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Value Sensitive Design (VSD) is the most well-known method to consider values in design. It consists of three iterative phases of investigation: conceptual, empirical, and technical. Although the approach is promising, the role of empirical research remains unclear. We address two opportunities for extending the role of empirical research in VSD. First, we argue that empirical research enables us to identify values in context. Second, we explain that empirical research enables us to anticipate how technology mediates the values of users. We make our point by means of an empirical study in a real-life controlled experimental context into the value mediation of virtual reality (VR) in patients with chronic low-back pain. Using value-oriented semi-structured interviews with twenty patients, we first analyze what values these patients consider important, and how the values are experienced. The second set of interviews held after all patients used VR four weeks at home, aims to provide insight into value changes as mediated by VR. We end the article by a comparison of our empirical results with previous, often speculative, literature into values in VR. We show that empirical research benefits the VSD process by providing in-depth insight into the effects of context and technology on values and the ability to translate these insights into recommendations for more responsible design and implementation of the technology.
Learn More >The comorbidity of chronic pain and mental dysfunctions such as depression and anxiety disorders has long been recognized, but the underlying mechanisms remain poorly understood. Here, using a mouse model of neuropathic pain, we demonstrated neuronal plasticity in the bed nucleus of the stria terminalis (BNST), which plays a critical role in chronic pain-induced maladaptive anxiety. Electrophysiology demonstrated that chronic pain increased inhibitory inputs to lateral hypothalamus (LH)-projecting BNST neurons. Chemogenetic manipulation revealed that sustained suppression of LH-projecting BNST neurons played a crucial role in chronic pain-induced anxiety. Furthermore, using a molecular genetic approach, we demonstrated that chronic pain elevated the excitability of a specific subpopulation of BNST neurons, which express cocaine- and amphetamine-regulated transcript (CART). The elevated excitability of CART-positive neurons caused the increased inhibitory inputs to LH-projecting BNST neurons, thereby inducing anxiety-like behavior. These findings shed light on how chronic pain induces psychiatric disorders, characterized by maladaptive anxiety.
Learn More >Given the economic burden of work-related neck pain and disability, it is important to understand its time course and associated risk factors to direct better management strategies. This study aimed to identify the 1-year trajectories of work-related neck disability in a high-risk occupation group such as sonography and to investigate which baseline biopsychosocial factors are associated with the identified trajectories.
Learn More >Pain neuroscience education (PNE) and exercise have emerged as potential interventions in adolescents with chronic pain; however, very few studies have explored their effectiveness. Blended-learning approaches combining face-to-face and online educational sessions have also emerged as facilitating methods of health education. This study aimed to compare the effectiveness of exercises and PNE versus exercise alone in adolescents with chronic neck pain.
Learn More >Spinal cord stimulation (SCS), an FDA-approved therapy for chronic pain, uses paresthesia (low frequency SCS (LF-SCS)) or paresthesia-free (such as high-frequency SCS (HF-SCS)) systems, providing analgesia through partially-elucidated mechanisms, with recent studies indicating a sexual dimorphism in pain pathogenesis (Bretherton et al., Neuromodulation, 2021; Paller et al., Pain Med 10:289-299, 2009; Slyer et al., Neuromodulation, 2019; Van Buyten et al., Neuromodulation 20:642-649, 2017; Mekhail et al., Pain Pract, 2021). We aim to evaluate SCS therapy sex effects based on paradigm, utilizing visual analog scores (VAS), perceived pain reduction (PPR), and opioid use.
Learn More >Chronic pain has a major impact on a patient's quality of life, affecting physical and psychological functioning. It has debilitating consequences on social and economic aspects too. This study aimed to explore the status of health-related quality of life (HRQoL) of Malaysian patients suffering from chronic non-malignant pain.
Learn More >Glutamate is implicated in migraine pathogenesis including central sensitization and pain transmission. Altered plasma glutamate levels has been noted in migraine. Chronic migraine (CM) presented a higher degree of central sensitization and pain transmission than episodic migraine (EM). However, no study has evaluated plasma glutamate levels separately in EM and CM. This study aimed to assess plasma glutamate levels in EM and CM compared to controls. An enzyme-linked immunosorbent assay was used to assess plasma glutamate levels in females with EM (n = 98) and CM (n = 92) as well as controls (n = 50). Plasma glutamate levels in participants with EM (median and interquartile range, 49.73 [40.82-66.12] μmol/L, p < 0.001) and CM (58.70 [44.64-72.46] μmol/L, p < 0.001) were significantly higher than those in controls (38.79 [29.50-53.60] μmol/L). Glutamate levels were not significantly different between participants with EM and CM (p = 0.075). There was no significant association of plasma glutamate levels with headache frequency (exponential and 95% confidence interval, 1.285 [0.941-1.755]) and intensity (mild, 59.95 [59.95-59.95] μmol/L vs. moderate, 52.76 [40.83-106.89] μmol/L vs. severe, 55.16 [42.34-68.03] μmol/L, p = 0.472). The plasma glutamate level is a potential indicator for EM and CM.
