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Progressive gray matter damage in patients with relapsing-remitting multiple sclerosis: a longitudinal diffusion
Celia Oreja-Guevara1, Marco Rovaris, Giuseppe Iannucci
1Neuroimaging Unit and Department of Neurology, Scientific Institute and University H San Raffaele, Milan, Italy.
Archives of Neurology
|April 13, 2005
Summary
Diffusion tensor MRI reveals progressive microstructural damage in the normal-appearing gray matter of patients with multiple sclerosis (MS). These changes occur independently of brain atrophy, highlighting gray matter pathology in MS.
Area of Science:
- Neuroimaging
- Biomedical Engineering
- Radiology
Background:
- Diffusion tensor magnetic resonance imaging (DT MRI) offers in vivo insights into tissue microstructure.
- DT MRI has identified subtle structural damage in normal-appearing brain tissues of multiple sclerosis (MS) patients.
Purpose of the Study:
- To assess DT MRI's sensitivity to longitudinal microstructural brain changes in relapsing-remitting MS.
- To detect early signs of damage in normal-appearing brain tissue beyond T2-weighted imaging resolution.
Main Methods:
- Twenty-six untreated relapsing-remitting MS patients underwent 18-month follow-up with serial MRIs.
- DT MRI, T2-weighted, and T1-weighted imaging were used to analyze brain tissue, lesions, and diffusivity.
- Mean diffusivity (D) histograms and fractional anisotropy were calculated for normal-appearing gray matter (GM) and white matter.
Main Results:
- Significant decreases in whole brain tissue volume and GM diffusivity histogram peak height were observed.
- Significant increases in normal-appearing GM diffusivity and T2-hyperintense lesion volumes were noted.
- Changes in GM diffusivity were independent of brain volume changes, indicating distinct pathological processes.
Conclusions:
- DT MRI demonstrates progressive microstructural alterations in the normal-appearing GM of MS patients.
- These findings underscore the significance of GM pathology in MS pathogenesis.
- Gray matter changes detected by DT MRI are not directly linked to concurrent brain atrophy.