Abstract

PurposeSodium MRI shows great promise as a marker for cerebral metabolic dysfunction in stroke, brain tumor, and neurodegenerative pathologies. However, cerebral blood vessels, whose volume and function are perturbed in these pathologies, have elevated sodium concentrations relative to surrounding tissue. This study aims to assess whether this fluid compartment could bias measurements of tissue sodium using MRI.MethodsDensity‐weighted and B1 corrected sodium MRI of the brain was acquired in 9 healthy participants at 4.7T. Veins were identified using co‐registered 1H T2∗‐weighted images and venous partial volume estimates were calculated by down‐sampling the finer spatial resolution venous maps from the T2∗‐weighted images to the coarser spatial resolution of the sodium data. Linear regressions of venous partial volume estimates and sodium signal were performed for regions of interest including just gray matter, just white matter, and all brain tissue.ResultsLinear regression demonstrated a significant venous sodium contribution above the underlying tissue signal. The apparent venous sodium concentrations derived from regression were 65.8 ± 4.5 mM (all brain tissue), 71.0 ± 7.4 mM (gray matter), and 55.0 ± 4.7 mM (white matter).ConclusionAlthough the partial vein linear regression did not yield the expected sodium concentration in blood (~87 mM), likely the result of point spread function smearing, this regression highlights that blood compartments may bias brain tissue sodium signals across neurological conditions where blood volumes may differ.

Highlights

  • All vein sodium signal calculations were significantly greater than the mean tissue signal of the region of interest (ROI) they were calculated from, as follows: Vein partial volume estimate (PVE) regression over all voxels within the brain tissue mask yielded a venous sodium signal 49 ± 3% of vitreous humor (VH) signal, or a VH normalized

  • The apparent tissue sodium concentration values measured in the white matter (WM) and gray matter (GM) ROIs were 39.1 ± 0.8 mM and 41.9 ± 0.9 mM, respectively

  • This method of apparent sodium concentration measurement is sensitive to the accuracy of the VH concentration value from the literature, absolute concentration values are not necessary to demonstrate through regression that sodium signal from veins contributes to brain tissue voxels

Read more

Summary

Introduction

Sodium plays a key role in neuronal action potentials, mediates the transport of metabolic substrates through cell membranes and is involved in osmoregulation and pH regulation.[1,2] Sodium (23Na) MRI shows promise as a marker for cerebral metabolic dysfunction in studying stroke,[3,4,5,6] brain tumor,[7,8,9,10,11] and neurodegenerative pathologies.[12,13,14,15,16,17] the 23Na MRI signal is greater in cerebrospinal fluid (CSF),[18,19,20,21] such that measurements of tissue sodium can be biased by tissue atrophy. By using a shift reagent in the rat brain, a significant 16% intravascular sodium signal increase was observed with NMR during a hypercapnia‐induced increase in cerebral blood volume (CBV).[26]

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call