Mechanistic basis of manual therapy in myofascial injuries ... · FASCIA SCIENCE AND CLINICAL APPLICATIONS e IMAGING: CLINICAL METHODS Mechanistic basis of manual therapy in myofascial

Journal of Bodywork & Movement Therapies (2013) 17, 221e234

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FASCIA SCIENCE AND CLINICAL APPLICATIONS e IMAGING: CLINICAL METHODS

Mechanistic basis of manual therapy in myofascialinjuries. Sonoelastographic evolution control

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Raul Martınez Rodrıguez, PT DO a,b,c,*, Fernando Galan del Rıo,PhD. PT DO a,d

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a Spanish National Football Federation, Physiotherapy Team, Urb. Av. Ramon y Cajal s/n, 28230 Las Rozas Madrid, SpainbTensegrity Center Physiotherapy & Osteopathy, Urb. Valdecabanas, Playa de Barro, 9, 28660 Boadilla del Monte,Madrid, SpaincHealth Area European University of Madrid, c/ Tajo s/n, 28670 Villaviciosa de Odon, Madrid, SpaindDepartment of Physical Therapy, Occupational Therapy, Rehabilitation and Physical Medicine, Rey Juan Carlos University,Av. de Atenas s/n, 28922 Alcorcon, Madrid, Spain

Received 5 March 2012; received in revised form 7 July 2012; accepted 17 August 2012

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Summary The term myofascia is referred to the skeleton of muscle fibres organized as an

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interconnected 3D network that surrounds and connects the musculoskeletal system. Extracel-
lular matrix muscle is relevant in tissue structural support and transmission of mechanicalsignals between fibres and tendons. Acute and chronic musculoskeletal injuries (muscle strain)are one of the major problems faced by those who practice any type of sport, regardless ofwhether they are professionals or amateurs. Therapeutic boarding is of uncertain value in mostcases because there are many contributing factors such as type, severity, functional implica-tion of the damaged tissue, progression or risk of relapse. Different studies suggest that themusculoskeletal cell matrix is essential for the development, maintenance and regenerationof skeletal muscle. In this article, we highlight the action of “non-contractile” structures, inparticular the myofascial system or muscle fascia, which can be responsible for the pathophys-iology and healing process of muscular injuries. Manual therapy plays a predominant role in thetreatment of these types of injuries and is key in the process of obtaining a scar capable oftransmitting mechanical information. The scientific basis of this process is described in thisarticle. Through real-time sonoelastography we have accurate information regarding thecurrent stage of the repair process and, thus, guide our treatment at all times. Some new

* Corresponding author. Tensegrity Center Physiotherapy & Osteopathy, Urb. Valdecabanas, Playa de Barro, 9, 28660 Boadilla del Monte,Madrid, Spain. Tel.: þ34 91 6324097.

E-mail address: [email protected] (R. Martınez Rodrıguez).

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222 R. Martınez Rodrıguez, F. Galan del Rıo

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concepts are introduced, including local elasticity, the relationship between fascial pretension
and the different stages of the physiological myofascia repair process, scar modelling tech-nique, and sonoelastographic evolution control.ª 2012 Elsevier Ltd. All rights reserved.
Muscular fascia or myofascia. Myofascialinterfaces

The term myofascia refers to the muscular supportingconnective tissue, skeleton of muscle fibres, or musculo-skeletal cell matrix. As such, myofascia consists of threedistinct layers of dense connective tissue (starting from themost external surface to the most interior): (1) theepimysium, which covers the muscle surface; (2) the peri-mysium, which consists of fascicles below the epimysium;and (3) the endomysium, which further divides thesefascicles into muscle fibres (Purslow, 2010) (see Fig. 1). It istherefore possible to find an injury not just on a musclefiber level but also at the endomysium, perimysium andepimysium level. Therefore, although an isolated conti-nuity solution at some fascial septa is possible, it is evidentthat muscular fiber strain with its corresponding epimysium

