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Persistent postsurgical pain: risk factors and prevention
Strategies for identification of patients at risk and for prevention and possible treatment of this important entity of chronic pain are outlined. Expand
Neuronal plasticity: increasing the gain in pain.
Here, a conceptual framework for the contribution of plasticity in primary sensory and dorsal horn neurons to the pathogenesis of pain is developed, identifying distinct forms of Plasticity, which are term activation, modulation, and modification, that by increasing gain, elicit pain hypersensitivity. Expand
Central sensitization: a generator of pain hypersensitivity by central neural plasticity.
The major triggers that initiate and maintain central sensitization in healthy individuals in response to nociceptor input and in patients with inflammatory and neuropathic pain are reviewed, emphasizing the fundamental contribution and multiple mechanisms of synaptic plasticity caused by changes in the density, nature, and properties of ionotropic and metabotropic glutamate receptors. Expand
TRPA1 Contributes to Cold, Mechanical, and Chemical Nociception but Is Not Essential for Hair-Cell Transduction
TRPA1 is apparently not essential for hair-cell transduction but contributes to the transduction of mechanical, cold, and chemical stimuli in nociceptor sensory neurons. Expand
Spared nerve injury: an animal model of persistent peripheral neuropathic pain
The spared nerve injury model differs from the Chung spinal segmental nerve, the Bennett chronic constriction injury and the Seltzer partial sciatic nerve injury models in that the co‐mingling of distal intact axons with degenerating axons is restricted, and it permits behavioral testing of the non‐injured skin territories adjacent to the denervated areas. Expand
p38 MAPK Activation by NGF in Primary Sensory Neurons after Inflammation Increases TRPV1 Levels and Maintains Heat Hyperalgesia
The activation of p38 in the DRG following retrograde NGF transport, by increasing TRPV1 levels in nociceptor peripheral terminals in a transcription-independent fashion, contributes to the maintenance of inflammatory heat hypersensitivity. Expand
Central sensitization: Implications for the diagnosis and treatment of pain
Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. Expand
Neuropathic pain: aetiology, symptoms, mechanisms, and management
We highlight current theories about peripheral neuropathic pain and show that progress in management is contingent on targeting treatment not at the aetiological factors or the symptoms but at theExpand
Neuropathic pain: a maladaptive response of the nervous system to damage.
Treatment needs to move from merely suppressing symptoms to a disease-modifying strategy aimed at both preventing maladaptive plasticity and reducing intrinsic risk. Expand
Central sensitization and LTP: do pain and memory share similar mechanisms?
Analysis of the molecular mechanisms underlying the generation and maintenance of central sensitization and LTP indicates that, although there are differences between the synaptic plasticity contributing to memory and pain, there are also striking similarities. Expand