第一章

緒論

　　肌肉痙攣是一種運動神經失調，使得牽張反射過度容易啟動，並伴隨過當的神經肌肉反應與肌肉牽張時阻力的異常增加[3][4]。在神經學上，肌肉痙攣為上運動神經元症狀的一種臨床表徵；控制脊髓反射的下行路徑包括興奮性與抑制性路徑，而因神經損傷造成的肌肉痙攣主要是抑制與興奮路徑失去平衡，整體來說是抑制性的訊號減少所致[1][2]。肌肉痙攣主要可分成兩種形式，分別為大腦形式與脊髓形式，可以中風病患與脊椎損傷病患為代表，這兩種不同形式主要是因為不同解剖位置的損傷，而造成生理學上的差異，其表現出來的症狀也會不同。目前已知在大腦形式上，抗地心引力的肌肉表現較為明顯，而脊髓形式在屈肌與伸肌都容易有肌肉痙攣的情形[2][6]。
　　被動拉長肌肉時感覺肌肉阻力增加的原因，主要有神經成分與機械成分，而影響肌肉痙攣的原因可分為三個層面，分別為上脊椎層面、脊椎層面(神經成分)與週邊層面(機械成分)，在神經成分上主要是alpha運動神經元過於興奮造成反射增大，而機械成分是因肌痙攣患者常有肌肉機械特質的改變，例如：第二類(type II)肌肉萎縮的情形、肌節數目減少使肌肉長度減少[10][14][15]，造成肌肉的剛性增加[12][13]，而之前研究顯示機械特質的改變無法直接由反射過大來解釋[16][17]。然而，現有量化肌肉痙攣的方式，不論是鐘擺測試(pendulum test)[20][21]、牽張反射(stretch reflex)[11]、肌腱反射(tendon reflex)[27][28]、H反射技術[25][26]等等，不是很難區分肌痙攣中神經與機械成分造成的交互影響，就是以偏蓋全地強調神經成分；同時這些評估與臨床上所觀察到病患肌痙攣程度、功能影響程度也有明顯之落差[40] [41] [42]。配合H反射技術的神經成分檢測，本研究將首次提出肌音訊號(MMG)應用，來定量人體肌肉痙攣機械成分。肌音訊號約在1800年被正式提出[47]，藉由肌肉收縮時肌纖維彼此間會產生滑動而產生類似音頻震動，反應肌肉張力、剛性等等肌肉內在機械特質[52][53][54]。
　　回顧過去相關的肌痙攣研究，迄今仍無研究同時量化肌痙攣中神經與機械成分，並進一步研究肌痙攣神經、機械成分在功能上之意義。所以本實驗將探討代表大腦形式的中風患者與代表脊髓形式的脊椎損傷患者肌痙攣中神經、機械成分的改變，並對神經、機械成分與臨床肌痙攣量測、功能量表結果的相關性做進一步研究。

