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研究生:姜雅齡
研究生(外文):Ya-Ling Chiang
論文名稱:單側肌肉疲勞於對側震顫動作及肌皮反射之影響
論文名稱(外文):Effects of Unilateral Muscle Fatigue on Contralateral Tremulous Movement and Cutaneomuscular reflex
指導教授:黃英俢
指導教授(外文):Ing-Shiou Hwang
學位類別:碩士
校院名稱:國立成功大學
系所名稱:物理治療研究所
學門:醫藥衛生學門
學類:復健醫學學類
論文種類:學術論文
論文出版年:2006
畢業學年度:94
語文別:英文
論文頁數:56
中文關鍵詞:疲勞施力震顫肌皮反射
外文關鍵詞:fatigueforce tremorcutaneomuscular reflex
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第一章
序論

當肌肉產生主動收縮時,若處於休息狀態下的對側同源肌肉(homologous muscle)出現非自主性的收縮,稱為對側動作溢流 (contralateral motor irradiation);一直以來動作溢流被視為缺乏功能性且可能影響動作靈活的半反射性動作。[15] 此種現象在兒童時期較易發現,隨著神經系統發展較成熟,可發展出抑制性的行為,避免執行單側肢體動作時受到對側不自主動作的影響,通常在十歲之後動作溢流就會逐漸消失。[24][48][50] 健康成年人在持續用力或是疲勞時可能出現對側動作溢流的現象,尤其在是執行手部動作時更為明顯。[1][4] 另外,有遺傳性疾病或大腦受損等中樞神經系統疾病時,也會導致過度的動作溢流發生。[50]
至目前為止,對於造成對側動作溢流的機制仍未完全清楚,被廣泛討論的有:1. 雙側活化模式(bilateral activation model),此模式以經胼胝體的誘發(transcallosal facilitation hypothesis),以及經胼胝體的抑制(transcaoolosal inhibition hypothesis)兩種假設為基礎,經胼胝體的誘發指的是當一側大腦產生活動時,興奮的訊號會經由連結兩側大腦的胼胝體(corpus callosum),興奮對側大腦內的相同區域,使其產生活動。[15] 此被誘發而產生的活動隨後會被同樣來自對側大腦的抑制訊息所抑制,此即稱為經胼胝體的抑制。[38][54][60] 因此,當經胼胝體的誘發過多,無法被隨後的抑制作用完全抑制,或是經胼胝體抑制減少時,被誘發所產生的大腦活動便會經由交叉到對側的腦脊髓路徑(crossed corticospinal pathway)傳到所支配的肌肉而引起對側動作溢流。[31] 2. 單側活化模式(unilateral activation model)指出,對側動作溢流的產生來自同側未交叉的腦脊髓路徑(ipsilateral corticospinal pathway)。[6] 當一側大腦活動時,會將訊號經由交叉的腦脊髓路徑傳到對側肌肉,產生收縮,同時同側未交叉的腦脊髓路徑會受到對側大腦的抑制,當此同側路徑未被完全抑制時,便會將活動傳到與活動大腦同側的肌肉而引起對側動作溢流。[25][48][57] 3. 除了上述兩種模式之外,有學者認為,對側動作溢流有可能發生於脊髓層級,藉由突觸前調節所造成。[40]
當肌肉主動收縮至疲勞時,除了週邊組織的機械特徵(包含肌肉以及粘彈組織特性)會發生疲勞性改變外,中樞神經也會產生興奮度下降的現象,稱為中樞疲勞(central fatigue)[23]。中樞疲勞可能伴隨非工作的大腦半球產生中樞神經興奮度改變:當一側肌肉因為主動收縮而產生疲勞時,會使控制主動動作的工作大腦對非工作大腦抑制減少,導致對側動作溢流產生[2][11][64]。
當肌肉產生疲勞的現象時,會造成同側肢體的施力震顫(force tremor)增加[23][64],施力震顫訊號中8-12 Hz頻帶由於不受週圍機械性因素影響(例如加重或缺血等),普遍被認為反應中樞神經震盪節律。[3][19][20] 先前的研究提出:平舉時兩側肢體的震顫訊號互相並沒有關聯[42],然而當一側肢體主動收縮至疲勞時,會同時造成兩側肢體震顫訊號中8-12 Hz頻帶的明顯增加,表示兩側的肢體震顫疲勞後,中樞神經震盪產生某些程度的關連性。[44] 除了因疲勞產生上脊髓神經的兩側關連之外,利用肌皮反射(cutaneomuscular reflex) 可了解疲勞所引起對側動作溢流改變的起源,因為肌皮反射E1成份普遍被認為是經由脊髓反射路徑而成,而I1以E2成份則來自上脊髓層級。[33][38][59]
本實驗目的利用施力震顫與肌皮反射的特徵變化,進一步探討單側肌肉疲勞時,對側動作溢流造成對側肢神經活性改變的可能機制。藉由非慣用手執行食指最大用力之主動外展等長收縮至疲勞後,兩側食指近端指間關節(proximal interphalangeal joint)所測量到的施力震顫,以及在非慣用手背側第一掌股間肌所觀察到肌皮反射成份的改變,來探討單側肌肉疲勞後,對側動作溢流產生時脊髓以及上脊髓層級神經興奮性的改變。

