THE EFFECT OF PATHOLOGICAL SUBSTRATE ON ICTAL EEG IN FOCAL EPILEPSY
Abstract number :
1.096
Submission category :
Year :
2002
Submission ID :
3532
Source :
www.aesnet.org
Presentation date :
12/7/2002 12:00:00 AM
Published date :
Dec 1, 2002, 06:00 AM
Authors :
Silvia B. Neme, Nancy R. Foldvary, George Klem, William Bingaman, Hans O. Luders. Department of Neurology, The Cleveland Clinic Foundation, Cleveland, OH; Department of Neurosurgery, The Cleveland Clinic Foundation, Cleveland, OH
RATIONALE: The purpose of this study is to analyze the effect of pathological substrate on the ictal EEG in patients with medically refractory focal epilepsy.
METHODS: Ictal scalp EEGs from 30 patients with neocortical focal epilepsy due to neoplasm (N=16) or malformation of cortical development (MCD, N=14) who were classified as Engel Class 1 following surgical resection involving one lobe were analyzed. Ictal onset patterns were classified as generalized, lateralized, regional or focal based on previously established criteria (Foldvary et al. Neurology 2001). Ictal EEGs were classified as localized (focal or regional), lateralized or generalized based on the earliest and most precise distribution of ictal activity during the entire event.
RESULTS: 275 seizures were analyzed (88 neoplasm and 187 MCD). Mean number of seizures recorded during VEEG was significantly greater for MCD (13.4) than neoplasm (5.5) groups. Ictal onset patterns (theta, delta, alpha, paroxysmal fast, repetitive spiking, suppression) did not differ significantly between groups. Lateralized ictal onsets were significantly more common in neoplasm (22.7% vs. 2.1%) and regional/focal onsets were more common in MCD (56.3% vs. 13.6%). Ictal EEGs were significantly more likely to be localized (regional/focal) in MCD than neoplasm (67.1% vs. 34.1%).
CONCLUSIONS: Ictal EEG patterns may vary depending upon the underlying pathological substrate. While other factors such as location of the epileptogenic lesion may be operative, these differences may provide insight into the epileptogenicity of lesions seen in patients with refractory epilepsy.