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This study aimed to develop culturally sensitive pain neuroscience education (PNE) materials for Hausa speaking patients with chronic spinal pain (CSP). PNE is a program of teaching patients about pain that has gained considerable attention in research and is increasingly used during physical therapy for patients with chronic pain. It helps in decreasing pain, disability, fear-avoidance, pain catastrophization, movement restriction, and health care utilization among patients with chronic pain. However, existing PNE materials and their application are limited to few languages and cultural inclinations. Due to the variations in pain perceptions, beliefs, and related outcomes among different population groups, culture-sensitive PNE materials addressing these outcomes are warranted. A focus-group discussion comprising 4 experts was used to adapt and develop preliminary PNE materials. Thereafter, an internet-based 3-round modified Delphi-study involving 22 experts ensued. Experts' consensus/recommendations concerning the content were used in modifying the PNE materials. Consensus was predefined as ≥75% level of (dis)agreement. Eighteen experts completed the Delphi rounds. Nineteen, 18 and 18 experts participated in rounds 1, 2 and 3 respectively, representing 86%, 94% and 100% participation rate respectively. Consensus agreement was reached in every round and content of the materials, including drawings, examples, figures and metaphors were adapted following the experts' suggestions. We therefore concluded that, culture-sensitive PNE materials for Hausa speaking patients with CSP were successfully produced. The present study also provides a direction for further research whereby the effects of culturally-sensitive PNE materials can be piloted among Hausa speaking patients with CSP.
Learn More >The nerve growth factor (NGF) plays an important role in the regulation of neuropathic pain. It has been demonstrated that calcitonin gene-related peptide (CGRP), a well-known contributor to neurogenic inflammation, increases neuroinflammatory pain induced by NGF. The inflammatory mediator that NGF most strongly induces is C-C chemokine ligand 19 (CCL19), which can recruit inflammatory cells by binding to the receptor CCR7 followed by promoting the response of neuroinflammation. However, the regulatory mechanism of NGF and CCL19 in tooth movement orofacial pain and the interaction between both are still unclear. In this study, male Sprague-Dawley rats were used to study the modulation of NGF on orofacial pain through CCL19 and the role of each in tooth movement pain in rats. The expression levels of CCL19 mRNA and protein were determined by real-time PCR and immunofluorescence, respectively. Pain levels were assessed by measuring the rats' bite force, which drops as pain rises. Meanwhile, by verifying the relationship between CGRP and CCL19, it was laterally confirmed that NGF could modulate tooth movement-induced mechanical hyperalgesia through CCL19. The results showed that the expression level of CCL19 rose with the increased NGF, and neurons expressing CGRP can express stronger CCL19. Compared with the baseline level, the bite force for all rats dropped sharply on day 1, reached its lowest level on day 3, and recovered gradually on day 5. All results indicated that NGF played an important role in tooth movement orofacial pain positively regulating CCL19 expression in the trigeminal ganglia of rats. Additionally, CCL19 increased the sensitivity to experimental tooth movement orofacial pain. NGF can regulate CCL19 expression, although it may regulate other inflammatory pathways as well. This is the first report on the interactions and modulations of tooth movement orofacial pain by NGF through CCL19 in rats.
Learn More >Cognition is defined as the brain's ability to acquire, process, store, and retrieve information. Pain has been described as an unpleasant sensory or emotional experience, and for experiencing pain consciously, cognitive processing becomes imperative. Moreover, evaluation of pain strongly depends on cognition as it requires learning and recall of previous experiences. There could be a possible close link between neural systems involved in cognition and pain processing, and studies have reported an association between pain and cognitive impairment. In this narrative review, we explore the available evidence that has investigated cognitive changes associated with pain. We also examine the anatomical, biochemical, and molecular association of pain and neuro-cognition. Additionally, we focus on the cognitive impairment caused by analgesic medications. There is a need to improve our understanding of pathophysiology and cognitive impairment mechanisms associated with chronic pain and its treatment. This area provides a diverse opportunity for grounding future research, aiding institution of timely interventions to prevent chronic pain and associated cognitive decline, ultimately improving patient care.
Learn More >Central sensitization (CS) is defined as the increased responsiveness of nociceptive neurons in the central nervous system to normal or subthreshold afferent input. CS has been proposed as an underlying mechanism of chronic pain in musculoskeletal disorders including low back pain (LBP). A Central Sensitization Inventory (CSI) has recently been developed for screening participants with CS. However, the association of CS with chronic LBP (cLBP) in the general population remains unknown. The purpose of this study was to investigate the association of CS with cLBP using the CSI in a population-based cohort of a Japanese mountain village.
Learn More >Research design considerations for chronic pain prevention clinical trials: IMMPACT recommendations.
