Recent pain research has concentrated heavily on excitatory processes. However, noxious stimuli activate excitatory and inhibitory systems. As failure of inhibition could underlie some forms of pathological pain, it may be argued that a full understanding of the mechanisms underlying the development of pain states can only come from a consideration of all the central sequelae of injurious stimuli. [berkley; blumberg et al.; coderre & katz; dickenson; mcmahon; weisenfeld-hallin et al.].

Evidence that central sensitization needs to be maintained in an ongoing manner by nociceptive input from the periphery makes the peripheral drive, rather than the central amplification process, the highest priority target for understanding and control. To stop the peripheral drives to kill two birds with one stone. Moreover, the amplification that central sensitization does provide is selective and not necessarily striking in intensity. A that neutralized central sensitization would probably be less effective in controlling persistent pain than many investigators (...) would like to believe. [berkley; blumberg et al.; coderre & katz; dickenson; mcmahon; weisenfeld-hallin et al.]. (shrink)