Imaging Poster Presentation

P0562 - Cortical lesions are not associated with leptomeningeal enhancement in a cohort of adults with MS. (ID 420)

Speakers
  • M. Morrison
Authors
  • M. Morrison
  • E. Beck
  • P. Sati
  • H. Kolb
  • D. Reich
Presentation Number
P0562
Presentation Topic
Imaging

Abstract

Background

Focal leptomeningeal enhancement (LME) on MRI is more commonly seen in neuroinflammatory diseases than in noninflammatory neurological diseases or healthy controls. In MS, meningeal inflammatory infiltrates sometimes overlie cortical demyelination in pathological samples, but studies linking cortical lesions to LME have had equivocal results to date.

Objectives

To evaluate the association between LME and cortical lesions in vivo and to assess the relationship between LME number and disease severity.

Methods

59 adults with MS (40 with relapsing remitting MS and 19 with primary or secondary progressive MS) underwent clinical testing (Multiple Sclerosis Functional Composite), 3 tesla (3T) MRI with gadolinium, and 7T non-gadolinium MRI within 6 months of the 3T MRI. 7T T1w MP2RAGE and T2*w gradient-echo images (both 0.5mm isometric) were used to identify cortical lesions, which were classified as leukocortical, intracortical, or subpial. Foci of LME were identified using post-gadolinium T2-FLAIR images and post–pre T2-FLAIR subtraction images. The spatial relationship between LME and cortical lesions was investigated, as was the clinical relationship between LME number and disease severity.

Results

66% of individuals (39/59) had no LME. 20% (12/59) had 1 focus of LME, and 14% (8/59) had >1 focus of LME. Median cortical lesion number was 20 in people without LME (IQR 91, range 0–206), 18 in people with 1 LME (IQR 12, range 0–182, p>0.05 vs no LME), and 39 in people with >1 LME (IQR 64, range 4–133, p>0.05 vs no LME). There was no difference in leukocortical, intracortical, or subpial lesion number between people with 0, 1, or >1 LME (p>0.05). None of the identified foci of LME was adjacent to a cortical lesion, though 13% of LME foci (4/31) were situated in the same sulcus as a cortical lesion. Median expanded disability status scale (EDSS) was higher in people with >1 focus of LME (5.5, range 1–7.5) compared to people without LME (median 1.5, range 0–7, p<0.05). EDSS was correlated with total cortical lesion number (rs=0.507, p<0.0001, ß=0.024) and subpial lesion number (rs=0.462, p<0.001, ß=0.028).

Conclusions

There was no association between number of LME foci and number of total cortical lesions or any cortical lesion subtype in our data. This suggests that LME cannot be taken to indicate ongoing inflammation overlying cortical demyelination. Further studies are needed to determine the histopathological basis of focal LME in MS and its relation, if any, to prior leptomeningeal inflammation.

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