Browse by Audience
To describe interictal brain structural and metabolic differences between patients with episodic migraine (EM), chronic migraine (CM) and healthy controls (HC).
Learn More >Aims of the study were to: Implement supported self-management for chronic primary orofacial pain in a clinical setting. Evaluate its impact on consultation rates, pain-severity, interference-with-life and patient experience.
Learn More >Neuroscience Education Therapy (NET) has been successfully used for numerous overlapping pain conditions, but few studies have investigated NET for migraine.
Learn More >Pain specialists treat patients with headache and interface with those who use opioids more so than neurologists and headache specialists. We assessed headache medicine knowledge and needs of pain specialists.
Learn More >To determine whether sociodemographic factors are associated with heterogeneity in pain evolution in inflammatory rheumatic diseases (IRDs) after accounting for disease-specific characteristics in a system with universal health care.
Learn More >Effective treatment of chronic pain, in particular neuropathic pain, without the side effects that often accompany currently available treatment options is an area of significant unmet medical need. A phenotypic screen of mouse gene knockouts led to the discovery that adaptor protein 2-associated kinase 1 (AAK1) is a potential therapeutic target for neuropathic pain. The synthesis and optimization of structure-activity relationships of a series of aryl amide-based AAK1 inhibitors led to the identification of , a brain penetrant, AAK1-selective inhibitor that proved to be a valuable tool compound. Compound was evaluated in mice for the inhibition of μ2 phosphorylation. Studies conducted with in pain models demonstrated that this compound was efficacious in the phase II formalin model for persistent pain and the chronic-constriction-injury-induced model for neuropathic pain in rats. These results suggest that AAK1 inhibition is a promising approach for the treatment of neuropathic pain.
Learn More >Chronic pain is highly prevalent in patients with rheumatoid arthritis (RA) and can cause various physical and psychological impairments. Unfortunately, the appropriate diagnosis of chronic pain syndromes in this population can be challenging because pain may be primary to RA-specific inflammation and/or secondary to other conditions, typically osteoarthritis (OA) and fibromyalgia (FM). This disparity further poses a clinical challenge, given that chronic pain can often be discordant or undetected with standard RA-specific surveillance strategies, including serological markers and imaging studies. In this review, we provide a robust exploration of chronic pain in the RA population with emphasis on epidemiology, mechanisms, and management strategies.
Learn More >It was reported that migraine was associated with increased vascular risks, and the association between high blood pressure (BP) and migraine was believed by some to be the missing link. The current review focused on the associations between migraine and hypertension and BP per se, and evidence on the directionality of the associations was also reviewed.
Learn More >While ketamine's analgesia has mostly been attributed to antagonism of N-methyl-D-aspartate receptors, evidence suggests multiple other pathways are involved in its antidepressant and possibly analgesic activity. These mechanisms and ketamine's role in the nociplastic pain paradigm are discussed. Animal studies demonstrating ketamine's neurotoxicity have unclear human translatability and findings from key rodent and human studies are presented.
Learn More >Chronic constriction injury (CCI) of the sciatic nerve was used to establish neuropathic pain (NP) models in rats. CCI rats were then treated with propofol and their paw withdrawal mechanical threshold (PWMT) and paw withdraw thermal latency (PWTL) were measured. In addition, the expression patterns of TNF-α, IL-1β and IL-10 were detected. CCI rats treated with propofol were further injected with antagomiR-140-3p to verify the role of miR-140-3p in propofol's analgesic actions. In addition to confirming the relationship between miR-140-3p and JAG1, the expression patterns of JAG1 itself were detected. Propofol-treated CCI rats were also injected with Ad-JAG1 to test the role of JAG1 in propofol's analgesic mechanism of action. Finally, the levels of JAG1 and Notch pathway-related proteins were detected.Results: Propofol was found to alleviate NP, including thermal hyperalgesia and mechanical pain threshold. Propofol could also ameliorate neuroinflammation by up-regulating the expression of IL-10 and inhibiting the release of TNF-α and IL-1β. Mechanically, propofol enhanced the amount of miR-140-3p in CCI rats via regulation of JAG1. Down-regulation of miR-140-3p, or up-regulation of JAG1, could reduce the protective effect of propofol against NP. Propofol inhibited the activation of Notch signaling via miR-140-3p/JAG1 to realize its analgesic effect. Conclusion: Our findings indicated that propofol inhibits inflammatory responses and the Notch signaling pathway via miR-140-3p/JAG1 to alleviate NP. These data provide evidence to support a potential clinical therapy for NP. This article is protected by copyright. All rights reserved.
Learn More >