Abstract
Pain is a warning that something is wrong. But for those who suffer from persistent, intense pain it loses any positive purpose and means only suffering and disability. Chronic pain becomes threatening and aversive, restricting mobility and shrinking the social world. A system that apparently evolved to warn and protect, to aid healing and ultimately to preserve life, can become a pathology, ‘have a life of its own’ (Daudet, 2002) and create an enormous human and economic burden (http://www.efic.org/costs-of-chronic-pain.php). The challenge to provide relief from pain runs through all branches of medicine and yet many physicians are surprisingly unaware or even uninterested in the complexity of pain. As a society we have turned to neuroscience, especially cellular and molecular neuroscience, which together with strong backing from the pharmaceutical industry promise the development of new analgesics targeted towards specific peripheral and central mechanisms of pain. While this has resulted in a huge escalation of knowledge in the neurobiology of pain, the practical application of this knowledge to the relief of pain has been disappointing—a fact that has led to considerable soul searching about the potential for translation of experimental laboratory-based pain research into clinical pain management (Mao, 2009; Mogil, 2009). In our enthusiasm for probing the biology of nocioception in laboratory models, we may have lost sight of the fundamental problem: pain intensity is not simply determined by how much noxious information arises from injured areas of the body—pain is the outcome of neural processing at multiple central nervous system sites in the spinal cord and brainstem, limbic system, hypothalamus and cortex (Kehlet et al. , 2006). The sensory component which makes it so clearly distinguishable from other sensations is only part of the pain experience. Reflex movements, autonomic reactions, altered attention, cessation of behaviour, a sense of unpleasantness …
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