第二章

方法

　　本實驗所使用的設備包括：(1)硬體部分：H反射電刺激器(Model S88, Grass Instruments, USA)、個人電腦、生理訊號濾波放大器(Model 7P511, Grass Instrument, USA)、3個肌電表面電極(Gereonics Inc., USA)與1個肌音表面電極(Nihon Kohden MT-3T, Japan)。(2)軟體部分：Labview 6.0(National Instruments, TX, USA)、Matlab 6.5(The Math Work Inc. USA)、SPSS 11.0(SPSS, USA)。
　　本實驗共計有4組受試者：(1)脊椎損傷病患組：11位男性、4位女性脊椎損傷病患，平均年齡為34.13 ± 11.46歲。(2)中風病患組：16位男性、3位女性中風病患，平均年齡為52.11 ± 8.82歲。(3)脊椎損傷病患之控制組：9位男性、7位女性與脊椎損傷病患年紀相符的健康受試者，平均年齡為34.13 ± 11.46歲。(4)中風病患之控制組：3位男性、11位女性與中風病患年紀相符的健康受試者，平均年齡為47.57 ± 9.60歲。將表面電極黏貼於慣用腳比目魚肌肌腹，電刺激之陰極置於後膝窩的後脛神經上、陽極黏貼於髕骨，受試者呈俯臥姿，踝關節固定於正中位置。
　　本實驗分成3個主要步驟，實驗過程中受試者皆為放鬆狀態：(1)尋找引起M反應的最小電量(MT)，以2.5倍MT電量刺激後脛神經引發最大M反應(Mmax)與最大M反應之肌音訊號值(Mmax_mmg)。(2)尋找最大M反應百分之十所需電量，引發H反射，所得之H反射振幅除以最大M反應振幅，定義為H/Mmax。(3)尋找最大H反射所需之電量，以雙H反射間隔200毫秒收取H反射恢復曲線參數(H2/H1)。步驟(1)(2)(3)以隨機順序方式施測，每個參數各重複收取8次。脊椎損傷與中風病患除上述電生理參數外，另外由一位具執照的治療師施測臨床量表，包括埃許瓦斯量表修改版(Modified Ashworth Scale, MAS)、巴氏量表(Barthel Index)、傅格梅爾動作量表(Fugl-Meyer motor assessment)的下肢部分、賓氏痙攣頻率自我評估量表(Penn spasm frequency)。
　　在訊號處理上所得之肌音訊號經由傅立葉轉換得中位頻率，以t檢定(Student t test)比較：1).脊椎損傷病患組與其控制組；2).中風病患組與其控制組；3).脊椎損傷病患組與中風病患組之間，前述各項電生理參數之組間差異。此外，各項電生理參數與臨床量表結果的相關性以斯皮爾曼等級相關(Spearman rank correlation)來檢測，由相關性的檢測中選取與埃許瓦斯量表修改版結果有顯著相關之電生理參數放入多重邏輯式回歸(multiple logistic regression)，探討其對埃許瓦斯量表修改版量測結果的解釋力。

第三章

結果

　　實驗結果共分兩部份陳述，第一部分為脊椎損傷病患、中風病患與其年齡相符之正常受試者在肌痙攣的神經與機械成分的比較，第二部分為代表肌痙攣神經與機械成分的各項電生理參數與臨床量表結果之相關性。
　　在最大M波之肌音訊號強度(Mmax_mmg)、H反射比值(H/Mmax)與雙H反射比值(H2/H1)上，脊椎損傷病患組與中風病患相對於其控制組都有明顯增加的情形(p < 0.05)，且脊椎損傷病患組與中風病患組間並無顯著差異，但在最大M反應(Mmax)上，只有脊椎損傷病患組的振幅小於其控制組(p < 0.05)，此外，肌音訊號的中位頻率(MDF)也只在中風病患組有顯著增加(p < 0.05)。此結果顯示脊椎損傷病患與中風肌痙攣病患其肌肉的神經、機械成分與健康受試者皆有不同。
　　各項電生理參數與臨床量表之相關性分析結果顯示：埃許瓦斯量表修改版(MAS)之結果除了與H反射比值(H/Mmax)有顯著相關(ρ = 0.540, p = 0.001)外，也和最大M波肌音訊號強度(Mmax_mmg)有明顯的相關性(ρ = 0.432, p = 0.011)，而賓氏痙攣頻率自我評估量表(Penn spasm frequency)與肌音訊號的中位頻率(MDF)有顯著負相關(ρ = -0.355, p = 0.039)、巴氏量表(Barthel Index)僅與最大M波肌音訊號強度(Mmax_mmg)有明顯的負相關(ρ = -0.397, p = 0.020)，但下肢部分之傅格梅爾動作量表(Fugl-Meyer motor assessment)與各項電生理參數並無相關。由多重邏輯式回歸(multiple logistic regression)的結果發現脊椎損傷與中風肌痙攣病患之H反射比值(H/Mmax)與肌音訊號強度(Mmax_mmg)可解釋埃許瓦斯量表修改版(MAS)之變異達百分之38.4(ρ = 0.620, p < 0.001)，因埃許瓦斯量表修改版(MAS)包含等級0，代表肌肉張力無增加情形，除肌痙攣病患外，再包含正常受試者資料於多重邏輯式回歸算式中，結果發現對於釋埃許瓦斯量表修改版(MAS)的變異解釋程度增加為百分之55.7(ρ = 0.746, p < 0.001)。

