Compensatory circuits in resting-state networks of epilepsy patients with left-sided hippocampus sclerosis.

Left-sided temporal lobe epilepsy (LTLE) causes bihemispheric dysfunctions in large networks and poor cognitive performance. To address possible compensatory mechanism in the resting-state we investigated the functional alteration in LTLE patients with histologically proven sclerosis in the left hippocampal CA1-field compared to healthy controls. Eight drug resistant LTLE-patients and eight sex and age matched healthy controls were included in the study. The patients' hemispherical language and verbal memory function was determined by intracarotid amytal testing. Additional cognitive abilities and depression-like symptoms were collected using standard questionnaires. 7 T-fMRI of the resting-state and graph-theoretical whole-brain analysis including hippocampal subfields enabled sensitive detection of highly specific resting-state modulations without predefinition of regions of interest. Graph-theoretical network parameter were correlated with patients' cognitive performance and depression-like symptoms. Functional connectivity of the hippocampus of LTLE patients was reduced interhemispheric and to the cortex. However, the whole-brain functional connectivity was strengthened, indicating a compensating mechanism for the above mentioned reduced hippocampus connectivity. The network's small-world index did not differ between groups. Graph-theoretical node-parameter were lateralized to the left hemisphere, reflecting interhemispheric neuroplasticity. A network component mediated by the left globus pallidus, the right inferior temporal gyrus and the left anterior corona radiata reinforced the functional connectivity between the impaired hippocampus and the bilateral cortex. The graph-theoretical resilience of the globus pallidus was correlated with improved depression-like symptoms. Therefore, we hypothesize, that the observed compensatory circuit reflects an allostatic adaptation of the brain to balance energy and disease-induced environmental stress rather than to improve cognitive impairments.