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重症肌无力是神经肌肉间兴奋传递功能障碍所引起的一种慢性疾病,以随意肌的无力及易疲劳为特点。近年来报告病例逐年增加,治疗上又较困难,复习有关文献把本病的治疗综述如下。一、胆碱脂酶抑制剂1934年开始应用胆碱脂酶抑制剂于临床。此类药物多用于早期轻症及急性恶化病例。(一) 理论根据:一般认为重症肌无力是由于自身免疫所致的神经—肌肉接头处有效的乙酰胆碱受体(AchR)的减少,即乙酰胆碱生成或释放不足,或胆碱脂酶活性增高,使乙酰胆碱破坏过快。在正常情况下,神经冲动达到运动神经末梢时,释放出乙酰胆碱,形成终板的动作电位,使肌肉收缩。重症肌无力时,乙酰胆碱释放减少,破坏增加,使终板微小电位
Myasthenia gravis is a chronic disease caused by dysfunction of neuromuscular transmission, characterized by weakness and fatigue of voluntary muscles. In recent years, reported cases increase year by year, the treatment is more difficult to review the relevant literature review of the treatment of the disease are as follows. First, cholinesterase inhibitors 1934 began to use cholinesterase inhibitors in clinical. Such drugs are used for early mild and acute exacerbations. (A) theoretical basis: It is generally believed that myasthenia gravis is due to decreased autoimmune neuronal - muscle acetylcholinergic receptors (AchR) decreased, that is, the production or release of acetylcholine or cholinesterase activity increased, so that Acetylcholine destruction too fast. Under normal circumstances, nerve impulses reach the motor nerve endings, the release of acetylcholine, forming the action potential of the end plate, so that muscle contraction. Myasthenia gravis, acetylcholine release decreased destruction increased, so that the end plate tiny potential