Critical illness polyneuropathy and critical illness myopathy are frequent complications of severe illness that involve sensorimotor axons and skeletal muscles, respectively. Clinically, they manifest as limb and resp...Critical illness polyneuropathy and critical illness myopathy are frequent complications of severe illness that involve sensorimotor axons and skeletal muscles, respectively. Clinically, they manifest as limb and respiratory muscle weakness. Critical illness polyneuropathy/myopathy in isolation or combination increases intensive care unit morbidity via the inability or difficulty in weaning these patients off mechanical ventilation. Many patients continue to suffer from decreased exercise capacity and compromised quality of life for months to years after the acute event. Substantial progress has been made lately in the understanding of the pathophysiology of critical illness polyneuropathy and myopathy. Clinical and ancillary test results should be carefully interpreted to differentiate critical illness polyneuropathy/myopathy from similar weaknesses in this patient population. The present review is aimed at providing the latest knowledge concerning the pathophysiology of critical illness polyneuropathy/myopathy along with relevant clinical, diagnostic, differentiating, and treatment information for this debilitat- ing neurological disease.展开更多
重症监护病房获得性肌无力(intensive care unit acquired weakness,ICUAW)是重症监护病房患者出现的进行性全身肢体无力,且除危重病本身外无其他原因可解释的一组临床综合征,主要表现为神经肌肉功能障碍。ICUAW的发病机制涉及中枢、周...重症监护病房获得性肌无力(intensive care unit acquired weakness,ICUAW)是重症监护病房患者出现的进行性全身肢体无力,且除危重病本身外无其他原因可解释的一组临床综合征,主要表现为神经肌肉功能障碍。ICUAW的发病机制涉及中枢、周围神经系统和肌纤维内复杂的功能、结构改变,但尚未完全明确。该文综述了目前关于ICUAW的潜在发病机制,以期对ICUAW的诊治提供新思路。展开更多
基金supported by grants from China Scholarship Council,No.2008102056the National Natural Science Foundation of China,No.81241147
文摘Critical illness polyneuropathy and critical illness myopathy are frequent complications of severe illness that involve sensorimotor axons and skeletal muscles, respectively. Clinically, they manifest as limb and respiratory muscle weakness. Critical illness polyneuropathy/myopathy in isolation or combination increases intensive care unit morbidity via the inability or difficulty in weaning these patients off mechanical ventilation. Many patients continue to suffer from decreased exercise capacity and compromised quality of life for months to years after the acute event. Substantial progress has been made lately in the understanding of the pathophysiology of critical illness polyneuropathy and myopathy. Clinical and ancillary test results should be carefully interpreted to differentiate critical illness polyneuropathy/myopathy from similar weaknesses in this patient population. The present review is aimed at providing the latest knowledge concerning the pathophysiology of critical illness polyneuropathy/myopathy along with relevant clinical, diagnostic, differentiating, and treatment information for this debilitat- ing neurological disease.
文摘重症监护病房获得性肌无力(intensive care unit acquired weakness,ICUAW)是重症监护病房患者出现的进行性全身肢体无力,且除危重病本身外无其他原因可解释的一组临床综合征,主要表现为神经肌肉功能障碍。ICUAW的发病机制涉及中枢、周围神经系统和肌纤维内复杂的功能、结构改变,但尚未完全明确。该文综述了目前关于ICUAW的潜在发病机制,以期对ICUAW的诊治提供新思路。
文摘目的分析危重症多发性神经病(critical illness polyneuropathy,CIP)患者的脑脊液及神经电生理特征。方法选取我中心2017年9月-2019年3月诊断为CIP且发病7~10 d的29例患者作为研究对象,分析其病因、脑脊液改变和肌电图电生理改变。结果29例中,男性16例,女性13例,平均年龄(50.4±19.3)岁。原发病因包括蛛网膜下腔出血8例(27.6%),病毒性脑炎14例(48.3%),重症肺部感染4例(13.8%),肿瘤晚期3例(10.3%)。选取21例脑脊液进行分析,其中9例(42.9%)存在脑脊液蛋白-细胞分离现象,提示周围神经病变可能有免疫因素参与。肌电图显示运动和感觉神经均有受损,神经轴索受损明显,上肢与下肢相比,运动神经波幅降低(30/58 vs 42/58,P=0.022)、传导速度减慢(12/58 vs 27/58,P=0.003)的神经条数有明显差异,下肢运动神经受损较上肢明显。上肢28条骨骼肌(28/44),下肢49条骨骼肌(49/73),早期针极肌电图可测得自发电位,差异无统计学意义(P=0.700)。5例CIP患者上肢运动神经波幅和传导速度均正常,而所支配的肌肉有90%出现明显自发电位,提示骨骼肌细胞膜电位改变早于神经轴索的损害。结论CIP患者脑脊液有蛋白细胞分离现象,可能存在免疫介导作用;CIP以轴索损害为主,运动神经下肢受累明显;早于轴索病变的自发电位是CIP早期特征性改变。
