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Dexmedetomidine (DEX) has showed significant analgesic effects in neuropathic pain, but the underlying mechanism has remained elusive. Our present study aimed to explore the effect of DEX on hyperalgesia with the involvement of p38MAPK signaling pathway a rat model of monoarthritis (MA).
Learn More >RATIONALE, AIMS AND OBJECTIVES: Portenoy and Foley's 1986 landmark case series 'Chronic use of opioid analgesics in non-malignant pain: report of 38 cases' has been reproached for opening the floodgates of opioid prescribing for chronic non-cancer pain and the attendant harms. This influential article has been cited over 500 times in the scientific literature over the last four decades. This study seeks to understand the impact of Portenoy and Foley's article on subsequent discussions and research about opioids.
Learn More >Rheumatoid arthritis (RA) considerably impacts patients' mental health. However, it is largely unclear how people suffering from RA experience psychological stress beyond depression or anxiety, and what drives stress in these patients.
Learn More >The role of spinal glia in the development and maintenance of chronic pain has become over the last years a subject of increasing interest. In this regard, toll-like receptor 4 (TLR4) signaling has been proposed as a major trigger mechanism. Hence, in this study we explored the implications of TLR4 inhibition in the periphery and primarily in the CNS, focusing on the impact this inhibition renders in pain development and glia activation in the dorsal horn in two models of pain. Making use of a synthetic cluster of differentiation 14 (CD14)/TLR4 antagonist, the effect of TLR4 blockade on tactile allodynia and heat hyperalgesia was evaluated in osteoarthritic and postoperative rat models. An in vitro parallel artificial membrane permeation assay was performed to determine the proneness of the drug to permeate the blood-brain barrier prior to systemic and central administration. Findings suggest a dominant role of peripheral TLR4 in the model of incisional pain, whilst both peripheral and central TLR4 seem to be responsible for osteoarthritic pain. That is, central and peripheral TLR4 may be differently involved in the etiopathology of diverse types of pain what potentially seems a promising approach in the management of pain.
Learn More >To evaluate the efficacy and safety of intra-articular injection of diclofenac etalhyaluronate (DF-HA) in patients with osteoarthritis (OA) of the hip, ankle, shoulder, or elbow.
Learn More >While the COVID-19 pandemic is affecting people's well-being worldwide, it may place a particularly high burden on people with chronic pain, as pain is known to be influenced by societal and psychological conditions.
Learn More >Muscles of the lumbar spine play an important role in controlling segmental intervertebral motion. This study aimed to evaluate the association between lumbar intervertebral motion and changes in lumbar morphology/composition in people with chronic low back pain (CLBP). A sample of 183 patients with CLBP participated in this cross-sectional study. Participants underwent lumbar flexion-extension X-Rays to determine vertebral motion (translational and/or rotational motion) of lumbar levels (L1-L2 to L5-S1) and lumbar spine Magnetic Resonance Imaging (MRI) to quantify total and functional cross-sectional areas (CSAs) and asymmetry of the multifidus, lumbar erector spinae and psoas muscles. The relationship between morphology/composition of the muscles and lumbar intervertebral motion was investigated. Smaller total and functional CSAs of the multifidus and greater CSAs of the lumbar erector spinae muscle were observed in participants with greater intervertebral motion. Muscle asymmetry was observed at different lumbar vertebral levels. The greatest amount of translational intervertebral motion was observed at the L3-L4 level, while the greatest amount of rotational translation occurred at the L4-5 level. Associations were observed between the morphology of the paraspinal muscles at the vertebral levels adjacent to the L3-L4 level and the increased intervertebral motion at this level. Relationships between measures of muscle morphology/composition and increased segmental vertebral motion were observed. The results may provide a plausible biological reason for the effectiveness of rehabilitating deficient paraspinal muscles in a subset of people with CLBP. This article is protected by copyright. All rights reserved.
