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Spinal cord stimulation is frequently used for the treatment of intractable chronic pain conditions. Trialing of the spinal cord stimulator device is recommended to assess the patient's response to neurostimulation before permanent implantation. The trial response is often assessed by Numeric Rating Scale changes and patient-reported percentage pain improvement. Using number rating scale changes between prespinal and postspinal cord stimulation trial, a calculated percentage pain improvement can be obtained. The aim of this study was to assess the difference between calculated and patient-reported percentage improvement in pain scale during spinal cord stimulation trials.
Learn More >Voltage-gated sodium channels are key players in neuronal excitability and pain signaling. Functional expression of the voltage-gated sodium channel Na1.7 is under the control of SUMOylated collapsin response mediator protein 2 (CRMP2). When not SUMOylated, CRMP2 forms a complex with the endocytic proteins Numb, the epidermal growth factor receptor pathway substrate 15 (Eps15), and the E3 ubiquitin ligase Nedd4-2 to promote clathrin-mediated endocytosis of Na1.7. We recently reported that CRMP2 SUMO-null knock-in (CRMP2) female mice have reduced Na1.7 membrane localization and currents in their sensory neurons. Preventing CRMP2 SUMOylation was sufficient to reverse mechanical allodynia in CRMP2 female mice with neuropathic pain. Here we report that inhibiting clathrin assembly in nerve-injured male CRMP2 mice precipitated mechanical allodynia in mice otherwise resistant to developing persistent pain. Furthermore, Numb, Nedd4-2 and Eps15 expression was not modified in basal conditions in the dorsal root ganglia (DRG) of male and female CRMP2 mice. Finally, silencing these proteins in DRG neurons from female CRMP2 mice, restored the loss of sodium currents. Our study shows that the endocytic complex composed of Numb, Nedd4-2 and Eps15, is necessary for non-SUMOylated CRMP2-mediated internalization of sodium channels in vivo.
Learn More >There is evidence that people with persistent shoulder pain exhibit findings consistent with the presence of sensorimotor dysfunction. Sensorimotor impairments can manifest in a variety of ways, and further developing our understanding of sensorimotor dysfunction in shoulder pain may improve current models of care. The Fremantle Back Awareness Questionnaire (FreBAQ) has been developed to assess disturbed body perception specific to the back. The purpose of the present study was to develop a shoulder-specific self-perception questionnaire and evaluate the questionnaire in people with persistent shoulder pain.
Learn More >Nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF) are essential for neuronal development and survival in embryo. However, after birth they play pivotal roles in generation of hyperalgesia in many painful conditions. Both factors are believed to act on different groups of primary afferents, and no interaction has been studied. Here we show a synergism of both factors. Intramuscular injection of a mixture of both factors of low concentration, each of which alone had no effect, induced a significant muscular mechanical hyperalgesia in rats. We show synergism occurs in the primary afferent neurons and find about 25 % primary afferents innervating the muscle express both TrkA (NGF receptor) and GFRα1 (GDNF receptor). We show by pharmacological means that afferent neurons with TrkA and GFRα1 express both TRPV1 and ASICs. Our data establish a basis for synergism of NGF and GDNF.
Learn More >Heterotrimeric guanine nucleotide-binding protein (G protein)-coupled receptors (GPCRs) are common drug targets and canonically couple to specific G protein subtypes and β-arrestin adaptor proteins. G protein- and β-arrestin-mediated signaling have been considered separable. We show GPCRs promote a direct interaction between G protein subtype family members and β-arrestins, regardless of their canonical G protein subtype coupling. G:β-arrestin complexes bound extracellular signal-regulated kinase (ERK) and their disruption impaired both ERK activation and cell migration, consistent with β-arrestins requiring a functional interaction with G for certain signaling events. These results introduce a GPCR signaling mechanism distinct from canonical G protein activation in which GPCRs cause the formation of G:β-arrestin signaling complexes.
Learn More >The aim of the present study was to investigate the analgesic effects of repetitive transcranial magnetic stimulation over the primary motor cortex (M1-rTMS) using different stimulation parameters to explore the optimal stimulus condition for treating neuropathic pain.
Learn More >Although evidence-based psychological treatments for chronic pain have been demonstrated to be effective for a variety of outcomes, modest effects observed in recent reviews indicate scope for improvement. Self-compassion promotes a proactive attitude towards self-care and actively seeking relief from suffering. Consequently, more compassionate people experience better physical, psychological, and interpersonal wellbeing.
Learn More >Studies have reported relief of chronic shoulder pain with non-ablative pulsed neuromodulatory [pRF] or ablative radiofrequency [aRF] procedures on innervation of the shoulder joint but interpretation of these reports is hampered by inconsistent indications, anatomic targets, and follow-up. This systematic review was conducted to synthesize the existing literature on procedures employing pRF or aRF for treating chronic shoulder pain.
Learn More >We investigated patients with chronic pain seeking medical cannabis. We assessed their demographics, patterns of cannabis use, and the long-term effectiveness of cannabis on their pain and functional domains.
Learn More >This study examined the prevalence of chronic pain alone, posttraumatic stress disorder (PTSD) alone, and both chronic pain and PTSD among U.S. Army soldiers during the postdeployment year.
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