[Neurobiology of pain]

An injury to the skin or to an internal organ evokes a discharge in the nociceptive afferents that innervate the damaged area and, as a consequence of the ensuing inflammatory process, sensitizes these nociceptive endings. The activity of sensitized nociceptors evokes two different alterations of pain sensation: 1. A change in the modality of the sensation evoked by low threshold mechanoreceptors, from touch to pain (allodynia) and 2. An increase in the magnitude of the pain sensations evoked by mechanically sensitive nociceptors (hyperalgesia). Allodynia and hyperalgesia show that pain sensation is a dynamic process whose presence and intensity depend on the past history of an affected area and not only on the magnitude of the stimulus. During the initial injury and for the duration of the repair process there will be increased nociceptive activity from the injured region. These afferent barrages cause, in turn, central changes in excitability mediated by positive feedback loops between spinal and supraspinal neurones and by the enhanced synaptic actions of certain neurotransmitters. Among these transmitters, attention has currently focused on the actions of NMDA receptors and neurokinins as putative mediators of the increases in central excitability induced by noxious stimuli.

The overall mechanism combines the features of the classical 'pain pathway' with the dynamic plastic changes mediated by non-conventional neurotransmitters.