Longitudinal Brain Atrophy Patterns in Early MOG‐Antibody Associated Disease and Relapsing Multiple Sclerosis

TL;DR

This study compares brain atrophy patterns in early MOG antibody disease and multiple sclerosis, finding that MOG disease does not show progressive brain volume loss over time.

Contribution

The study is the first to show no longitudinal brain volume loss in MOG antibody disease using voxel-based morphometry.

Findings

MOG antibody disease showed no longitudinal gray or white matter changes over 2 years.

Multiple sclerosis patients had thalamic atrophy linked to clinical relapses.

MOG disease showed atrophy in the bilateral fornix and stria terminalis compared to controls.

Abstract

Myelin oligodendrocyte glycoprotein antibody‐associated disease can manifest as a relapsing or monophasic condition. Although several MRI studies have shown evident gray and white matter atrophy compared to healthy controls, little is known about regional brain volume dynamics in myelin oligodendrocyte glycoprotein antibody‐associated disease over time.

In this study, we performed an explorative voxel‐based morphometry to detect brain volumetric differences between myelin oligodendrocyte glycoprotein antibody‐associated disease (N = 27), relapsing multiple sclerosis (N = 40)—both in early disease stages—and healthy controls (N = 45). Furthermore, we investigated the longitudinal brain volume changes over a 2‐year follow‐up period in myelin oligodendrocyte glycoprotein antibody‐associated disease (N = 15) and relapsing multiple sclerosis (N = 40).

We identified distinct patterns of regional brain volume loss in the patient subgroups compared to healthy controls. In multiple sclerosis patients, bilateral thalamic atrophy was observed, whereas patients with myelin oligodendrocyte glycoprotein antibody‐associated disease showed atrophy of the bilateral fornix and stria terminalis. Our results confirmed longitudinal volume loss in thalamic and infratentorial regions in the relapsing multiple sclerosis group, which was partly related to clinical relapses during the 2‐year follow‐up period. In contrast, no longitudinal gray or white matter changes were found in the myelin oligodendrocyte glycoprotein antibody‐associated disease group.

To our knowledge, this is the first MRI study demonstrating no evidence of regional brain volume loss over time in patients with myelin oligodendrocyte glycoprotein antibody‐associated disease using voxel‐based morphometry, suggesting a different—probably not progressive—pathophysiological background compared to relapsing multiple sclerosis.

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