Leptomeningeal enhancement in multiple sclerosis demonstrates posterior predilection and T1 alterations in the adjacent cortex

Ashley A Thommana; Erin S Beck; Matthew A Greenwald; Gina Norato; Hallie Gaitsch; Dzung L Pham; Steven Jacobson; María I Gaitán; Govind Nair; Daniel S Reich; Serhat V Okar

doi:10.1177/20552173251408625

Leptomeningeal enhancement in multiple sclerosis demonstrates posterior predilection and T₁ alterations in the adjacent cortex

Mult Scler J Exp Transl Clin. 2026 Jan 20;12(1):20552173251408625. doi: 10.1177/20552173251408625. eCollection 2026 Jan-Mar.

Authors

Affiliations

¹ Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA.
² Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
³ Clinical Trials Unit, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA.
⁴ Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.

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 T₁-maps at 7T. T₁ 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 T₁ 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 T₁ relaxation time observed in the cortex adjacent to LME may signify subtle tissue changes in the absence of cortical lesions.

Keywords: MRI; Multiple sclerosis; blood-cerebrospinal fluid barrier; leptomeningeal enhancement; real inversion-recovery MRI.