| 研究生: |
黃柏憲 Haung, Po-Hsien |
|---|---|
| 論文名稱: |
皮質電刺激技術在腦損傷中的應用 Application of cortical electrical stimulation technology in brain injury |
| 指導教授: |
蔡坤哲
Tsai, Kuen-Jer |
| 學位類別: |
碩士 Master |
| 系所名稱: |
醫學院 - 臨床醫學研究所 Institute of Clinical Medicine |
| 論文出版年: | 2021 |
| 畢業學年度: | 109 |
| 語文別: | 英文 |
| 論文頁數: | 47 |
| 中文關鍵詞: | 缺血性中風 、創傷性腦損傷 、皮質電刺激 |
| 外文關鍵詞: | ischemic stroke, traumatic brain injury, cortical electrical stimulation |
| 相關次數: | 點閱:144 下載:0 |
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大腦是人體最脆弱的器官之一,這和它有限的自我修復能力有很大的關係。因此,罹患神經退化性疾病或是遭受大腦損傷的患者能夠完全康復的機會很低。大腦損傷可能由各種原因造成,包括車禍、運動傷害、槍擊、中風等。大腦損傷發生的七天內屬於病發的急性期,也是治療效果最好的時段,然而大腦的結構和功能牽涉了複雜的細胞、分子以及神經網路,這導致臨床上尚無有效的配套措施。研究出能應用於大腦損傷急性期的治療手段是相當迫切的事情。電刺激是現行被認為具有潛力的治療方法之一,各種型式的電刺激裝置、刺激位點、電流參數和刺激時間都被廣泛的嘗試。在本研究中,我們旨在發掘皮質電刺激在腦傷模型中的應用。首先,我們發現應用於初級軀體感覺皮層的電刺激能減少缺血性中風模型的梗塞體積、改善其神經功能障礙、抑制促發炎細胞的招募以及提高神經元的存活。其中的機制可能涉及到腦源性神經營養因子的分泌增加以及PI3K/AKT的訊號路徑。接著,我們在創傷性腦損傷模型中觀察到針對病灶的連續電刺激不僅減少病灶體積、改善動物的神經功能障礙,還促進sox2陽性的細胞聚集在病灶周圍的皮質。總而言之,我們的研究提供了初級軀體感覺皮層作為新的有效電刺激位點,以及連續性電刺激促進大腦自我修復的可行性。
The brain is one of the most fragile organs of the human body because it has much to do with its limited self-repair ability. Therefore, patients suffering from neurodegenerative diseases or brain injuries have a low chance of complete recovery. Brain injuries can be caused by a variety of reasons, such as car accidents, sports injuries, gunshots, strokes, and so on. Within seven days after the onset of the brain injury, it is the acute stage of the disease and the best treatment period. However, the structure and function of the brain involve complex cells, molecules, and neural networks, which has led to the lack of effective supporting measures in clinical practice. It is very urgent to develop treatments that can be applied to the acute phase of brain injury. Electrical stimulation (ES) is currently considered as one of the potential therapeutic methods. Various types of electrode devices, stimulation sites, current parameters and stimulation time have been widely tried. In this study, we aim to explore the application of cortical electrical stimulation in brain injury models. First, we found that electrical stimulation applied to the primary somatosensory cortex could reduce the infarct volume of the ischemic stroke model, improve its neurological dysfunction, inhibit the recruitment of pro-inflammatory cells, and enhance the survival of neurons. The mechanism may involve the increased secretion of brain-derived neurotrophic factor and the signal pathway of PI3K/AKT. Next, we observed in the traumatic brain injury model that continuous electrical stimulation of the lesion not only reduced the lesion volume and improved the animal's neurological dysfunction, but also promoted the accumulation of sox2-positive cells in the perilesional cortex. All in all, our research suggests that the primary somatosensory cortex as a new effective electrical stimulation site and the feasibility of continuous electrical stimulation to promote the self-repair of the brain.
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