Abstract
Acute mechanical, thermal, and chemically induced pains in the skin are signalled by a set of specific nociceptive afferents, which encode the magnitude of the perceived pain by their discharge intensity. After tissue injury or inflammation, a number of changes in the properties of the primary afferent occur parallel to profound changes in the central nervous system. Primary hyperalgesia (within the area of tissue injury) is best explained by changes of the properties of primary nociceptive afferents, whereas secondary hyperalgesia (increased pain sensitivity outside the area of tissue injury) critically requires functional changes in the central nervous system. Collectively, these changes are the basis for the many forms of hyperalgesia that can present clinically as incident pain. Knowledge of the various types of hyperalgesia and their underlying mechanisms is required for better treatment of this challenging aspect of chronic pain.
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