Abstract Details

Title The Association Between Cortical Gray Matter Lesions and Leptomeningeal Enhancement on 7-Tesla MRI in Multiple Sclerosis

Topic Multiple Sclerosis

Presentation(s) S31 - MS and CNS Inflammatory Disease: Imaging (4:47 PM-4:58 PM)

Poster/Presentation
Number 008

Background

Post-contrast FLAIR MRI has emerged as a potential biomarker of meningeal inflammation in MS. Autopsy studies suggest a link between CLs and meningeal inflammation.

Objective

To determine the relationship between meningeal inflammation and cortical demyelination in multiple sclerosis (MS) using leptomeningeal enhancement (LME) and cortical lesions (CLs) as imaging biomakers on 7-Tesla (7T) MRI.

Design/Methods Forty-one MS patients (31 relapsing, 10 progressive) underwent MRI on a 7T scanner. MP2RAGE and MPFLAIR images were acquired pre- and post-contrast. CLs identified as hypointensities on MP2RAGE were classified as leukocortical, intracortical, subpial, or hippocampal. LME foci were identified as hyperintensities on post-contrast MPFLAIR in the subarachnoid space and characterized as nodular or spread/fill. Cortical gray matter (GM) volume was derived from Lesion-TOADS segmentation. Relationships were explored with Spearman correlation and Wilcoxon rank-sum.

Results

Thirty-three (80%) participants had at least one focus of LME. Nodular foci were present in 13 (32%) participants, whereas 31 (76%) had spread/fill foci. All had CLs with a median of 23 (range 2 – 82) lesions per subject. Hippocampal lesions were higher in those with spread/fill LME compared to those without (median 23.32 vs. 13.80, p = 0.02). No significant relationships between LME and other CL subtypes were found. Although cortical GM volume did not significantly correlate with LME in the full cohort, cortical GM volume negatively correlated with LME focus count in relapsing MS-only (rho = -0.45, p = 0.01).

Conclusions

These results do not strongly support a relationship between LME and CLs; perhaps except for hippocampal lesions. The correlations between cortical GM volume and LME support a link between widespread, non-lesional cortical atrophy and meningeal inflammation. This relationship may be decoupled later in the disease course – hence the lack of this finding when including those with progressive MS phenotypes.

Authors/Disclosures
PRESENTER	No disclosure on file
	No disclosure on file
	No disclosure on file
	No disclosure on file
	No disclosure on file
	No disclosure on file
Daniel M. Harrison, MD (University of Maryland School of Medicine)	Dr. Harrison has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Horizon Therapeutics. Dr. Harrison has received personal compensation in the range of $500-$4,999 for serving as an Editor, Associate Editor, or Editorial Advisory Board Member for American College of Physicians. The institution of Dr. Harrison has received research support from Roche-Genentech. Dr. Harrison has received publishing royalties from a publication relating to health care.

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