Browse by Audience
Research on social disparities in pain care has been mainly focused on the role of race/racism and sex/sexism. Classism in pain assessment and management practices has been much less investigated. We aimed to test the effect of patient socioeconomic status (SES; a proxy of social class) on nurses' pain assessment and management practices and whether patient SES modulated the effects of patient distress and evidence of pathology on such practices.
Fear of pain resonates with most people, in particular in relation to dying. Despite this, there are still people dying with unrelieved pain.
Studies to date have not comprehensively examined pain experience after total knee arthroplasty (TKA). Discrete patterns of pain in this period might be associated with pain outcomes at 6 to 12 months after TKA.
Pain is a widely experienced symptom of inflammatory bowel disease (IBD), which has significant psychological and functional impacts on patients. Understanding the aetiology and management of chronic pain is a poorly understood area of IBD research. This qualitative study aimed to explore the experiences of individuals with IBD and pain, the pain management strategies they use and any needs for future pain management interventions.
Chronic pain is one of the commonest reasons individuals seek medical attention. It is a major issue because of the wide inter-individual variability in the analgesic response. This might be partly explained by the presence of variants in genes encoding molecules involved in pharmacodynamics and pharmacokinetics. The aim was to analyze opioid effectiveness in chronic low-back pain (CLBP) relief after opioid titration, unveiling the impact of pharmacogenetics.
The role of soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) in atopic dermatitis (AD) is unknown. This study is envisioned to lead to the previously unreported SNARE function in AD-related cytokine secretion and epidermis-nerve communication. Herein, we report that various cytokines were simultaneously upregulated and co-released in the innate immunity-activated primary human keratinocytes (phKCs). AD-related cytokines thymic stromal lymphopoietin (TSLP), endothelin-1 (ET-1) or inflammatory TNF-α activated distinct but overlapping sensory neurons. Interestingly, TNF-α potentiated TSLP-induced Ca-influx, whereas ET-1 caused itch-selective B-type natriuretic peptide (BNP) release. In phKCs, BNP upregulated genes promoting dermatological and neuroinflammatory diseases and conditions. VAMP3, SNAP-29 and syntaxin4 proved important in driving cytokine release from phKCs. Depletion of VAMP3 inhibited nearly all the cytokine release including TSLP and ET-1. Accordingly, VAMP3 co-occurred with ET-1 in AD patient skin. Our study pinpoints the pivotal role of SNAREs in mediating cytokine secretion related to AD. VAMP3 is identified as a suitable target for developing broad-spectrum anti-cytokine therapeutics for controlling itch and atopic skin inflammation.
The classification of temporomandibular disorders (TMD) has progressed substantially over the past 25 years due to the strategic implementation of an initial classification system based on core taxonomic principles. In this article we describe the development of the DC/TMD and its translation into the multidimensional ACTTION-American Pain Society Pain Taxonomy (AAPT) for chronic pain disorders. The initial scientific classification system (RDC/TMD) relied upon a boot-strapping process that did not attempt to solve all known clinical problems but, rather, focused on problems that could be solved at that time. The core design principles included using epidemiological data, operationalized concepts, reliable methods, and incorporation of the biopsychosocial model into a dual-axis system. This system led to sufficient data collection internationally that the system itself could be revised, first by critical evaluation of all aspects, second by review from invited experts, and third by the construction of a revised taxonomy (DC/TMD) that maintained the core design principles of the RDC/TMD. The resultant disorders with pain as a dominant feature exhibit substantial sensitivity and specificity, and they have been translated into the AAPT framework. The AAPT TMD criteria are part of an evidence-based classification system providing a systematic structure that includes five dimensions: diagnostic criteria, common features, comorbidities, consequences, and putative mechanisms. Future research will attempt to extend this AAPT domain from solely TMDs to include other orofacial pain conditions. PERSPECTIVE: The painful TMDs have well-established sensitivity and specificity, as based on the DC/TMD; their translation to the AAPT framework for chronic pain conditions provides a structure for consistent clinical application within the broader health care settings and for future research on the TMDs.
Patients with migraine frequently report ocular or visual symptoms including aura, photophobia, and eye pain. Using validated instruments, our group previously reported that due to these symptoms, patients have marked reductions in visual quality of life. In chronic migraine, these reductions can be as substantial as those reported for other neuro-ophthalmic diseases such as multiple sclerosis with optic neuritis and idiopathic intracranial hypertension. Because the instruments take several different dimensions into account, we were unable to determine which ocular symptom(s) contributed to reduced visual quality of life. The purpose of this investigation was to attempt to determine which ocular symptom(s) were driving the observed reduction in visual quality of life.
Depression is a well-recognised effect of long-term treatment with interferon-alpha (IFN-α), a widely used treatment for chronic viral hepatitis and malignancy. In addition to the emotional disturbances, high incidences of painful symptoms such as headache and joint pain have also been reported following IFN-α treatment. The endocannabinoid system plays an important role in emotional and nociceptive processing, however it is unknown whether repeated IFN-α administration induces alterations in this system. The present study investigated nociceptive responding in the IFN-α-induced mouse model of depression and associated changes in the endocannabinoid system. Furthermore, the effects of modulating peripheral endocannabinoid tone on inflammatory pain-related behaviour in the IFN-α model was examined. Repeated IFN-α administration (8,000IU/g/day) to male C57/Bl6 mice increased immobility in the forced swim test and reduced sucrose preference, without altering body weight gain or locomotor activity, confirming development of the depressive-like phenotype. There was no effect of repeated IFN-α administration on latency to respond in the hot plate test on day 4 or 7 of treatment, however, formalin-evoked nociceptive behaviour was significantly increased in IFN-α treated mice following 8 days of IFN-α administration. 2-Arachidonoyl glycerol (2-AG) levels in the periaqueductal grey (PAG) and rostroventromedial medulla (RVM), and anandamide (AEA) levels in the RVM, were significantly increased in IFN-α-, but not saline-, treated mice following formalin administration. There was no change in endocannabinoid levels in the prefrontal cortex, spinal cord or paw tissue between saline- or IFNα-treated mice in the presence or absence of formalin. Furthermore, repeated IFN-α and/or formalin administration did not alter mRNA expression of genes encoding the endocannabinoid catabolic enzymes (fatty acid amide hydrolyase or monoacylglycerol lipase) or endocannabinoid receptor targets (CB CB or PPARs) in the brain, spinal cord or paw tissue. Intra plantar administration of PF3845 (1μg/10μl) or MJN110 (1μg/10μl), inhibitors of AEA and 2-AG catabolism respectively, attenuated formalin-evoked hyperalgesia in IFN-α, but not saline-, treated mice. In summary, increasing peripheral endocannabinoid tone attenuates inflammatory hyperalgesia induced following repeated IFN-α administration. These data provide support for the endocannabinoid system in mediating and modulating heightened pain responding associated with IFNα-induced depression.