尿毒症相关性不安腿综合征的发病机制研究进展  

Research advances in the pathogenesis of restless legs syndrome in uremia

作　　者：王茜茜 倪凌燕 邱孟瑶 吴云成[1] WANG Xi-Xi;NI Ling-Yan;QIU Meng-Yao;WU Yun-Cheng(Department of Neurology,Shanghai General Hospital,Shanghai Jiao Tong University School of Medicine,Shanghai 200080,China;Shanghai General Hospital of Nanjing Medical University,Shanghai 200080,China;Department of Neurology,Taicang First People's Hospital,Taicang,Jiangsu 215400,China)

机构地区：[1]上海交通大学附属第一人民医院神经内科,上海200080 [2]南京医科大学附属上海市第一人民医院临床医学院,上海200080 [3]太仓市第一人民医院神经内科,江苏太仓215400

出　　处：《国际神经病学神经外科学杂志》2020年第4期422-425,共4页Journal of International Neurology and Neurosurgery

摘　　要：尿毒症是继发性不安腿综合征最常见的病因之一,但相关机制尚未完全阐明。在尿毒症相关性不安腿综合征的发病机制中,间脑多巴胺能神经元受损所致的功能障碍、铁缺乏对运动障碍的直接调控及通过影响多巴胺能系统的间接调控、持续性的血液透析所致的静息状态、对硫铵代谢的影响等扮演重要角色。此外,周围神经病变、钙磷不平衡、基因、毒素刺激等因素可能也参与了尿毒症相关性不安腿综合征的发生与发展。Uremia is one of the most common causes of secondary restless leg syndrome(RLS),but its mechanism has not been fully elucidated so far.Functional impairment caused by diencephalic dopaminergic neuron damage,direct regulation of dyskinesia by iron deficiency and indirect regulation through the dopaminergic system,resting state caused by continuous hemodialysis,and influence on ammonium sulfate metabolism play an important role in the pathogenesis of RLS in uremia.In addition,factors such as peripheral neuropathy,calcium-phosphorus imbalance,gene,and toxin stimulation may also be involved in the development and progression of RLS in uremia.

关 键 词：不安腿综合征 尿毒症 发病机制 多巴胺能系统功能障碍 缺铁 

分 类 号：R745.1[医药卫生—神经病学与精神病学]