| Project/Area Number |
09670789
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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 |
Pediatrics
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| Research Institution | Toyama Medical and Pharmaceutical University |
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Principal Investigator |
KONISHI Tohru Toyama Medical and Pharmaceutical University, Pediatrics, Associate Prof., 医学部, 助教授 (30115167)
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| Co-Investigator(Kenkyū-buntansha) |
YAGI Shinichi Toyama Medical and Pharmaceutical University, Pediatrics, Assistant Professor, 医学部, 助手 (30182299)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | childhood / epilepsy / higher brain dysfunction / cognitive function / maturation / electroencephalography / power spectrum / event-related potential / 年齢発達 / Epilepsy / Electroencephalography / Power spectrum / Event-related potential / Cognitive bunction |
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| Research Abstract |
The onset and clinical course of childhood epilepsy generally showed age-dependency, so may be related to the CNS maturation. Contrary, disadvantage factors associated with epilepsy may affect to the CNS maturation, In this study, we studied the higer bain dysfunction in children with epilepsy using electrophysiological methods : 1) power-spectral analysis of BEG background activity for an indicator of whole brain neuronal activity, and 2) event-related potential (P300) for an indicator of cognitive function.
The longitudinal evaluation was done in 150 children with epilepsy, being compared with those in 50 normal children. Results were as follows : 1) Significant slowing of background activity and prolongation of P300 latency were widely observed in children with epilepsy. 2) The degree and age- change of these abnormalities were quite different between each epileptic syndrome. it indicates that the higher brain dysfunction mainly depended on epileptogenesis itself. 3) The dysfunction was more prominent during active phase of epilepsy, and became to be lesser after seizure control. 4) The direct effect of seizure occurrence was a littel, but the dysfunction tended to be related to the long-term seizure prognosis. 5) The effect of anticonvulsant therapy was transient at early phase of therapy, but being a little during chronic medication.
Our results suggest that some minimaI higher brain dysfunction generally combined in children with epilepsy, even if being no distinct retardation. These dysfunction may be originated from epileptogenesis itself. Preventive education or habitation programs from ealy phase of therapy is necessary for comprehensive therapy of epilepsy.
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