Muscle is electrically inexcitable in acute quadriplegic myopathy

Abstract

We directly stimulated muscle in three patients with acute quadriplegic myopathy to determine whether paralyzed muscle in this syndrome is electrically excitable. Two of the patients had been treated with neuromuscular blocking agents and corticosteroids, and one patient had been treated with corticosteroids alone. We found that paralyzed muscle is electrically inexcitable in affected patients. Muscle regained electrical excitability over weeks to months. The recovery of muscle excitability paralleled the clinical recovery of patients, suggesting that paralysis in this syndrome is secondary to electrical inexcitability of muscle membrane.

Neuromuscular Disorders in Critically-Ill Patients – Approaches to Electrophysiologic Changes in Critical Illness Neuropathy and Myopathy

“…Therefore, the following three factors contributing to reduction in muscle membrane excitability are introduced [7]:…”

Mechanisms of Neuromuscular Dysfunction in Critical Illness

“…This electrophysiologic technique is based upon the comparison of the motor response amplitude obtained by directly stimulating muscle with the response obtained by stimulating nerve and relies on the finding that skeletal muscle is electrically inexcitable in CIM [29,30]. Direct muscle stimulation is most useful early in the course of illness when the traditional MUP assessment on EMG is not possible due to delirium or sedation.…”

“…The causes of muscle atrophy and loss of myosin are complex and are still poorly understood [5,39] and while very important, will not be discussed further. The third factor is loss of the ability of muscle fibers to generate action potentials, which results in electrical inexcitability of muscle [29,30,40]. Atrophy and loss of myosin are likely more important in chronic weakness of patients with CIM, whereas loss of muscle excitability may be more important in the acute setting.…”

“…For example, if a negative shift in sodium channel gating occurs in both nerve and muscle then both tissues might become inexcitable and cause neuropathy or myopathy respectively. It is now relatively well established that skeletal muscle becomes electrically inexcitable in septic patients [11,29,30,63]. There is also evidence of inexcitability of sensory nerves.…”

16.5 Critical-Illness-Myopathie

“…Protein catabolism and muscle wasting are observed in CIM. Proteolytic pathways involving calpain [63] and the ubiquitin-proteasome pathway [64,65] are upregulated due to pro-inflammatory cytokines in conjunction with increased apoptosis [66]. As calpain is a calcium-activated protease, altered cellular calcium homeostasis due to endotoxemia and inflammation might play a role [60,67].…”