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研究生:陳若佟
研究生(外文):Jo-Tong Chen
論文名稱:自發性電位活動的電生理分析以特徵量化肌膜疼痛症候群引痛點敏感度
論文名稱(外文):Electrophysiological Analysis of the Spontaneous Electrical Activity for Characterizing the Sensitivity of Myofascial Trigger Points of Myofascial Pain Syndrome
指導教授:鍾高基鍾高基引用關係
指導教授(外文):Kao-Chi Chung
學位類別:博士
校院名稱:國立成功大學
系所名稱:醫學工程研究所
學門:工程學門
學類:綜合工程學類
論文種類:學術論文
論文出版年:2001
畢業學年度:90
語文別:中文
論文頁數:99
中文關鍵詞:肌膜疼痛症引痛點終板電位頻譜分析自發性電位活動
外文關鍵詞:myofascial pain syndromemyofascial trigger pointend-plate potentialsspectral analysisspontaneous electrical activity
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肌膜疼痛徵候群為最常見的肌肉疼痛疾病,其特徵為在肌肉緊繃帶上有一特定敏感的引痛點 (myofascial trigger point)。近年來隨著發生率大幅上升,肌膜疼痛徵候群成為造成長期失能的主因之一,且往往嚴重影響患者生活品質及日常工作。引痛點的概念為目前臨床、基礎研究及復健治療的主流,但由於引痛點病生理相關機轉尚不清楚,限制了肌膜疼痛徵候群的正確診斷與治療成效。
肌膜疼痛徵候群常常肇因或相關於重覆或持續的不當肌肉收縮。如果在引痛點上給與機械性刺激,可以誘發局部抽搐反應(local twitch response)及引傳痛。肌膜疼痛徵候群可能是神經肌肉交接處異常的一種表現,且引痛點內含有多個活化小點(不正常的運動終板),使用肌電圖儀於此活化小點可記錄到具特徵化的自發性電位活動(spontaneous electrical activity)。目前學者咸認為自發性電位活動為一種不正常的終板電位(end-plate noise),因神經肌肉交接處有過多的乙醯膽鹼釋放,引起局部去極化及鈣離子增加,漸漸形成肌肉緊繃帶或進一步使其更加惡化。自發性電位活動的大小和病人的疼痛程度相關,然而於引痛點的領域中,應用訊號分析方法來特徵化自發性電位活動的研究相當罕見。
本研究計畫利用兔子實驗模式,經由自發性電位活動的電生理分析來特徵化引痛點。本研究假說:“數位訊號處理有助於量化、驗證自發性電位活動乃是因過多的乙醯膽鹼釋放所致之不正常的終板電位,且引痛點敏感度會受到交感神經、鈣離子及機械刺激的調節。”本實驗第一階段為利用引痛點自發性電位活動的平均積分面積來探討交感神經阻斷劑(phentolamine)、鈣離子阻斷劑(verapamil)及機械刺激(針刺療法)對引痛點敏感度之影響;第二階段利用自發性電位活動的功率頻譜分析來量化乙醯膽鹼離子通道開啟時間。使用肌電圖儀紀錄一秒鐘的自發性電位活動,經由時域及頻域訊號處理,分析引痛點自發性電位活動的平均積分面積及乙醯膽鹼離子通道開啟時間,提供本研究實驗之特徵化參數。
第一階段實驗:於兔子外髂動脈注射phentolamine或verapamil前、後過程中,在股二頭肌的引痛點紀錄單一活化小點的自發性電位活動變化,再於股二頭肌分別紀錄二十五個不同活化小點的自發性電位活動;對照組則於外髂動脈注射生理食鹽水,並重複以上之步驟。在針刺實驗過程中,實驗組以快速針刺激來儘量誘發局部抽搐反應,對照組則以緩慢針速於引痛點中移動,分別於針刺前、後紀錄股二頭肌引痛點中十五個活化小點的自發性電位活動。利用平均積分面積,以 t-檢定及二項變異數分析來驗證實驗組效果。第二階段實驗:於兔子股二頭肌的引痛點紀錄十個活化小點的自發性電位活動。自發性電位活動的功率頻譜係經由羅倫氏方程式(Lorentzian function)上的截頻(cut-off frequency)分析可推導求得乙醯膽鹼離子通道開啟時間,並利用回歸來驗證乙醯膽鹼離子通道開啟時間及平均積分面積這二個參數之間的關係。
實驗結果顯示:單一活化小點於注射phentolamine或verapamil後, 其自發性電位活動隨時間呈線性衰減;而對照組則呈穩定狀態。Phentolamine和verapamil實驗組中二十五個不同活化小點自發性電位活動的平均積分面積顯著比對照組的小(分別為7.92mV vs. 9.89mV 及 6.72mV vs. 8.99mV)。施予針刺療法,對引痛點具有顯著的抑制作用,其標準化平均積分面積分別為0.565 vs. 0.983。乙醯膽鹼離子通道開啟時間平均值為0.414±0.010ms,且其值與平均積分面積值呈負線性相關。
結論:引痛點自發性電位活動的平均積分面積及乙醯膽鹼離子通道開啟時間相當適合做為量化引痛點敏感度的參數。本實驗結果不但認同自發性電位活動是一種不正常的終板電位,並驗證引痛點病生理機轉確受到交感神經、鈣離子及機械刺激的調節。本實驗進一步釐清肌膜疼痛徵候群的病生理機轉,並應用於臨床上,提供有價值的最新基礎資料。

Myofascial pain syndrome (MPS), the most common cause of painful muscular dysfunction in clinics, is usually caused by or associated with obvious stress episode, repeated or sustained overload. Myofascial trigger point (MTrP), a hyperirritable spot within a palpable taut band of skeletal muscle, is the most important characteristic of MPS. Referred pain and local twitch response can be elicited by mechanical stimulus to the MTrP. MPS is suggested to represent a neuromuscular disorder and