Abstract

Summary In this article, we have reviewed the different stages of acquisition and processing of nociceptive information from peripheral receptor to brain and underline the plastic changes that accompany tissue injury. For instance, the subclassification of peripheral receptors in nociceptors and non-nociceptors (e.g., mechanoreceptors, thermoreceptors) must be understood in light of peripheral sensitization. This phenomenon is the probable explanation for primary hyperalgesia, the decrease in pain threshold at the site of injury. The observation that substance P enhances NMDA-elicited responses suggests that these two receptor systems may operate in concert to prolong and amplify the afferent input generated by peripheral tissue injury. Such afferent barrage induces a state of central sensitization. In this phenomenon, the subliminal zone of the receptive fields of many dorsal horn neurons becomes suprathreshold. These peripheral and central sensitizations probably induce permanent changes in central circuits associated with some chronic pain states. In fact, it is tempting to extrapolate from Bach et al5 that preventive treatment of acute pain will prevent the development of chronic pain syndromes in surgical patients.

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