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There is evidence that secondary mechanical hyperalgesia, which develops in healthy tissue surrounding injury or in distant tissue to which pain is referred, can be mediated by the thick tactile sensory fibres. These pains are probably provoked by impulses in normal low-threshold afferents entering the central nervous system, where they encounter highly abnormal central nervous circuits that amplify or reroute the signals of normally innocuous events. The afferent fibres convey information to the central nervous system in two quite different ways. Sensory fibres which have been changed by their contact with damaged or inflamed tissue discharge impulses in a characteristic spatial and temporal pattern. The second way is by transport of chemicals from the tissues along axons towards the dorsal root ganglion. In response to changes in these relatively slowly transported chemicals the chemistry and metabolism of the cytoplasm and cell membrane, including its central terminal arborizations, is altered. This consequently affects the post-synaptic cells of the central nervous system. Pain and the central nervous system The first cells of the central nervous system on which the afferents terminate are not exclusively simply relay cells. They form integrated groups with both summation and differentiation functions as well as inhibitory and facilitatory mechanisms. The facilitatory functions appear to become active following noxious inputs and this results in the development of a hyperalgesic state (Treede et al., 1992; Woolf & Doubell, 1994). In addition, there are also powerful inhibitory systems in this region and their failure may contribute to hyperalgesia. The modulator role of the spinal cord in transmission of nocioceptive signals from the periphery to the brain has been known for many years, and new evidence as to the complexity of the system and both the excitatory and inhibitory influence of many different neurotransmitter substances emerges continually (Dickenson, 1995, Marsh et al., 1997). Knowledge of these pathways forms the basis for the provision of pain relief by the epidural or intrathecal administration of analgesic drugs. To date the opioid pathways remain the most important system involved in the production of analgesia at the spinal level, although noradrenaline, the natural ligand acting at α2 adrenoceptors, also has a major role in the spinal modulation of nocioception. Opioid receptors and α2 adrenoceptors are present in laminae 1 and 2 of the dorsal horn, the area involved in the reception and modulation of incoming nocioceptive signals, and their density and, in the case of opioid, the proportion of each type of receptor differ at different levels of the spinal cord (Bouchenafa & Livingston, 1987, 1989; Khan et al., 1999).
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