Introduction

The nociceptive system was previously thought of as a hard—wired system, mediating information about tissue damage to the brain in a fixed and static manner. However, injury to the peripheral or central nervous system (CNS) triggers a cascade of changes, which alter the structure and function of the nervous system. The result is a high degree of plasticity in those systems that mediate information about tissue damage, with neuronal modifications occurring at several levels of the neuraxis from the peripheral receptor to the cortex. These changes after nerve damage may result in peripheral or central neuropathic pain.

Neuropathic pain is characterized by pain in an area with sensory loss corresponding to the damaged nerve or central lesion. The qualities may be burning, smarting, shooting, aching, and pricking. The pain may be accompanied by dysesthesia (unpleasant abnormal sensations), allodynia (the elicitation of pain in the affected area by non-noxious stimulation with light touch or innocuous cold or warmth), and hyperalgesia (increased pain response to a normal noxious stimulus). Other features frequently seen in neuropathic pain are wind-up-like pain (abnormal temporal summation of pain), aftersensations (pain continuing after stimulation has ceased), and referred pain (pain felt in a place apart from the stimulated area).