16. fMRI and eeg studies of the role of basal ganglia in epilepsy

Abstract

(1) In the fMRI study the impact of epilepsy on the functional brain connectivity (FC) of the BG in two large-scale networks, the default mode network (DMN) and somatomotor network (SMN), was studied in 10 healthy control subjects (HC) and 24 patients with epilepsy. In HC, the BG were functionally negatively correlated with typical DMN regions. This negative correlation as well as the FC between the BG and SMN was significantly lower in patients ( Rektor et al., 2013 ). (2) SEEG studies: The human striatum and pallidum did not generate specific epileptic EEG activity, not even when the seizures were generalized. The visually observed slowing and amplitude increase in the BG was found with the spread of the epileptic activity from the hippocampus to other areas ( Rektor et al., 2002 ). Significant frequency components of 2–10 Hz, with the maximum in the 5–10 Hz range, were constantly observed in the BG ( Rektor et al., 2011 ). The frequency of this component slowed by around 2 Hz during seizures. There was a significant ictal increase of power spectral density in all frequency ranges. The changes in the BG were consistent while the seizure activity spread over the cortex, and they partially persisted after the clinical seizure ended. They were inconsistently present in the first period after the seizure onset. Conclusion Unlike in HC, in TLE the BG are not correlated with a DMN component, and the FC of the BG is decreased with SMN. The epileptic process reduces the FC between the BG and large-scale brain networks. This may reflect an altered function of the BG in epilepsy. Based on our SEEG studies, the time course of the oscillatory activities together with the absence of the epileptiform EEG activities in the BG lead us to suggest an inhibitory role of the BG in temporal lobe seizures. This “filtering effect” of the BG may act as an obstacle to the spread of ictal activity. The BG should be seriously considered as a potential target for neuromodulatory and pharmacological treatment of TLE.