What question did this study set out to answer?

The study aims to understand the prevalence of leptomeningeal enhancement (LME) across brain regions and its connection to cortical pathology in multiple sclerosis (MS).

January 22, 2026Open Access

Leptomeningeal enhancement in multiple sclerosis demonstrates posterior predilection and T 1 alterations in the adjacent cortex

Key Points

The study aims to understand the prevalence of leptomeningeal enhancement (LME) across brain regions and its connection to cortical pathology in multiple sclerosis (MS).
Recorded LME distribution patterns using 3T Real-IR MRI in 90 adults with MS.
Analyzed T1 relaxation times in normal-appearing cortex near LME for a subset of 15 participants with 7T MRI.
Compared T1 times in the cortex beneath LME to adjacent and homologue cortex.
Identified 243 LME foci in 65 out of 90 participants, indicating a prevalence of 73%.
Noted that 66.3% of LME foci were located posterior to the central sulcus.
Observed elevated mean T1 times beneath LME compared to adjacent (p < 0.0001) and homologue (p = 0.0052) cortex.

Abstract

Background Leptomeningeal enhancement (LME) is a putative magnetic resonance imaging (MRI) marker of meningeal inflammation in multiple sclerosis (MS). 3D inversion-prepared fast-spin-echo sequence with real-reconstruction inversion recovery (Real-IR) MRI at 3 tesla (T) is highly sensitive to LME. Objectives To assess LME prevalence across brain regions and characterize the relationship between LME and subtle cortical pathology. Methods LME distribution patterns across brain regions were recorded for 90 adults (Age: 51 ± 11; women: 57; MS: 78) using 3T Real-IR. A subset of 15 participants had corresponding T 1 -maps at 7T. T 1 relaxation times were calculated in the normal-appearing cortex subjacent to the LME, in comparison to the adjacent and homologue cortex. Results 243 LME foci were found across 65 participants (73%). One hundred and sixty-one (66.3%) LME foci were posterior to the central sulcus. Three of 15 7T participants had a cortical lesion nearby LME (3/49 foci). Mean T 1 times within cortex beneath LME (1734 ± 135 ms) were elevated compared to homologue (1668 ± 167 ms, p = .0052) and adjacent cortex (1651 ± 133 ms, p < .0001). Conclusions Regional variations in LME distribution may point to topographical differences in the blood-meningeal barrier. Alterations in T 1 relaxation time observed in the cortex adjacent to LME may signify subtle tissue changes in the absence of cortical lesions.

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