Abstracts

Rationale: Memory impairment is one of the most prominent cognitive deficits in temporal lobe epilepsy (TLE). The overall goal of this study was to explore the contribution of cortical and hippocampal (subfield) damage to impairment of auditory immediate recall (AIMrecall), auditory delayed recall (ADMrecall) and auditory delayed recognition (ADMrecog) of the Wechsler Memory Scale-III in TLE with (TLE-MTS) and without hippocampal sclerosis (TLE-no). It was hypothesized that volume loss in CA1 and CA3 and dentate gyrus (CA3&DG) determine memory impairment in TLE-MTS and temporal mesial neocortical thinning in TLE-no. Furthermore, it was assumed that frontal lateral cortical thinning aggravates memory impairment in both groups. Methods: T1 whole brain and T2-weighted high resolution hippocampal MRI and WMS-III were acquired in 22 controls, 14 TLE-MTS and 19 TLE-no. Hippocampal subfield volumes, i.e., entorhinal cortex, subiculum, CA1, CA1-2 transition zone and CA3&DG volumes were determined on the T2 image using a manual parcellation scheme. Freesurfer was used to obtain cortical thickness averages of temporal (fusiform (FUSI), parahippocampal gyrus), frontal (superior, caudal and rostral medial gyrus, pars opercularis (POP), orbitalis and triangularis) and parietal (precuneus, inferior and superior parietal region, supramarginal gyrus) cortical regions of interest (ROI). MANOVA and stepwise regression analysis were used to identify hippocampal subfields and cortical ROI significantly contributing to AIMrecall, ADMrecall and ADMrecog. Results: All three memory scores were significantly lower in TLE-MTS and TLE- no compared to controls but not different between the two TLE groups. In TLE-MTS, AIMrecall (p = 0.0016) was associated with CA3&DG, ADMrecall with CA3&DG (p = 0.002) and POP (p = 0.01) and ADMrecog with CA1 (p = 0.023). In TLE-no CA3&DG (p = 0.019) and FUSI thickness (p = 0.029) were associated with AIMrecall, ADMrecall with FUSI (p = 0.044) and POP (p = 0.041) thickness and ADMrecog with FUSI (p = 0.036). Conclusions: The study provided evidence for a different structural correlate of the verbal memory impairment in TLE-MTS and TLE-no and thus further supports the notion that TLE-no is not just a mild form of TLE-MTS but a different entity of TLE. In TLE-MTS the impairment was associated with neuron loss in the hippocampus. CA3&DG was associated with impaired recall (AIMrecall, ADMrecall) and CA1 with impaired recognition (ADMrecog) suggesting a functional specialization by different hippocampal subfields. In TLE-no memory deficits were associated with CA3&DG and FUSI, i.e., involved a more wide-spread and less well defined hippocampal-mesial-temporal cortical regions. POP thinning, indicating frontal dysfunction, influenced ADMrecall performance in both TLE groups. Despite the different structural correlate, the memory impairment was of similar severity in both groups. This indicates that it is the interruption of the network supporting a specific function and less the anatomical localization of the interruption within the network which determines the memory impairment.