Abstract

Background: The resting-state networks (RSNs) are sets of biological neuronal ensembles, demonstrating a synchronized low frequency BOLD (Blood Oxygenation Level Dependent) signal fluctuations (<0.08−0.1Hz). The Default Mode Network (DMN) is a RSN that is active when an individual is not focused on the outside world and the brain is at wakeful rest. It has been shown that DMN is involved in emotional processing and may play a significant role in the origin of affective symptoms. Affective symptoms (depression and anxiety) are common in temporal lobe epilepsy and DMN functional connectivity (FC) have been found to be altered in patients with this pathology. Aim: To investigate FC in TLE patients with and without comorbid anxiety-depressive symptoms. Materials and Methods: 28 patients with TLE, confirmed by EEG, aged between 18 and 50, without any significant brain alterations and history of other psychiatric disorders were included in this study. Affective symptoms were assessed during comprehensive psychiatric interview. Beck Depression Inventory, Hospital Anxiety Depressive Scale, Hamilton Anxiety Scale and Montgomery-Asberg Depressive Rating Scale were additionally used to quantify symptom severity. All subjects underwent routine MRI procedure and 9-min resting-state fMRI scanning session, during which they were asked to keep their eyes closed. The images were processed and analyzed using SPM8 and ‘GIFT’ toolbox. Independent component analysis was used to isolate DMN. The resulted maps were compared in groups using one-way ANOVA with post-hoc pairwise comparisons. The results were considered as statistically significant according to threshold of p< 0.005 with a 10-voxel cluster size [1]. Results: All patients were divided into three groups: patients with current affective symptoms and left-sided epileptic focus (left-sided ‘affective’ group (LSAG), n = 18), patients with current affective symptoms and right-sided focus (right-sided ‘affective’ group (RSAG), n = 18), and patients without affective symptoms (‘non-affective’ group (NAG), n = 18). In both groups with affective symptoms, a moderate level of depressive and anxiety symptoms was found, with higher ‘anxiety’ score in LSAG and higher ‘depressive’ score and ‘dysphoric’ symptoms in RSAG. ANOVA revealed significant group differences in the left insula, superior parietal and left frontal cortex. Post-hoc analysis identified increased FC in the right precuneus, parahippocampal and frontal cortex in RSAG compared to NAG. Higher FC in LSAG group demonstrated higher FC in the left insular and parietal cortex compared to RSAG. Conclusions: Increased insular and frontal FC, observed in LSAG, may determine more severe anxiety symptoms in this group. The results are consistent with the data from recent studies, indicating higher anxiety level in patients with left-sided epileptic focus localization. Increased FC in the right precuneus, parahippocampal and frontal area in RSAG may explain the presence of depressive symptoms in this groups and their association with impaired self-control and self-awareness. To finalize, TLE can be considered as a good model to investigate mechanisms underlying anxiety and depression not only in epilepsy, but also in many other neurological and psychiatric disorders.

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