肌筋膜疼痛触发点内理化环境的改变及其作用

背景:以往研究对肌筋膜疼痛触发点的研究主要集中在发病特点和临床治疗方面,有关肌筋膜疼痛触发点局部组织的理化环境变化及其作用的研究较少.目的:总结并讨论肌筋膜疼痛触发点局部组织的理化环境变化及各种理化因子在肌筋膜疼痛中的作用.方法:由第一作者用计算机检索中国期刊全文数据库(CNKI:2000/2010)和Medline数据库(2000/2010),检索词分别为"肌筋膜疼痛触发点、致痛因子、神经系统致敏、伤害性感受器"和"myofascial trigger points,algogenic substance,nervous system sensitization,nociceptors".共检索到159篇文章,按纳入和排除标准对文献进行筛选,共纳入30篇文章.从肌筋膜疼痛触发点局部理化环境变化及各种理化因子的作用两方面进行总结,对理化环境在肌筋膜疼痛触发点发病中的重要作用进行介绍.结果与结论:肌筋膜疼痛触发点局部肌肉组织各种理化因子发生显著性变化,表现为各神经血管反应物质增多,炎症递质和致痛因子浓度明显升高.但是国内外对肌筋膜疼痛触发点理化环境变化及其作用的相关研究较少,了解仍不深入.     

颈肌筋膜触发点疼痛和头部牵涉痛的诊断与治疗

目的:调查颈肌触发点疼痛和其头部牵涉痛的特征,观察利用不同部位颈肌在不同辅助镇痛下的牵张治疗效果。方法:对80例不同颈部肌筋膜触发点疼痛患者,明确触发点疼痛和其头部牵涉痛的位置,并做正确诊断;根据诊断对这些病人在不同镇痛方法下进行不同的肌牵张疗法,有些病例在牵张前加用针刺破坏触发点或扎断挛缩增粗的纤维。治疗后教病人在家做自我牵张法和随访,并对治疗前后做VAS评分。结果:治疗前后VAS评分差异有显著性(P<0.001)。结论:本法对颈部肌触发点疼痛和其头部牵涉痛的治疗有效,并且方便易行。但治疗者必须理解其致痛病理和牵张治疗的基本原理,同时需要积累诊断经验。     

损伤性大鼠肌筋膜疼痛触发点的肌电活动和组织形态学特征

目的:观察损伤性大鼠肌筋膜疼痛模型触发点的肌电活动特征和组织形态学改变。方法:16只雄性SD大鼠(7周龄),随机分成对照组(A组)和实验组(B组)两组,实验组采取打击结合离心运动的实验方法对其进行连续8周造模干预。造模结束后,实验组与对照组均正常饲养4周。12周结束后对大鼠进行寻找触发点、记录触发点的肌电活动、病理解剖取材,然后进行触发点肌电分析和观察肌纤维病理组织形态。结果:A组大鼠没有出现触发点,B组大鼠平均出现2个触发点。正常对照组未发现自发肌电活动,实验组除了出现自发肌电活动外,其肌电电位是一种纤颤电位,与对照组的正常肌电电位有明显的区别。实验组的病理切片发现聚集的圆形或椭圆形肌纤维结节以及粗细相间的连续梭形肌纤维。结论:肌筋膜触发点是一种区域性堆集并具有肌电信号异常的挛缩肌纤维。此特征也反证了打击结合离心运动方法建立的大鼠触发点动物模型是有效的。     

肌筋膜触发点的热象图

<正> Travell和Simons提出了第一个有关肌肉综合征的诊断框架。他们描述的肌筋膜触发点(TrPs)是一些对刺激过敏的斑块,通常位于一束绷紧的骨骼肌肉或肌筋膜内。它们在加压时出现疼痛,并产生特征性的牵涉痛、触痛和自主神经现象。活动性TrPs 常有触痛,防碍肌肉完全伸展,降低肌力,直接加压时产生牵涉痛。当受到适当的刺激时,活动性TrPs 引起肌纤维的局部抽搐反应,并对疼痛     

