| Project/Area Number |
11670809
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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 | Tokyo Metropolitan Institute for Neuroscience |
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Principal Investigator |
HAYASHI Masaharu Director, Department of Clinical Neuroscience, Tokyo Metropolitan Institute for Neuroscience, 東京都神経科学総合研究所, 副参事研究員 (00280777)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2001: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2000: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1999: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | infantile spasms / Lennox syndrome / brainstem / neurotransmitter / limbic system / progressive myoclonic epilepsy / dentatorubral-pallidoluysian atrophy / severely handicapped / ウエスト症候群 / 大脳皮質形成異常 / ウェスト症候群 / 重障児・者 / 扁桃体 / 滑脳症 / 新生児仮死後遺症 / 側頭葉 / グルタミン酸トランスポーター / カルシウム結合たん白 |
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| Research Abstract |
Previously, we reported the common functional brainstem lesions in the autopsy cases of lissencephaly (LIS) and perinatal hypoxic ischemic encephalopathy (HIE) having both infantile spasms (IS) and Lennox-Gastaut Isyndrome (LGS). To investigate the pathogenesis of IS and LGS, we immunohistochemically examined the expression of neiuotransmitters, neuropeptides, calcium-binding proteins and/or glutamate transporters in the brainstem and limbic system in child autopsy cases. In cases of LIS and HIE suffering from both epileptic syndromes, there were no IS/LGS-specific changes in the expressions of either calcium-binding proteins or glutamate transporters in the brainstem and limbic system. The brainstem showed reduced expressions of neurotransmitters in both the cases of hereditary dentatorubral-pallidoluysian atrophy suffering from another refractory progressive myoclonic epilepsy and the cases of subtle cerebral dysgenesis having IS but not LGS, although the changes were not related to the severity of epileptic seizures. In addition, the amygdaloid lesions in the severely handicapped were clarified to have relationships with the etiology but not either the severity of epileptic seizures or the hippocampal lesions. It is suggested that the brainstem lesions in IS and/or LGS can be involved in the disease progression more than the limbic lesions.
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