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Persistent postsurgical pain: risk factors and prevention
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.
Central sensitization: a generator of pain hypersensitivity by central neural plasticity.
Spared nerve injury: an animal model of persistent peripheral neuropathic pain
Central sensitization: Implications for the diagnosis and treatment of pain
- C. Woolf
- Biology, MedicinePAIN
- 1 March 2011
TRPA1 Contributes to Cold, Mechanical, and Chemical Nociception but Is Not Essential for Hair-Cell Transduction
p38 MAPK Activation by NGF in Primary Sensory Neurons after Inflammation Increases TRPV1 Levels and Maintains Heat Hyperalgesia
Neuropathic pain: aetiology, symptoms, mechanisms, and management
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.
The neuropathic pain triad: neurons, immune cells and glia
Immunosuppression and blockade of the reciprocal signaling pathways between neuronal and non-neuronal cells offer new opportunities for disease modification and more successful management of pain.