No association between cortical lesions and leptomeningeal enhancement on 7-Tesla MRI in multiple sclerosis

Mehrnaz Ighani1, Samuel Jonas2, Izlem Izbudak3

  • 1University of Maryland, College Park, MD, USA.

Multiple Sclerosis (Houndmills, Basingstoke, England)
|October 2, 2019
PubMed
Abstract

Insights

Leptomeningeal enhancement (LME) on MRI is linked to gray matter atrophy in multiple sclerosis (MS), suggesting meningeal inflammation contributes to neurodegeneration rather than focal lesion formation.

Area of Science:

  • Neuroimaging
  • Neurology
  • Pathology

Background:

  • Autopsy studies suggest a link between meningeal inflammation and cortical lesions (CLs) in multiple sclerosis (MS).
  • Understanding this relationship is crucial for MS pathogenesis research.

Purpose of the Study:

  • To investigate the association between meningeal inflammation, indicated by leptomeningeal enhancement (LME), and cortical pathology in MS using 7-Tesla (7T) MRI.
  • To explore the correlation between LME and CLs, as well as cortical atrophy measures.

Main Methods:

  • Forty-one participants with MS underwent 7T MRI brain scans.
  • Cortical lesions (CLs) and foci of leptomeningeal enhancement (LME) were quantified.
  • Correlations between LME, CLs, cortical thickness, and gray matter volume were analyzed.

Main Results:

  • All MS participants exhibited CLs, with 65.8% showing multiple LME foci.
  • A significant correlation was found between LME and hippocampal CL count (ρ=0.32, p=0.042).
  • Mean cortical thickness negatively correlated with the number of LME foci (ρ=-0.43, p=0.005).
  • In relapsing-remitting MS (RRMS), LME correlated with hippocampal lesion count, reduced gray matter volume, and decreased cortical thickness.

Conclusions:

  • The study supports a relationship between LME and cortical gray matter atrophy in MS.
  • No significant association was found between LME and neocortical CLs.
  • Findings suggest meningeal inflammation may drive neurodegenerative processes in MS rather than focal lesion development.

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