BrainPrint captures stage-specific lateral shape asymmetry in autoimmune limbic encephalitis

Antonia Harms1, Tobias Bauer1, Leon Ernst1, Bastian David1, Bernd Weber2, Albert J. Becker3, Martin Reuter4, Rainer Surges1, Theodor Rüber5

1 Department of Epileptology, University of Bonn Medical Center, Bonn, Germany
2 Institute of Experimental Epileptology and Cognition Research, University of Bonn Medical Center, Bonn, Germany
3 Department of Neuropathology, Section for Translational Epilepsy Research, University of Bonn Medical Center, Bonn, Germany
4 German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany; 3Martinos Center for Biomedical Imaging, Radiology, MGH / Harvard Medical School, Boston, USA
5 Department of Epileptology, University of Bonn Medical Center, Bonn, Germany; Epilepsy Center Frankfurt Rhine-Main, Department of Neurology, Goethe University Frankfurt, Frankfurt am Main, Germany; Center for Personalized Translational Epilepsy Research (CePTER), Goethe-University Frankfurt, Frankfurt am Main, Germany

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Limbic Encephalitis (LE) is an autoimmune disease often associated with temporal lobe epilepsy. It is categorized by serological subgroups, that differ in clinical progress, therapy and prognosis. We aimed to investigate lateral shape asymmetry of an ensemble of 11 cortical and subcortical structures by applying BrainPrint, a surface-based method that uses Eigenvalues of the Laplace-Beltrami operator on triangular (boundary) and tetrahedral (volumetric) meshes as shape descriptors. Intraindividual lateral shape asymmetry for each structure was computed as normalized Euclidean distance between vectors containing the first 50 Eigenvalues sorted by magnitude. We compared lateral shape asymmetry of patients with autoantibodies against glutamic acid decarboxylase (GAD, n=41), leucine-rich glioma-inactivated protein 1 (LGI1, n=22),  contactin-associated protein-like 2 (CASPR2, n=12), voltage gated potassium channel (VGKC, n=16), and N-methyl-D-aspartate receptor (NMDAR, n=8) in acute and chronic disease stages to 94 healthy controls. While we did not find any lateral volumetric asymmetry, the following significant (p<0.05) differences between groups regarding the shape were identified using a Kruskal-Wallis test and post-hoc Dunn-tests for pairwise comparisons. In the acute disease stage: thalamus, amygdala and in the cerebellar white matter surface. In the chronic disease stage: thalamus, amygdala, putamen, cerebellar white matter surface, pial surface and lateral ventricles. Our findings mirror the higher sensitivity of shape information as compared to volumetry. Since we have already found volumetric features reflecting the serostatus of LE in earlier studies, we now aim to develop accurate imaging biomarkers for clinical and scientific implementation.