Abstracts

Rationale: The anterior thalamic radiations (ATR) are a fiber bundle that course from the mediodorsal and anterior thalamic nuclei to the frontal and cingulate cortices. These thalamocortical fibers play an essential role in seizure spread and, along with the thalamus, may be involved in network pathology that contributes to cortical damage in patients with MTLE. In this study, we aimed to investigate the relative contributions of thalamic volume (TV) and microstructure of the ATR, as measured by fractional anisotropy (FA), to explaining patterns of gray matter cortical thinning (GMT) in patients with left and right MTLE. Methods: Diffusion tensor imaging (DTI) and volumetric MRI were performed in 27 patients with MTLE (15 left; 12 right) who all showed evidence of mesial temporal sclerosis (MTS) on MRI, and 27 age and gender-matched healthy controls. FA of the ATR, cortical thickness, and thalamic and hippocampal volume were calculated for all subjects. Surface-based correlational analysis was used to determine the vertex-wise relationship between volumes or FA of the ATR and GMT. Results: Patients with left and right MTLE both showed significant ipsilateral hippocampal and thalamic volume loss, and the magnitude of ipsilateral volume loss did not differ between left and right MTLE. However, patients with left MTLE showed more widespread cortical thinning relative to patients with right MTLE in both hemispheres. Patients with left MTLE also had lower FA of the ATR bilaterally, whereas patients with right MTLE demonstrated no difference in FA of the ATR compared to controls. In left MTLE, the volume of the thalamus and the FA of the ATR correlated with GMT in bilateral superior frontal areas. Where TV alone was correlated with bilateral supramarginal and ipsilateral middle temporal areas, and FA of ATR alone was correlated with contralateral temporal and precentral regions. In contrast in right MTLE, only the FA of ATR correlated with GMT in ipsilateral frontal regions. Volume and FA were not correlated with clinical-seizure related variables of reported seizure frequency, age of onset, or years of disease duration in either group. Conclusions: Patients with MTLE show pathology within thalamocortical networks, but the pattern of pathology differs between left and right MTLE. These findings may reflect differences in structural connectivity between patients with left and right MTLE that complement previous findings of functional connectivity differences between these groups. Whether or not thalamocortical seizure spread contributes to neocortical atrophy or whether cortical atrophy is the result of an aberrant developmental process or some other disease-related mechanism remains unknown.