Muscle is electrically inexcitable in acute quadriplegic myopathy
- 1 March 1996
- journal article
- Published by Wolters Kluwer Health in Neurology
- Vol. 46 (3) , 731-736
- https://doi.org/10.1212/wnl.46.3.731
Abstract
The absence of significant neuropathy [3,5] or persistent decrement following repetitive nerve stimulation [3,5-7,10] suggests that the decrease in CMAP amplitude associated with acute quadriplegic myopathy is caused by an abnormality in muscle. This abnormality could simply be secondary to loss of muscle, because in some patients there is a dramatic increase in CK, and muscle biopsy reveals widespread necrosis. [5,11,12] In most patients, however, there is a marked decrease in CMAP amplitude with only a minor increase in CK, and muscle biopsy does not reveal necrosis. [3,5] We postulated that the decrease in CMAP amplitude in these patients may be secondary to loss of muscle membrane excitability. To test this hypothesis, we directly stimulated muscle in three patients with acute quadriplegic myopathy to determine whether the muscle was electrically excitable. We also directly stimulated denervated muscle in three patients who had not received corticosteroids to determine the threshold of denervated muscle for direct excitation.Keywords
This publication has 4 references indexed in Scilit:
- Dystrophin–glycoprotein complex: Its role in the molecular pathogenesis of muscular dystrophiesMuscle & Nerve, 1994
- Message from the editor's officeMuscle & Nerve, 1992
- Different localization of dystrophin in developing and adult human skeletal muscleMuscle & Nerve, 1991
- Huntington diseaseNeurology, 1979