The most important clinical development in chronic pain during the past decade has not been new treatments but a thoroughly revised interpretation of the mechanisms that act to maintain pain. Pain is no more seen as a predetermined result of simple activation of certain neural structures. It is now understood to be a dynamic phenomenon due to myriad pathophysiological changes in the peripheral and central nervous system in response to disease, injury, or loss of function1 (box 1). These changes reflect the surprising but indisputable fact that the human nervous system is adaptable and capable of substantial plasticity. Initially reversible, the changes tend to become fixed depending on the nature and duration of the original cause, as well as the age and perhaps the genetic susceptibility of the patient

In chronic pain the abnormal activity in the altered pain mediating afferent system continues irrespective of its original causation. Simple blocking or severing of neural pathways is not helpful: the locus of abnormal barrages is simply shifted more centrally. Recent advances in the pharmacology of pain have unravelled some of the mediators of chronic pain, and they offer potential targets for treatments that are currently being developed (box 2). New investigative techniques are also being developed for improved detection of factors maintaining chronic pain. Alongside pharmacological advances, stimulation treatments and psychological approaches have seen innovative developments.