Electron spin resonance spectroscopy was used to substantiate the presence of a membrane defect in myotonic erythrocytes. There was increased membrane fluidity and decreased polarity in myotonic membranes. Phenytoin (formerly diphenylhydantoin) normalizes fluidity differences in spectra derived from myotonic erythrocytes but has no significant effect on normal spectra. These experiments demonstrate the applicability of biophysical methods to human erythrocyte membranes and support the concept of a membrane defect in myotonic dystrophy that does not have a primary myopathic, neuropathic, or vascular cause.

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