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Interictal Slow and High-Frequency Oscillations

Is it an Epileptic Slow or Red Slow?

Inoue, Takeshi*; Inouchi, Morito; Matsuhashi, Masao‡,§; Matsumoto, Riki*; Hitomi, Takefumi*,∥; Daifu-Kobayashi, Masako*; Kobayashi, Katsuya*; Nakatani, Mitsuyoshi*; Kanazawa, Kyoko*,¶; Shimotake, Akihiro§; Kikuchi, Takayuki#; Yoshida, Kazumichi#; Kunieda, Takeharu**; Miyamoto, Susumu#; Takahashi, Ryosuke*; Ikeda, Akio§

Journal of Clinical Neurophysiology: March 2019 - Volume 36 - Issue 2 - p 166–170
doi: 10.1097/WNP.0000000000000527
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Purpose: We reported the presence of interictal slow and high-frequency oscillations (HFOs) (IIS + HFO) and its temporal change so as to elucidate its clinical usefulness as a surrogate marker of epileptogenic zone in a patient with intractable focal epilepsy.

Methods: We focused on one of the core electrodes of epileptogenicity, and investigated IIS + HFO in the pre- and post-segment of 30 minutes to all the 6 seizures. We adopted interictal slow in duration of 0.33 to 10 seconds, amplitude ≥50 μV and co-occurring with HFOs, and then divided into 5 groups depending on the amplitude of slow wave.

Results: Before and after all the 6 seizures, the number of IIS + HFO was 2,890 at one electrode in the core epileptogenic zone. The number of IIS + HFO significantly decreased for 30 minutes after seizures. Furthermore, the number of IIS + HFO with the amplitude of 200 to 399 μV significantly decreased after seizures.

Conclusions: IIS + HFO with the amplitude of 200 to 399 μV was influenced by and decreased after seizures. It may reflect the core part of epileptogenic area as similarly as ictal direct current shifts and ictal HFOs do. IIS + HFO could be called as the term “red slow,” which may be useful to delineate at least a part of the epileptogenic zone.

*Department of Neurology, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto, Japan;

Department of Respiratory Care and Sleep Control Medicine, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto, Japan;

Human Brain Research Center, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto, Japan;

§Department of Epilepsy, Movement Disorders and Physiology, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto, Japan;

Department of Clinical Laboratory Medicine, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto, Japan;

Department of Neurology, National Center Hospital, National Center of Neurology and Psychiatry, Kodaira-shi, Tokyo, Japan;

#Department of Neurosurgery, Kyoto University Graduate School of Medicine, Sakyo-ku, Kyoto, Japan; and

**Department of Neurosurgery, Ehime University Graduate School of Medicine, Shitsukawa Toon City, Ehime, Japan.

Address correspondence and reprint requests to Akio Ikeda, MD, PhD, FACNS, Department of Epilepsy, Movement Disorders and Physiology, Kyoto University Graduate School of Medicine, 54, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan; e-mail: akio@kuhp.kyoto-u.ac.jp.

Department of Epilepsy, Movement Disorders and Physiology, which A. Ikeda and A. Shimotake are currently affiliated, is an endowment department, supported with a grant from GlaxoSmithKline K.K., Nihon Kohden Co, Otsuka Pharmaceutical Co, and UCB Japan Co, Ltd.

A. Ikeda has received support from the Japan Ministry of Education, Culture, Sports, Science and Technology (MEXT) KAKENHI Grant Number 15H05874 and Japan Society for the Promotion of Science (JSPS) KAKENHI Grant Numbers 26293209, 26462223, 25350691, and 23500484. M. Matsuhashi has received support from MEXT KAKENHI 15H05875 and JSPS KAKENHI 26330175. R. Matsumoto has received support from MEXT KAKENHI 17H05907 and JSPS KAKENHI 26282218. T. Hitomi has received support from MEXT KAKENHI 17K09798. K. Kanazawa has received support from Intramural Research Grant (28-4): Clinical Research for Diagnostic and Therapeutic Innovations in Developmental Disorders for Neurological and Psychiatric Disorders of NCNP. For the remaining authors, none were declared.

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© 2019 by the American Clinical Neurophysiology Society