Browse by Audience
Various approaches have been developed with a view to treating the back pain component in patients with chronic low back pain (CLBP) and persistent spinal pain syndrome (PSPS). Emerging evidence shows that peripheral nerve field stimulation (PNFS) may be an efficacious therapeutic modality against axial low back pain. Hence, the aim of the review was to evaluate the analgesic efficacy and safety of PNFS, when used alone or as an adjunct to spinal cord stimulation (SCS), for managing CLBP and PSPS.
Learn More >We investigated whether lidocaine can increase the pain threshold of rats with trigeminal neuralgia by affecting the expression of P2X7, p-p38 and IL-Iβ proteins in the thalamus. Thirty-three male Sprague-Dawley (SD) rats were randomly divided into three groups ( = 11): Sham group, Ion-CCI (infraorbital nerve chronic constriction injury) group and Ion-CCI+L group(Ion-CCI+lidocaine 10 mg/kg/day, i.p.). The mechanical pain threshold of rats was measured preoperatively and at 1, 3, 5, 7, 9, 11 and 14days after operation with the von Frey filament sensor tester. Fourteen days after operation, the rats were dissected to collect their whole brain, thalamus and trigeminal ganglion to detect IL-1β, P2X7, p38, and p-p38 protein expression. The pain threshold of rats in Ion-CCI+L group was lower than that in Sham group ( < 0.01) and higher than that in Ion-CCI group ( < 0.01).ELISA showed that IL-1β in the thalamus and trigeminal ganglion in Ion-CCI+L group were lower than those in ion-CCI group ( < 0.05) but higher than those in Sham group ( < 0.05). Western blot showed that the expression levels of P2X7 and p-p38 in the thalamus of rats in Ion-CCI+L group were lower than those in Ion-CCI group ( < 0.01) and higher than thaose in Sham group ( < 0.01),while the expression levels of IL-1β in the thalamus in Ion-CCI+L group were lower than those in Ion-CCI group ( < 0.05) and higher than those in Sham group ( < 0.01). Immunofluorescence showed that p-p38 in the thalamus in Ion-CCI+L group was lower than that in Ion-CCI group ( < 0.05) and higher than that in Sham group ( < 0.05). Lidocaine can reduce the inflammatory response of the central nervous system and increase the pain threshold of trigeminal neuralgia rats by inhibiting p2x7-p38-IL-1β signaling pathway.This pathway play an important role in the pathogenesis of trigeminal neuralgia, and it may be one of the targets for the treatment of trigeminal neuralgia.
Learn More >Osteoarthritis (OA) is a leading cause of disability, the most common form of chronic disease in the temporomandibular joint (TMJ), and the most severe disease type of temporomandibular disorders (TMD). The etiology of TMD is multifactorial, considering parafunctional habits, sleep bruxism, or sleep disturbance as common factors. Insomnia and apnea are the two most frequent forms of sleep disorders in TMD patients. Due to this, the objective of this systematic review was to highlight whether there is currently scientific evidence in the literature describing that patients with temporomandibular joint osteoarthritis (TMJ-OA) are associated with increased sleep disorders or impaired sleep quality.
Learn More >The diagnosis of cervicogenic headache (CGH) remains a challenge for clinicians as the diagnostic value of detailed history and clinical findings remains unclear.
Learn More >Currently, there is a significant unmet need for novel analgesics with fewer side effects. In this study, we carried out structural modification of a hit compound previously identified in an artificial-intelligence (AI) virtual screening and discovered the potent analgesic, benzo[b]thiophene-2-carboxamide analog (compound 25) with new structural scaffold. We investigated the signaling pathways of opioid receptors mediated by compound 25, and found this racemic compound activated mu-opioid receptor through the cyclic adenosine monophosphate (cAMP) and β-arrestin-2-mediated pathways with strong potency and efficacy, and accompanying nociceptin-orphanin FQ opioid peptide and delta-opioid receptors through the cAMP pathway with weak potencies. Compound 25 elicited potent antinociception in thermal-stimulated pain (ED value of 127.1 ± 34.65 μg/kg) and inflammatory-induced allodynia models with less gastrointestinal transit inhibition and antinociceptive tolerance than morphine. Overall, this study revealed a novel analgesic with reduced risks of side effects.
