Mechanisms of cutaneous hyperalgesia
Rolf‐Detlef Treede
Abstract
Rolf‐Detlef Treede
Abstract
Abstract Hyperalgesia is the psychophysical counterpart of sensitization (either peripheral or central) of the nociceptive system (for review see Cervero and Laird 1991, Treede et al. 1992, Woolf and Salter 2000).ȃ3 As such, it is characterized by a decrease in pain threshold, increased pain to suprathreshold stimuli, and spontaneous pain. Increased pain sensitivity at a site of tissue damage is called primary hyperalgesia: in normal skin surrounding a site of tissue damage it is called secondary hyperalgesia. The antonym to hyperalgesia is hypoalgesia (decreased pain sensitivity), which may occur as a consequence of damage to the peripheral or central nociceptive system.
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Abstract Hyperalgesia is the psychophysical counterpart of sensitization (either peripheral or central) of the nociceptive system (for review see Cervero and Laird 1991, Treede et al. 1992, Woolf and Salter 2000).ȃ3 As such, it is characterized by a decrease in pain threshold, increased pain to suprathreshold stimuli, and spontaneous pain. Increased pain sensitivity at a site of tissue damage is called primary hyperalgesia: in normal skin surrounding a site of tissue damage it is called secondary hyperalgesia. The antonym to hyperalgesia is hypoalgesia (decreased pain sensitivity), which may occur as a consequence of damage to the peripheral or central nociceptive system.
Key concepts: Hyperalgesia, Hypoalgesia, Nociception, Sensitization, Peripheral, Central sensitization, Medicine, Threshold of pain