第四章

討論

　　實驗結果顯示脊椎損傷病患與中風病患最大M波之肌音訊號強度(Mmax_mmg)大於正常受試者，由物理模型上得知，肌音電極產生的波動壓力與其感受到的肌纖維之加速度成正比，因此肌痙攣病患最大M波之肌音訊號強度變大代表肌肉剛性增加，此肌肉剛性增加的推論印証之前學者發現肌痙攣肌肉在生物力學特徵上的改變；另外本研究發現僅有中風病患的中位頻率高於其控制組，因頻率的改變主要受肌肉長度與張力影響，推測可能是中風病患伸肌張力較強使其踝關節容易維持在蹠屈位置，造成比目魚肌肌節數減少與肌肉長度變短所致，綜觀以上論述，肌音訊號時閾與頻閾的改變代表肌痙攣病患的機械成分與正常受試者確有不同，且其機械成分的改變可能會因病源學而異。
　　在神經成分上，脊椎損傷病患與中風病患的H反射比值(H/Mmax)與雙H反射比值(H2/H1)明顯高於正常受試者，此結果與之前多數研究類似，代表肌痙攣病患的運動神經元過度興奮與上脊椎傳入訊息異常；此外，脊椎損傷病患最大M反應(Mmax)減小可能是肌纖維萎縮、運動單元數減少所致。
　　在相關性研究分析上，埃許瓦斯量表修改版(MAS)與H反射比值(H/Mmax)、最大M波之肌音訊號強度(Mmax_mmg)皆有顯著相關，且後兩者間為統計獨立變項；多變數邏輯迴歸分析顯示，H反射比值與最大M波之肌音訊號在統計上可共同有效地解釋埃許瓦斯量表修改版的迴歸變異數，表示H反射比值與最大M波之肌音訊號強度代表不同之肌痙攣成分，而且除神經成分外，機械成分的改變同是影響肌痙攣嚴重程度的要素；至於無法完全解釋的埃許瓦斯量表修改版變異數的部分，部分導因可能為埃許瓦斯量表修改版量表在下肢測試信度較低所造成。在日常活動評估上，巴氏量表(Barthel Index)僅與代表肌痙攣機械成分的最大M波之肌音訊號強度相關；賓氏痙攣頻率自我評估量表(Penn spasm frequency)與肌音訊號的中位頻率(MDF)有顯著負相關，顯示病患日常生活活動缺損、痙攣頻率與肌肉機械特質的關聯大於神經成分；此外，下肢部分之傅格梅爾動作量表(Fugl-Meyer motor assessment)與各項電生理參數並無相關，雖然如此，並不一定代表動作功能與肌痙攣成分全然無關，需考慮本研究肌痙攣的各項評估均在肌肉放鬆狀態進行，然而肌痙攣表現在肌肉放鬆與活動時可能有明顯的差異。

