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Published on: November 20, 2015
Dura mater enhancement on 3T MRI is associated with cortical lesion burden in multiple sclerosis
Robert Zivadinov1,2, Mehak Semy3, Alexander Bartnik3
1Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, 77 Goodell Street, Suite 450, Buffalo, NY, 14203, USA. rz4@buffalo.edu.
Background:
Post-contrast FLAIR MRI can demonstrate meningeal signal enhancement in people with multiple sclerosis (pwMS), including enhancement along the leptomeninges and dura mater. Although these enhancement patterns have been variably interpreted as reflecting inflammatory processes, their biological specificity and relationship to cortical lesion pathology remain uncertain.
Objective:
To evaluate the association between cortical lesion burden and distinct patterns of meningeal enhancement (ME), including dura mater enhancement (DME), leptomeningeal enhancement (LME), and meningeal perivascular enhancement (MPVE) on MRI in pwMS.
Methods:
214 pwMS (173 relapsing-remitting, 41 progressive) underwent 3T MRI including 3D FLAIR pre- and post-contrast, and subtraction imaging. ME (LME + DME) and MPVE were visually classified. Cortical lesions were quantified using a validated multi-modal approach incorporating MMCLE, FLAIR-squared, AI-DIR, and T1/T2 ratio maps, with expert verification. Analyses were adjusted for age, sex, disease duration, disease subtype, and disease-modifying treatment, and corrected for multiple comparisons.
Results:
142 (66.4%) pwMS showed combined ME/MPVE, 121 (56.5%) ME, including 97 (45.3%) with DME and 48 (22.4%) with LME. Additionally, 46 (21.5%) exhibited MPVE. A higher prevalence and frequency of LME + pwMS were observed in older age groups (p = 0.002), whereas no such age-related pattern was found for DME + or MPVE + pwMS. DME + pwMS showed greater cortical lesion number (9.6 vs. 4.9, p = 0.003) and volume (374.1 mm3 vs. 187.6 mm3, p = 0.019) compared to DME - pwMS. DME frequency correlated with cortical lesion number (r = 0.59, p < 0.001) and volume (r = 0.56, p < 0.001). Stepwise regression identified DME as an independent predictor of cortical lesion number (β = 0.45, p < 0.001) and volume (β = 0.41, p < 0.001), explaining 12-15% of variance beyond conventional MRI measures.
Conclusions:
DME on 3T MRI is associated with increased cortical lesion burden in pwMS.
Insights
Dura mater enhancement (DME) on MRI in people with multiple sclerosis (pwMS) is linked to a higher burden of cortical lesions. This finding helps clarify the relationship between meningeal changes and brain pathology in MS.
Area of Science:
- Neurology
- Radiology
- Neuroimmunology
Background:
- Post-contrast FLAIR MRI shows meningeal signal enhancement in people with multiple sclerosis (pwMS).
- The biological specificity and relationship of these enhancement patterns to cortical lesion pathology are uncertain.
Purpose of the Study:
- To evaluate the association between cortical lesion burden and distinct patterns of meningeal enhancement (ME) on MRI in pwMS.
- Specific patterns investigated include dura mater enhancement (DME), leptomeningeal enhancement (LME), and meningeal perivascular enhancement (MPVE).
Main Methods:
- 214 pwMS underwent 3T MRI, including 3D FLAIR pre- and post-contrast imaging.
- Meningeal enhancement (ME) and MPVE were visually classified; cortical lesions were quantified using a validated multi-modal approach.
- Analyses were adjusted for covariates and corrected for multiple comparisons.
Main Results:
- DME was observed in 45.3% of pwMS, and was significantly associated with a higher number and volume of cortical lesions.
- DME frequency correlated strongly with cortical lesion number (r=0.59) and volume (r=0.56).
- DME independently predicted cortical lesion number and volume, explaining 12-15% of variance.
Conclusions:
- Dura mater enhancement (DME) on 3T MRI is associated with increased cortical lesion burden in people with multiple sclerosis.
- This association provides further insight into the pathological mechanisms underlying MS.
