The Contribution of Both the Peripheral and Central Nervous Systems to the Pain that Follows Peripheral Nerve Injury

Abstract

Pain, as a sensory state, is not simply the inevitable consequence of the activation of a defined set of sensory pathways in the periphery. Rather, pain is a descriptor that we choose to identify a variety of different unpleasant, uncomfortable and distressing sensations that may be elicited in quite a number of different ways. It is useful to look at pain in terms of its pathogenesis as consisting of three different types: physiological, inflammatory and neuropathic pain (the latter two constituting clinical pain; Woolf 1987 a). Physiological pain is that sensation elicited by transient non-tissue-damaging noxious stimuli that activate high threshold A-delta and C nociceptors. This type of pain, which we commonly experience as pin prick, pinch, or excessive heat or cold, has a distinct threshold and a quantifiable stimulus-response relationship. These properties of physiological pain have led to the idea that there are specific pain pathways in the peripheral and central nervous systems that are similar to the specific pathways that are considered to mediate the innocuous somatosensations such as touch, pressure, vibration, hot or cold. However, what this analysis fails to take account of is that physiological pain is very different from inflammatory and neuropathic pain. Clinical pain is not simply excessive or prolonged ‘physiological’ pain; it is a qualitatively different sensory experience with different neural mechanisms.