第二章
方法

本實驗所使用的設備包括:(1)硬體部分:固定裝置、推拉力計(Model FT-10, Grass-Telefactor, USA及Model 9820P, AIKOH, Japan)、單頻訊號放大器(Model PS-30A-1, Entrain, UK及Model P122, Grass-Telefactor, USA)、示波器(Instek GOS-620, Taiwan)、可重複使用的銀/氯化銀肌電表面電極(Model F-E9M-40-5, Grass-Telefactor, USA)、生理訊號濾波放大器(Model P511, Grass-Telefactor, USA)、表皮肌肉反射電刺激器(Model S88, Grass Instruments, USA)。(2)軟體部分:Labview 7.0(National Instruments, TX, USA)、Matlab 6.5(The Math Work Inc. USA)、SPSS 11.0(SPSS Inc. USA)。
本實驗共有15位健康自願受試者,8位女性、7位男性,平均年齡為23.53 ± 2.39歲。14位受試者慣用手為右手、一位為左手。非慣用手為執行疲勞測試的肢體,為動作手,慣用手則為非動作手。實驗分為兩個部分,中間相隔約兩個月。其中一名受試者因無法前往執行第二次實驗,因此以另一名年紀及慣用手相符之受試者代替。受試者於坐姿下,受測食指呈指向(pointing)姿勢固定在副木內,將表面電極黏貼於雙手背側第一掌股間肌肌腹,受試者經由推拉力計執行食指外展的動作,收縮力量會同步顯示在示波器的螢幕上。
第一個實驗為測試單手疲勞後,兩側施力震顫改變情形。實驗開始前先分別測試兩邊背側第一掌股間肌的最大自主收縮力量(MVC),作為之後施力標準。實驗可分成四個部分:(1) 疲勞前單側肢體動作,受試者以慣用手食指執行10% MVC等長外展動作,持續五秒,重複六次,每次中間間隔一分鐘避免疲勞,六次結束後休息兩分鐘再開始下一個測試。(2) 疲勞前雙側肢體動作,慣用手食指以10% MVC,非慣用手食指以100% MVC同時執行等長外展動作,持續五秒,重複六次,每次間隔一分鐘避免疲勞,結束後休息五分鐘再開始下一個測試。(3) 疲勞後雙側肢體動作,非慣用食指持續持行兩分鐘循環的疲勞測試,包括一分鐘100% MVC以及一分鐘30% MVC等長外展動作,同時慣用手執行10% MVC等長外展動作,動作持續直到非慣用手執行一分鐘的100% MVC動作時無法達到目標線75%值,此後即為疲勞後雙側肢體動作狀況。施力震顫訊號只在執行100% MVC時紀錄。(4) 疲勞後單側肢體動作,在疲勞測試後,受試者的慣用手繼續執行10% MVC食指等長外展動作,而非慣用手則休息不動,持續30秒。分別在四個狀況下紀錄雙側的施力訊號以及表面肌電訊號作為之後施力震顫的分析。
第二個實驗利用肌皮反射來探討,輔助因為單側肌肉疲勞而產生對側動作溢流時,在脊髓以及上脊髓層級的進一步確定。受試者的姿勢與第一個實驗相同,除了慣用手食指多了一組環狀電極以用來給予電刺激,陰極置於近端指骨,陽極置於中間指骨,利用頻率5 Hz、持續0.1毫秒、約2到2.5倍引起感覺的最小電量,刺激指神經,引發肌皮反射。實驗步驟與第一個實驗相同,但只測試疲勞前以及疲勞後兩個狀況,均為雙側肢體動作,執行動作的同時並收集慣用手的肌皮反射,而疲勞後狀況的肌皮反射只在非慣用手執行100% MVC的情況下收集。
在訊號處理部份,第一個實驗所收集到的施力訊號經去趨勢(detrend)及濾波(6-50 Hz)處理之後成為施力震顫訊號,計算均方根值(root mean square, RMS)以及利用Welch's method估計震顫訊號之功率頻譜密度(power spectrum density, PSD),從功率頻譜密度中找出在8-12 Hz頻帶中最大值所在的頻率,定義為高峰頻率(peak frequency),以及所對應的頻譜強度。表面肌電訊號則經去趨勢及濾波(1-400 Hz)處理後,計算均方根值。第二個實驗將所收集到的表面肌電訊號去趨勢且翻正(rectified)後,依據電刺激發生的時間點將表面肌電訊號分割並重疊,產生取樣時間為145毫秒的肌皮反射。取電刺激產生前20毫秒的平均值為背景表面肌電訊號,作為標準化的基準,找出標準化後肌皮反射中的三個高峰,計算其與背景表面肌電訊號間的差值,分別紀錄為E1、I1以及E2,以百分比表示。
以威氏符號等級檢定(Wilcoxon signed ranks test)比較不同狀況下,施力震顫訊號、表面肌電訊號以及肌皮反射的差異。

