Lesion Heterogeneity In Multiple Sclerosis: Relations Between Appearances On T1 Weighted Images, T1 Relaxation Times, And Metabolite Concentrations

Brex PA, Parker GJ, Leary SM, Molyneux PD, Barker GJ, Davie CA, Thompson AJ, Miller DH
J Neurol NeuroSurg Psychiatry 2000 May;68(5):627-632
Institute of Neurology, NMR Research Unit, 6th floor, Univ, College London, Queen Square, London WC1N 3BG, UK
PMID# 10766895; UI# 20229924
Abstract

Objectives
Multiple Sclerosis lesions appear as areas of high signal on T2 weighted MRI. A proportion of these lesions, when viewed on T1 weighted MRI, appear HypoIntense compared with surrounding White Matter.

These HypoIntense T1 lesions are thought to represent areas of greater tissue damage compared with the more non-specific, total T2 lesion load.

This study aimed to better characterize the properties of high signal T2 lesions with differing appearances on T1 weighted MRI using quantitative MR techniques.

Methods
Eleven patients with Secondary/Progressive Multiple Sclerosis were studied.

Two high signal T2 lesions were selected from each patient-one of which appeared HypoIntense and one IsoIntense on a T1 weighted image.

A Voxel (volume element) was positioned around each Lesion and for this volume of Brain the metabolite concentrations were estimated using Proton MR Spectroscopy ((1)H-MRS).

And, the T1 relaxation time within each Voxel calculated from a T1 map generated using a multislice technique.

Results
Compared with IsoIntense T1 lesions, HypoIntense T1 lesions exhibited a significantly lower absolute concentration of N-AcetylAspartate derived metabolites (tNAA) and a significantly higher absolute concentration of Myo-Inositol (Ins).

T1 relaxation time correlated significantly with both tNAA (r=-0.8, p < 0.001) and Ins (r=0.5, p=0.012).

There was no correlation between T1 relaxation times and Creatine/PhosphoCreatine or Choline containing compounds.

Conclusions
Prolonged T1 relaxation times seem to reflect the severity of Axon damage or dysfunction (inferred by a low tNAA) and possibly also Gliosis (inferred by a high Ins) in chronic Multiple Sclerosis Lesions.



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