Abstract
ObjectivesThe mechanisms underlying the anterior nucleus of the thalamus (ANT) deep brain stimulation (DBS) for the treatment of drug-resistant epilepsy (DRE) have not been fully explored. The present study aimed to measure the changes in whole-brain activity generated by ANT DBS using interictal electroencephalography (EEG). Materials and methodsInterictal EEG signals were retrospectively collected in 20 DRE patients who underwent ANT DBS surgery. Patients were classified as responders or non-responders depending on their response to ANT DBS treatment. The power spectrum (PS) and Phase Lag Index (PLI) were determined and data analyzed using a paired sample t-test to evaluate activity differences between pre-and-post-treatment on different frequency categories. Student's t-test, Mann-Whitney test (non-parametric test) and Fisher exact test were used to compare groups in terms of clinical variables and EEG metrics. P values < 0.05 were considered statistically significant, and FDR-corrected values were used for multiple testing. ResultsPS analysis revealed that whole-brain spectral power had a significant decrease in the beta (p = 0.005) and gamma (p = 0.037) bands following ANT DBS treatment in responders. The analysis of scalp topographic images of all patients showed that ANT DBS decreases PS in the beta band at the F3, F7 and Cz electrode sites. The findings indicated a decrease in PS in the gamma band at the Fp2, F3, Cz, T3, T5 and Oz electrode sites. After ANT DBS treatment, PLI analysis showed a significant decrease in PLI between Fp1 and T3 in the gamma band in responders. ConclusionThe findings showed that ANT DBS induces a decrease in power in the left frontal lobe, left temporal lobe and midline areas in the beta and gamma bands. Lower whole-brain power in the beta and gamma bands can be used as biomarkers for a favorable therapeutic response to ANT DBS, and decreased synchronization between the left frontal pole and temporal lobe in the gamma band can also be used as a biomarker for effective clinical stimulation to guide postoperative programming.
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