Psychophysical evidence that central sensitization contributes to secondary mechanical hyperalgesia in human subjects

Tissue damage as a consequence of traumatic and inflammatory processes can, in many instances, increase pain sensitivity in areas of the body remote from the site of injury. Increased pain sensitivity in the uninjured tissue surrounding the primary site of injury is referred to as secondary hyperalgesia. In most experimental models of tissue injury, secondary hyperalgesia is characterized psychophysically as enhanced pain to mechanical, but not heat stimuli. It is generally accepted that mechanisms related to the neurophysiologic phenomenon of central sensitization correspond to the psychophysical phenomenon of hyperalgesia. The purpose of this article is to review recent human psychophysical data supporting the hypothesis that secondary mechanical hyperalgesia reflects mechanisms related to central sensitization. Novel therapeutic approaches for a number of chronic pain conditions can be expected to evolve as the central mechanisms of secondary hyperalgesia become better understood.