GENERATION OF ACUTE PAIN - CENTRAL MECHANISMS

Pain can either be 'nociceptor-mediated', produced as a consequence of the activation of high threshold nociceptors, or 'A-fibre mediated', resulting from the activation of low threshold A-beta afferent fibres. Under normal circumstances nociceptor mediated pain only occurs in response to high intensity noxious stimuli. Following peripheral tissue injury the inflammatory reaction generates a complex set of chemical signals that alter the transduction properties of nociceptors such that they can be activated by low intensity stimuli, the phenomenon of peripheral sensitization. Pain in this circumstance is still nociceptor mediated but can be generated by low intensity or innocuous stimuli. The nociceptive input to the spinal cord in these circumstances however produces activity-dependent alterations in the response properties of neurones in the dorsal horn. This means that they begin to repond to normal inputs, including that generated by A-beta low threshold afferents, in an abnormal and exaggerated way. This is the phenomenon of central sensitization. Because afferent inputs can provoke prolonged alterations within the central nervous system, optimal treatment of acute pain states should be directed both at abolishing peripheral sensitization and to preventing the establishment of central sensitization. The latter involves the strategy of pre-emptive analgesia.