Figure 1 Scanning electron micrographs of the collagen fiberscaffolding in ECM structures in bovine sternomandibularismuscle. Upper panel: low-magnification view, showing thickerperimysial sheets surrounding fascicles. Lower panel: high-magnification oblique view, showing endomysial networks.From Purslow and Trotter (1994) with permission.

is inevitable. In other words, when there is a mechanicalovercharge at this level, should we talk about muscularinjuries or myofascial injuries? In this article, we highlightthe action of “non-contractile” structures, the myofascialsystem or muscle fascia, and their decisive participation inthe physiopathology and healing process of muscularinjuries (Kaariainen et al., 2000).

Kjaer et al. (2006) suggest common signaling pathwaysthat stimulate contractile and extracelular matrix (ECM)components. In fact, in developing skeletal muscle, animportant interplay between muscle cells and ECM can bepresent. In addition to the fascial layers described above,recent scientific research has shown the existence ofinterfaces or connective bonds precisely connecting thefascial tunics between them and the muscle’s cells. Theselinks have been traditionally omitted in conventionaldescriptive anatomy because they are obliterated in normaldissections. In studies from Passerieux et al. (2006) loopswere found between the perimysium and epimysium andnamed epi-perimisial junctions. Muscle physiologyadvances suggest that the perimysium plays a role in thecross-transmission of contraction forces (Huijing, 2009).This interfascial trabecular system may provide mechan-ically competent links for transmitting forces from theperiphery to the inside of the muscle. In addition to theabove loops, links called perimysialeperimysial junctionsexist that facilitate the longitudinal slip of fasciclesbetween themselves (Passerieux et al., 2007). However,the more relevant junctions appear to be the adhesionbetween the perimysium and the myofiber endomysium.These structures are introduced into the honeycombstructure formed by the endomysium and make their way tothe muscle cell surface, forming ‘‘perimysial junctionalplates’’ (for more information please refer to Passerieuxet al., 2007). The importance of these structures lies intheir ability to penetrate the inside of the muscle cell andstop at places with a high concentration of myonuclei andmitochondria. Thereby, as described later, externalmechanical forces that could affect gene expression, aredirected into the muscle cell and the musculoskeletal cellmatrix (Kjaer, 2004).

Myofascial repair. Local elasticity concept

The muscle wound, healing after myofascial injury (musclestrain), is a complex process including three overlappingphases: degeneration and inflammation, muscle regenera-tion and fibrosis (Jarvinen et al., 2000; Serrano and Munoz-Canoves, 2010). Following acute tissue injury, infiltratinginflammatory cells and resident stem cells orchestrate theiractivities to restore tissue homeostasis. It is known thatwhen myofascia is damaged, myogenic satellite cells acti-vate, divide, differentiate, and finally fuse with healthymuscle fibres to repair the injured tissue and to enhancehypertrophy of muscle fibres (Jarvinen et al., 2005; Filippin

Sonoelastographic evolution control. Scar modelling technique 223

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et al., 2009). Other non-muscle stem cells such as hepa-tocyte growth factor (HGF), fibroblast growth factors(FGFs), transforming growth factor-betas (TGF-betas), andothers, are released during muscle repair and guide muscleregeneration (Smith et al., 2007; Karalaki et al., 2009).

At the same time, the myofascial repair process leavesbehind a connective tissue scar in the injured muscle.Fibrosis can be defined as the replacement of the normalstructural elements of the tissue by distorted, non-functional and excessive accumulation of fibrotic tissue(Diegelmann and Evans, 2004). Thereby, because of anexcessive proliferation of collagen, dense scar tissue canform within the injured muscle. Unfortunately, the gradualdevelopment of fibrotic scar tissue within the injured areahinders muscle regeneration, and ultimately leads toincomplete functional recovery in relation to decrease ofcontractile function and muscle extensibility, along with anincreased risk of reinjury (Ciciliot and Schiaffino, 2010;Baoge et al., 2012).

