secondary hyperalgesia

secondary hyperalgesia

long-term tissue hypersensitivity beyond area of original injury; due to excitation of dorsal horn N-methyl-d-aspartate (NMDA) receptors (see syndrome, complex regional pain)
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Additionally, we also evaluated the analgesic effect of the chronic treatment with CT-[beta]CD in animals induced with non inflammatory chronic muscle pain, which is suggested to be an animal model of FM, for 7 days through the digital analgesimeter, once, in this model, there is a significant decrease in mechanical withdrawal threshold of the paw, being interpreted as secondary hyperalgesia (Da Silva et al.
Secondary hyperalgesia was believed to be the basis of chronic post surgical pain (CPSP).
Systemic gabapentin and S (+)-3-isobutyl-[gamma]- aminobutyric acid block secondary hyperalgesia.
This stimulation led to secondary hyperalgesia, also known as enhanced pain sensitivity, common in burns.
The stimulation generated secondary hyperalgesia, or enhanced pain sensitivity beyond the site of an injury - a common feature of burns.
In such cases, local nociceptive excitation and peripheral sensitization may coexist with a state of secondary hyperalgesia, leading to diffuse pain experience.
A novel model of primary and secondary hyperalgesia after mild thermal injury in the rat.
Secondary hyperalgesia is thought to be a basis for chronic post surgical pain.
Primary hyperalgesia is defined as changes in the area of injury, while secondary hyperalgesia is changes to pain thresholds in the undamaged tissue surrounding the injury, which can become hypersensitive to touch (Campbell et al.
There is also evidence that surgery and opioid share NMDA receptor activation, therefore adequate blockade of these receptors by ketamine as an adjuvant to opioids might benefit the patients by evoking attenuation of pain, secondary hyperalgesia and opioid sparing effects.
Ketamine, as NMDA-receptor antagonist, when administered intravenously and epiduraly, inhibits long lasting secondary hyperalgesia induced by surgery.
The most well known action is reversible NMDA receptor antagonism thought to be responsible for suppression of secondary hyperalgesia and central sensitisation.
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