Abstracts

Exit Patterns in Subdural EEG, A Potential Pitfall

Abstract number : 1.116
Submission category : 3. Clinical Neurophysiology
Year : 2011
Submission ID : 14530
Source : www.aesnet.org
Presentation date : 12/2/2011 12:00:00 AM
Published date : Oct 4, 2011, 07:57 AM

Authors :
N. K. So, A. Alexopoulos, D. Nair, J. Bulacio, I. Najm, J. Gonzalez-Martinez, W. Bingaman

Rationale: Rationale: Intracranial subdural electrode investigation has been a proven and valuable technique for the localization of the epileptogenic zone. However at our center, this goal was not achieved in 15% of patients and resective surgery could not be performed. We would like to highlight the appearance of subdural exit patterns at electroencephalography (EEG) onset as a potential cause of false non-localization in extratemporal neocortical epilepsy, due to propagation of ictal activity from a deep source to the cortical surface.Methods: Methods: retrospective review and identification of patients with extratemporal epilepsy investigated by intracranial EEG recordings at the Cleveland Clinic from 2006 to the present and who had (a) an exit pattern at EEG onset on subdural EEG defined as the simultaneous onset of ictal activity at 2 or more non-contiguous sites in one or more lobes, and (b) surgical resection primarily outside the areas marked by exit patterns, (c) seizure-free after a cortical resection. Results: Results: Six patients were identified who became seizure free for a minimum follow-up period of 6 months (range 6 to 44 months) despite appearance of exit patterns on subdural EEG (Table). Surgical localization was possible because: (i) simultaneous placement of depth electrodes revealed a deeper site of ictal onset, 2 patients; (ii) subsequent repeat intracranial stereotactic-depth EEG investigation gave localization of the ictal onset zone, 2 patients; (iii) Magnetic Resonance Imaging (MRI) visualization of a structural abnormality deep to the cortical surface showing the exit patterns , 2 patients. In common to all six patients, the epileptogenic zone resected was deep to the cortical surface: in a sulcus, or in the opercular-insular, or deep mesial interhemispheric cortex. The pathology was malformation of cortical development in 5 of 6 patients in which pathological examination was obtained. Conclusions: Conclusions: Exit patterns on subdural EEG can be a cause of false non-localization. They reflect rapid cortical surface propagation from a deeper ictal onset zone. When a deeper cortical focus is suspected in neocortical epilepsy, it is essential to supplement subdural with depth EEG sampling when planning intracranial EEG evaluation, or consider stereotactic-depth-EEG
Neurophysiology