Abstract
Pre-emptive analgesia is based on the idea that analgesia initiated before a nociceptive event will be more effective than analgesia commenced afterwards, and that its effects will outlast the pharmacological duration of action of the analgesic used. The idea of pre-emptive analgesia is based upon experimental neurophysiological work demonstrating that afferent nociceptive impulses result in alterations of central nervous system function. These changes, most easily elicited by C-fibre afferents, particularly affect the spinal dorsal horn. Termed central sensitisation, they are reflected by reduced pain thresholds (allodynia), increased responses to pain (hyperalgesia), after-discharging or spontaneous activity of dorsal horn neurons (wind-up), and extension of hypersensitivity to unaffected tissues (secondary hyperalgesia). Their biochemical basis is now being unravelled, with excitatory amino acid (e.g. NMDA) and neuropeptide (e.g. substance P) neurotransmitters playing prominent roles. Blockade of these receptors has recently been shown to depress the central sensitisation associated with nociception. Ketamine, a non-competitive NMDA receptor blocker, for example, has been shown modulate postoperative pain in a positive way. ...Continue Reading
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