MECHANISMS OF TOUCH-EVOKED PAIN (ALLODYNIA) - A NEW MODEL

In this paper we review the current neurophysiological models of touch -evoked pain and present a new proposal that addresses the mechanisms of allodynia. The new model is based on the notion that alpha-beta mec hanoreceptors can gain access to nociceptive neurones by means of a pr esynaptic link, at central level, between low threshold mechanorecepto rs and nociceptors. We propose that the excitation of nociceptors prov oked by a peripheral injury activates the spinal interneurones that me diate primary afferent depolarization (PAD) between low threshold mech anoreceptors and nociceptors. As a consequence of the increased and pe rsistent barrage driving these neurones their excitability is increase d such that, when activated by low threshold mechanoreceptors from are as surrounding the injury site, they produce a very intense PAD in the nociceptive afferents which is capable of generating spike activity. This activation would be conducted antidromically in the form of dorsa l root reflexes (DRRs) but would also be conducted forward activating the second order neurones normally driven by nociceptors. The sensory consequence of this mechanism is pain evoked by the activation of low threshold mechanoreceptors from an area surrounding an injury site (al lodynia).