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

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...

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Bibliographic Details
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
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Summary: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
ISSN:0148-639X
1097-4598
DOI:10.1002/mus.20884