Abstracts

Rationale: High-frequency oscillations (HFOs) can be recorded in epileptic patients using intracranial EEG recordings. HFOs have been correlated to the seizure onset zone and are thought to represent epileptogenic tissue. They are usually detected at the beginning of seizure and during slow-wave-sleep. Although they co-occur with epileptic spikes, not all spikes generate HFOs and not all HFOs show simultaneous spikes. To improve our understanding of the underlying pathophysiology, we studied whether HFOs are influenced by antiepileptic medication levels and by the occurrence of seizures. Methods: Forty-two adult patients with intractable focal epilepsy were studied with intracerebral depth EEG between 2004 and 2007. EEG was sampled at 2000Hz after filtering at 500Hz, and only patients with five or more artifact-free nights were selected. From each night, one minute of slow-wave-sleep was selected and ripples (80-250 Hz), fast ripples (250-500 Hz) and spikes were identified on all artifact-free channels. The rates of ripples, fast ripples and spikes, and of HFOs without co-occurring spikes, corrected for the number of recorded channels, were compared before and after seizures with stable dose of medication and during a decrease of medication but while there were no intervening seizures (paired t-test). Results: Twelve patients (seven with temporal lobe epilepsy) were included with five to eight artifact-free nights of recording. In ten patients we could compare the pre- and post-ictal epileptiform activity while medication was stable: there was a significant increase in rate of spikes after seizures, while there was no change in HFO rates (2-tailed t-test, p<0.05). In six patients, comparison of epileptiform activity before and after decreased medication, but without intervening seizures, showed no difference in spike rates, but a significant increase in ripples and of both ripples and fast ripples without co-occurring spikes (2-tailed t-test, p<0.05). Figures 1 and 2 show rates of ripples and fast ripples during medication withdrawal, while no seizure had occurred yet. Conclusions: We confirmed earlier reports that spikes increase after seizures and do not increase after medication withdrawal in the absence of intervening seizures. HFOs respond differently to seizures and antiepileptic medication compared to spikes. While HFOs show no rate increase after seizures, they increase after medication reduction. This implies that spikes and HFOs have different underlying pathophysiological mechanisms, HFOs behaving more like seizures when antiepileptic drugs are decreased.