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Transient Receptor Potential Ankyrin-1-expressing vagus nerve fibers mediate IL-1β induced hypothermia and reflex anti-inflammatory responses.

Inflammation, the physiological response to infection and injury, is coordinated by the immune and nervous systems. Interleukin-1β (IL-1β) and other cytokines produced during inflammatory responses activate sensory neurons (nociceptors) to mediate the onset of pain, sickness behavior, and metabolic responses. Although nociceptors expressing Transient Receptor Potential Ankyrin-1 (TRPA1) can initiate inflammation, comparatively little is known about the role of TRPA1 nociceptors in the physiological responses to specific cytokines.

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An exploratory study evaluating the 30 medications most commonly associated with headaches in the FDA Adverse Event Reporting System.

This project seeks to identify the top 30 drugs most commonly associated with headaches in the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS), as well as their respective reporting odds ratios (RORs).

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Pain education and pain management skills in virtual reality in the treatment of chronic low back pain: A multiple baseline single-case experimental design.

Chronic lower back pain is a major health problem and current treatments do not always lead to adequate pain control. Virtual reality (VR) is an upcoming technology that has shown to be effective in reducing acute pain. However, the value of VR in reducing chronic pain is still unknown. Therefore, the current study focuses on the effects of a recently developed VR application 'Reducept' using a multiple baseline single-case experimental design in 8 patients (N = 8). Reducept is a VR-training program aiming to improve pain management skills and providing pain education in patients with (chronic lower) back pain. Results based on visual and statistical analyses indicated that Reducept has the potential to reduce chronic lower back pain, although its clinical relevance was small. This study is one of the first that focuses on the possible effects of Reducept using sophisticated visual and statistical analyses. Our study shows a detailed overview of individual changes in pain intensity over time. Further research is necessary to investigate the working mechanism of Reducept and its impact on chronic pain conditions.

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Virtual issue: Recent advances in pediatric headache: Bridging the data gap.

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Socioeconomic and geographic inequalities in headache disability in Brazil: The 2019 National Health Survey.

To map the socioeconomic and geographic inequalities in headache disability in Brazil.

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Developing multivariable models for predicting headache improvement in patients with acute post-traumatic headache attributed to mild traumatic brain injury: A preliminary study.

Post-traumatic headache (PTH) is a common symptom after mild traumatic brain injury (mTBI). Although there have been several studies that have used clinical features of PTH to attempt to predict headache recovery, currently no accurate methods exist for predicting individuals' improvement from acute PTH. This study investigated the utility of clinical questionnaires for predicting (i) headache improvement at 3 and 6 months, and (ii) headache trajectories over the first 3 months.

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Graded Sensorimotor Retraining and Pain Intensity in Chronic Low Back Pain-Reply.

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Electroacupuncture ameliorates depression-like behaviors comorbid to chronic neuropathic pain via Tet1-mediated restoration of adult neurogenesis.

Although electroacupuncture (EA) stimulation is a widely used therapy for chronic pain and comorbid psychiatric disorders, its long-term effects on chronic neuropathic pain-induced depression and the underlying mechanisms remain elusive. In the present study, we found that EA stimulation was able to restore adult neurogenesis in the ventral dentate gyrus (DG), by both increasing neuronal differentiation and restoring the normal morphology of newborn dendrites, in mice with spared nerve injury (SNI) surgery. By ablating the Nestin + neural stem cells (NSCs) via DTA expression, we further proved that neurogenesis in the ventral DG was crucial to the long-term, but not the immediate antidepressant effect of EA, nor was it associated with nociception. Furthermore, we found that the restoration of neurogenesis was dependent on Tet1-mediated epigenetic modification upon EA treatment. Tet1 could bind to the promoter of the Prox1 gene, thus catalyzing its demethylation and facilitating its expression, which finally contributed to the restoration of neurogenesis and amelioration of depression-like behaviors induced by chronic neuropathic pain. Thus, we conclude that EA stimulation restores inhibited Tet1 expression in hippocampal NSCs of mice with chronic neuropathic pain, and increased Tet1 expression ameliorates hypermethylation of Prox1 and restores normal adult neurogenesis in the ventral DG, which contributes to the long-term antidepressant effect of EA.

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Fear Learning in Genital Pain: Toward a Biopsychosocial, Ecologically Valid Research and Treatment Model.

Although fear learning mechanisms are implicated in the development, maintenance, exacerbation, and reduction of genital pain, systematic research on how fear of genital pain emerges, spreads, persists, and reemerges after treatment is lacking. This paper provides an overview of the literature on pain-related fear, integrates the ideas on learning and sexual arousal responding, and specifies the pathways through which compromised learning may contribute to the development and persistence of genital pain. In order to refine theories of genital pain and optimize treatments, we need to adopt a biopsychosocial framework to pain-related fear learning and uncover potential moderators that shape individual trajectories. This involves examining the role of physiological processes, subjective experiences, as well as partner and relational cues in fear acquisition, excessive generalization and impaired safety learning, extinction of fear, counterconditioning, and return of fear. Recent methodological advances in fear conditioning and sex research are promising to enable more symptom-specific and ecologically valid experimental paradigms.

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Differential regulation of Cav3.2 and Cav2.2 calcium channels by CB1 receptors and cannabidiol.

Cannabinoids represent a promising therapeutic avenue for chronic pain, however clinical trials often fail to report analgesic efficacy of cannabinoids. Inhibition of voltage-gated calcium channels is one mechanism through which cannabinoids may produce analgesia. We hypothesized that cannabinoids and cannabinoid receptor agonists target different types of voltage gated calcium channels through distinct mechanisms.

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