Abstracts

Rationale: Deep brain stimulation (DBS) has been used in an increasing frequency in the treatment of refractory epilepsy in men. On the other hand, the ideal parameters for stimulation and the actual mechanism of action of DBS are poorly understood. Both low and high frequency stimulation could be applied intra- and postoperative but their acute and chronic effects are not adequately known. We study the acute effects of low and high frequency DBS in normal rats.Methods: Four adult Wistar rats were implanted with both stimulation and recording electrodos. Six screw skull electrodes were used: 4 for electrocorticography (2 on each side) and 2 as references. The hippocampal formation was targeted bilaterally with one monopolar electrode (recording) and 1 bipolar electrode (stimulation). Stimulation was carried out using a Kinetra (Medtronic) pulse generator. Mean intensity was 1.5V, pulse width was 300usec and frequency was 6Hz (for low frequency stimulation) or 130Hz (high frequency stimulation). Results: Unilateral hippocampal low frequency stimulation disclosed time-locked recruiting responses over the contralateral hippocampus at very low voltages (< 0.5V). It also triggered time-locked recruiting responses initially seen over the ipsilateral cortex (1V) and also over the contralateral one after stimulation voltage was increased (1.5V). No visually detectable EEG modification was noted after high frequency stimulation with 1.5V. No behavioral modification was noted during low or high frequency DBS.Conclusions: Time-locked recruiting responses have also been recorded intra-operatively during hippocampal DBS electrode insertion in man. Contrary to humans, activation of the contralateral hippocampus is easily obtained after unilateral hippocampal stimulation. This might be related to the large thickness of the hippocampal commissure in the rat, compared to that in humans. High frequency DBS yielded similar results as those in man. Adequate DBS animal models might help to understand its mechanisms of action.