Volumetric and structural connectivity abnormalities co-localise in TLE

TL;DR

This study investigates the relationship between grey matter volume loss and white matter connectivity disruptions in temporal lobe epilepsy, revealing that abnormalities tend to co-localize and are driven by neighboring regions, indicating shared underlying mechanisms.

Contribution

It provides a comprehensive analysis of how volumetric and connectivity abnormalities co-localize in TLE, highlighting their interrelation and potential shared mechanisms.

Findings

White matter abnormalities are greater between regions with grey matter volume loss.

Grey matter abnormalities are greater when connected by abnormal white matter tracts.

Co-localization of abnormalities is mainly driven by neighboring regions in the same hemisphere.

Abstract

Patients with temporal lobe epilepsy (TLE) exhibit both volumetric and structural connectivity abnormalities relative to healthy controls. How these abnormalities inter-relate and their mechanisms are unclear. We computed grey matter volumetric changes and white matter structural connectivity abnormalities in 144 patients with unilateral TLE and 96 healthy controls. Regional volumes were calculated using T1-weighted MRI, while structural connectivity was derived using white matter fibre tractography from diffusion-weighted MRI. For each regional volume and each connection strength, we calculated the effect size between patient and control groups in a group-level analysis. We then applied hierarchical regression to investigate the relationship between volumetric and structural connectivity abnormalities in individuals. Additionally, we quantified whether abnormalities co-localised within individual patients by computing Dice similarity scores. In TLE, white matter connectivity abnormalities were greater when joining two grey matter regions with abnormal volumes. Similarly, grey matter volumetric abnormalities were greater when joined by abnormal white matter connections. The extent of volumetric and connectivity abnormalities related to epilepsy duration, but co-localisation did not. Co-localisation was primarily driven by neighbouring abnormalities in the ipsilateral hemisphere. Overall, volumetric and structural connectivity abnormalities were related in TLE. Our results suggest that shared mechanisms may underlie changes in both volume and connectivity alterations in patients with TLE.