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|Title:||The future: new concepts and potential therapies|
|Citation:||Neuropathic pain: causes, management and understanding, 2013 / Toth, C., Moulin, D. (ed./s), Ch.29, pp.341-356|
|Publisher:||Cambridge University Press|
|Publisher Place:||United Kingdom|
|Nicole M. Sumracki, Lauren Nicotra, Yuen Hei Kwok, Liang Liu, Krista van Steeg, Linda R. Watkins, and Mark R. Hutchinson|
|Abstract:||Introduction: Chronic pain is a complicated, multifaceted disease process affecting millions of people worldwide. Neuropathic pain specifically, as a subset of chronic pain, is defined as pain resulting as a direct consequence from a lesion or disease affecting the somatosensory system, and is estimated to affect 3-4.5% of the global population, with an estimated annual cost of $100 billion in the USA alone . Critically, the somatosensory system has previously been thought to consist merely of neuronal networks, and it was believed that the dysregulation of this wiring led to the chronic pain pathologies. However, data developed during the past two decades has shed light on neuronal and non-neuronal origins of neuropathic pain . Despite many preclinical and clinical advances the precise mechanisms underlying neuropathic pain are still not well understood and the efficacy of current pharmacological therapies is at present symptomatically suppressive, rather than disease modifying or curative. All seven currently approved treatments for neuropathic pain are designed to target neuronal contributors of the disease. Given the discovery of non-neuronal pro-inflammatory central immune signaling mediators of neuropathic pain, the less-than-optimal success of existing therapies is perhaps not surprising.|
|Rights:||© Cambridge University Press 2013|
|Appears in Collections:||Aurora harvest 2|
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