Abstracts

Rationale: Investigation of hippocampal subfield atrophy patterns could provide useful information about distinct structural changes within the hippocampus in medial temporal lobe epilepsy with hippocampal sclerosis (HS-MTLE). We aimed to investigate atrophy patterns of hippocampal subfields by using volumetric measurement and vertex-based shape analysis, and their relationships with clinical factors in patients with unilateral HS-MTLE. Methods: High-resolution volumetric MR images were acquired for 24 left HS-MTLE patients, 23 rightHS-MTLE patients, and 41 controls. Automated volumetric measurement of the hippocampal subfields and vertex-based hippocampal shape analysis were performed and compared between the groups (ANCOVA with Bonferroni-corrected p < 0.05 for subfield volumes and familywise error-corrected p < 0.05 for shape analysis). Within-group correlations were performed between clinical variables (disease duration, seizure frequency) and subfield volumes and hippocampal shape changes (partial correlation, p < 0.05). Results: Compared to controls, both left and right HS-MTLE patients had significant volume reductions in ipsilateral CA1, CA2-3, CA4-DG, presubiculum, and subiculum (corrected p < 0.05). Disease duration negatively correlated with volumes of left CA1 (r = −0.508, p = 0.013), presubiculum (r = −0.501, p = 0.015), and subiculum (r = −0.487, p = 0.018) in left HS-MTLE group, and right CA1 (r = −0.566, p = 0.006) in right HS-MTLE group. Inward deformation of ipsilateral CA1 subfield was observed in left and right HS-MTLE patients relative to controls (FWE-corrected p < 0.05). Conclusions: Using automated volumetric analysis, we have shown diffuse atrophy of ipsilateral hippocampal subfields in patients with chronic unilateral HS-MTLE, in good accordance with previously reported pathologic findings. Our findings of ipsilateral CA1 atrophy on shape analysis and a negative correlation between disease duration and ipsilateral CA1 volume further support the notion that CA1 subfield is more vulnerable to neuronal damage associated with longer disease duration in HS-MTLE.