Abstracts

RATIONALE: Forecasting seizure onset on the basis of analysis of running EEG signals is feasible in temporal lobe epilepsy (TLE). However, earlier work by our group (Lopes da Silva FH, et al. Rhytms of the brain: between randomness and determinism. In: Lehnertz K et al., ed. [italic]Chaos in the brain?[/italic] Singapore: World Scientific, 2000:63-76.) has indicated that it might not always be possible to anticipate seizure onset in TLE even when the transition from the interictal to ictal activity proceeds according to the so-called attractor deformation scenario. We investigated whether we could reliably extend the horizon for forecasting seizures by probing for trends in local tissue excitability changes and signal modulation to external inputs in continuously sampled intracranial EEG in TLE.
METHODS: Informed consent was obtained from 4 pharamacoresistant TLE patients who were candidates for epilepsy surgery undergoing video/SEEG seizure monitoring for lateralization of ictal onset. A paired pulse paradigm involving biphasic electrical stimulation and registration from adjacent intracerebral contacts in the pes hippocampi in either temporal lobe was carried out to determine local changes in tissue excitability over time. Patients received 3 paired pulses per minute with interpulse intervals varying between 20 and 500 msec and current intensities between 0.5 and 1 mA for up to 12 hours per recording session. Furthermore 5-sec-long trains of biphasic stimulation having a frequency and intensity related to the interstimulus distance of the paired-pulse paradigm were administered on the same contacts during the same sessions in addition to the paired pulse paradigm in 2 of these patients. Amplitude ratios of the paired-pulse evoked responses and carrier signal modulation by tetanic stimulation were compared for purposes of seizure onset lateralization as well as for attempting to forecast seizure onset.
RESULTS: Correctly lateralizing interictal state paired pulse suppression response in hippocampal signals was obtained in 3 patients but was bilaterally absent in the fourth one. When present pre-ictal loss of paired pulse suppression response reliably coincided with extended periods of time when epileptic seizures did occur. Carrier signal modulation was more affected for signals obtained from the hippocampus of ictal onset than from the one in the other hemisphere in both patients tested with this active probing paradigm.
CONCLUSIONS: Active probing for loss of carrier signal modulation in intracranial EEG signals correctly lateralizes the hippocampus of ictal onset in the interictal period. Measurement by the paired pulse paradigm of changes in local tissue excitability thought to result from failure of local inhibitory factors leading to an ictal event may extend the horizon for reliable seizure forecasting in TLE patients. Reliable forecasting of seizures in such patients will ultimately lead to efficient closed loop counterstimulation paradigms and effective seizure control.
[Supported by: SEIN Scientific Research, Heemstede, The Netherlands. The authors express their gratitude to the patients who consented to participate in this study and to the neurosurgeons of the [italic]Dutch Collaborative Epilepsy Surgery Program[/italic] for implanting the intracranial electrodes used.]