Abstracts

Rationale: Intracranial electroencephalography has been traditionally used to record spontaneous seizures and perform brain mapping in preparation for epilepsy surgery. We present a case where stimulation of intracranial leads triggered a patient's typical clinical seizure, which improved localization of the epileptogenic zone for surgical resection that ultimately resulted to ongoing seizure freedom. Methods: The patient was diagnosed with epilepsy at 5 years of age and underwent left parietal resection at 17 years of age after failing multiple antiepileptic drugs (AED). After a questionable period of seizure freedom, he presented to our clinic at 24 years of age having developed recurrent complex partial seizures with similar features. His typical seizure started with "face flushing" and involved an aura of dizziness and "lifting sensation" followed by right sided blurred vision, confusion, blank staring, inability to speak, hand wringing, and right head tilt lasting less than 3 minutes. The patient was refractory to treatment with 10 attempted AEDs and subsequently underwent a second surgical evaluation. Video EEG recording noted intermittent slowing over the left parietal and temporal regions with frequent spikes at F3-C3-T7 associated with occasional right frontal synchrony. Multiple seizures arose from the left parietotemporal lobe. His brain MRI was unrevealing. Wada testing confirmed left hemisphere language dominance and bitemporal memory function support. Electrocorticography involved coverage of the left lateral parietal, posterior lateral frontal, mesial posterior frontal and mesial parietal lobe, subtemporal, and lateral temporal lobe. Monitoring revealing frequent spikes at inferior interhemispheric (IIH) leads 4-8 overlying the cingulate gyrus, superior interhemispheric (SIH) leads 6-8 overlying the mesial left parietal lobe, grid 12/13 overlying lateral parietal lobe, lateral temporal leads and anterior subtemporal leads. Most seizures had an ictal onset zone at SIH 6-8 with rapid spread to IIH leads 4-8 (skipping the middle interhemispheric strip) and grid 11-13. During brain mapping, stimulation of IIH leads 6-8 triggered symptoms characteristic of the patient's typical clinical seizures including dizziness, face flushing, and confusion. The EEG however exhibited no electrographic correlate, after-discharges, or immediate propagation in any other areas covered by intracranial electrodes. With this knowledge, the patient underwent partial surgical resection of the left lateral and mesial parietal lobe including the cingulate gyrus under IIH leads 6-8 where we had triggered the patient's typical clinical seizure. The final pathology showed cortical dysplasia. Results: The patient has been seizure free since surgery. No significant post-surgical symptoms were noted except for mild short term memory loss which improved to baseline within 4 months. Even more, the patient reported significant improvement in mood. Conclusions: Our case study indicated that the stimulation of intracranial leads can be utilized beyond their current function of brain mapping and recording of spontaneous seizures. By stimulating intracranial leads to elicit patients' typical seizures, we may be able to better localize seizure onset zones and facilitate the identification of involved networks. In our case study, the patient's stereotypic seizure was triggered by stimulation of IIH leads over the left cingulate gyrus allowing for ongoing seizure freedom after resection of this area. Our hypothesis regarding the lack of electrographic correlate was that the seizure propagated from the cingulate gyrus to the mesial temporal lobe, which was presumed very focal and therefore undetectable by sub-temporal strips. Funding: None