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The current treatments of primary musculoskeletal low back pain (LBP) have a low to moderate efficacy, which might be improved by looking at the contribution of placebo effects. However, the size of true placebo effects in LBP is unknown. Therefore, a systematic review and meta-analysis were executed of randomized controlled trials investigating placebo effects in LBP.
Learn More >Mechanical hyperalgesia and allodynia incidence varies considerably among neuropathic pain patients. This study explored whether sensory or psychological factors associate with mechanical hyperalgesia and brush allodynia in a human experimental model.
Learn More >Both spinal tumor necrosis factor (TNF) and interleukin-6 (IL-6) contribute to the development of "mechanical" spinal hyperexcitability in inflammatory pain states. Recently we found that spinal sensitization by TNF was significantly reduced by blockade of spinal IL-6 signaling suggesting that IL-6 signaling is involved in spinal TNF effects. Here we explored whether spinal interleukin-1β (IL-1β), also implicated in inflammatory pain, induces "mechanical" spinal hyperexcitability, and whether spinal IL-1β effects are related to TNF and IL-6 effects. We recorded the responses of spinal cord neurons to mechanical stimulation of the knee joint in vivo and used cellular approaches on microglial and astroglial cell lines to identify interactions of IL-1β, TNF, and IL-6. Spinal application of IL-1β in anaesthetized rats modestly enhanced responses of spinal cord neurons to innocuous and noxious mechanical joint stimulation. This effect was blocked by minocycline indicating microglia involvement, and significantly attenuated by interfering with IL-6 signaling. In the BV2 microglial cell line, IL-1β, like TNF, enhanced the release of soluble IL-6 receptor, necessary for spinal IL-6 actions. Different to TNF, IL-1β caused SNB-19 astrocytes to release interleukin-11. The generation of "mechanical" spinal hyperexcitability by IL-1β was more pronounced upon spinal TNF neutralization with etanercept, suggesting that concomitant TNF limits IL-1β effects. In BV2 cells, TNF stimulated the release of IL-1Ra, an endogenous IL-1β antagonist. Thus spinal IL-1β has the potential to induce spinal hyperexcitability sharing with TNF dependency on IL-6 signaling, but TNF also limited IL-1β effects explaining the modest effect of IL-1β.
Learn More >New daily persistent headache (NDPH) is a primary headache disorder characterized by an intractable, daily, and unremitting headache lasting for at least 3 months. Currently, there are limited studies in the pediatric population describing the characteristics of NDPH.
Learn More >Chronic pain is a major healthcare issue that often requires an interdisciplinary treatment approach. Defining relevant treatment goals is one of the crucial steps in creating successful rehabilitation schemes. Therefore, the first aim is to explore goals that patients suffering from chronic pain aim to achieve. The second aim is to translate those goals into measurable functional outcome variables which can be used to measure treatment success.
Learn More >Pain catastrophizing underpins several psychosocial theories of pain, but there is limited evidence to support the proposal that changes in pain catastrophizing cause changes in pain. Results from mediation analyses have conflicting results, and one reason for these might be the timing of the assessment of pain catastrophizing. This study aimed to test the effect of the timing of pain catastrophizing on pain intensity.
Learn More >Mirogabalin besylate has been approved in several countries to treat peripheral neuropathic pain. This pooled analysis, using data from the two pivotal Phase III studies in Asian patients with diabetic peripheral neuropathic pain and post-herpetic neuralgia, aimed to provide clinicians with more detailed and precise information relating to mirogabalin's safety and efficacy.
Learn More >The pleiotropic cytokine interleukin-6 (IL-6) is emerging as a molecule with both beneficial and destructive potentials. It can exert opposing actions triggering either neuron survival after injury or causing neurodegeneration and cell death in neurodegenerative or neuropathic disorders. Importantly, neurons respond differently to IL-6 and this critically depends on their environment and whether they are located in the peripheral or the central nervous system. In addition to its hub regulator role in inflammation, IL-6 is recently emerging as an important regulator of neuron function in health and disease, offering exciting possibilities for more mechanistic insight into the pathogenesis of mental, neurodegenerative and pain disorders and for developing novel therapies for diseases with neuroimmune and neurogenic pathogenic components.
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