Abstracts

Rationale:
Intracranial EEG is widely used for localization in patients with drug resistant focal epilepsy, but imprecise electrode placement impairs the utility of this practice. This is due to the limited sensitivity of each electrode, which captures activity from only a small volume of the brain, resulting in ""tunnel vision"". Due to the limited recording volume of intracranial electrodes, the question whether epileptiform activity seen in these electrodes reflects onset or propagation often remains unanswered. Scalp EEG, on the other hand, records from greater areas of the brain but is biased by brain currents closer to head surface compared to deep currents, and a low spatial resolution. It has been shown that spike-locked averaging (SLA) from intracranial electrodes may eliminate noise and expose the contribution of these intracranially-identified currents to scalp EEG. We attempted to unmask the scope of contribution of intracranial interictal epileptiform activity to scalp EEG, and use it to delineate the scalp field of interictal epileptiform activity, which may have a primary source other than that identified using stereo-EEG (SEEG).
Method:
EEG data from two patients with drug resistant epilepsy who underwent concurrent intracranial monitoring with depth electrodes and 21 scalp electrodes in the 10-20 locations were analyzed. For each patient, 50 interictal sharp waves recorded using the depth electrodes and belonging to the same cluster according to their distribution, were manually annotated. Intracranial SLA of the intracranial and scalp EEG in all recorded electrodes was performed, obtaining a 3-second timeframe flanking the spike. The averaged intracranial and scalp signal was inspected for novel and significant alterations in the scalp signal, and the electric field distribution was described.
Results:
In both patients, while pre-averaging scalp electrodes showed no discernible epileptiform activity, intracranial SLA revealed a clear sharp and slow wave on scalp EEG. In patient 1 a population of spikes involving the posterior frontal operculum and posterior insula were seen intracranially. SLA resulted in a perceptible spike on the scalp EEG, spanning the ipsilateral fronto/centro/parietal regions and a bilateral diffuse slow wave. In patient 2, SLA of a population of intracranial spikes with possibly left posterior subtemporal neocortical onset propagating to the left hippocampus resulted in an ipsilaterally distributed sharp and slow wave on scalp EEG.
Conclusion:
Scalp and depth electrode SLA may aid in epileptic networks lateralization and localization by reforming the hypotheses used in positioning depth electrodes. In the future, adding frequency domain analysis rather than averaging the synchronized spike may help overcome imprecise spike synchronization which may result from the variability in spikes within a single spike population. Combining data from several spike populations belonging to a single patient may also be of value in mapping the epileptic network. Finally, we plan to implement the SEEG-triggered SLA scalp spikes in source localization algorithms.
Funding:
:No funding was received.