Conclusions

Pain can have detrimental effects on almost every organ system. The most readily apparent effects are those on the respiratory and cardiovascular systems. More prolonged effects develop via the expression of genes for neuropeptides, cytokines, growth factors, and other compounds. Interactions between the immune and nervous systems are the basis for the development and also the control of inflammatory pain. Immediately after tissue injury, a cascade of local events is initiated that leads to increased sensitivity. In parallel, intrinsic counteractive mechanisms, which are capable of controlling pain by central and peripheral opioid actions, can come into play. The transition from acute to chronic pain may critically depend on disturbances of intrinsic control mechanisms as well as on effective therapeutic measures initiated at the earliest possible time.

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