基于电刺激的大鼠肌筋膜疼痛触发点的发生机制

目的:探究电刺激下肌筋膜疼痛触发点肌纤维的兴奋性和耐疲劳表现。方法:将48只雄性SD大鼠随机分为对照组(CG1、CG2、CG3)和触发点组(TG1、TG2、TG3)。CG1和TG1测试刺激阈值强度和最大收缩力量(MCF)以及其最适刺激强度;CG2和TG2测试不同刺激强度下MCF的变化;CG3和TG3测试不同刺激频率下MCF的变化。钝性打击结合离心运动造模8周,恢复4周后将大鼠接入生物机能测试系统,给予肌纤维一系列电刺激,测量比较各组引起肌肉收缩的阈值强度、MCF、刺激强度和频率诱导的肌肉疲劳等指标。结果:TG1组引起肌肉开始收缩的阈值强度和最大收缩力量(MCF)的最适刺激强度比CG1组低,具有显著性差异(P0.05);TG1组与CG1组的MCF无显著性差异(P0.05)。TG2组电刺激引起的MCF第15、20次增量电刺激低于第1、5、10次增量,具有高度显著性差异(P0.01);TG2组电刺激引起的MCF第10、15、20次增量CG2组,具有高度显著性差异(P0.01);TG2组电刺激引起的MCF第1、5、10次增量无显著性差异(P0.05);TG2组电刺激引起的MCF第1、5次增量与CG2组相比无显著性差异(P0.05)。TG3组电刺激引起MCF所需的刺激频率比CG3组低,呈高度显著性差异(P0.01);TG3组电刺激引起的MCF比CG3组低,具有显著性差异(P0.05)。结论:与正常肌纤维相比,触发点肌纤维对电刺激反应更敏感,受到连续电刺激时更易疲劳。     

肌筋膜触发点疼痛特征的要点分析

介绍肌筋膜触发点疼痛的病理和临床特点及怎样理解其诊断和治疗方法。肌筋膜触发点是受累骨骼肌上能够激惹疼痛的局限小区，挤压时疼痛和拉紧的带，引起牵涉痛和交感现象。静息下运动终板神经末梢处乙酰胆碱浓度增高，引起肌后连接持续去极化和持续性肌节缩短和收缩结节。慢性持续肌节缩短增加局部能量的消耗和血循环的减少，神经血管反应物质释放，致敏传入神经引起触发点疼痛。触发点诊断常依赖病理生理学的诊断标准。触发点治疗的可能原则是对受累肌的牵张，其次是想法刺激或破坏触发点。常用的方法有肌疗法、肌肉牵张和冷喷雾疗法、针刺法加肌肉牵张法、肉毒素注射加肌肉牵张法。同时，常需要辅以补充各种维生素和改善周围循环和提高免疫功能的药物。     

肌肉牵张与冷敷对颈部肌筋膜触发点针刺后疼痛的效果

目的 探讨肌肉牵张与冷敷对颈部肌筋膜触发点针刺后疼痛的应用效果。 方法 选取2016年6月-2017年6月行颈肌筋膜触发点针刺治疗后的80例患者为研究对象,采用随机数字表法将其分为实验组及对照组各40例。比较2组疼痛评分及随访3个月内颈肌筋膜疼痛复发情况。 结果 2组疼痛评分在时间效应及组间效应上比较,差异有统计学意义(F_时间=23.703,P<0.001;F_组间=29.395,P<0.001);3个月内实验组颈肌筋膜疼痛复发例数少于对照组(χ²=26.593,P<0.001)。 结论 肌筋膜触发点针刺治疗后进行肌肉牵张加冷敷能够有效地改善患者的疼痛症状,降低颈部肌筋膜疼痛的复发率,提升患者满意度。     

基于H反射通路探究大鼠慢性肌筋膜疼痛触发点的发病机制

目的:基于H反射探究大鼠慢性肌筋膜疼痛触发点(myofascial trigger points,MTrPs)的发病机制。方法:16只7周龄雄性SD大鼠随机分为实验组和对照组,实验组采取对腓肠肌定点钝性打击结合离心运动的模式进行连续8周造模。造模结束后两组均正常饲养4周。12周结束后,检测MTrPs造模成功指标(即紧张带、局部抽搐反应和自发肌电活动),并在此基础上进行H反射的诱发实验,采集引发H波的阈值、Mmax、Hmax、M波和H波潜伏期、Hmax/Mmax等。结果:与非MTrPs相比,MTrPs处诱发的H反射Mmax(4.28±1.27 mV)较低,Hmax(1.01±0.34 mV)较高,H波潜伏期(4.60±0.89 ms)较短,Hmax/Mmax比值(0.21±0.19)较大(P<0.05)。结论:H反射与慢性MTrPs形成的病理生理机制有关,MTrPs大鼠脊髓中枢可能存在高度致敏,Iα类传入神经兴奋性较高,肌梭敏感性可能也较高。     

