Abstracts

Rationale: Temporal lobe epilepsy with hippocampal sclerosis is a chronic disease with frequent neuropsychological deficits. It is widely acknowledged that physiological brain function in these patients is jeopardized both by acute epileptic activity and changes in neuronal circuitry. The latter changes have received much recent interest with the advent of diffusion tensor imaging (DTI). Several DTI-studies showed correlations between alterations of white matter connectivity and memory impairment, most notably in cases of left hippocampal sclerosis. However, the precise functional topography of the changes in memory circuitry remains yet to be established. Our study intended to probe common patterns of functional memory activations in left and right hippocampal sclerosis and relate them to the underlying structural connectivity of the affected hippocampus. Methods: We have gathered a large data base on a homogeneous group of patients with unilateral sclerosis, comprising 22 patients with left and 22 patients with right sided lesions and 22 matched control subjects. We recorded DTI sequences with 50 directions and functional MRI (fMRI) of memory function. In short, nameable object stimuli were encoded 24h prior to the recognition session, which was scanned at 3T. Over all subjects, bilateral dorsolateral prefrontal and temporal occipital cortex as well as Broca s area were implicated in delayed object recognition. These cortical hotspots serve as regions of interest in a current second analysis. Here individual hippocampi are segmented and used as seed regions for probabilistic tractography between the hippocampus and the said cortical regions of interest. Results: Second level analysis between groups of patients revealed differential activation of distributed memory landmarks. Patients with right hippocampal sclerosis had enhanced BOLD signal in the left sided memory network, most notably in temporo occipital regions. Patients with left hippocampal sclerosis, on the contrary, showed enhanced activation in the inferior parietal region ipsilateral to the lesion. This area has been implicated in hippocampo parietal networks of episodic memory (Vincent et al., 2006). These data suggest differential remodeling of the cortical memory circuitry, which is more pronounced in left temporal lobe epilepsy. Preliminary analysis of structural connectivity points to a de-afferentation of the lesioned hippocampus from ipsilateral frontal and temporal occipital areas. Conclusions: Patients with left or right hippocampal sclerosis show differential reorganization of memory circuitry which essentially concerns the left hemisphere of patients with left sided lesion, possibly due to de-afferentation of the affected hippocampus. These results improve our insight into the interaction of epileptic and cognitive networks and help to establish a blueprint of individual functional and structural memory topography in hippocampal sclerosis.