Moore David M, McCrory Connail
Phase Ih Ward, St. James Hospital, Dublin 8, Ireland.
Curr Neuropharmacol. 2017;15(2):198-205. doi: 10.2174/1570159x14666160224124446.
Chronic pain remains a challenging clinical problem with a growing socio-economic burden for the state. Its prevalence is high and many of the patients are of work age. Our knowledge regarding the pathophysiology of chronic pain is poor. The consensus view is that the central nervous system plays a key role in the persistence of pain after an initiating event has long ceased. However the specifics of this biological response to an initiating event remains unclear. There is a growing body of evidence to support the concept that a central neuroimmune response is initiated and a number of small peptides have been implicated in this process following cerebrospinal fluid analysis in patients with chronic pain. This central biosynthetic peptide response leads to a process called central sensitization. Therapy is aimed at modulating and even inhibiting this response. However current pharmacological therapeutic options are limited in efficacy with significant deleterious side effect profiles. Proteomic studies extend single molecule analysis by identifying the components of biological networks and pathways and defining their interactions. This tool offers the potential to provide a molecular overview of the biological processes involved in chronic pain. It will also facilitate examination of gene-drug interactions. This technique offers a mechanism of defining the central biological responses that result in chronic pain and this information may facilitate the development of better therapies.
慢性疼痛仍然是一个具有挑战性的临床问题,给国家带来日益沉重的社会经济负担。其患病率很高,且许多患者处于工作年龄。我们对慢性疼痛病理生理学的了解不足。目前的共识是,在引发疼痛的事件早已结束后,中枢神经系统在疼痛持续过程中起关键作用。然而,这种对引发事件的生物学反应的具体情况仍不清楚。越来越多的证据支持这样一种观点,即中枢神经免疫反应被启动,并且在对慢性疼痛患者进行脑脊液分析后,一些小肽与这一过程有关。这种中枢生物合成肽反应会导致一种称为中枢敏化的过程。治疗旨在调节甚至抑制这种反应。然而,目前的药物治疗选择疗效有限,且有明显的有害副作用。蛋白质组学研究通过识别生物网络和途径的组成部分并确定它们之间的相互作用,扩展了单分子分析。这个工具有可能提供一个涉及慢性疼痛的生物学过程的分子概述。它还将有助于研究基因与药物的相互作用。这项技术提供了一种确定导致慢性疼痛的中枢生物学反应的机制,这些信息可能有助于开发更好的治疗方法。