Critical illness myopathy: Further evidence from muscle-fiber excitability studies of an acquired channelopathy

• Published in: Muscle & nerve 2008-01, Vol.37 (1), p.14-22
• Main Authors: Allen, David C., Arunachalam, Ramamurthy, Mills, Kerry R.
• Format: Article
• Language: English
• Subjects: Action Potentials - physiology; Acute Disease; Adult; Biological and medical sciences; Cell Membrane - physiology; Channelopathies - metabolism; Channelopathies - pathology; Channelopathies - physiopathology; compound muscle action potential; Critical Illness; critical illness myopathy; Diagnosis, Differential; direct muscle stimulation; Disease Progression; Electromyography; Fundamental and applied biological sciences. Psychology; Humans; hypokalemic periodic paralysis; Ion Channels - physiology; Male; Middle Aged; Muscle Fibers, Skeletal - physiology; Muscle Weakness - etiology; Muscle Weakness - metabolism; Muscle Weakness - physiopathology; Muscle, Skeletal - metabolism; Muscle, Skeletal - physiopathology; muscle-fiber conduction velocity; Muscular Diseases - etiology; Muscular Diseases - metabolism; Muscular Diseases - physiopathology; Striated muscle. Tendons; Vertebrates: osteoarticular system, musculoskeletal system
• ISSN: 0148-639X; 1097-4598
• 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. Muscle Nerve, 2007