Council on Science and Public Health, American Medical Association, Chicago, Illinois 60654, USA.
Pain Med. 2010 Nov;11(11):1635-53. doi: 10.1111/j.1526-4637.2010.00986.x.
Because of disparate taxonomic arrays for classification, the American Academy of Pain Medicine has proposed categorizing pain on a neurobiologic basis as eudynia (nociceptive pain), Greek for "good pain," or maldynia (maladaptive pain), Greek for "bad pain." The latter has been viewed as maladaptive because it may occur in the absence of ongoing noxious stimuli and does not promote healing and repair.
To address recent findings on the pathogenesis of pain following neural injury and consider whether the development of maladaptive pain justifies its classification as a disease and to briefly discuss the scope of pharmacologic and non-pharmacologic approaches employed in patients with such pain.
English language reports on studies using human subjects were selected from a PubMed search of the literature from 1995 to August 2010 and from the Cochrane Library. Further information was obtained from Internet sites of medical specialty and other societies devoted to pain management.
Neural damage to either the peripheral or central nervous system provokes multiple processes including peripheral and central sensitization, ectopic activity, neuronal cell death, disinhibition, altered gene expression, and abnormal sprouting and cellular connectivity. A series of neuro-immune interactions underlie many of these mechanisms. Imaging studies have shown that such damage is characterized by functional, structural, and chemical changes in the brain. Such pain is maladaptive in the sense that it occurs in the absence of ongoing noxious stimuli and does not promote healing and repair.
As defined, maldynia is a multidimensional process that may warrant consideration as a chronic disease not only affecting sensory and emotional processing but also producing an altered brain state based on both functional imaging and macroscopic measurements. However, the absolute clinical value of this definition is not established.
由于分类的分类学数组不同，美国疼痛医学学院提出根据神经生物学基础对疼痛进行分类，即 eudynia（伤害性疼痛），希腊语为“好的疼痛”，或 maldynia（适应性不良的疼痛），希腊语为“坏的疼痛”。后者被认为是适应性不良的，因为它可能发生在没有持续有害刺激的情况下，并且不会促进愈合和修复。
解决神经损伤后疼痛发病机制的最新发现，并考虑适应性不良的疼痛的发展是否证明其作为疾病的分类合理，并简要讨论在患有此类疼痛的患者中使用的药理学和非药理学方法的范围。
从 1995 年至 2010 年 8 月，使用人类受试者的英语语言报告从 PubMed 文献搜索和 Cochrane 图书馆中选择。从医学专业和专门从事疼痛管理的其他学会的互联网网站获取了更多信息。
外周或中枢神经系统的神经损伤会引发多种过程，包括外周和中枢敏化、异位活动、神经元细胞死亡、去抑制、基因表达改变以及异常发芽和细胞连接。许多这些机制的基础是一系列神经免疫相互作用。影像学研究表明，这种损伤的特征是大脑的功能、结构和化学变化。这种疼痛是适应性不良的，因为它发生在没有持续有害刺激的情况下，并且不会促进愈合和修复。
按照定义，maldynia 是一个多维度的过程，不仅可能影响感觉和情绪处理，而且还会根据功能成像和宏观测量产生改变的大脑状态，因此可能需要被视为一种慢性疾病。然而，该定义的绝对临床价值尚未确定。
