Primary hyperalgesia corresponds to the increased sensitivity to pain that develops at the site of an injury, whereas secondary hyperalgesia corresponds to the increased sensitivity that occurs in a large, uninjured area surrounding the site of injury. As indicated in Table I, the properties of primary and secondary hyperalgesia differ. In the primary zone, hyperalgesia occurs in response to both mechanical and heat stimuli. In contrast, in the secondary zone, hyperalgesia occurs to mechanical stimuli but not heat stimuli (Ali et al. 1996). This dichotomy suggests that the neural mechanisms underlying primary and secondary hyperalgesia differ. At the site of injury, primary afferents become sensitized, which may account for certain aspects of primary hyperalgesia. For example, a burn injury produces marked sensitization of nociceptors to heat and a corresponding hyperalgesia to heat (Meyer and Campbell 1981). However, nociceptors with receptive fields outside the injury zone do not become sensitized after an injury (e.g., Thalhammer and LaMotte 1'983; Schmelz et al. 1996). Sensitization does not spread, so peripheral sensitization does not account for secondary hyperalgesia. Secondary hyperalgesia develops as a result of plasticity in the central nervous system (CNS), which we globally call central sensitization. It can contribute to both primary and secondary hyperalgesia.
展开▼
