3 Tesla Sodium Inversion Recovery Magnetic Resonance Imaging Allows for Improved Visualization of Intracellular Sodium Content Changes in Muscular Channelopathies

Abstract

To implement different sodium (²³Na)-magnetic resonance imaging (MRI) contrasts at 3 Tesla and to evaluate if a weighting toward intracellular sodium can be achieved, using 2 rare muscular channelopathies as model diseases. Both lower legs of 6 patients with hypokalemic periodic paralysis (HypoPP), 5 patients with paramyotonia congenita (PC), and 5 healthy volunteers were examined on a 3 Tesla system with 3 different ²³Na-MRI pulse sequences. HypoPP and PC are rare muscle diseases, which are well characterized by elevated myoplasmic sodium at rest and after cooling, respectively. Intra- and interindividual comparisons were performed before and after provocation of one lower leg muscle. Three different ²³Na-MRI sequences were applied: (i) The total tissue sodium concentration was measured using a spin-density sequence (²³Na-TSC). (ii) A T1-contrast was applied to assess whether the known changes of the intracellular sodium concentration can be visualized by T1-weighting (²³Na-T1). (iii) An inversion recovery (²³Na-IR) sequence was used to utmost suppress the sodium signal from extracellular or vasogenic edema. Furthermore, a potential influence of the temperature dependency of the sodium relaxation times was considered. Additionally, H-MRI was performed to examine potential lipomatous or edematous changes. In HypoPP, all Na sequences showed significantly (P<0.05) higher signal intensities compared with PC patients and healthy subjects. In muscles of PC patients, provocation induced a significant (P=0.0007) increase (>20%) in the muscular ²³Na-IR signal and a corresponding decrease of muscle strength. Additionally, a tendency to higher ²³Na-T1 (P=0.07) and ²³Na-TSC (P=0.07) signal intensities was observed. Provocation revealed no significant changes in ¹H-MRI. In volunteers and in the contralateral, not cooled lower leg, there were no significant signal intensity changes after provocation. Furthermore, the ²³Na-IR sequence allows for a suppression of signal emanating from intravascular sodium and vasogenic edema. Our results indicate that the ²³Na-IR sequence allows for a weighting toward intracellular sodium. The combined application of the ²³Na-TSC and the ²³Na-IR sequence enables an improved analysis of pathophysiological changes that occur in muscles of patients with muscular channelopathies.