Pain
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Previously, we demonstrated that placebo analgesia (PA) accompanies reductions in neural activity during painful stimulation. This study investigated areas of the brain where the neural activity was increased during PA. The literature has associated PA with two potential mechanisms of action; one sustained (e.g., engaged for the duration of PA), the other, transitory (e.g., a feedback mechanism). ⋯ Conversely, brain regions with transient activity included linguistic centers in the left hemisphere and frontal regions of the right hemisphere generally associated with executive functioning. Together, these mechanisms likely engage analgesic processes and then simply monitor the system for unexpected stimuli, effectively liberating resources for other processes. Identifying brain regions associated with pain-modulation with different temporal profiles is consistent with the multidimensionality of PA and highlights the need for continued investigation of this construct.
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Chronic pain is a public health problem with high impact on various population segments. There are few population studies with the aim of delineating the profile of the chronic pain patient, and generating data for actions to prevent, control and minimize the problem. The aim of this study was to estimate the prevalence of chronic pain in the population of Salvador, Bahia, Brazil and identify independent predictors associated with this morbidity. ⋯ Among the studied factors, in the gross analysis, the following were shown to be associated with chronic pain: conjugal situation, smoking, excessive alcohol consumption, presence of central obesity and age, all with p<0.05. In the multivariate analysis, female sex, smoking, excessive alcohol consumption, and age were sustained as independent predictors. The presence of chronic pain was predominant in women, the elderly, smokers or ex-smokers and excessive alcohol consumers.
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The synaptic vesicle protein synapsin II is specifically expressed in synaptic terminals of primary afferent nociceptive neurons and regulates transmitter release in the spinal cord dorsal horn. Here, we assessed its role in nerve injury-evoked molecular and behavioral adaptations in models of peripheral neuropathic pain using mice genetically lacking synapsin II. Deficiency of synapsin II resulted in reduced mechanical and cold allodynia in two models of peripheral neuropathic pain. ⋯ In addition, the expression of the vesicular glutamate transporters, VGLUT1 and VGLUT2, was strongly reduced in synapsin II knockout mice in the spinal cord. Conversely, synapsin II knockout mice showed a stronger and longer-lasting increase of GABA in lamina II of the dorsal horn after nerve injury than wild type mice. These results suggest that synapsin II is involved in the regulation of glutamate and GABA release in the spinal cord after nerve injury, and that a imbalance between glutamatergic and GABAergic synaptic transmission contributes to the manifestation of neuropathic pain.
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EphBs receptors and ephrinBs ligands are present in the adult brain and peripheral tissue and play a critical role in modulating multiple aspects of physiology and pathophysiology. Ours and other studies have demonstrated that spinal ephrinBs/EphBs signaling was involved in the modulation of nociceptive information and central sensitization. However, the role of ephrinBs/EphBs signaling in peripheral sensitization is poorly understood. ⋯ EphrinB1-Fc-induced hyperalgesia is accompanied with the NMDA receptor-mediated increase of expression in peripheral and spinal phosphorylated mitogen-activated protein kinases (phospho-MAPKs) including p-p38, pERK and pJNK, and also is prevented or reversed by the inhibition of peripheral and spinal MAPKs. Furthermore, in formalin inflammation pain model, pre-inhibition of EphBs receptors by the injection of EphB1-Fc reduces pain behavior, which is accompanied by the decreased expression of peripheral p-p38, pERK and pJNK. These data provide evidence that ephrinBs may act as a prominent contributor to peripheral sensitization, and demonstrate that activation of peripheral ephrinBs/EphBs system induces hyperalgesia through a MAPKs-mediated mechanism.
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The objective of this study is to identify subgroups of patients with non-specific neck pain who are more likely to benefit from either physiotherapy, spinal manipulation therapy, or usual care, on the short- and long-term. Data of three recently finished randomised controlled trials, with similar design and setting, were combined. The combined study population consisted of 329 patients with non-specific neck pain in an adult (18-70years) primary care population in the Netherlands. ⋯ The analysis revealed three predictors for recovery of which the effect is modified by treatment: pain intensity (0-10 scale) in the short-term model, age and (no) accompanying low back pain in the long-term model. With these predictors a clinically relevant improvement in recovery rate (up to 25% improvement) can be established in patients receiving a tailored instead of a non-advised treatment. In conclusion we identified three characteristics that facilitate a deliberate treatment choice, to optimise benefit of treatment in patients with non-specific neck pain: age, pain intensity, and (no) accompanying low back pain.