there are multiple active loci (dysfunctional motor end-plates) within an MTrP area, in which the spontaneous electrical activity (SEA) is shown by electromyography. SEA is considered as end-plate noise due to excessive acetylcholine (ACh) leakage. Although magnitudes of SEA are closely related to pain intensity/MTrP sensitivity in patients, signal analysis has seldom applied to characterize the SEA for MTrP investigation.
This research was to characterize the MTrP through electrophysiological analysis of SEA using a rabbit model. The hypothesis tested: “Digital signal processing is potentially useful to quantify and validate the SEA as end-plate noise due to excessive ACh leakage, and the sensitivity of MTrP modulated by sympathetic activity, calcium and mechanical stimulus”. More specifically, Phase I: study the effect of a sympathetic blocking agent (phentolamine), a calcium channel blocker (verapamil) and mechanical stimulation (dry needling) on MTrP sensitivity by the average integrated value of SEA (AIV); and Phase II: estimate the channel open time of end-plate ACh receptors (AChR) by power spectral analysis of SEA. Raw data of 1-sec SEA were recorded by electromyography for time/frequency signal analysis. The AIV and AChR channel open time were used as characteristic index.
Phase I: Initially, SEA from the same active locus before and after an injection of phentolamine or verapamil into the external iliac artery was recorded from biceps femoris muscle of rabbits. Then, SEA was also recorded from 25 active loci in MTrP region. Control study was conducted on the other side with the same procedure except that normal saline was used. In dry needling study, SEA was recorded from 15 active loci before and after MTrP needling. The AIV was used to analyze the treatment effect with t-test and Two-way ANOVA (p<.05). Phase II: SEA was recorded by electromyography from 10 active loci in biceps femoris muscle of rabbits. The AChR channel open time on end-plates was estimated from the cut-off frequency by fitting the power spectrum distribution of SEA through a Lorentzian function.
The results demonstrated that in the same active locus, the AIV of phentolamine or verapamil group showed a linear decay with time after injection, but control group showed no statistical change of the AIV with time. The AIV of 25 loci in phentolamine or verapamil group was significantly lower than that of control group (7.92mV vs. 9.89mV and 6.72mV vs. 8.99mV, respectively). The mean of normalized AIV of dry needling group (0.565) was significantly lower than that of control (0.983). The mean and SD of AChR channel open time was 0.414±0.010ms for 8 rabbits. The regression analysis results have revealed an inverse linear relationship between the AChR channel open time and the AIV of SEA.
