| Project/Area Number |
09470297
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
NISHIO Shunji Kyushu University, Faculty of Medicine, Assistant Professor, 医学部, 講師 (10180580)
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| Co-Investigator(Kenkyū-buntansha) |
FUKUI Masashi Kyushu University, Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (10038713)
MORIOKA Takato Kyushu University, Faculty of Medicine, Assistant Professor, 医学部, 助手 (10260697)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥7,900,000 (Direct Cost: ¥7,900,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1997: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | cerebral cortical dysplasia / neurotrohin / epilepsy / histopathology / neuronal cell tumor |
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| Research Abstract |
Background : With modern neuroimaging modalities, important subtle pathologic changes can now be identified with a high degree of confidence. Among them, focal cortical dysplasia (FCD), is often associated with intractable epilepsy, is now distinguished from other cortical dysplasias because of its distinct clinical and phenotypical features. Materials and Methods : In this study, we performed magenetoencephalography (MEG) and electrocorticography (ECoG) on patients with FCD-associated epilepsy to confirm the "intrinsic" epileptogenecity of FCD. The immunohistochemical expression of Trk receptors, which interact with neurotrophins and results in both growth and maturational changes in neuronal cells, was also investigated on the FCD tissues obtained at surgery. In addition, experimental induction of FCD was tried. Results and Conclusions : (1) On MEG, the clusters of the dipoles generated in paroxysmal activities were located in the FCD lesions themselves. Paroxysmal activities were re
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corded from the ECoG electrodes which were placed over the surface of the FSD lesion. Intraoperative depth recordings with a needle electrode inserted into the FCD lesion revealed paroxysmal foci to be located in the FCD lesion. These findings suggest that FCD lesions to be highly and intrinsically epileptogenic lesions. (2) In FCD lesions, the TrkA expression was localized in large dysplastic sytomegalic neurons, and TrkB expression was observed in large dysplastic and relatively small neuronal cells within the affected cortex. Although the exact roles of neurotrophins and their receptors in the pathogenesis of FCD remain uncertain, its development might be governed by such neurotrophic influences, and thus possibly prevent the death of abnormal neuronal cells. In addition, Trk receptors in FCDs may also a role in establishing in the intrinsic epileptogenecity of FCDs. (3) Intraoperative electrophysiological examinations on cerebral benign neuronal cell tumors with intractable epilepsy, no definite epileptogenic abnormalities were observed at the tumor site, while the epileptogenic zone was identified adjacent to the region of the tumor. A histological examination of the epileptogenic cortex revealed the presence of minute cortical dysplasia. (4) Experimental studies to induce FCD on fetal rats were failed. Less
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