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Characteristics of EEG Seizure-Onset Patterns Recorded From Subdural Electrodes Over MRI-Visible Frontal Focal Cortical Dysplasia Type IIb Lesions

Hirozawa, Daisuke*,†; Terada, Kiyohito*; Matsuda, Kazumi*; Usui, Keiko*; Usui, Naotaka*; Tottori, Takayasu*; Kondo, Akihiko*; Araki, Yasukiyo*; Omote, Yoshio*; Kashida, Yumi*; Mochizuki, Hideki; Inoue, Yushi*

Journal of Clinical Neurophysiology: September 2017 - Volume 34 - Issue 5 - p 427–433
doi: 10.1097/WNP.0000000000000384
Original Research

Purpose: Focal cortical dysplasia (FCD) is intrinsically epileptogenic, and an MRI-visible lesion typically constitutes the core part of the epileptogenic zone. We aimed to identify ictal EEG patterns that represent the epileptogenic zone by using subdural electrodes placed over the MRI-visible FCD lesion.

Methods: We selected seven patients with frontal lobe epilepsy caused by pathologically proven FCD type IIb who underwent preoperative intracranial EEG evaluation with subdural electrodes followed by resection surgery with seizure-free outcome. The characteristics of ictal EEG patterns, interictal/ictal high-frequency oscillations, and ictal direct current shifts from intracranial electrodes placed over the MRI-visible lesion were analyzed.

Results: Two seizure-onset patterns (low voltage fast activity and fast spike activity) were identified. Low voltage fast activity was seen in all patients with a lateral frontal lesion, and it was always preceded by preictal spikes. Fast spike activity occurred only in patients with a mesial frontal lesion. Interictal/ictal high-frequency oscillations and ictal direct current shifts were seen in all patients.

Conclusions: The epileptogenic zone of frontal FCD type IIb may be characterized by EEG seizure-onset patterns consisting of low voltage fast activity and fast spike activity accompanied by ictal high-frequency oscillations and ictal direct current shifts. Further study is needed to determine whether other seizure-onset patterns exist in patients with FCD type IIb.

*National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, Shizuoka, Japan; and

Department of Neurology, Osaka University, Osaka, Japan.

Address correspondence and reprint requests to Kiyohito Terada, MD, PhD, National Epilepsy Center, Shizuoka Institute of Epilepsy and Neurological Disorders, Urushiyama 886, Aoi-ku, Shizuoka 420-8688, Japan; e-mail: kyht-terada@umin.net.

The authors have no funding or conflicts of interest to disclose.

© 2017 by the American Clinical Neurophysiology Society