PGF2α对大鼠肌筋膜疼痛触发点自发肌电活动的影响

目的:观察肌筋膜疼痛触发点(MTrPs)模型大鼠外周血中前列腺素F2α(PGF2α)浓度变化情况,并通过体外注射PGF2α观察其对触发点肌电活动的影响,探究PGF2α与触发点的关系。方法:40只雌性SD大鼠随机分为对照组(CG组)、造模组(MG组)、生理盐水组(SG组)和PGF2α组(PG组),每组10只。除CG组外,其余三组采取打击结合离心运动进行干预8周,恢复4周,检测受累肌结节、紧绷带、局部抽搐反应和自发性电位;CG组正常饲养12周。12周后ELISA法测量各组大鼠血清PGF2α浓度。之后分别对SG组局部肌肉注射生理盐水,PG组局部肌肉注射PGF2α,CG组和MG组分别作为空白对照和模型对照不注射任何物质。干预后即刻记录各组静息状态下的自发性电活动。结果:与CG组相比,其余三组大鼠血清PGF2α浓度均显著性增加(P0.05)。给药后即刻,MG组、SG组和PG组大鼠均能记录到异常的自发电位,对照组大鼠基本无电活动,肌电波形形似一条直线。与CG组相比,MG组、SG组和PG组的肌电波频、波幅以及波长均有显著性差异(P0.05);PG组显著高于MG组和SG组(P0.05)。MG组和SG组之间相比各指标均无显著性差异。结论:PGF2α能增加触发点肌纤维的肌电活动,促使触发点活性增加。     

肌筋膜触发点疼痛特征的要点分析

介绍肌筋膜触发点疼痛的病理和临床特点及怎样理解其诊断和治疗方法。肌筋膜触发点是受累骨骼肌上能够激惹疼痛的局限小区,挤压时疼痛和拉紧的带,引起牵涉痛和交感现象。静息下运动终板神经末梢处乙酰胆碱浓度增高,引起肌后连接持续去极化和持续性肌节缩短和收缩结节。慢性持续肌节缩短增加局部能量的消耗和血循环的减少,神经血管反应物质释放,致敏传入神经引起触发点疼痛。触发点诊断常依赖病理生理学的诊断标准。触发点治疗的可能原则是对受累肌的牵张,其次是想法刺激或破坏触发点。常用的方法有肌疗法、肌肉牵张和冷喷雾疗法、针刺法加肌肉牵张法、肉毒素注射加肌肉牵张法。同时,常需要辅以补充各种维生素和改善周围循环和提高免疫功能的药物。     

Uncovering the biochemical milieu of myofascial trigger points using in vivo microdialysis: An application of muscle pain concepts to myofascial pain syndrome

This article discusses muscle pain concepts in the context of myofascial pain syndrome (MPS) and summarizes microdialysis studies that have surveyed the biochemical basis of this musculoskeletal pain condition. Though MPS is a common type of non-articular pain, its pathophysiology is only beginning to be understood due to its enormous complexity. MPS is characterized by the presence of myofascial trigger points (MTrPs), which are defined as hyperirritable nodules located within a taut band of skeletal muscle. MTrPs may be active (spontaneously painful and symptomatic) or latent (non-spontaneously painful). Painful MTrPs activate muscle nociceptors that, upon sustained noxious stimulation, initiate motor and sensory changes in the peripheral and central nervous systems. This process is called sensitization. In order to investigate the peripheral factors that influence the sensitization process, a microdialysis technique was developed to quantitatively measure the biochemical milieu of skeletal muscle. Biochemical differences were found between active and latent MTrPs, as well as in comparison with healthy muscle tissue. In this paper we relate the findings of elevated levels of sensitizing substances within painful muscle to the current theoretical framework of muscle pain and MTrP development.     