The fibrotic phase of the repair process depends ongeneral factors including the type, severity, location andfunctional implication of the damaged myofascia; as well asthe appropriate inflammatory response, and treatmentprotocol, including early mobilisation (dense scar formationin the injury area may prohibit muscle regeneration),immobilisation (improves the penetration of muscle fibresthrough the connective tissue but their orientation is notparallel with the uninjured muscle fibres) or mobilizationstarted after short immobilisation (better penetration ofmusclefiber throughconnective tissueandbetterorientationof regenerated muscle fibres) (Jarvinen and Lehto, 1993).

More specifically, in the balance of the processes ofremodelling and fibrosis, the influence of particular growthfactors, including transforming growth factor-b1 (TGF-b1) isrelevant. This is a potent stimulator of collagen prolifera-tion, leading to the formation of fibrotic scar tissue afterinjury (Desmouliere et al., 1993). Tomasek et al. (2002)suggest that TGF-b1 induces myofibroblastic differentia-tion of fibroblasts both in vitro and in vivo. The resultingover-growth of myofibroblasts is responsible for the ensuingexcessive accumulation of fibrotic tissue. Interestingly,TGF-b1 can induce the differentiation of myogenic cells intofibrotic cells in injured skeletal muscle, increasing skeletalmuscle fibrosis (Li et al., 2004; Cencetti et al., 2010).

Furthermore, by means of mechanical stimuli being con-verted into chemical activity (Ingber, 1997) studies haveshown that the mechanical properties of a cell’s microenvi-ronment can have a great impact on cell structure and func-tion (Engler et al., 2006). One of the recent paradigm shifts instem cell biology has been the discovery that stem cells canbegin to differentiate into mature tissue cells when exposedto intrinsic properties of the ECM, such as matrix structure,elasticity, and composition (Reilly and Engler, 2010). Localelasticity refers to the ability of a tissue to return to its orig-inal length after a stretch, measured in kPa in a defined areaof soft tissue. In this context, recent findings (Wipff and Hinz,2009; Hinz, 2009; Meyer-ter-Vehn et al., 2011) suggest thatTGF-b1 activation is partly controlled by tissue stiffness andmyofibroblast contractile forces. This mechanical cue formyofibroblast differentiation establishes a vicious cyclebecause the excessive extracellular matrix secreting andremodelling activities of myofibroblasts are the cause and

effect of further connective tissue contracture and stiffening(Hinz, 2009). In other words, fibroblasts can alter theirmorphology and gene expression profile when grown onchemically equivalent surfaces, with different rigidities(Solon et al., 2007).

Fascial pretension and tensional homeostasis

Development of the tensegrity theory allows us to definethe relationship between mechanics and biochemistry atthe molecular level (Ingber, 2003). Tensegrity, which is anabbreviation for “tension integrity”, is an architecturalconcept developed by Fuller (1961). Tensegrity structuresare based on the presence of discontinuous compressionelements that balance the force generated or received bycontinuous tension elements. A significant characteristic ofthis tensegrity model is the tensile prestress (pretension) ofcontinuous tension elements, that ensures constant struc-ture stability against both compression and traction forces(Ingber, 2008a, b). This pretension can be variable, and itvaries, based on different mechanical demands, such asabsorption and management of forces. Moreover, in livingorganisms, all components are arranged according toa hierarchical organization that spans from the helical DNAstructure on the molecular level, to the cellular andnuclear cytoskeleton on the microscopic level to themusculoskeletal system on the macroscopic level, andfinally to the entire organism. The biotensegrity modelincorporates the compression-resistant bones of the skel-eton and the surrounding tension-generating muscles, andtension-resisting fascia (Ingber, 2008a, b). This is a physi-cally integrated framework that supports the weight of thebody, allowing rapid adjustment to external forces, whilepermitting freedom of movement (Ingber, 2008a, b).