In conclusion, the AIV and AChR channel open time seem to provide useful index to characterize the sensitivity of MTrP. The results of this study support the research hypothesis: “SEA is abnormal end-plate noise due to excessive ACh leakage and the sensitivity of MTrP is modulated by sympathetic activity, calcium and mechanical stimulus”. The digital signal processing and spectral analysis technique developed provide a simple and rapid estimation of the dominant AChR ion channel kinetics from in vivo SEAs recording for characterizing the MTrPs.

TABLE OF CONTENTS
中文摘要……………………………………………………………… I
Abstract………………………………………………………………III
誌謝……………………………………………………………………V
CONTENTS………………………………………………………………VI
LIST OF TABLES …………………………………………………………IX
LIST OF FIGURES…………………………………………………………X
CHAPTER 1. INTRODUCTION………………………………… 1
1.1 Prevalence and Clinical Aspects of MPS ………………… 4
1.2 Etiology and Pathophysiology of MTrPs …………………… 6
Hypothetical Mechanism of MTrP…………………………………… 7
Energy Crisis Theory…………………………………………… 7
Motor End-plate Hypothesis…………………………………… 8
Multiple Loci Hypothesis………………………………….……10
Muscle Spindle Hypothesis………………………………………11
Fibrotic Scar Tissue Hypothesis………………………………12
Neuropathic Hypothesis…………………………………………13
Sympathetic Modulation on MTrP Sensitivity …………1
Calcium Effect on MTrP …………………………………14
LTR Eliciting During MTrP Injection………………………………15
Animal Model for MTrP………………………………………………18
1.3 Spontaneous Electrical Activity of MTrPs …………………20
Electrodiagnostic characteristics of MTrP ……………………20
End-plate Noise in Electromyography ………………………….22
Modeling of Bioelectricity and Channel Kinetics ……………25
Time Domain Signal Analysis of MEPPs / MEPCs …………………27
Frequency Domain Signal Analysis of MEPPs / MEPCs ………29
1.4 Motivation and Objectives…………………………………………32
Purpose and Specific Aims……………………………………………32
Research Hypothesis………………………………………………….32
Significances…………………………………………………………..33
CHAPTER 2. MATERIALS AND METHODS ………..…….34
2.1 Animal Subjects ……………………………………………………35
2.2 Instrumentation and Equipment ………………………………36
2.3 Methodology and Experimental Procedures ………………..37
Animal Preparation ……………………………………………………37
Identification of Myofascial Trigger Spot (MTrS)………………38
Electrophysiological Recordings of SEA ………………………39
Phentolamine (Group 1) and Verapamil (Group 2)…………….41
Dry Needling (Group 3)……………………………………………42
Spectral Analysis of SEA (Group 4)……………………………43
Data Acquisition and Signal Processing ………………………43
Phase I Time Domain Analysis of SEA……………………… 44
Phase II Frequency Domain Analysis of SEA…………………….44
Statistical Analysis ………………………………………………45
Phase I Time Domain Analysis of SEA…………………………46
Phase II Frequency Domain Analysis of SEA…………………47
CHAPTER 3. RESULTS ………………………………………………48
3.1 SEA Signal characteristics …………………………… 50
Heterogeneity of the AIV of SEA…………………………………50
3.2 The Phentolamine Effect on MTrP Sensitivity …………….53
Stage I: Changes of SEA in the same locus……………………53
Stage II: Changes of SEA in 25 different loci………………….56
3.3 The Verapamil Effect on MTrP Sensitivity ………………58
Stage I: Changes of SEA in the same locus………………………58
Stage II: Changes of SEA in 25 different loci…………………60
3.4 The Dry Needling Effect on MTrP Sensitivity ………………62
3.5 AChR Channel Open Time………………………….………………65
Power spectral analysis of SEA………………………………………65
Regression analysis of AChR channel open time and AIV of SEA65
CHAPTER 4. DISCUSSION……………………………………………….70
4.1 Sympathetic Effect on SEA………………………………73
4.2 Calcium Channel Blocker Effect on SEA………………………75
4.3 Dry Needling Effect on SEA…………………………………77
4.4 AChR Channel Open Time……………………………………78
CHAPTER 5. CONCLUSIONS and RECOMMENDATION………83
References ………………………………………………………………85
List of suppliers………………………………………………………95
Appendix………………………………………………………………..96

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