中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/1056
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    題名: 前大腦動脈梗塞中風患者，動作關聯皮質電位的改變;Altered Movement-Related Cortical Potentials in Stroke Patients with Anterior Cerebral Artery Territory Infarct
    作者: 黃偉師;Wei-Shih Huang
    貢獻者: 中國醫藥大學：醫學研究所碩士班
    關鍵詞: 動作關聯;皮質電位;中風;前大腦動脈;內側額葉梗塞;MRCP;Stroke;ACA;Medial frontal lobe infarct
    日期: 2006-06-26
    上傳時間: 2009-08-13 14:50:28 (UTC+8)
    摘要: 動作關聯皮質電位(MRCP)由腦電圖(EEG)組成，是一種緩慢負向位移，啟始於意志動作之前的1~1.5 秒。它包含至少三項次組成﹕動作準備電位(Bereitschaftspontial，BP）、負斜波(negative slope，NS’）、及動作電位(motor potential，MP）。一般認為BP的產生是源自內側前額葉皮質，NS’是由雙側感覺運動皮質區所產生，而MP則被視為源自對側中央區。這些MRCP次組成的產生源頭乃依據皮質或頭皮記錄到的波形所作成的推論，然而這些理論性假設應該進一步經由是否改變這些可能源頭的神經活性可以導致MRCP波形的改變來做進一步印證。至少有兩種方法可以檢測此問題。其一是研究這些區域的病變或損傷對MRCP的影響。其二是經由外部的電生理功能性擾動(例如重複式經顱磁刺激術)來調節這些可能的源頭區域，觀察這些干擾如何影響MRCP的型態。在這個研究中，我們是使用第一種的病變研究，利用前大腦動脈梗塞中風病人和正常人在動作準備皮質電位的不同，研究前大腦動脈梗塞中風病人動作開始準備過程是如何受到影響。前大腦動脈梗塞中風是一種較不常見部位的腦血管阻塞型中風。缺血性腦中風造成的大腦內側額葉局部病灶，不僅造成大腦內側額葉區域的功能障礙，同時也干擾了連結到此病變區域構造完整的神經網絡。因此，我們假設，內側額葉缺血性腦中風後，大腦皮質運動神經網絡的失能，造成前大腦動脈梗塞後的區域，動作關聯皮質電位的改變。在此計畫中，進行了七位病人的實驗組及符合年齡配對的七位正常人控制組動作關聯皮質電位的研究。有三項結果可以提出: (1) 病人組某些動作關聯皮質電位的次組成，相對於控制組，皆表現出較為明顯的負波; (2) 病人組兩側腦部，特別是左側腦部，的負斜波相對於控制組，有明顯的增大現象; (3) 病人組腦部的負斜波，在任何一側手腕活動時，皆沒有出現「對側顯著」的現象。我們的結論如下:經由運用動作關聯皮質電位在時間過程上會有顯著變化的優點，我們呈現了左側前大腦動脈灌流區域內側額葉梗塞中風病人在動作發生前及動作執行中，於兩側腦部會出現動作關聯皮質電位作用活性明顯增強的現象。這些結果符合先前的大腦前額葉會媒介動作早期準備過程的概念，而且推測是經由大腦前額葉內側區域的影響。這種影響可藉由本實驗---前大腦動脈灌流區域內側額葉梗塞運動功能缺損後，代償的發生來印証;機轉可能是來自於輔助運動區-前區部分(pre-SMA)，傳送至運動區的抑制性輸入訊息，因病灶而減少，或者是招募病灶周圍興奮性皮質區域而增加代償。

    The movement-related cortical potential (MRCP) is an electroencephalography (EEG) component related to voluntary movement, which is a slow negative shift starting 1-1.5 sec before volitional movement. MRCPs consist of at least 3 subcomponents, the Bereitschaftspontial (BP), the negative slope (NS’), and the motor potential (MP). It is generally agreed that the generator for the BP is from the mesial prefrontal cortex and that for the NS’ can be sufficiently explained by the activation of generators in the sensorimotor cortex bilaterally. The MP can be accounted for by the activation of a source in the contralateral central region. The generating sources of these subcomponents of MRCP were deduced from the scalp or subdural recordings and the hypothesis should be further verified by determining whether functional perturbation of the candidate regions could actually modulate the behavior of MRCP. At least 2 methods may be adopted for this purpose. The first is lesion study of MRCP over the target sites. The second way is to modulate the candidate regions by external electrophysiological functional perturbation (e.g. repetitive transcranial magnetic stimulation, rTMS) to observe how the interference would affect the MRCP conformation. The present research is designed to elucidate the MRCP issue relying on lesion study in stroke patients with anterior cerebral artery (ACA) territory infarct. ACA territory is an uncommon site for occlusive vascular strokes. We hypothesized a deficit in the neuronal motor network after ACA infarct would lead to alterations in the movement related cortical network in the ACA infarct patients. We conduct the study in 7 patients and 7 age matched control. Three main results can be summarized as following: (1) some of the MRCP subcomponents showed a more pronounced negativity in the patient group than could be observed in the control group; (2) the amplitudes of NS’ were especially noted to be increased over the bilateral hemispheres in the patient group on the right hand movement as compared with the controls; (3) loss of lateralization of NS’ was noted in the patient group on the right hand movement, similar trend can also be observed on the left hand movement.
    The results could be due to diminution of pre-SMA (Area F6) inhibitory inputs to the subsequent motor regions or due to the recruitment of the nearby excitatory cortical regions for the compensation of motor impairment of the medial frontal lobe infarct. These results are in line with the idea of prefrontally mediated early preparatory processes prior to the execution of motion and illustrate that medial frontal region are crucial for the modulation or generation of MRCP.
    顯示於類別:[醫學研究所] 博碩士論文

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