Abstracts

Rationale: Motor seizures can be pharmaco-resistant but resective surgery, although possible, is usually not offer as a therapeutic option because of the motor deficit that occur postoperatively and in these cases alternative therapy is required. Deep brain stimulation is supposed to be a promising therapy but requires better understanding of the physiology of new target such as basal ganglia (BG). Although BG have been proposed to be involved in the propagation and the control of seizure, the electrophysiological mechanisms underlying the control of seizure have not been yet elucidated. Here we aimed at determining the effect of neocortical seizures on BG structures involved in the motor loop. To address this issue, we used a monkey model of penicillin-induced cortical motor epilepsy. Extra cellular activities (ECA) and local field potential (LFP) of the putamen, subthalamic nucleus (STN), external and internal part of the globus palllidus (GPe and GPi) were all recorded simultaneously with EEG. Methods: Two monkeys were equipped with a recording chamber, epidural screw for EEG recording and a cannula inserted in the motor cortex. Awake monkeys were placed on a restrain chair and motor seizures were induced using single injection of 10-40 μl of Penicillin G injected through the cannula in the motor cortex. Electro-clinical motor seizures arose every 1-2minutes and usually lasted 20seconds. Results: During the ictal period, ECA of BG structures were characterised by: 1) an increase of the firing rate (FR) in all nuclei exception of the GPi; 2) the appearance of an oscillatory firing mode in STN and GPi and 3) an increase of the oscillatory frequency in all structures. Furthermore, the frequency oscillation of the putamen and GPi were lower and higher respectively compared to the FR of spikes EEG. Using time frequency analyses of the LFP, obtained during ictal period, we showed an increase of the power of oscillations in the delta and beta band in all the structures. The coherence analysis between EEG and STN, GPE activities, showed a strong relationship during all the duration of the seizure in the delta and beta band. In the putamen, the coherence in the delta band appeared at the onset of the seizure while in the beta band, the coherence was significant only in the middle of the seizure. In GPi, the coherence in the delta and beta band appeared just at the end of the seizure. Conclusions: We conclude that these major modifications constitute an evidence of BG reorganization during focal motor seizure. The fact that oscillatory frequency in the putamen and Gpi differ with the cortical EEG frequency and that the coherence between GPi, the Putamen and the cortex appears only at the end of the seizure (especially for Gpi, while it appears at the onset of the seizure for the STN and GPe) might create an imbalance between the direct and the indirect BG pathway at the onset of seizure, facilitating its propagation. Whether the modulation of BG will restore a balance between the 2 systems, leading to a cessation of the seizure, is still a scientific and therapeutical challenge.