Mechanisms of touch-evoked pain (allodynia): a new model.

Abstract

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 A-beta mechanoreceptors can gain access to nociceptive neurones by means of a presynaptic link, at central level, between low threshold mechanoreceptors and nociceptors. We propose that the excitation of nociceptors provoked by a peripheral injury activates the spinal interneurones that mediate primary afferent depolarization (PAD) between low threshold mechanoreceptors and nociceptors. As a consequence of the increased and persistent barrage driving these neurones their excitability is increased such that, when activated by low threshold mechanoreceptors from areas 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 dorsal 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 (allodynia).