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Preclinical and clinical pain science have since long suffered from lack of joint ventures that, as securely as possible, have approached problems that are relevant for the understanding of clinical pain phenomenologies and treatment (Yezierski & Hansson, 2018), the core of translational pain medicine. The uncoupling of the two has led to loss of momentum and few novel efficacious treatment remedies where needed the most, i.e., in long term pain states. Here, the area of translational pain medicine is craving for a road map so that preclinical and clinical scientists can walk hand in hand into the future with a common agenda on how to approach the search for much needed improved treatment strategies.
Learn More >To assess the prevalence of migraine or severe headache among US adults by inflammatory bowel disease (IBD) status.
Learn More >Most SARS-CoV-2-infected individuals never require hospitalization. However, some develop prolonged symptoms. We sought to characterize the spectrum of neurologic manifestations in non-hospitalized Covid-19 "long haulers".
Learn More >Numerous studies support the effectiveness of Acceptance and Commitment Therapy (ACT) for chronic pain, yet little research has been conducted about its underlying mechanisms of change, especially regarding patients with comorbid mental disorders. The present investigation addressed this issue by examining associations of processes targeted by ACT (pain acceptance, mindfulness, psychological flexibility) and clinical outcomes (pain intensity, somatic symptoms, physical health, mental health, depression, general anxiety).
Learn More >As in other fields of medicine, development of new medications for management of neuropathic pain has been difficult since preclinical rodent models do not necessarily translate to the clinics. Aside from ongoing pain with burning or shock-like qualities, neuropathic pain is often characterized by pain hypersensitivity (hyperalgesia and allodynia), most often towards mechanical stimuli, reflecting sensitization of neural transmission.
Learn More >Compared to racism and sexism, classism in pain assessment and management practices (PAMP) has been less investigated and its mediating mechanisms are still unknown. Drawing upon a social psychological model of dehumanization, this research aimed to test: (1) the effect of patient socioeconomic status (SES; a proxy of social class) on PAMP and (2) whether patient dehumanization and perceived life hardship mediated these effects. Two online experimental studies were conducted, in which patient SES was manipulated (Low vs. High) within-subjects. One-hundred sixty-two female medical students (study 1) and 105 female nurses (study 2) were presented with vignettes/pictures depicting two cases of women with chronic low-back pain, followed by videos of them performing a pain-inducing movement. Participants reported on patient dehumanization, perceived life hardship and PAMP. The Low SES patient was perceived as less pain sensitive (medical students only) but more disabled, credible and her pain more attributed to psychological causes (by nurses only). Medical students recommended less non-pharmacological treatments but prescribed slightly stronger medication. Medical students were less willing to provide individualized care to the Low SES patient, whereas nurses showed the opposite pattern. Patient mechanistic dehumanization mediated SES effects on pain disability (medical students only). Perceived life hardship mediated SES effects on pain disability, credibility (nurses only) and intentions of providing individualized care (nurses only). These finding bear novel contributions to the fields of pain, health service research and social psychology, and have important implications to the development of more effective future interventions to reduce classism in PAMP.
Learn More >The German Research Network on Neuropathic Pain (DFNS) quantitative sensory testing (QST) method for sensory phenotyping is used to stratify patients by mechanism associated sensory phenotype, theorised to be predictive of intervention efficacy. We hypothesised that change in pain and sensory dysfunction would relate to change in sensory phenotype. We investigated the responsiveness of sensory phenotype to surgery in patients with an entrapment neuropathy.With ethical approval and consent, this observational study recruited patients with neurophysiologically confirmed carpal tunnel syndrome. Symptom and pain severity parameters and DFNS QST were evaluated prior to and after carpal tunnel surgery. Surgical outcome was evaluated by patient-rated change. Symptom severity score of the Boston Carpal Tunnel Questionnaire and associated pain and paraesthesia subgroups were comparators for clinically relevant change.QST results (n=76) were compared to healthy controls (n=54). At 6 months post-surgery 92% participants reported a good surgical outcome and large decrease in pain and symptom severity (p<.001). Change in QST parameters occurred for thermal detection, thermal pain and mechanical detection thresholds with a moderate to large effect size. Change in mechanical pain measures were not statistically significant. Change occurred in sensory phenotype post-surgery (p<.001); sensory phenotype was associated with symptom subgroup (p=.03) and patient-rated surgical outcome (p =.02).QST derived sensory phenotype is sensitive to clinically important change. In an entrapment neuropathy model, sensory phenotype was associated with patient-reported symptoms and demonstrated statistically significant, clinically relevant change after disease modifying intervention. Sensory phenotype was independent of disease severity and may reflect underlying neuropathophysiology.
Learn More >Neuropathic pain affects up to 10% of the total population and no specific target is ideal for therapeutic need. The sodium leak channel (NALCN), a non-selective cation channel, mediates the background Na leak conductance and controls neuronal excitability and rhythmic behaviors. Here, we show that increases of NALCN expression and function in dorsal root ganglion (DRG) and dorsal spinal cord contribute to chronic constriction injury (CCI)-induced neuropathic pain in rodents. NALCN current and neuronal excitability in acutely isolated DRG neurons and spinal cord slices of rats were increased after CCI which were decreased to normal levels by NALCN-siRNA. Accordingly, pain-related symptoms were significantly alleviated by NALCN-siRNA-mediated NALCN knockdown and completely prevented by NALCN-shRNA-mediated NALCN knockdown in rats or by conditional NALCN knockout in mice. Our results indicate that increases in NALCN expression and function contribute to CCI-induced neuronal sensitization; therefore, NALCN may be a novel molecular target for control of neuropathic pain.
Learn More >chronic pain, a common complaint among older adults, affects physical and mental well-being. While opioid use for pain management has increased over the years, pain management in older adults remains challenging, due to potential severe adverse effects of opioids in this population.
Learn More >Diabetic neuropathic pain (DNP) is a common complication of diabetes characterized by persistent pain. Emerging evidence links astrocytes to mechanical nociceptive processing, and the motor cortex (MCx) is a cerebral cortex region that is known to play a key role in pain regulation. However, the association between MCx astrocytes and DNP pathogenesis remains largely unexplored. Here, we studied this association using designer receptors exclusively activated by designer drugs (DREADDs) to specifically manipulate MCx astrocytes. We proved that the selective inhibition of MCx astrocytes reduced DNP in streptozocin (STZ)-induced DNP models and discovered a potential mechanism by which astrocytes release cytokines, including tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β), to increase neuronal activation in the MCx, thereby regulating pain. Together, these results demonstrate a pivotal role for MCx astrocytes in DNP pathogenesis and provide new insight into DNP treatment strategies.Astrocytes are critical for maintaining CNS homeostasis. In recent years, astrocytes have been demonstrated to play roles in pain signaling modulation and neuropathic pain maintenance, with studies showing that they inhibit pain transmission at the spinal level. This work suggests that astrocytes also modulate pain at the supraspinal level. Indeed, we show that chemogenetically manipulated MCx astrocytes affect the mechanical withdrawal thresholds of rats and elucidate a potential mechanism by which astrocytes release inflammatory mediators to increase neuronal activation in the MCx, thereby regulating pain. Together, our data support that inhibition of astrocytes in the MCx region might have broad prospects for diabetic neuropathic pain treatment.
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