3 Tesla Sodium Inversion Recovery Magnetic Resonance... : Investigative Radiology (original) (raw)

Original Articles

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

Nagel, Armin Michael PhD*; Amarteifio, Erick MD†,‡; Lehmann-Horn, Frank MD§; Jurkat-Rott, Karin MD§; Semmler, Wolfhard MD, PhD*; Schad, Lothar R. PhD¶; Weber, Marc-André MD†,‡

From the Departments of *Medical Physics in Radiology and †Radiology, German Cancer Research Center (DKFZ), Heidelberg, Germany; ‡Department of Diagnostic and Interventional Radiology, University Hospital Heidelberg, Heidelberg, Germany; §Division of Neurophysiology, University of Ulm, Ulm, Germany; and ¶Computer Assisted Clinical Medicine, University of Heidelberg, Mannheim, Germany.

Received February 8, 2011; accepted for publication (after revision) May 12, 2011.

Conflicts of interest and sources of funding: Frank Lehmann-Horn is an endowed Senior Research Professor for Neurosciences of the non-profit Hertie-Foundation. The other authors have nothing to declare.

Reprints: Armin Michael Nagel, PhD, Department of Medical Physics in Radiology, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany. E-mail: [email protected].

Abstract

Objectives:

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.

Materials and Methods:

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, 1H-MRI was performed to examine potential lipomatous or edematous changes.

Results:

In HypoPP, all 23Na 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.

Conclusions:

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.