ABSTRACT
I. INTRODUCTION Perhaps the most significant advance in the field of pain research has been the realization that pain is not a single sensory experience and that the different forms of pain are mediated by different neurological mechanisms. Some years ago we proposed a conceptual framework and a series of models that addressed the mechanisms of both acute and chronic pain and the interrelation between different pain states (1). We argued that the neurophysiological mechanisms responsible for all of the various pain states are different and that normal (nociceptive) and abnormal (neuropathic) pain represent the endpoints of a sequence of possible changes that can occur in the nervous system. Normally, a steady state is maintained in which there is a close correlation between injury and pain. However, changes or oscillations induced by nociceptive input or by changes in the environment can result in variations in the quality and quantity of pain sensation produced by a particular noxious stimulus. Such changes would be temporary, unless there was further noxious input, as the system would always tend to restore the normal balance between injury and pain. However, long-lasting or very intense nociceptive input or the removal of a portion of the normal input would distort the nociceptive system to such an extent that the close correlation between injury and pain would be lost.