第三章
結果

實驗結果共分兩個部分,第一部分為施力震顫實驗,探討單手疲勞後,兩側施力震顫以及表面肌電訊號的改變情形。實驗資料收集與分析共有四種狀況:疲勞前單側肢體動作、疲勞前雙側肢體動作、疲勞後雙側肢體動作以及疲勞後單側肢體動作;第二部分為肌皮反射實驗,探討單側肌肉疲勞後,對側手所測量到肌皮反射中三個成份的改變,實驗資料收集與分析有兩種狀況:疲勞前以及疲勞後。在本實驗中,均由非慣用手執行疲勞測試,因此稱為動作手,慣用手則為非動作手。
動作手施力震顫的均方根值(RMS)在疲勞產生後有明顯下降的情形(p < 0.05),雖然功率頻譜密度(PSD) 8-12 Hz頻帶間的高峰頻率(peak frequency)在疲勞產生前後並沒有明顯的改變,然而其所對應的頻譜強度在疲勞產生後則有顯著的下降(p < 0.05)。非動作手的施力震顫訊號部分,疲勞前在雙側以及單側肢體動作狀況之間,均方根值並沒有顯著差異,疲勞測試之後,不論在雙側或單側動作的狀況下,疲勞後施力震顫的均方根值較疲勞前均有明顯的增加(p < 0.05)。疲勞後非動作手的比較發現,單側動作狀況的均方根值明顯大於雙側動作時的值(p < 0.05)。只有在單側動作的狀況下,疲勞後8-12 Hz頻帶中的高峰頻率比疲勞前明顯下降(p < 0.05),其他狀況之下8-12 Hz高峰頻率則都沒有顯著差異。在雙側以及單側動作的情況下,疲勞後高峰頻率頻譜強度均比疲勞前強度明顯增加(p < 0.05)。不論是在疲勞前或疲勞後,單側與雙側動作之間高峰頻率的頻譜強度並沒有顯著差異。在表面肌電訊號部分,動作手在疲勞後,均方根值有明顯下降的情形(p < 0.05)。然而非動作手不論是在疲勞前後,雙側或單側動作的狀況下均沒有顯著差異。
標準化後的肌皮反射結果顯示:非動作手在動作手疲勞後只有代表脊髓反射路徑的E1振幅有明顯的增加(p < 0.05),而與上脊髓層級有關的I1以及E2在疲勞前後則沒有明顯的改變(p > 0.05)。

