Gur Ali, Oktayoglu Pelin
Department of Physical Medicine and Rehabilitation, Medical Faculty, Dicle University, 21280 Diyarbakir, Turkey.
Curr Pharm Des. 2008;14(13):1274-94. doi: 10.2174/138161208799316348.
Fibromyalgia (FM) and chronic fatigue syndrome (CFS) are poorly understood disorders that share similar demographic and clinical characteristics. The etiology and pathophysiology of these diseases remain unclear. Because of the similarities between both disorders it was suggested that they share a common pathophysiological mechanisms, namely, central nervous system (CNS) dysfunction. Current hypotheses center on atypical sensory processing in the CNS and dysfunction of skeletal muscle nociception and the hypothalamic-pituitary-adrenal (HPA) axis. Researches suggest that the (CNS) is primarily involved in both disorders in regard to the pain, fatigue and sleep disturbances. Many patients experience difficulty with concentration and memory and many others have mood disturbance, including depression and anxiety. Although fibromyalgia is common and associated with substantial morbidity and disability, there are no US Food and Drug Administration (FDA)-approved treatments except pregabalin. Recent pharmacological treatment studies about fibromyalgia have focused on selective serotonin and norepinephrine (NE) reuptake inhibitors, which enhance serotonin and NE neurotransmission in the descending pain pathways and lack many of the adverse side effects associated with tricyclic medications. CFS is a descriptive term used to define a recognisable pattern of symptoms that cannot be attributed to any alternative condition. The symptoms are currently believed to be the result of disturbed brain function. To date, no pharmacological agent has been reliably shown to be effective treatment for CFS. Management strategies are therefore primarily directed at relief of symptoms and minimising impediments to recovery. This chapter presents data demonstrating CFS, abnormal pain processing and autonomic nervous system (ANS) dysfunction in FM and CFS and concludes by reviewing the new concepts in treatments in CFS and FM.
纤维肌痛(FM)和慢性疲劳综合征(CFS)是了解甚少的疾病,它们具有相似的人口统计学和临床特征。这些疾病的病因和病理生理学仍不清楚。由于这两种疾病之间存在相似性,有人提出它们具有共同的病理生理机制,即中枢神经系统(CNS)功能障碍。目前的假说是以中枢神经系统中非典型的感觉处理、骨骼肌伤害感受功能障碍以及下丘脑 - 垂体 - 肾上腺(HPA)轴为中心。研究表明,中枢神经系统在疼痛、疲劳和睡眠障碍方面主要与这两种疾病有关。许多患者存在注意力不集中和记忆困难的问题,还有许多人有情绪障碍,包括抑郁和焦虑。尽管纤维肌痛很常见,且与相当高的发病率和残疾率相关,但除了普瑞巴林外,没有美国食品药品监督管理局(FDA)批准的治疗方法。最近关于纤维肌痛的药物治疗研究集中在选择性5-羟色胺和去甲肾上腺素(NE)再摄取抑制剂上,这些药物可增强下行疼痛通路中的5-羟色胺和去甲肾上腺素神经传递,并且没有许多与三环类药物相关的不良副作用。慢性疲劳综合征是一个描述性术语,用于定义一种无法归因于任何其他疾病的可识别症状模式。目前认为这些症状是脑功能紊乱的结果。迄今为止,没有可靠证据表明任何药物对慢性疲劳综合征有效。因此,管理策略主要针对缓解症状并尽量减少恢复的障碍。本章展示了有关慢性疲劳综合征、纤维肌痛中异常疼痛处理和自主神经系统(ANS)功能障碍的数据,并通过回顾慢性疲劳综合征和纤维肌痛治疗的新概念来作总结。