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Pain Research: What Have We Learned and Where Are We Going
| Content Provider | Semantic Scholar |
|---|---|
| Author | Pr, Pinto Mcintyre, Timothy Fonseca, Camilla Almeida A. Araujo-Soares V. Ml, Peters Bruce J. Hf, Gramke Preopera, Marcus Ma Felice Sanoja, Raul Wang R. Stokes, J. R. Pirie E. Skahen J. Shtaerman Y. Persist, Yaksh Tl Viisanen H. Amorim D. Koivisto A. Dissociated, Pertovaara A. Baron R. Forster M. Subgrouping, Binder A. Cerveró, Fernando |
| Abstract | Effects of spinally delivered N-and P-type voltage-dependent calcium channel antagonists on dorsal horn neuronal responses in a rat model of neuropathy. Central sensitization: a generator of pain hypersensitivity by central neural plasticity. Transient receptor potential channel polymorphisms are associated with the somatosensory function in neuropathic pain patients. Genetically determined P2X7 receptor pore formation regulates variability in chronic pain sensitivity. health-related quality of life and pain in patients with chronic fibro-myalgia and neuropathic pain. Asymmetric time-dependent activation of right central amygdala neurones in rats with peripheral neuropathy and pregabalin modulation. functional imaging evidence supporting the presence of central sensitization in a cohort of osteoarthritis patients. Arthritis Rheum 2009; 61: 1226– 34 23 Yarnitsky D. Conditioned pain modulation (the diffuse noxious in-hibitory control-like effect): its relevance for acute and chronic pain states. Pre-and post-surgical factors that predict the provision of rescue analgesia following hysterectomy.tive anxiety and catastrophizing: a systematic review and meta-analysis of the association with chronic postsurgical pain. Inhibition of neuropathic pain by selective ablation of brainstem medullary cells expressing the mu-opioid receptor. Engagement of descending inhibition from the rostral ventromedial medulla protects against chronic neuropathic pain. Central sensitization: a biopsychosocial explanation for chronic widespread pain in patients with fibromyalgia and chronic fatigue syndrome.ent hyperalgesia in the cisplatin-treated mouse as defined by threshold measures, the conditioned place preference paradigm, and changes in dorsal root ganglia activated transcription factor 3: the effects of gabapentin, ketorolac, and etanercept. modulation of conditioned place-preference and mechanical hypersensitivity by a TRPA1 channel antagonist in peripheral neur-opathy. of patients with neuro-pathic pain according to pain-related sensory abnormalities: a first step to a stratified treatment approach. We have always wondered why do we feel pain, how is it caused, what it means to us and, more importantly, how can we prevent or reduce it. We can trace the origin of pain research back to the beginning of our time on earth. From spiritual |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://bja.oxfordjournals.org/content/111/1/6.full.pdf |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
