Allen David C, Arunachalam Ramamurthy, Mills Kerry R
Academic Unit of Clinical Neurophysiology, Guy's, King's & St. Thomas' School of Medicine, King's College Hospital, London SE5 9RS, UK.
Muscle Nerve. 2008 Jan;37(1):14-22. doi: 10.1002/mus.20884.
Recent studies have demonstrated acquired muscle inexcitability in critical illness myopathy (CIM) and have used direct muscle stimulation (DMS) techniques to distinguish neuropathy from myopathy as a cause of weakness in the critically ill. The mechanisms underlying weakness in CIM are incompletely understood and DMS is only semiquantitative. We report results from a series of 32 patients with CIM and demonstrate significant slowing of muscle-fiber conduction velocity (MFCV) and muscle-fiber conduction block during the acute phase of CIM, which correlates with prolonged compound muscle action potential (CMAP) duration, clinical severity, and course. We also used a paired stimulation technique to explore the excitability of individual muscle fibers in vivo. We demonstrate altered muscle-fiber excitability in CIM patients. Serial studies help define the course of these pathophysiological changes. Parallels are made between CIM and hypokalemic periodic paralysis. Our findings provide further evidence for muscle membrane dysfunction being the principal underlying abnormality in CIM.
近期研究已证实危重病性肌病（CIM）存在获得性肌肉兴奋性缺失，并运用直接肌肉刺激（DMS）技术来区分神经病变与肌病，以明确其作为危重症患者肌无力病因的情况。CIM导致肌无力的潜在机制尚未完全明确，且DMS仅为半定量检测。我们报告了32例CIM患者的系列研究结果，证实在CIM急性期肌肉纤维传导速度（MFCV）显著减慢以及肌肉纤维传导阻滞，这与复合肌肉动作电位（CMAP）时限延长、临床严重程度及病程相关。我们还采用配对刺激技术来探究体内单个肌肉纤维的兴奋性。我们证实CIM患者的肌肉纤维兴奋性发生改变。系列研究有助于明确这些病理生理变化的过程。同时将CIM与低钾性周期性麻痹进行了对比。我们的研究结果为肌膜功能障碍是CIM主要潜在异常这一观点提供了进一步证据。
