Abstracts

To date, Vagus Nerve Stimulation (VNS) is the only form of chronic, intermittent neuroelectrical stimulation that is FDA approved and has been demonstrated to be safe and efficacious for the treatment of epilepsy in prospective, randomized, controlled trials. Although recent studies have been published hypothesizing how VNS effectively reduces seizure frequency in many medication refractory patients, its exact mechanism of action remains unclear.
Human studies with scalp EEG recordings have shown variable results with respect to VNS related changes in activity. Koo, et al. (2001) demonstrated a decrease in the frequency of interictal scalp recorded discharges up to one year after VNS implantation. However, Hammond, et al. (1992) found no noticeable changes in the EEG background activity in the nine patients they studied, but they did find that VNS can interrupt ongoing ictal EEG activity. Kuba and colleagues (2002) observed a reduction of interictal epileptiform discharges during stimulation periods and interstimulation periods, as compared with baseline in 15 of their patients with VNS.
ECoG studies of VNS are virtually nonexistent. Olejniczak, et al. (2001) found a significant decrease in the occurrence of hippocampal recorded epileptiform activity in one patient with VNS compared to that occurring at baseline.
Our objective is to further study the effects of VNS on interictal epileptiform discharges recorded with intracranial EEG.
Two patients with medication refractory seizures and functioning VNS were admitted to our epilepsy monitoring unit for intracranial EEG monitoring as part of their evaluation for epilepsy surgery. Electrocorticography (ECoG) was recorded with subdural electrodes placed over the most active cortical regions, as determined by prior video-EEG scalp recordings. 12 hours of continuous video-ECoG were recorded, 6 hours prior to turning the VNS ON, and 6 hours after. Two hours of EEG recording were analyzed, one half of this data with the VNS ON and one-half with it OFF. The frequency of manually counted interictal epileptiform spikes (IES) during these two epochs were compared.
In our first patient, the average IES frequencies decreased from 2.5 per second for the VNS OFF period to less than 0.9 per second at the end of the VNS ON period. For the second patient the IES frequencies decreased from 0.7 per second to less than 0.2 per second with VNS treatment. It was also noted that epileptiform activity was more easily detected by means of ECoG than from previous scalp recordings. Further quantitative assessment of VNS ON and VNS OFF ECoG characteristics will be presented to include power spectral and coherence analysis.
1. VNS significantly decreased ECoG spike frequency in our two patients.
3. These results suggest that VNS diminishes the epileptogenic capacity of interictal epileptiform activity.
3. Intracranial EEG recording was more revealing of epileptiform activity than scalp EEG recording.