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研究生:陳香君
研究生(外文):Shiang-Jiun Chen
論文名稱:以神經電生理學探討黑質紋狀體多巴胺徑路功能不全時感覺運動系統之運作
論文名稱(外文):Neuroelectrophysiological Evaluation of the Sensorimotor System in Dopaminergic Nigrostriatal Dysfunction
指導教授:陳 贊 如陳 順 勝
指導教授(外文):Tsan-Ju ChenShun-Sheng Chen
學位類別:碩士
校院名稱:高雄醫學大學
系所名稱:醫學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2001
畢業學年度:89
語文別:中文
論文頁數:73
中文關鍵詞:體感覺誘發電位運動誘發電位神經電生理學巴金森氏病
外文關鍵詞:somatosensory evoked potentials (SEPs)motor evoked potentials (MEPs)NeuroelectrophysiologicalParkinson's disease (PD)
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中文摘要
黑質內的多巴胺神經元變性導致紋狀體多巴胺缺乏是造成巴金森氏病的主要原因,而巴金森氏病的運動障礙問題和患者無法產生適當的運動命令以及建立動作執行前的促進作用有關。以往的研究已顯示傳入的感覺訊息會被用來啟動、控制、或偵測正在進行中的動作,因此巴金森氏病患者的運動障礙可能部分是導因於黑質紋狀體多巴胺徑路缺損所造成的感覺運動統合功能改變。就此觀點而言,學者建議誘發電位的記錄可能會在患者與正常人之間顯現出差異。本論文的目的即是以非侵犯性的神經電氣生理學方法評估單側巴金森氏病患者的感覺運動統合功能,將採用體感覺誘發電位(SEPs)及運動誘發電位(MEPs)進行檢測。SEPs是指在週邊神經給予電刺激以誘發軀體感覺徑路之傳導;而MEPs則是在運動皮質給予經顱磁刺激後誘發出來的一個短潛時肌肉反應,代表皮質脊髓徑路的傳導情形。當在被記錄的骨骼肌持續收縮的狀態下給予經顱磁刺激,結果會在MEP反應後緊跟著出現一段肌電圖活動停止的期間,稱之為靜止期(SP),此期與脊髓和皮質內的抑制性機轉有關。在本論文中,選取二十二名偏單側巴金森氏病患者進行研究,同時募集四十二名健康志願者以便與患者進行比較,同時,在患者本身的健患側之間、以及服藥期(ON期)和停藥期(OFF期)之間亦將進行統計分析。
結果顯示,刺激患者正中神經後記錄到的SEPs各波潛時均正常,顯示患者的軀體感覺徑路傳導未受到影響。不過患者在ON期時,健側N30波的波振幅會顯著增加。由於N30波的主要發生區被認為是在附加運動皮質區(SMA),因此N30波可作為是檢視由基底核、前運動區及SMA等所構成的皮質-皮質下-皮質迴路功能的一個指標。患者的健側N30波在服藥情況下變大顯示L-dopa會促進支配健側的SMA的反應。相反地,患側N30波的波振幅不受藥物影響,顯示患側可能因SMA-基底核-視丘神經迴路功能缺損造成對多巴胺治療沒有反應。
至於MEPs方面,患者健患側的磁刺激閾值並無不同,但健康志願者在慣用側則比非慣用側有較高的閾值。波潛時方面,患者與健康志願者間並無差異,顯示這些患者的錐體運動徑路傳導為正常,但MEP的波振幅則在患者顯著較大,顯示患者的皮質興奮性較高。此外,患者在OFF期時,患側在100%閾值刺激下的靜止期會縮短,此現象與前述患者有較高的皮質興奮性相呼應,兩者可能同樣導因於皮質抑制性的降低。ON期時,患側縮短的靜止期又會回復到接近正常。
總之,本論文結果顯示黑質紋狀體多巴胺徑路功能不全時會影響到感覺運動的統合,而N30波和靜止期的變化可作為評估此統合功能的有效指標。

