| Project/Area Number |
13670640
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
IKEDA Akio Kyoto University, Graduate School of Medicine, Lecturer, 医学研究科, 講師 (90212761)
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| Co-Investigator(Kenkyū-buntansha) |
NAGAMINE Takashi Kyoto University, Graduate School of Medicine, Associate Professor, 医学研究科, 助教授 (10231490)
MIYAMOTO Susumu Kyoto University, Graduate School of Medicine, Associate Professor, 医学研究科, 助教授 (70239440)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2002: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2001: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Epileptic excitation / Epileptic inhibition / Supplementary motor area / Transcraial magnetic stimulation / Epileptic seizures / transcorical associaion / 脱力発作 / 経頭蓋的磁気刺激刺激法 / 皮質電気刺激法 |
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| Research Abstract |
Epileptic inhibitory process causes so-called atonic seizures, and inhibitory mechanism within the normal cortices may be responsible for seizure inhibition. We investigated the pathomechanism of the two phenomena
(1) Atonic seizures in patients with partial epilepsy were investigated by means of prolonged video/EEG monitoring, MRI and FDG-PET. Rostral, non-primary motor area and perirolandic areas were responsible for developing atonic seizures in patients with partial epilepsy. As opposed to atonic seizures in generalized epilepsy in which a sudden atonia leads to the falling and significant trauma, atonic seizures in partial epilepsy developed not so suddenly and thus less severe trauma was caused. This difference could reflect the cortical involvement responsible for atonia in the cortical level. (2) Inhibitory effects on the epileptic foci by electrical or magnetic cortical stimulation: In order to clarify the degree of inhibitory effects and the mechanism on the epileptic foci by
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magnetic or electrical cortical stimulation, we first employed low-frequency (0.9Hz) electric stimulation through a pair of subdural electrodes in patients with intractable partial epilepsy who had chronic subdural implantation before epilepsy surgery. As the results, significantly interictal epileptiform discharges decreased when epileptic focus was stimulated. When epileptic foci were stimulated by means of high frequency elctric currents as done for usual cortical mapping, interictal epileptiform discharged also decreased and background power of ECoG also significantly decreased mainly between 20 to 40Hz selectively at the stimulated cortical area. It may reflect the augmentation of the intrinsic inhibitory mechanism. We also employed low-frequency (0.9Hz,15min, 4 times in a week) transcranial magnetic stimulation in patients with intractable neocortical epilepsy. As the results, habitual seizures decreased in the following 2 weeks after stimulation by 44%. Both epileptic and magnetic cortical stimulation can suppress inhibitory activity at least partly by means of common physiological mechanism Less
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