Under physiological circumstances muscle cell excitation involves the rapid shift of ions across membranes at the myoneural junction and at the cell surface.1-6 Membrane depolarization is associated with net potassium loss as sodium enters the cell, while the reverse exchange occurs upon repolarization. Neuromuscular excitability is dependent upon absolute electrolyte concentrations on either side of the cell membrane.7 Furthermore, it is likely that the achievement and maintenance of optimal muscle contractility is a function of the rate of ionic transfer. To some degree this rate may be regulated by hormonal agents as insulin and mineralocorticoids.8
Although an anatomical lesion at the myoneural junction has recently been reported in myasthenia gravis,9 the lability of strength and the rapid changes induced by pharmacological agents and physiological variables raise the question that this disorder may reflect a defect in ionic exchange. Acetylcholine is thought to alter the motor end
FRENKEL M. The Effect of Insulin and Potassium in Myasthenia Gravis. Arch Neurol. 1963;9(5):447–457. doi:10.1001/archneur.1963.00460110015001
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