SUMMARY
Objective
To evaluate superficial (superficial-WM) and deep white matter (deep-WM) MRI diffusion tensor imaging (DTI) metrics and identify distinctive patterns of microstructural abnormalities in focal epilepsies of diverse etiology, localization and response to antiseizure medications (ASM).
Methods
We examined DTI data for 113 healthy controls and 113 patients with focal epilepsies: 51 patients with temporal lobe epilepsy and hippocampal sclerosis refractory to ASM (refractory-TLE-HS), 27 with pharmacoresponsive TLE-HS, 15 with temporal lobe focal cortical dysplasia (tFCD), and 20 with frontal lobe focal cortical dysplasia (fFCD). To assess white matter (WM) microstructure, we used a multi-contrast multi-Atlas parcellation of DTI. We evaluated fractional anisotropy (FA), mean diffusivity (MD), radial diffusivity (RD) and axial diffusivity (AD), and assessed within-group differences ipsi and contralateral to the epileptogenic lesion, as well as between-group differences, in regions-of-interest (ROI).
Results
The TLE-HS groups presented more widespread superficial and deep WM diffusion abnormalities than both FCD groups. Concerning superficial-WM, TLE-HS groups showed multilobar ipsi and contralateral abnormalities, with less extensive distribution in pharmacoresponsive patients. Both refractory-TLE-HS and pharmacoresponsive-TLE-HS groups also presented pronounced changes in ipsilateral frontotemporal ROIs (decreased FA and increased MD, RD, and AD). Conversely, FCD patients showed diffusion changes almost exclusively adjacent to epileptogenic areas.
Significance
Our findings add further evidence of widespread abnormalities in WM diffusion metrics in patients with TLE-HS compared to other focal epilepsies. Notably, superficial-WM microstructural damage in patients with FCD is more restricted around the epileptogenic lesion, while TLE-HS groups showed diffuse WM damage with ipsilateral frontotemporal predominance. These findings suggest the potential of superficial-WM analysis for better understanding the biological mechanisms of focal epilepsies, identifying dysfunctional networks, and their relationship with the clinical-pathological phenotype. In addition, lobar superficial-WM abnormalities may aid in the diagnosis of subtle FCDs.
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