Abstracts

Rationale: Non-lesional epilepsy cases provide diagnostic and therapeutic challenges in epilepsy surgical planning and extent of electrode placement. Scalp EEG recording is the most common initial source of localization of epilepsy. Seizure onset EEG patterns and correlating interictal epileptiform discharges (IED) in intracranial EEG have been linked with epileptogenic mechanisms in temporal lobe epilepsy but correlating pathology has not extensively been reviewed. We present our experience of reviewing IEDs on scalp EEG and correlating intracranial subdural and depth electrode monitoring to determine underlying pathology. Methods: We reviewed 10 patients with intractable focal epilepsy who underwent scalp EEG and intracranial subdural/depth electrode placement and resection. IEDs were blindly reviewed on scalp and then intracranial EEG and categorized by morphology, amplitude and propagation patterns. Surgical pathology and seizure outcomes were then collected after EEG was reviewed and descriptive analysis was performed. Results: Ten patients with focal epilepsy were subdivided into categories based on interictal characteristics. Two patients had asynchronous bilateral hemisphere IEDs with high frequency, high amplitude sinusoidal waves preceded or followed by slow waves and they had either malformation of cortical development. One patient had high frequency sinusoidal waves with focal onset that may also spread to the contralateral side without attached slow wave. This same patient also had 2-3 Hz delta slow waves or repetitive irregular spike and slow-wave discharges. This patient had periventricular heterotopias. Four patients had single spike and slow wave complex IEDs regionalized to the temporal chains with/without ipsilateral propagation. This pattern was associated with mesial temporal sclerosis, though when associated with propagation also tended to have neocortical temporal gliosis. Three patients had irregular 2-3 Hz spike-sharp-slow waves with broad field on the ipsilateral and contralateral hemisphere and also may have had mixed slow waves for 1-2 seconds and had neocortical temporal gliosis on pathology. Conclusions: Our findings are significant for showing that IED patterns on scalp EEG may correlate with pathology of epileptogenic tissue. Careful review of these patterns recorded before the seizure onset suggesting pathology may help with seizure localization and intracranial electrode placement as well as prognosis for seizure freedom for those undergoing surgical resection. Further large-volume prospective studies are needed. Funding: No funding