Abstract
Depletion of striatal dopamine secondary to degeneration of dopaminergic neurons within the substantia nigra is the main cause of Parkinson's disease (PD). The movement disorders in PD patients is related to their inability to generate the appropriate motor command and to build up the premovement facilitation of the motor system. As the sensory input might be used to initiate, control, or monitor ongoing movement, an altered sensorimotor integration due to the impairment of the nigrostriatal dopaminergic pathway has been thought to be partly responsible for their motor deficits. In this respect, it has been suggested that evoked potential recording might display some differences from healthy controls. Therefore, the aim of this study is to examine the possible contribution of noninvasive neuroelectrophysiological methods in evaluating the functionality of sensorimotor integration mechanisms in (predominantly) unilateral PD patients. The techniques of somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) that provide information on the transmission of afferent and efferent pathways respectively were used in the present study. SEPs reflect the electric brain potentials elicited by an electric stimulus applied to a mixed nerve, that is, conduction of the afferent volley to the primary somatosensory cortex. On the other hand, transcranial magnetic stimulation (TMS) of the motor cortex produces MEPs, which are generated by excitation of cortical motoneurons and mediated via corticospinal pathways. When TMS is performed during voluntary muscle contraction, the MEP is followed by a transient pause in electromyographic activity (silent period, SP). Both spinal and intracortical inhibitory mechanisms contribute to the SP. In this study, a total of twenty-two patients were examined and forty-two healthy controls were also studied for comparative purposes. Comparisons were made between patients and healthy controls. Most importantly, statistical tests were made within the group of patients, that is, examining data between affected and non-affected sides and between ON (L-dopa) phase and OFF phase.
In patients, no significant changes could be found in all latencies of respective median nerve SEP components, which indicate that the transmission of somatosensory pathway is not involved. However, the amplitude of N30 on the non-affected side was significantly increased at the ON phase. Because the generator of N30 was supposed to be the supplementary motor area (SMA), it has been suggested that N30 is a marker of the functionality of a cortico-subcortico-cortical loop that includes the basal ganglia as well as the premotor area and SMA. Enhanced effects on N30 amplitude were seen on the non-affected side at ON phase indicating that L-dopa facilitates the response of SMA. On the other hand, no change of N30 amplitude on the affected side indicates that the previously mentioned loop was dopamine unresponsive probably due to a defective function of neural structures involved in the SMA-BG-thalamic circuitry.
As for the MEP study, a physiologically higher TMS threshold (T) was shown in the dominant hand of normal controls, but the PD patients had the same threshold on both sides of the body. Normal MEP latencies in PD patients indicates that patient's pyramidal motor tract conduction was normal, however, larger MEP amplitudes shown in PD patients indicates that their cortical excitability is higher than that of normal controls. Besides, during OFF phase, the SP of 100%T was shortened on the affected side of PD patients, which coincided with the previously mentioned suggestion that PD patients had higher cortical excitation probably owing to decreased cortical inhibition. However, the shortened SP in PD patients could recover in the ON phase.
In conclusion, the results in this study showed that dopaminergic nigrostriatal dysfunction could affect sensorimotor integration, which could be evaluated by using the useful indicators of N30 and SP.

目 錄
英文縮寫對照表
中文摘要………………………………………1
英文摘要………………………………………3
第一章 緒 論
前 言…………………………………………5
重要文獻回顧…………………………………5
一、多巴胺系統在腦內的分佈及其功能……5
二、中紋狀體系統缺損與運動障礙…………6
三、利用誘發電位評估運動障礙……………7
體感覺誘發電位………………………………8
運動誘發電位…………………………………10
研究目的………………………………………12
研究設計………………………………………12
圖1-1∼1-6……………………………………13-19
第二章 材料與方法
研究對象………………………………………20
研究步驟………………………………………20
檢測前之準備…………………………………21
記錄體感覺誘發電位…………………………21
記錄運動誘發電位……………………………23
數據處理及統計分析…………………………25
表2-1∼2-2……………………………………26-27
圖2-1∼2-5……………………………………28-32
第三章 結 果
基本資料之比較………………………………33
體感覺誘發電位之比較………………………33
運動誘發電位之比較…………………………35
表3-1∼3-7……………………………………37-43
圖3-1∼3-5……………………………………44-48
第四章 討 論
感覺誘發電位…………………………………49
運動誘發電位…………………………………55
總結……………………………………………60
參考文獻………………………………………62

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