Background: Autopsy data suggest a causative link between meningeal inflammation and cortical lesions (CLs) in multiple sclerosis (MS). Objective: To use leptomeningeal enhancement (LME) and CLs on 7-Tesla (7T) magnetic resonance imaging (MRI) to investigate associations between meningeal inflammation and cortical pathology. Methods: Forty-one participants with MS underwent 7T MRI of the brain. CLs and foci of LME were quantified. Results: All MS participants had CLs; 27 (65.8%) had >1 focus of LME. Except for hippocampal CL count (ρ = 0.32 with spread/fill-sulcal pattern LME, p = 0.042), no significant correlations were seen between LME and CLs. Mean cortical thickness correlated with the number of LME foci (ρ = –0.43, p = 0.005). Participants with relapsing–remitting multiple sclerosis (RRMS) showed no correlation with neocortical CLs, but significant correlations were seen between LME and hippocampal lesion count (ρ = 0.39, p = 0.030), normalized cortical gray matter (GM) volume (ρ = –0.49, p = 0.005), and mean cortical thickness (ρ = –0.59, p < 0.001). Conclusion: This study supports a relationship between LME and cortical GM atrophy but does not support an association of LME and neocortical CLs. This may indicate that meningeal inflammation is involved with neurodegenerative inflammatory processes, rather than focal lesion development.

Background and Purpose: Preliminary research has demonstrated that post-gadolinium 3D FLAIR MRI at 7T may be a valuable tool for detecting abnormal meningeal enhancement and inflammation in MS; however, researchers have not systematically investigated its longitudinal persistence. We hypothesize that persistence of meningeal enhancement in MS varies based on pattern of enhancement as well as demographic and clinical factors such as treatment status, disease phenotype, and disability score. Materials and Methods: Thirty-one subjects with MS were prospectively scanned before and after intravenous contrast administration at 2 time points, approximately 1 year apart. Fifteen subjects in the cohort were scanned another time approximately 1 year later. Foci of enhancement were categorized into four subtypes: subarachnoid spread/fill, subarachnoid nodular, vessel wall, and dural foci. We reviewed follow-up scans to determine whether foci changed between time points and then compared persistence to demographic and clinical variables. Results: Persistence ranged from 71–100% at 1 year, and 73–100% at 2 years depending on enhancement pattern. Subarachnoid spread/fill and subarachnoid nodular subtypes persisted less often than vessel wall and dural foci. Persistence was not significantly different between those on/off treatment and those with progressive/non-progressive diseases phenotypes. Number of persisting foci was significantly different in subjects with/without increasing Expanded Disability Status Scale scores (median 12 v 7.5, p=0.04). Conclusion: Longitudinal persistence of meningeal enhancement on 3D FLAIR at 7T in MS varies by pattern of enhancement and correlates with worsening disability; however, it is not significantly different in those on/off treatment or those with progressive/non-progressive disease phenotypes.

No abstract

No abstract

No abstract