Abstract
The classical perception that the pain state reflects the response to a stimulus-dependent activation of a specific anatomically-defined system, and that the magnitude of the pain state is strictly proportional to the magnitude of the stimulus, was challenged conceptually by the early formulations of Melzack and Wall leading to the gate control theory. Clinical experience indicates that there are frequent examples of dissociation between the magnitude of the physical stimulus and the perceived pain response. Thus, protracted small afferent input can induce a state of hyperalgesia and hyperesthesia [allodynia]. Nerve injury of changes in spinal cord processing can similarly result in anomalous states where otherwise innocuous input may be perceived as aversive. Current interest in myofascial pain states suggests that such conditions may represent an alteration in afferent processing, leading to unexpected severe pain behaviors in spite of an apparently modest triggering stimulus. While the mechanisms of this pain state remain obscure, there is a growing pre-clinical literature which sheds light on several systems that may account for changes in the input and output function of the spinal cord. These systems will be discussed in the following sections.