Learn More >Upregulation of P2X3 receptor (P2X3R) has been strongly implicated in nociceptive signaling including bone cancer pain (BCP). The present study, using rat bone cancer model, aimed to explore the role of P2X3R in regulating rat pain behavior under the intervention of electroacupuncture (EA). The BCP model was successfully established by injection with MRMT-1 breast cancer cell into the medullary cavity of left tibia for 3 × 10 cells/3 μL PBS in rats as revealed by obvious bone destruction, decreased paw withdrawal thresholds (PWTs), and reduced paw withdrawal latencies (PWLs). Western blot analyses showed that P2X3R expression was significantly upregulated in ipsilateral lumbar 4-6 (L4-6) dorsal root ganglia (DRG), but the difference not seen in spinal cord dorsal horn (SCDH). With the in-depth study of P2X3R activation, we observed that intrathecal injection of P2X3R agonist α,β-meATP aggravated MRMT-1 induced BCP, while injection of P2X3R inhibitor A-317491 alleviated pain. Subsequently, we demonstrated that BCP induced mechanical allodynia and thermal hyperalgesia were attenuated after EA treatment. Under EA treatment, total P2X3R protein expression in ipsilateral DRGs was decreased, and it is worth mentioning that decreased expression of P2X3R membrane protein, which indicated that both the expression and membrane trafficking of P2X3R were inhibited by EA. The immunofluorescence assay showed that EA stimulation exerted functions by reducing the expression of P2X3R-positive cells in ipsilateral DRGs of BCP rats. Ca imaging analysis revealed that the EA stimulation decreased the percentage of α,β-meATP responsive neurons in DRGs and inhibited calcium influx. Notably, the inhibitory effect of EA on mechanical allodynia and nociceptive flinches was abolished by intrathecal injection of α,β-meATP. These findings demonstrated EA stimulation ameliorated mechanical allodynia and thermal hyperalgesia in rat model of MRMT-1-induced BCP. EA exerts analgesic effect on BCP by reducing the overexpression and functional activity of P2X3R in ipsilateral DRGs of BCP rats. Our work first demonstrates the critical and overall role of P2X3R in EA's analgesia against peripheral sensitization of MRMT-1-induced BCP and further supports EA as a potential therapeutic option for cancer pain in clinic.
Learn More >Mitochondria is an autonomous organelle that plays a crucial role in the metabolic aspects of a cell. Cortical Spreading Depression (CSD) and fluctuations in the cerebral blood flow have for long been mechanisms underlying migraine. It is a neurovascular disorder with a unilateral manifestation of disturbing, throbbing and pulsating head pain. Migraine affects 2.6 and 21.7% of the general population and is the major cause of partial disability in the age group 15-49. Higher mutation rates, imbalance in concentration of physiologically relevant molecules, oxidative stress biomarkers have been the main themes of discussion in determining the role of mitochondrial disability in migraine. The correlation of migraine with other disorders like hemiplegic migraine, MELAS, TTH, CVS, ischemic stroke and hypertension has helped in the assessment of the physiological and morphogenetic basis of migraine. Here, we have reviewed the different nuances of mitochondrial dysfunction and migraine. The different mtDNA polymorphisms that can affect the generation and transmission of nerve impulse has been highlighted and supported with research findings. In addition to this, the genetic basis of migraine pathogenesis as a consequence of mutations in nuclear DNA that can in turn affect the synthesis of defective mitochondrial proteins is discussed along with a brief overview of epigenetic profile. This review gives an overview of the pathophysiology of migraine and explores mitochondrial dysfunction as a potential underlying mechanism. Also, therapeutic supplements for managing migraine have been discussed at different junctures in this paper.
Learn More >Neuropathic pain is a complex condition that can be refractory to conventional management and can cause persistent suffering in patients. Current pharmacologic treatments can provide temporary symptomatic relief; however, the mechanism of these therapies does not address the underlying cause of neuropathic pain. The use of injectable biologics for neuropathic pain has multiple proposed mechanisms for analgesia including attenuation of inflammatory mediated processes, arrest or delay of the degenerative process, inhibition of apoptotic pathways, and augmentation of the survival and recovery of injured and uninjured nerves.
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