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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
Gray matter T2 hypointensity is related to plaques and atrophy in the brains of multiple sclerosis patients
R Bakshi1, J Dmochowski, Z A Shaikh
1Department of Neurology, University at Buffalo, State University of New York, Buffalo, NY, USA. rbakshi@buffalo.edu
Abstract:
Cortical and subcortical gray matter hypointensities on T2-weighted MR images (T2WI) occur commonly in MS brains and have been related to disease duration, clinical course, and the level of neurologic disability. These hypointensities have been reported to occur in the thalamus, basal ganglia, and rolandic cortex. We assessed whether T2 hypointensity is associated with the severity of white matter plaques and atrophy of MS brains. In 114 MS patients, hypointensity of the thalamus, putamen, caudate, and sensorimotor cortex was ordinally rated against age- and gender-matched normal controls on 1.5-T MRI fast spin-echo axial T2WI. Regional and global T2 hyperintense and T1 hypointense parenchymal lesion loads were ordinally rated. Enlargement of subarachnoid and ventricular spaces (atrophy) was ordinally rated vs. age- and gender-matched normal controls. T2 hypointensity was highly, positively correlated with many other MRI variables. Regression modeling showed that T2 hypointensity was related to total atrophy, total T2 lesion load, third ventricular enlargement, parietal atrophy, and to a lesser extent, frontal T1 lesions and cerebellar T2 lesions, but not related to gadolinium enhancement. Ordinal ratings of T2 lesions and central atrophy showed high correlations with quantitative computerized assessments. We conclude that gray matter hypointensity on T2WI may reflect pathologic iron deposition and brain degeneration in MS. This T2 hypointensity is associated with brain atrophy and other MR markers of tissue damage. Further study is warranted to determine if T2 hypointensity is predictive of disease course in MS and is a useful surrogate outcome measure in therapeutic trials.
Insights
Gray matter hypointensities on T2-weighted MRI in multiple sclerosis (MS) brains are linked to brain atrophy and tissue damage. These findings suggest T2 hypointensity may indicate degeneration and iron deposition in MS patients.
Area of Science:
- Neuroimaging
- Neurology
- Radiology
Background:
- Gray matter hypointensities on T2-weighted MRI (T2WI) are common in multiple sclerosis (MS) and linked to disease progression and disability.
- These abnormalities have been observed in various brain regions, including the thalamus, basal ganglia, and cortex.
Purpose of the Study:
- To investigate the association between T2 hypointensity in gray matter and the severity of white matter lesions and brain atrophy in MS patients.
- To explore the relationship between T2 hypointensity and other magnetic resonance imaging (MRI) markers of MS pathology.
Main Methods:
- 114 MS patients underwent 1.5-T MRI with fast spin-echo axial T2WI.
- Ordinal ratings were used to assess T2 hypointensity in specific gray matter regions (thalamus, putamen, caudate, sensorimotor cortex) compared to controls.
- White matter lesion load (T2 hyperintense, T1 hypointense) and brain atrophy (enlargement of subarachnoid and ventricular spaces) were also ordinally rated.
Main Results:
- T2 hypointensity showed a strong positive correlation with various MRI variables.
- Regression analysis revealed associations between T2 hypointensity and total atrophy, total T2 lesion load, third ventricular enlargement, parietal atrophy, and some T1 and T2 lesions in specific regions.
- No significant relationship was found between T2 hypointensity and gadolinium enhancement.
Conclusions:
- Gray matter hypointensity on T2WI in MS may indicate pathological iron deposition and neurodegeneration.
- T2 hypointensity is associated with brain atrophy and other MRI indicators of tissue damage in MS.
- Further research is needed to determine if T2 hypointensity can predict MS disease course or serve as a surrogate outcome in clinical trials.
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