第四章
討論

實驗結果顯示,當動作手執行最大主動收縮至疲勞時,非動作手的施力震顫訊號在均方根值以及8-12 Hz頻帶的高峰頻率頻譜強度均有明顯增加,且當動作手停止收縮後,非動作手的施力震顫訊號仍明顯增加。本研究的發現與之前學者研究的結果相若,顯示當一側肢體執行主動收縮至疲勞時,工作大腦產生疲勞後對非工作大腦的抑制能力減少,導致非動作手的施力震顫訊號振幅增加。即使動作手在停止收縮後,非動作手的施力震顫訊號仍明顯增加,表示動作結束後此抑制減少的現象仍會持續一段時間。
當動作手疲勞後,在非動作手所測得之肌皮反射E1成份有明顯增加,顯示疲勞溢流與脊髓神經元的興奮性增加有關,。先前研究發現,當一側肢體執行主動動作時,對側休息肢體的H反射會有下降的情形,推測是因為動作肢體會藉由脊髓層級內的中間神經單位(interneuron)對對側肢體的脊髓運動神經池(spinal motoneuron pool)產生突觸前抑制(presynaptic inhibition)所造成,當動作肢體疲勞後,對對側肢體的抑制現象減少,因此非動作肢體脊髓層級的神經元興奮性增加。然而代表上脊髓層級的神經元興奮性的肌皮反射I1以及E2成份沒有明顯改變,,與施力震顫8-12 Hz高峰頻率頻譜強度增加的發現不一致。推測I1以及E2的傳導路徑經由背索(dorsal column)往上傳到感覺運動皮質(sensorimotor cortex)再往下傳到脊髓層級的運動神經池,雖然在上脊髓層級神經元的興奮性下降,但可能被脊髓層級神經元興奮性上升所抵銷,導致肌皮反射的I1以及E2部分沒有明顯改變。

第五章
結論

本研究以食指的施力震顫訊號、肌皮反射為探討工具,分析施力震顫訊號均方根值、8-12 Hz頻帶的高峰頻率與所對應的頻譜強度、以及標準化後肌皮反射三個高峰E1、I1以及E2等參數,探討單側肌肉疲勞引起對側動作溢流產生時,對側非作用肢施力震顫訊號的影響以及脊髓與上脊髓層級神經元興奮性的改變。
研究結果顯示作用手執行最大主動收縮至疲勞後,對側非動作手的施力震顫訊號不論是均方根值或是8-12 Hz頻帶的高峰頻率及頻譜強度均有明顯增加,顯示當動作手疲勞後,中樞疲勞的現象會影響對側大腦,改變非動作手的施力震顫表現。另外,從肌皮反射的結果發現,當動作手疲勞後,非動作手所測量到的E1部分有明顯增加,表示當疲勞而產生對側動作溢流時,非動作側脊髓層級的神經元興奮度會增加。對照施力震顫8-12 Hz頻譜強度增加的發現,在I1, E2的部分沒有明顯的改變可能是因為肌皮反射在上脊髓層級的靈敏度不夠,因此無法觀察到I1, E2的改變。綜合震顫訊號與肌皮反射實驗結果,可推測當一側肌肉因最大主動收縮導致疲勞而造成對側動作溢流時,對側非動作肢體的脊髓以及上脊髓層級均可能有所改變。
未來研究的發展可探討不同的族群,例如老年人或中風患者,在因單側肢體疲勞而引發對側動作溢流時,脊髓以及上脊髓層級的改變,藉此進一步瞭解肌肉疲勞與神經誘發技術的機制與臨床應用的實際成效。
Introduction: It is of theoretical interest to characterize changes in contralateral motor irradiation after unilateral muscle fatigue, though most studies draw attention to cross-over effect of central fatigue that would possibly mediate neuronal excitability of the unexercised limb. The objectives of this study were 1) to investigate the post-exercise effect of the exhausted FDI on feature alternation in the contralateral force tremor and muscle activity, and 2) to gain a better insight into spinal and supraspinal mechanisms of muscle fatigue on contralateral motor irradiation by using cutaneomuscular reflex (CMR).