第五章

結論

　　本研究以H反射技術為探討工具，配合H/Mmax、H2/H1與肌音訊號參數(Mmax_mmg)，研究脊椎損傷與中風病患其肌痙攣的神經與機械成分，並進一步探討神經、機械成分與臨床觀察之肌痙攣程度、功能損傷的相關性。
　　研究結果顯示病患的H/Mmax與H2/H1比值明顯高於正常受試者，代表肌痙攣病患在運動神經元興奮度異常，此外，病患在肌音訊號強度與中位頻率的改變顯示其肌肉機械特質與正常肌肉確有不同。在相關性研究結果發現同時考慮Mmax_mmg與H/Mmax兩項參數可解釋臨床常使用之埃許瓦斯量表修改版(MAS)量測的肌痙攣結果達百分之38.4，而代表基本日常生活功能的巴氏量表(Barthel Index)僅與Mmax_mmg有顯著相關，此結果顯示相較於肌痙攣的神經成分，病患日常生活功能損傷與其肌肉機械特質異常有更顯著的關係；然而代表動作功能的傅格梅爾動作量表(Fugl-Meyer motor assessment)卻與肌痙攣各項參數皆無明顯相關性。
　　因肌痙攣程度在肌肉放鬆與活動的情況會有不同，病患動作功能損傷情形或許與肌肉活動下的肌痙攣表現較有相關性，所以未來研究的發展，可於肌肉活動情況下研究病患肌痙攣的情形。

　　Introduction: The Hoffmann reflex (H reflex) is often used to study spasticity, but it does not correlate well with clinical observation and spasticity-related impairment in motor functions, since H reflex accounts primarily for spinal pool excitability. The objectives of this study were 1) to characterize the changes in neural and mechanical components of spasticity for neurological patients with cerebral and spinal lesions using modified H reflex which included innovative use of mechanomyogram (MMG), and 2) to related two components with several clinical scales corresponding to severity of spastic and functional impairments. Methods: Four groups were recruited with consent including spinal cord injury (SCI) group, stroke group and their age-matched control groups. The neural component of spasticity was represented with the adjusted ratio of H reflex to the maximal M response (H/Mmax) and the ratio of paired H reflexes with interpulse interval of 200 msec (H2/H1). To characterize mechanical component in spasticity, amplitude and median frequency of maximal M response recorded with MMG signal were assessed. Clinical functional scales such as Modified Ashworth Scale (MAS), Barthel index, Fugl-Meyer motor assessment and Penn spasm frequency were evaluated by another licensed physical therapist for blind purpose. Results: Significant larger H/Mmax ratio, H2/H1 ratio and amplitude of Mmax_mmg were observed in SCI and stroke groups than their age-matched groups (p < 0.05), but no significant difference in above-mentioned measurements was found between both patient groups. The only exceptions were Mmax which was significantly decreased only in SCI group (p = 0.027) and MDF of Mmax_mmg was significantly increased in stroke group (p = 0.006) in comparison with their control groups. These findings strongly indicated that there were obvious neurophysiological and biomechanical changes in a spastic muscle for patients in SCI and stroke groups. The connection between neural and mechanical components with clinical assessment was scale-dependent. MAS correlated significantly with H/Mmax (ρ = 0.540, p = 0.001) and amplitude of Mmax_mmg (ρ = 0.432, p = 0.011) accounting for the variance of MAS for 55.7% (ρ = 0.746, p < 0.001), if normal subjects whose muscle tone were grade 0 were included. For the other clinical functional scales, Barthel index merely correlated with the amplitude of Mmax_mmg (ρ = -0.397, p = 0.020) and Penn spasm frequency related inversely to MDF of Mmax_mmg (ρ = -0.355, p = 0.039), but Fugl-Meyer motor assessment did not correlate with any spasticity measurement. Conclusion: With the use of modified H reflex, the present study quantitatively identified neural and mechanical components intrinsic with spasticity in patients with SCI and stroke. Only mechanical component of spasticity related to daily activities evaluated with Barthel index, but functional outcomes of patients scored by Fugl-Meyer test was surprisingly independent of any parameters in spasticity quantification. As spasticity measurement in this study was performed on a spastic muscle in relaxed condition, further development will focus on characterizing spasticity dynamically when a spastic muscle activates for motor tasks. It might give better insight into spasticity and explore appropriately the relationship between functional outcomes and spasticity.

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