MRI analysis in temporal lobe epilepsy: Cortical thinning and white matter disruptions are related to side of seizure onset

Abstract

Summary Purpose Past studies reported more widespread structural brain abnormalities in patients with left compared to right temporal lobe epilepsy (TLE), but the profile of these differences remain unknown. This study investigated the relationship between cortical thinning, white matter compromise, epilepsy variables, and the side of seizure onset, in patients with TLE. Methods We performed diffusion tensor imaging tractography and cortical thickness analyses of 18 patients with left TLE (LTLE), 18 patients with right TLE (RTLE), and 36 controls. We investigated the relationship between brain structural abnormalities, side of seizure onset, age of seizure onset, and disease duration. Key findings TLE groups displayed cortical thinning and white matter compromise, predominately on the side ipsilateral to the seizure onset. Relative to RTLE, patients with LTLE showed more widespread abnormalities, particularly in white matter fiber tracts. Greater compromise in white matter integrity was associated with earlier age of seizure onset, while cortical thinning was marginally associated with disease duration. Significance These data support previous findings of LTLE showing greater structural compromise than RTLE, and suggest that mechanisms may not be uniform for gray and white matter compromise in patients with LTLE and RTLE. These results may indicate that LTLE is different than RTLE, possibly due to greater vulnerability of the left hemisphere to early injury and the progressive effects of seizures.

Machine learning classification of mesial temporal sclerosis in epilepsy patients

“…2). Similar to previous studies on cortical thickness, the distribution of effects was relatively broad but had a predominance of effects in nearby frontal, temporal and limbic regions (Lin et al, 2007;Bernhardt et al, 2010;Kemmotsu et al, 2011). Additionally, measures of curvature and folding were found to be abnormal in ipsilateral temporal and frontal cortices, concordant with prior work (Voets et al, 2011;Alhusaini et al, 2012).…”

“…findings of more widespread alterations in cortical morphology that extend beyond the hippocampus are consistent with TLE's comorbid deficits in executive, intellectual and language functioning (Oyegbile et al, 2004). More recently, using methods that reconstruct the cortical surface to more precisely measure gray matter structure, researchers found up to 30% reductions in cortical thickness bilaterally in multiple frontal, temporal and occipital regions in TLE patients with MTS compared to controls (Lin et al, 2007;Bernhardt et al, 2010;Kemmotsu et al, 2011). These findings are present in TLE patients with and without MTS but have been shown to be stronger in patients with MTS (Labate et al, 2011).…”

Functional Connectivity of the Hippocampus in Temporal Lobe Epilepsy: Feasibility of a Task-Regressed Seed-Based Approach

“…Pereira et al (2010) reported decreased FC in hippocampal networks in patients with unilateral mesial TLE (mTLE) comorbid with ipsilateral hippocampal sclerosis (HS), and noted a more pronounced ipsilateral decrease in those with left mTLE compared to right. These findings parallel recent MRI studies that indicate greater gray and white matter atrophy in patients with left compared to right TLE (Kemmotsu et al, 2011;Kucukboyaci et al, 2011). However, other studies have shown reductions in hippocampal FC ipsilateral to right hippocampal seed (Morgan et al, 2011) that differentiate right versus left TLE patients.…”

A meta-analysis on progressive atrophy in intractable temporal lobe epilepsy

“…Although the remaining studies addressed aging, no consistent method was chosen: 3 reported no significant effects of age on morphometric measures in controls, 15,32,48 3 found no effect of age or no effect of age at epilepsy onset in patients, 19,29,53 2 corrected for age at onset, 18,28 5 corrected for age in patients, 17,26,47,49,54 4 utilized MRI measures adjusted for age 13,31,39,46 (based on regression models derived from controls), 1 calculated epilepsy duration/age ratios, 23 2 statistically compared chronological age effects between patients and controls. 41,45 Among the longitudinal studies, 3 were singlecohort studies of patients without controls (interscan interval ranging from 2.3 to 3.4 years 27,41,44 ). One study followed a multicohort design with a median interscan interval of 3.3 years, but without statistically comparing patients to controls.…”