Learn More >Theoretical frameworks explain how pain-related psychological factors may influence physical performance. In this systematic review and meta-analysis, we evaluated the evidence regarding the relationship between pain-related psychological factors and maximal physical performance in patients with low back pain (LBP). Pubmed, Embase, CINAHL and Web of Science databases were searched from inception to May 2022. Cross-sectional or longitudinal studies reporting cross-sectional measures of association between at least one pain-related psychological factor and a quantitatively measured outcome of maximal physical performance in patients with LBP were eligible for inclusion. Thirty-eight studies (n=2490; 27 cross-sectional studies, n=1647 (66%); 11 longitudinal studies, n=843 (34%)) were included, with 92% of participants (n=2284) having chronic LBP. Results showed that pain-related fear, pain catastrophising and anticipated pain were consistently and negatively associated with maximal physical performance in chronic LBP, whereas pain-self efficacy showed positive correlations. Overall, magnitudes of absolute pooled r-values were small (r≤0.25), except for anticipated pain, which was moderately associated with maximal physical performance (r=-0.34 to -0.37). Subanalyses and sensitivity analyses yielded similar pooled correlation coefficients. Certainty of evidence using the GRADE recommendations was very low to moderate for pain-related fear, and very low to low for the other pain-related psychological factors. Prospero registration: CRD42021227486. Perspective: Overall, small pooled correlation coefficients were shown between pain-related psychological factors and maximal physical performance in chronic LBP. Certainty of evidence was very low to low for all pain-related psychological factors other than pain-related fear. Future studies taking into account limitations of the current literature may therefore change these conclusions.
Learn More >The phenomenon of alcohol analgesia and tolerance can facilitate misuse and lead to the development of alcohol use disorder (AUD). Numerous alcohol-induced behaviors are genetically influenced; however, it is unknown if alcohol analgesia has a genetic contribution. Rodent studies have shown that alcohol responses differ vastly between two widely studied inbred strains of mice, C57BL/6J (B6) and DBA/2J (D2). Here, we used B6 and D2 mice as an initial behavioral genetic analysis of acute alcohol-induced antinociception.
Learn More >To evaluate the effect of neuromodulatory drugs on the intensity of chronic pelvic pain (CPP) in women.
Learn More >Veterans Health Administration implemented the Opioid Safety Initiative (OSI) in 2013 to promote safe/rational opioid prescribing. West Palm Beach VA Healthcare System (WPBVAHCS) has been an outlier for the percentage of Veterans with chronic non-cancer pain receiving ≥90 mg Morphine Equivalent Daily Dosing (MEDD) in Veterans Integrated Service Networks (VISN) 8 since the 2016 fiscal year. The purpose was to determine the utility of a Pain Clinical Pharmacist Practitioner (CPP) identifying, reviewing, and approaching Veterans utilizing high-dose opioids for dose reevaluation and the impact on OSI metric post-opioid reevaluation. Pain CPP opioid education resulted in 28% (11/39) of Veterans undergoing an average 17.7 mg MEDD opioid dose reduction. For Veterans evaluated by Pain CPP, 83% (15/18) reported no change or improvement in average pain and PEG score. Pain CPP's implemented 48 interventions outside of opioid dose reduction, the most common related to naloxone. No documented opioid overdose events, hospitalizations for uncontrolled pain or mental health, suicide attempts or pain-related crisis interventions were reported. Pain CPP's are equipped to provide opioid education, address risk mitigation strategies, reassess pain regimens, and refer for non-pharmacologic modalities. Utilization of Pain CPP resources helps improve OSI metrics while providing safe comprehensive medication management (CMM) for chronic pain.
Learn More >Increased tetrahydrobiopterin (BH4) generated in injured sensory neurons contributes to increased pain sensitivity and its persistence. GTP cyclohydrolase 1 (GCH1) is the rate-limiting enzyme in the de novo BH4 synthetic pathway, and human single-nucleotide polymorphism studies, together with mouse genetic modeling, have demonstrated that decreased GCH1 leads to both reduced BH4 and pain. However, little is known about the regulation of expression upon nerve injury and whether this could be modulated as an analgesic therapeutic intervention. We performed a phenotypic screen using about 1000 bioactive compounds, many of which are target-annotated FDA-approved drugs, for their effect on regulating expression in rodent injured dorsal root ganglion neurons. From this approach, we uncovered relevant pathways that regulate expression in sensory neurons. We report that EGFR/KRAS signaling triggers increased expression and contributes to neuropathic pain; conversely, inhibiting EGFR suppressed GCH1 and BH4 and exerted analgesic effects, suggesting a molecular link between EGFR/KRAS and pain perception. We also show that GCH1/BH4 acts downstream of KRAS to drive lung cancer, identifying a potentially druggable pathway. Our screen shows that pharmacologic modulation of GCH1 expression and BH4 could be used to develop pharmacological treatments to alleviate pain and identified a critical role for EGFR-regulated GCH1/BH4 expression in neuropathic pain and cancer in rodents.
Learn More >