Documentation of myofascial trigger points

Two basic diagnostic features of myofascial trigger points (TPs), namely, local tenderness and alteration of tissue consistency (such as in taut bands, muscle spasm), can be documented quantitatively by simple hand-held instruments. A pressure threshold meter (algometer) assists in location of TPs and their relative sensitivity. A side-to-side difference exceeding 2kg in comparison with normal values indicates pathologic tenderness. The effect of treatment can be quantified. Pressure tolerance, measured over normal muscles and shin bones, expresses pain sensitivity. Myopathy is suspected if muscle tolerance drops below bone tolerance. Tissue compliance measurement documents objectively and quantitatively alteration in soft tissue consistency. Muscle spasm, tension, spasticity, taut bands, scar tissues, or fibrositic nodules can be documented. The universal clinical dynamometer is used as part of a physical examination to quantify weakness. Thermography (heat imaging) demonstrates discoid shaped hot spots over TPs. Muscle activity, spasm, or contraction is visualized as increased heat emission in the shape of the active muscle.     

Differences between myofascial trigger points and tender points

The article describes and compares the characteristics of myofascial trigger points (MTrPs) of the myofascial pain syndrome and the tender points (TePs) of the fibromyalgia syndrome. Many statements are hypothetical, because not all aspects of the disorders have been clarified in solid studies. Signs and symptoms of MTrPs: (1) palpable nodule, often located close to the muscle belly, (2) often single, (3) allodynia and hyperalgesia at the MTrP, (4) referral of the MTrP pain, (5) normal pain sensitivity outside the MTrPs, (6) local twitch response, (7) local contracture in biopsy material, (8) peripheral mechanism probable. Signs and symptoms of TePs: (1) no palpable nodule, (2) location often close to the muscle attachments, (3) multiple by definition, (4) allodynia and hyperalgesia also outside the TePs, (5) enhanced pain under psychic stress, (6) unspecific histological changes in biopsy material, (7) central nervous mechanism probable. The multitude of differences speak against a common aetiology and pathophysiology.     

Thermographic imaging of myofascial trigger points

Thermographic findings in two patients suffering from myofascial trigger points are presented. These are shown as discrete foci of increased thermal emission, with corresponding areas of diffuse hyperthermia. These thermal findings correlate highly with the classic locations of specific trigger points and their areas of pain referral, respectively, as described in literature. Not only do these cases describe a thermal pattern that varies somewhat from previous reports, but they also illustrate the previously unreported imaging of areas of pain referral from specific trigger points.     

Contribution of myofascial trigger points to migraine symptoms.

This study evaluated the contribution of myofascial trigger points (TrPs) to migraine pain. Seventy-eight migraine patients with cervical active TrPs whose referred areas (RAs) coincided with migraine sites (frontal/temporal) underwent electrical pain threshold measurement in skin, subcutis, and muscle in TrPs and RAs at baseline and after 3, 10, 30, and 60 days; migraine pain assessment (number and intensity of attacks) for 60 days before and 60 days after study start. Fifty-four patients (group 1) underwent TrP anesthetic infiltration on the 3rd, 10th, 30th, and 60th day (after threshold measurement); 24 (group 2) received no treatment. Twenty normal subjects underwent threshold measurements in the same sites and time points as patients. At baseline, all patients showed lower than normal thresholds in TrPs and RAs in all tissues (P < .001). During treatment in group 1, all thresholds increased progressively in TrPs and RAs (P < .0001), with sensory normalization of skin/subcutis in RAs at the end of treatment; migraine pain decreased (P < .001). Threshold increase in RAs and migraine reduction correlated linearly (.0001 < P < .006). In group 2 and normal subjects, no changes occurred. Cervical TrPs with referred areas in migraine sites thus contribute substantially to migraine symptoms, the peripheral nociceptive input from TrPs probably enhancing the sensitization level of central sensory neurons. PERSPECTIVE: This article shows the beneficial effects of local therapy of active myofascial trigger points (TrPs) on migraine symptoms in patients in whom migraine sites coincide with the referred areas of the TrPs. These results suggest that migraine pain is often contributed to by myofascial inputs that enhance the level of central neuronal excitability.     

Understanding effective treatments of myofascial trigger points

This article considers specific treatment approaches and the role of etiological mechanisms in terms of clinical feature characteristics of MTrPs: increased muscle tension, pain and tenderness, painful stretch range of motion, initiating causes of MTrPs. Final sections note additional treatments that are currently used, and summarize the etiological and clinical distinctions between MTrPs and fibromyalgia.