Although certain risk factors can identify individuals who are most likely to develop chronic pain, few interventions to prevent chronic pain have been identified. To facilitate the identification of preventive interventions, an IMMPACT meeting was convened to discuss research design considerations for clinical trials investigating the prevention of chronic pain. We present general design considerations for prevention trials in populations that are at relatively high risk for developing chronic pain. Specific design considerations included subject identification, timing and duration of treatment, outcomes, timing of assessment, and adjusting for risk factors in the analyses. We provide a detailed examination of 4 models of chronic pain prevention (ie, chronic postsurgical pain, postherpetic neuralgia, chronic low back pain, and painful chemotherapy-induced peripheral neuropathy). The issues discussed can, in many instances, be extrapolated to other chronic pain conditions. These examples were selected because they are representative models of primary and secondary prevention, reflect persistent pain resulting from multiple insults (ie, surgery, viral infection, injury, and toxic or noxious element exposure), and are chronically painful conditions that are treated with a range of interventions. Improvements in the design of chronic pain prevention trials could improve assay sensitivity and thus accelerate the identification of efficacious interventions. Such interventions would have the potential to reduce the prevalence of chronic pain in the population. Additionally, standardization of outcomes in prevention clinical trials will facilitate meta-analyses and systematic reviews and improve detection of preventive strategies emerging from clinical trials.
Learn More >Ulinastatin, a broad-spectrum serine protease inhibitor, has been widely used to treat various diseases clinically. However, so far, the antinociceptive effect of ulinastatin remains less studied experimentally and the underlying mechanisms of ulinastatin for pain relief remain unclear. This study aimed to find evidence of the analgesic effect of ulinastatin on acute somatic and visceral pain.
Learn More >Pain and joint deformity are the most common symptoms of hip osteoarthritis (OA). However, no significant association between pain and severity of radiographic lesions has been reported. Recently, central sensitization has been suggested as an underlying mechanism of pain in OA. We investigated the involvement of radiologic severity or central sensitization in the clinical manifestation of hip OA with various degrees of joint deformity.
Learn More >People with chronic low back pain (LBP) exhibit changes in postural control. Stereotypical muscle activations resulting from external perturbations include anticipatory (APAs) and compensatory (CPAs) postural adjustments. The aim and objective of this study was to determine differences in postural control strategies (peak amplitude, APAs and CPAs) between symptomatic and asymptomatic adults with and without Lumbar Disc Degeneration (LDD) using surface electromyography during forward postural perturbation. Ninety-seven subjects participated in the study (mean age 50 years (SD 12)). 3T MRI was used to acquire T2 weighted images (L1-S1). LDD was determined using Pfirrmann grading. A bespoke translational platform was designed to deliver horizontal perturbations in sagittal and frontal planes. Electromyographic activity was analysed bilaterally from 8 trunk and lower limb muscles during four established APA and CPA epochs. A Kruskal-Wallis H test with Bonferroni correction for multiple comparisons was conducted. Four groups were identified: no LDD no pain (n = 19), LDD no pain (n = 38), LDD pain (n = 35) and no LDD pain (n = 5). There were no significant differences in age or gender between groups. The most significant difference between groups was observed during forward perturbation. In the APA and CPA phases of predictable forward perturbation there were significant differences ankle strategy between groups (p = 0.007-0.008); lateral gastrocnemius and tibialis anterior activity was higher in the LDD pain than the LDD no pain group. There were no significant differences in the unpredictable condition (p>0.05). These findings were different from the remaining groups, where significant differences in hip strategy were observed during both perturbation conditions (p = 0.004-0.006). Symptomatic LDD patients exhibit different electromyographic strategies to asymptomatic LDD controls. Future LBP electromyographic research should benefit from considering assessment of both lower limbs in addition to the spine. This approach could prevent underestimation of postural control deficits and guide targeted rehabilitation.
Learn More >Primary nociceptors are a heterogeneous class of peripheral somatosensory neurons, responsible for detecting noxious, pruriceptive, and thermal stimuli. These neurons are further divided into several molecularly defined subtypes that correlate with their functional sensory modalities and morphological features. During development, all nociceptors arise from a common pool of embryonic precursors, and then segregate progressively into their mature specialized phenotypes. In this review, we summarize the intrinsic transcriptional programs and extrinsic trophic factor signaling mechanisms that interact to control nociceptor diversification. We also discuss how recent transcriptome profiling studies have significantly advanced the field of sensory neuron development.
Learn More >The effect of spinal cord stimulation (SCS) amplitude on the activation of dorsal column fibres has been widely studied through the recording of Evoked Compound Action Potentials (ECAPs), the sum of all action potentials elicited by an electrical stimulus applied to the fibres. ECAP amplitude grows linearly with stimulus current after a threshold, and a larger ECAP results in a stronger stimulus sensation for patients. This study investigates the effect of stimulus frequency on both the ECAP amplitude as well as the perceived stimulus sensation in patients undergoing SCS therapy for chronic back and/or leg pain.
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