Methods: Fifteen healthy volunteers performed a series of two-minute fatiguing contraction, each consisted of one-minute sustained isometric index abduction at 100% MVC following one-minute abduction at the 30% MVC of the exercised index. Force tremor of bilateral index, electromyographic (EMG) activities and CMR of the first dorsal interosseous (FDI) were recorded before and after the fatigue paradigm. A number of fatigue neurophysiological responses were assessed, including root mean square (RMS) of force tremor and EMG, spectral power and spectral peaks of force tremor in the range of 8-12 Hz, as well as E1, I1 and E2 components of CMR.

Results: The RMS and 8-12 Hz peak amplitude of force tremor in the non-exercised limb was significantly increased after fatiguing contraction of the contralateral FDI (p< 0.05). Muscle fatigue leaded to a marked decline in RMS of force tremor (p=0.001) and EMG activity (p=0.001), 8-12 Hz peak amplitude of the exhausted limb (p=0.001). Maximal fatiguing contraction of the FDI resulted in a significant increase in the size of the E1 short-latency component of the contralateral non-exercised limb (p=0.008), while neither significant change in the I1 nor E2 component of CMR was noted.

Conclusion: The increase in the 8-12 Hz tremor in the non-exercised limb after muscle fatigue indicates that the cross-over effect was centrally mediated. In addition to supraspinal involvement, the present study suggested an increase in the spinal motoneuron pool of the non-exercised limb after contralateral muscle fatigue, in the context of significant upsurge in E1 of the CMR. Collectively, there existed a cross-over effect upon neuronal excitability of the unexercised limb following unilateral fatiguing contraction, and both spinal and supraspinal mechanisms are responsible for the fatigue-induced modulation of contralateral overflow.
Abstract................................................................. ..Ⅰ
Chinese abstract...........................................................Ⅲ
List of tables.............................................................ⅩⅧ
List of figures............................................................ⅩⅨ
Acknowledgement............................................................ⅩⅣ
Chapter 1: Introduction.....................................................1
1.1 Contralateral motor irradiation.........................................1
1.1.1 Introduction.......................................................1
1.1.2 Possible mechanisms................................................2
1.1.2.1 Bilateral activation model.........................................2
1.1.2.2 Unilateral activation model........................................3
1.1.2.3 Other models.......................................................4
1.2 Contralateral motor irradiation after fatigue......................5
1.2.1 The effects of unilateral muscle fatigue on bilateral force tremor.6
1.3 Cutaneomuscular reflex.............................................7
1.4 Rationales.........................................................9
1.5 Significance of the Problems.......................................10
1.6 Hypotheses.........................................................11
Chapter 2: Methods..........................................................12
2.1 Subjects................................................................12
2.2 Experiment I............................................................13
2.2.1. The objective of the study...........................................13
2.2.2. Physiological recording..............................................15
2.2.3 Procedures............................................................16
2.3 Experiment II...........................................................18
2.3.1. The objective of the study...........................................18
2.3.2 Cutaneomuscular Reflex Recording......................................19
2.3.3. Procedures...........................................................21
2.4 Data and Statistical Analysis...........................................22
2.4.1 The Force Signals.....................................................22
2.4.2 The EMG signals.......................................................23
2.4.3 Cutaneomuscular Reflex................................................24
2.4.4 Statistics............................................................25
2.4.4.1 Experiment I........................................................25
2.4.4.2 Experiment II.......................................................26
Chapter 3: Results..........................................................27
3.1 Force signals...........................................................27
3.1.1 Root mean square of force tremor......................................29
3.1.2 Power spectrum density of force tremor................................31
3.2 The EMG signals.........................................................36
3.3 Cutaneomuscular reflex..................................................39
Chapter 4: Discussion.......................................................41
4.1 Force tremor and EMG activity...........................................41
4.1.1 Increased force tremor of the non-exercised limb in with contralateral movement....................................................................42
4.2 Cutaneomuscular reflex..................................................43
4.2.1 Increased E1 component after contralateral muscle fatigue.............44
4.2.2 Paradoxical insignificant change in the I1 and E2 components after contralateral muscle fatigue................................................46
Chapter 5: Conclusion.......................................................47
References..................................................................48
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