Subcortical grey matter volume and asymmetry in the long-term course of Rasmussen’s encephalitis

Author:

Bauer Tobias1ORCID,Reiter Johannes T1,Enders Selma1,Keil Vera C W2345,Radbruch Alexander2,Helmstaedter Christoph1,Surges Rainer1,Rüber Theodor1ORCID

Affiliation:

1. Department of Epileptology, University Hospital Bonn , 53127 Bonn , Germany

2. Department of Neuroradiology, University Hospital Bonn , 53127 Bonn , Germany

3. Department of Radiology and Nuclear Medicine, Amsterdam UMC Location Vrije Universiteit Amsterdam , 1081 HV Amsterdam , Netherlands

4. Brain Imaging, Amsterdam Neuroscience , Amsterdam UMC, 1081 HV Amsterdam , Netherlands

5. Cancer Center Amsterdam , Amsterdam UMC, 1081 HV Amsterdam , Netherlands

Abstract

Abstract Rasmussen’s encephalitis is characterized by drug-resistant focal seizures and chronic inflammation of one hemisphere leading to progressive loss of hemispheric volume. In this cohort study, we aimed to investigate subcortical grey matter volumes and asymmetries in Rasmussen’s encephalitis longitudinally in clinically relevant subgroups. We retrospectively included all T1-weighted MRI scans of all people with Rasmussen’s encephalitis who were treated at the University Hospital Bonn between 1995 and 2022 (n = 56, 345 scans, median onset 8 years, 36 female). All cases were classified as type 1 (onset ≤ 6 years) or type 2 (onset > 6 years). Subcortical segmentations were performed using FreeSurfer. Longitudinal trajectories of subcortical volumes and hemispheric ratios (ipsi-/contralesional) were assessed using linear mixed-effect models. Unihemispheric cortical degeneration was accompanied by ipsilesional atrophy of the nucleus accumbens, caudate nucleus, putamen, thalamus and contralesional atrophy of the nucleus accumbens and caudate nucleus both in type 1 (all P ≤ 0.014) and type 2 (all P < 0.001). In type 1, however, contralesional volume increase of the amygdala, hippocampus, pallidum and thalamus was found (all P ≤ 0.013). Both ipsilesional and contralesional subcortical atrophies, like cortical atrophy, are most probably caused by neurodegeneration following chronic neuroinflammation. We speculate that contralesional volume increase in type 1 could be related to either neuroplasticity or ongoing acute neuroinflammation, which needs to be investigated in further studies.

Funder

BONFOR

Medical Faculty of the University of Bonn

Publisher

Oxford University Press (OUP)

Subject

Neurology,Cellular and Molecular Neuroscience,Biological Psychiatry,Psychiatry and Mental health

Reference29 articles.

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