Introduction

Pre-emptive analgesia is a therapeutic strategy designed to relieve pain by administration of treatment in advance of pain (Woolf et al., 1993). The rationale for this approach comes from the discovery that the sensory barrage initiated by tissue damage and carried by C-fibers sets in train changes in the excitability or sensitivity of neurons within the central nervous system that outlast the initiating stimulus; the phenomenon of central sensitization (Woolf, 1983; Coderre et al., 1993; Dubner and Ruda, 1992; McMahon et al., 1993; Woolf, 1994). Central sensitization manifests as a reduction in the pain threshold, an amplification of the intensity and duration of the pain response to noxious stimuli, the spread of abnormal sensitivity to uninjured tissue, and the generation of pain by normally innocuous inputs (Torebjork et al., 1992; Koltzenburg et al., 1992, 1994; Woolf, 1995).

If tissue damage can be anticipated, as in the case of elective surgery, there may be a clinical advantage in minimizing the establishment or maintenance of central sensitization in the intraoperative and postoperative period. Three potential approaches can be adopted to do this. The first is to block sensory inflow during surgery using regional anesthesia with sodium channel blockers to block conduction in C-nociceptor sensory fibers. The second is to target specifically those transmitters and receptors in the dorsal horn of the spinal cord responsible for initiating central sensitization with, for example, N-methy1-D-aspartic acid receptor antagonists like ketamine or neurokinin receptor antagonists to block the action of glutamate and substance P.