We read with interest the report by Road and colleagues concerning generalized weakness following neuromuscular blockade and corticosteroid use. They describe an evolving electrophysiologic pattern in which early needle EMG suggests denervation, but later studies that, during recovery, reveal myopathic recruitment. We routinely see similar EMG evolution in our patients and believe that our observation of muscle fiber inexcitability in this setting fully explains these findings.
Muscle fibers are inexcitable even to direct muscle stimulation in patients with acute quadriplegic myopathy (AQM). Furthermore, individual muscle fibers are inexcitable to intracellular stimulation in an animal model of AQM. The principle explanation for muscle inexcitability in the animal model appears to be a reduction in sodium current. This mechanism of weakness is analogous to that of periodic paralysis where there is profound weakness, markedly decreased CMAP amplitudes, and relatively normal muscle morphology. The analogy between AQM and periodic paralysis is also instructive when trying to understand the presence of spontaneous activity in AQM. Fibrillations are common in hyperkalemic periodic paralysis and may increase during attacks when most muscle fibers are inexcitable. Although the mechanism of electrical inexcitability in AQM remains uncertain, it is possible that severely affected individual muscle fibers exist in a state of inexcitability, whereas less severely affected fibers might have poorly regulated excitability and may fibrillate. In this setting, motor unit recruitment may appear neuropathic as some motor units may have no electrically excitable fibers. As recovery progresses all motor units have at least a few excitable fibers and recruitment then appears myopathic. The presence of fibrillation potentials adds to the illusion of denervation in early AQM.
The observation that muscle is electrically inexcitable in AQM deserves to be included in any discussion of electrophysiologic findings in this disorder.