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A treat-to-target strategy, in which strictly defined treatment targets facilitate decision making in clinical practice, is advocated as an optimised management approach for some chronic disorders. The aim of the STARDUST trial was to assess whether a treat-to-target strategy with early endoscopy, regular biomarker and clinical symptom monitoring, and dose intensification for persistent inflammatory activity, was more successful in achieving endoscopic improvement at week 48 than a clinically driven maintenance strategy in patients with moderate-to-severe active Crohn's disease receiving ustekinumab.
Learn More >The anterior cingulate cortex (ACC) is a core brain region processing pain emotion. In this study, we performed RNA sequencing analysis to reveal transcriptomic profiles of the ACC in a rat chronic constriction injury (CCI) model. A total of 1628 differentially expressed genes (DEGs) were identified by comparing sham-operated rats with rats of 12 hours, 1, 3, 7, and 14 days after surgery, respectively. Although these inflammatory-related DEGs were generally increased after CCI, different kinetics of time-series expression were observed with the development of neuropathic pain affection. Specifically, the expression of and continued to increase following CCI. The expression of , and were initially upregulated after CCI and subsequently decreased after 12 hours. Similarly, the expression of , and increased after 12 hours but reduced after 1 day. However, the expression of the above genes increased again 7 days after CCI, when the neuropathic pain affection had developed. Furthermore, gene ontology analysis, Kyoto Encyclopedia of Genes and Genomes pathway enrichment and interaction network analyses further showed a high connectivity degree among these chemokine targeting genes. Similar expressional changes in these genes were found in the rat spinal dorsal horn responsible for nociception processing. Taken together, our results indicated chemokines and their targeting genes in the ACC may be differentially involved in the initiation and maintenance of neuropathic pain affection. These genes may be a target for not only the nociception but also the pain affection following nerve injury.
Learn More >Long-term opioid therapy (>12 months) is not effective for improving chronic non-cancer pain and function. Where patients are not experiencing pain relief with long-term opioids, the opioid should be tapered and discontinuation considered. Practitioners may find it challenging to tell patients experiencing pain that they are better off reducing or not taking medicines that do not help. This review aims to ascertain what is published about: (1) the interaction and (2) the nature of the relationship between practitioners and patients when prescribing opioids for chronic non-cancer pain in primary care.
Learn More >Mechanistic studies principally focusing on primary afferent nociceptive neurons uncovered the upregulation of collapsin response mediator protein 2 (CRMP2)-a dual trafficking regulator of N-type voltage-gated calcium (Cav2.2) as well as Nav1.7 voltage-gated sodium channels-as a potential determinant of neuropathic pain. Whether CRMP2 contributes to aberrant excitatory synaptic transmission underlying neuropathic pain processing after peripheral nerve injury is unknown. Here, we interrogated CRMP2's role in synaptic transmission and in the initiation or maintenance of chronic pain. In rats, short-interfering RNA-mediated knockdown of CRMP2 in the spinal cord reduced the frequency and amplitude of spontaneous excitatory postsynaptic currents, but not spontaneous inhibitory postsynaptic currents, recorded from superficial dorsal horn neurons in acute spinal cord slices. No effect was observed on miniature excitatory postsynaptic currents and inhibitory postsynaptic currents. In a complementary targeted approach, conditional knockout of CRMP2 from mouse neurons using a calcium/calmodulin-dependent protein kinase II alpha promoter to drive Cre recombinase expression reduced the frequency and amplitude of spontaneous excitatory postsynaptic currents, but not miniature excitatory SCss. Conditional knockout of CRMP2 from mouse astrocytes using a glial fibrillary acidic protein promoter had no effect on synaptic transmission. Conditional knockout of CRMP2 in neurons reversed established mechanical allodynia induced by a spared nerve injury in both male and female mice. In addition, the development of spared nerve injury-induced allodynia was also prevented in these mice. Our data strongly suggest that CRMP2 is a key regulator of glutamatergic neurotransmission driving pain signaling and that it contributes to the transition of physiological pain into pathological pain.
Learn More >Addressing severe maternal morbidity (SMM) is a public health priority in the US. Use of labor neuraxial analgesia for vaginal delivery is suggested to reduce the risk of postpartum hemorrhage (PPH), the leading cause of preventable severe maternal morbidity.
Learn More >Virtual consultations (VC) have been embraced by healthcare organisations during the COVID-19 pandemic. VC allows continuation of patient care while adhering to government advised restrictions and social distancing measures. Multidisciplinary pain management programmes (PMPs) are a core element of many pain services and utilising virtual methods to deliver PMPs has allowed them to continue to provide care. This systematic review aimed to explore the content of existing virtually delivered PMPs and discuss if and how these findings can be used to guide clinical delivery.
Learn More >We conducted a Mendelian randomization study to assess whether alcohol and coffee consumption and smoking are causally associated with risk of developing migraine. Independent single-nucleotide polymorphisms associated with the potential risk factors at P < 5 × 10-8 in large-scale genome-wide association studies were selected as instrumental variables. Summary-level data for the associations of the selected single-nucleotide polymorphisms with migraine were obtained from the FinnGen consortium comprising 6687 cases and 144,780 noncases and the UK Biobank study comprising 1072 cases and 360,122 noncases. Estimates derived from the FinnGen and UK Biobank cohorts were combined using fixed-effects meta-analysis. We found evidence for associations of genetically predicted alcohol consumption (odds ratio [OR] 0.54 per SD increase in log-transformed alcoholic drinks per week, 95% confidence interval [CI], 0.35-0.82; P = 0.004), coffee consumption (OR 0.56 per 50% increase in coffee consumption, 95% CI, 0.45-0.70; P < 0.001), and smoking initiation (OR 1.15 for one SD increase in the prevalence of smoking initiation, 95% CI, 1.01-1.31; P = 0.038). These associations persisted in sensitivity analyses, including mutual adjustment in multivariable Mendelian randomization analyses. In reverse Mendelian randomization analyses, genetic liability to migraine was inversely associated with alcohol consumption but was not associated with coffee consumption or smoking initiation. This study provides genetic evidence in support of a protective role of moderate coffee consumption and a detrimental role of cigarette smoking in the etiology of migraine. The inverse association between alcohol consumption and migraine risk may be attributable to reverse causality.
Learn More >An evidence-practice gap exists for cancer pain management, and cancer pain remains prevalent and disabling.
Learn More >People with chronic pain frequently have difficulties in completing everyday tasks to maintain independence and quality of life. Informal caregivers may provide support to these individuals. However, the effectiveness of interventions to train and support these individuals in caregiving remains unclear. The purpose of this study was to systematically review the evidence to determine the effectiveness of caregiver interventions to support informal caregivers of people with chronic pain.
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