| Project/Area Number |
17K17843
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurosurgery
Orthopaedic surgery
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| Research Institution | Nara Medical University (2019-2021)
Osaka University (2017-2018) |
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Principal Investigator |
Mano Tomoo 奈良県立医科大学, 医学部, 准教授 (70778026)
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| Project Period (FY) |
2017-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2019: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2017: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 非侵襲脳刺激 / 神経リハビリテーション / 脳血管障害 / 経頭蓋磁気刺激 / ニューロリハビリテーション / 反復経頭蓋磁気刺激 / 脳卒中 / 脳・神経 / 脳神経疾患 / リハビリテーション / 脳の可塑性 / 非侵襲脳刺激療法 |
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| Outline of Final Research Achievements |
The effect of rTMS on neural activity depends on the frequency of stimulation. High frequencies above 5 Hz enhance neural activity, and low frequencies below 1 Hz suppress it. It is necessary to increase the neural activity of the site that compensates for cerebrovascular diseases. Therefore, we proposed two approaches: (i) applying high-frequency rTMS to the affected primary motor cortex (M1), and (ii) applying inhibitory low-frequency rTMS to non-affected M1. Both the high-frequency group and the low-frequency group had significantly higher motor function in the Rotarod test and swimming distance than in the control group, but there was not signifincant difference between the high-frequency group and the low-frequency group. Application of inhibitory low frequencies weakens interhemispheric inhibition from the stimulated cerebral hemisphere to the functional compensation site. It indirectly activates the functional compensation site by releasing from interhemispheric inhibition.
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| Academic Significance and Societal Importance of the Research Achievements |
脳血管障害は要介護の原因疾患の上位を占めていおり、片麻痺回復への新たなリハビリテーション療法が必要とされている。脳卒中後の機能回復は、神経の可塑的変化により、脳内に新しい神経ネットワークを作ることで、残存した正常組織が働くことで機能回復するとされているが、そのメカニズムは未知である。機能回復促進を科学的方法に基づくニューロリハビリテーションがあるが、その実現化として期待が大きいのが、rTMS療法である。本研究にてrTMS療法の脳内メカニズムの一部を解明することができ、今後の臨床応用の可能性を期待できる。
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