE, Web of Science and Scopus, using terms related to total joint arthroplasty and QST. Prospective studies were included if they reported an association between presurgical QST and postsurgical pain in adults with osteoarthritis undergoing primary unilateral total joint arthroplasty.From 2994 identified studies, 18 met the inclusion criteria (1869 patients). Total knee arthroplasty was the most common surgery (16 studies) and pressure pain threshold (PPT) was the most common test (11 studies), followed by dynamic measures (9 studies). Postsurgical pain was assessed at acute (5 studies), subacute (2 studies) and chronic (13 studies) time points. Risk of bias was assessed using the Quality in Prognosis Studies Tool, and evaluated as low-to-moderate in most domains. Fourteen studies reported at least one statistically significant association between QST and pain (acute: 4 studies, subacute: 1 study, chronic: 9 studies). PPT was associated with postsurgical pain in 6 studies (out of 11, 55%), heat pain threshold in 2 (out of 6, 33%), conditioned pain modulation in 1 (out of 6, 17%) and temporal summation of pain in 5 (out of 8, 63%). The predictive role of presurgical QST for post-arthroplasty pain remains unclear, mainly due to heterogeneous methodologies and inconsistent results.
Learn More >Exercise and physical activity are an evidence-based practice for chronic pain. Health professionals need instruments to assess self-efficacy for this practice taking into account the specific barriers of patients with these health problems.
Learn More >The efficacy of onabotulinumtoxinA (OnaB-A) as a preventative treatment for chronic migraine, emerging fortuitously from clinical observation is now supported by class one evidence and over two decades of real-world clinical data. There is still limited ability to predict a clinically meaningful response to OnaB-A for individual patients, however. This review summarises briefly the proposed mechanism of OnaB-A in chronic migraine, the literature of predictors of clinical response, and recent developments in the field.
Learn More >Neurophysiological investigation of nociceptive pathway has so far been limited to late cortical responses. We sought to detect early components of the cortical evoked potentials possibly reflecting primary sensory activity.
Learn More >This study examined the prevalence of suicidality and associations with pain characteristics (i.e., presence of usual pain/discomfort, pain intensity) among those with chronic pain conditions (i.e., arthritis, migraine, back pain).
Learn More >Exercise is the most common treatment recommended by health care providers for treatment of musculoskeletal pain. We examined whether voluntary running wheel exercise improves pain and bone remodeling in rats with monosodium iodoacetate (MIA)-induced unilateral knee joint pain. During acquisition of wheel running prior to OA treatment, rats separated into two groups characterized by either high or low levels of voluntary wheel running as indicated by distance and peak speed. Following induction of knee joint OA, all rats showed diminished voluntary wheel running throughout the study. Voluntary wheel running failed to alter evoked nociceptive responses evaluated as weight asymmetry or hindpaw tactile thresholds at any time-point of the study. In contrast, relief of ongoing pain was demonstrated by conditioned place preference produced by lidocaine injection into the MIA-treated knee in high but not low running rats. Both high and low voluntary runners showed diminished trabecular bone loss compared to sedentary controls. These observations indicate that both high and low intensity exercise is beneficial in protecting against bone remodeling in advanced OA. The data suggest that similar to clinical observation, bone remodeling does not correlate with pain. Additionally, these results suggest that higher intensity exercise may relieve persistent ongoing OA pain while maintaining movement-evoked nociception. The relief of ongoing pain can potentially offer significant improvement in quality of life while preservation of responses to movement-evoked pain may be especially important in protecting the joint from damage due to overuse.
Learn More >The role that inflammation plays in human nerve injury and neuropathic pain is incompletely understood. Previous studies highlight the role of inflammation in the generation and maintenance of neuropathic pain, but the emerging evidence from the preclinical literature for its role in the resolution of neuropathic pain remains to be explored in humans. Here, we use carpal tunnel syndrome (CTS) as a human model system of nerve injury and neuropathic pain to determine changes in serum cytokine protein levels and gene expression levels before (active stage of disease) and after carpal tunnel decompression surgery (recovery). Fifty-five CTS patients were studied and 21 healthy age and gender matched participants served as controls. In the active stage of the disease (CTS before surgery vs healthy controls), PTGES2 mRNA was decreased in patients (adjusted p=0.013), while TGF-β and CCL5 protein levels were increased (adjusted p=0.016 and p=0.047 respectively). In the resolution phase (CTS before surgery vs after surgery), IL-9 mRNA was increased after surgery (adjusted p=0.014) and expression of IL-6 mRNA and IL-4 protein levels were increased before surgery (adjusted p=0.034 and p=0.002 respectively). IL-9 mRNA expression negatively correlated with several (neuropathic) pain scores. In contrast, protein levels of IL-4 positively correlated with pain scores. In conclusion, we demonstrate specific dysregulation of systemic cytokine expression both in the active and resolution phases of nerve injury and neuropathic pain. IL-9 represents an interesting candidate associated with resolution of nerve injury and neuropathic pain.
Learn More >Multicentre cross-sectional study.
Learn More >Evidence suggests that Δ-tetrahydrocannabinol (Δ-THC), the intoxicating component of cannabis, may cause enduring changes in the structure and function of adolescent brain circuits implicated in nociceptive responding. Yet, whether such changes might persistently disrupt nociceptive behaviors remains unknown. In the present study, we subjected C57BL6/J mice of both sexes to once-daily injections of Δ-THC (5 mg-kg, intraperitoneal) or vehicle throughout adolescence (PND 30-43) and, when the animals had reached adulthood (PND 70), assessed nociceptive behavior using the formalin and chronic constriction injury (CCI) tests. We also investigated, using the tail immersion test, the antinociceptive effects of morphine and the development of tolerance to such effects. The results show that adolescent Δ-THC exposure does not significantly impair nociceptive responding or morphine-related antinociception and tolerance. The findings suggest that frequent exposure to a moderate dose of Δ-THC during adolescence does not permanently alter nociceptive circuits in male or female mice. The endocannabinoid system serves critical functions in the central and peripheral nervous systems, including regulation of pain, and can be modified by prolonged exposure to the intoxicating constituent of cannabis, Δ-tetrahydrocannabinol (Δ-THC). This raises the possibility that regular use of Δ-THC-containing cannabis during adolescence might cause changes in nociception that persist into adulthood. We found that frequent early-life exposure to a moderate dose of Δ-THC does not permanently alter nociceptive function in male or female mice.
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