Clinical pain is not simply the consequence of a “switching on” of the “pain system” in the periphery by a particular pathology, but instead reflects to a substantial extent, the state of excitability of central nociceptive circuits. The induction of activity-dependent increases in synaptic function in these circuits, triggered and maintained by dynamic nociceptor inputs, shifts the sensitivity of the pain system such that normally innocuous inputs can activate it and the perceptual responses to noxious inputs are exaggerated, prolonged and spread widely. These sensory changes represent the manifestation of central sensitization, and extensive experimental medicine and clinical investigations over the past twenty years, have revealed it to be an important component of the pain hypersensitivity present many patients. While considerable progress has been made in teasing out the cellular and molecular mechanism responsible [148], much remains still to be learned, particularly which genetic and environmental contributors increase the risk of developing central sensitization in particular systems, exactly what triggers and sustains the phenomenon, and what is responsible in some individuals for its persistence. Nevertheless, the identification of the contribution of central sensitization to many “unexplained” clinical pain conditions has both provided a mechanistic explanation, and offered a therapeutic target.
Posted on: Thu, 15 Jan 2015 00:04:47 +0000
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