Learn More >Chronic migraine (CM) is one of the most disabling diseases, and it is commonly misdiagnosed and mistreated. Despite the importance of a timely and accurate diagnosis for the effective management of CM, recent surveys have shown that only 20-25% of individuals with CM receive a correct diagnosis. The obvious consequences of misdiagnosed CM are prolongation of symptoms and their associated effects on disability and health-related quality of life. Additionally, mistreatment of CM can lead to acute medication overuse headache with escalation of headache and end organ damage. Ideally, a diagnosis of CM should be made in the primary care setting, based on a thorough medical history including detailed descriptions of headaches occurring earlier in life as well as current headaches, and the range of headaches (not just the worst headaches). In our experience, it is often equally informative to ask the patient about the number of headache-free days (HFDs) and no accompanying symptoms (i.e., crystal-clear days) to quantify headache days and accurately estimate headache frequency/impact. Headache frequency is important, as this count is one key means of diagnosing CM, which requires ≥ 15 headache days/month, noting that these do not need to be migraine days. A headache day is defined as more than 4 h a day of headache. Comorbidities are common in CM and may affect the treatment choice and increase disability. Every CM patient should be offered a preventive migraine treatment. In this commentary, we provide practical insights and tips for diagnosing CM and cover issues of medication overuse, patient communication, diagnostic testing, and when to make a referral. Our key message to physicians for a patient who comes to the clinic with frequent disabling headaches having features of migraine is to assume CM until proven otherwise.
Learn More >Few studies have investigated factors associated with acute postsurgical pain (APSP) trajectories, and whether the APSP trajectory can predict chronic postsurgical pain (CPSP) remains unclear. We aimed to identify the predictors of APSP trajectories in patients undergoing gastrointestinal surgery. Moreover, we hypothesised that APSP trajectories were independently associated with CPSP. We conducted a prospective cohort study of 282 patients undergoing gastrointestinal surgery to describe APSP trajectories. Psychological questionnaires were administered 1 day before surgery. Meanwhile, demographic characteristics and perioperative data were collected. Average pain intensity during the first 7 days after surgery was assessed by a numeric rating scale (NRS). Persistent pain intensity was evaluated at 3 and 6 months postoperatively by phone call interview. CPSP was defined as pain at the incision site or surrounding areas of surgery with a pain NRS score ≥ 1 at rest. The intercept and slope were calculated by linear regression using the least squares method. The predictors for the APSP trajectory and CPSP were determined using multiple linear regression and multivariate logistic regression, respectively. Body mass index, morphine milligram equivalent (MME) consumption, preoperative chronic pain and anxiety were predictors of the APSP trajectory intercept. Moreover, MME consumption and preoperative anxiety could independently predict the APSP trajectory slope. The incidence of CPSP at 3 and 6 months was 30.58% and 16.42% respectively. APSP trajectory and age were predictors of CPSP 3 months postoperatively, while female sex and preoperative anxiety were predictive factors of CPSP 6 months postoperatively. Preoperative anxiety and postoperative analgesic consumption can predict APSP trajectory. In addition, pain trajectory was associated with CPSP. Clinicians need to stay alert for these predictors and pay close attention to pain resolution.
Learn More >Chronic multisite musculoskeletal pain (CMP) is common and highly morbid. However, vulnerability factors for CMP are poorly understood. Previous studies have independently shown that both small hippocampal brain volume and genetic risk alleles in a key stress system gene, FKBP5, increase vulnerability for chronic pain. However, little is known regarding the relationship between these factors and CMP. Here we tested the hypothesis that both small hippocampal brain volume and FKBP5 genetic risk, assessed using the tagging risk variant, FKBP5rs3800373, increase vulnerability for CMP. We used participant data from 36,822 individuals with available genetic, neuroimaging, and chronic pain data in the UK Biobank study. Although no main effects were observed, the interaction between FKBP5 genetic risk and right hippocampal volume was associated with CMP severity (β = -0.020, p = 0.002, p = 0.01). In secondary analyses, severity of childhood trauma further moderated the relationship between FKBP5 genetic risk, right hippocampal brain volume, and CMP (β = -0.081, p = 0.016). This study provides novel evidence that both FKBP5 genetic risk and childhood trauma moderate the relationship between right hippocampal brain volume and CMP. The data increases our understanding of vulnerability factors for CMP and builds a foundation for further work assessing causal relationships that might drive CMP development.
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