One of the most significant characteristics of this bio-tensegrity model can be fascial pretension that ensuresconstant structural stability. This notion of acquiredpretension raises the following questions: in the healingprocess, could we consider fascial pretension increase to bea local etiological factor of increasing the fibrotic phase? Inother words, what happens in the healing process when westart with excessive pretension of the myofascia? Addi-tionally, can we measure the local pretension increase?

In this context, if physical forces play an important rolein tissue development and remodelling it is necessary toknow how fibroblasts respond to different pretension statesin the extracellular matrix. The biotensegrity model can beapplicable at the cellular level, considering the cell asa pretensed structure with cytoskeletal filament networksthat mechanically couple specific cell surface receptors,such as integrins, to matrix scaffolds (Ingber, 1998). Duringthe in vitro culture of fibroblasts, in 3D collagen matriceswith different states of substrate pretension, it wasobserved that fibroblasts have a high level of mechano-sensitivity (Rhee, 2009). Recent studies on fibroblasts inthree-dimensional (3D) collagen matrices have revealed theimportance of biomechanical conditions, in addition tobiochemical cues, for cell shape, signaling and migration(Solon et al., 2007; Langevin et al., 2010).

When cultured on 3D high-tension matrices, fibroblastsexhibit stress fibres, permanent focal adhesions and signal


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activation of focal adhesions. In the same culture with 3Dhigh-tension matrices, fibroblasts can adopt a laminar formby flattening and spreading (Gabbiani, 2003; Hinz, 2007;Chiquet et al., 2009). This laminar form will have importantimplications for cellular functionby activating aproliferativephenotype with high level of collagen biosynthesis activity(Grinnell, 2003; Kjaer et al., 2006). Additionally, conjunctivepresence of mechanical stress (high-tension matrix) andactive transforming growth factor b1 (TGF-b1) is essential toconvert fibroblasts into contractile myofibroblasts, whichcontribute to the reconstruction of injured tissue bysecreting new extracellular matrices, and by exerting highcontractile force (Hinz, 2007). Conversely, fibroblasts grownon low-tension matrices (relaxed) adopt a dendritic form, inwhich the dendritic extensions expand to allow for physicalcommunication among the fibroblasts. Low-tension culturesexperience changes in cell function in the same way thatchanges occur in cell function and shape in 3D high-tensionmatrices cultures. In this case (low-tension), biosyntheticactivity is inhibited, leading to a quiescent cellular state.

Additionally, this relationship between fibroblasts and theextracellular membrane through focal adhesions that ismediated by integrin receptors involves a bidirectional rela-tionship precisely conditioned by pretension (Grinell, 2008).

Manual therapy in myofascial injuries

If fibroblast behavior depends on surrounding mechanicalprocesses, it is relevant to understand these processes asfully as possible, when treating myofascial injury. Mostimportantly, can pretension states be modified by manualtherapy? Could cell and tissue physiology be influenced,using fascial therapy? And moreover, in the clinical context,to guide a correct treatment in myofascial injury, howmight we measure the relevant local elasticity changes inmyofascial tissues, before and after treatment?

In normal tissue response injury, wound healing isdirected by chemical and mechanical signals. Once theregenerative phase has started, isometric tension isgenerated in the repair area that stimulates a localincrease in collagen biosynthesis. Finally, it progresses tothe contracture phase, which can be induced by myofi-broblast contractile activity. When this final phase persistsover time, it can create pathological situations if thecontraction produced by the myofibroblasts smooth actinalpha-1 fibres also persists (Grinnell, 2003).

It is therefore essential to return the matrix from a high-tension state, to a low-tension one. It might be possible toinduce myofibroblast apoptosis, or to halt the trans-formation to myofibroblasts, although this hypothesis hasnot yet been proven (Hinz, 2007). Similarly, any manualaction that returns the matrix to a low-tension state mightbe able to inhibit biosynthetic activity by the fibroblast(excessive pathologic collagen crossovers), which woulddistort mobility between the fascial interfaces and, ulti-mately, would lead hypertrophic scars.

In order to reduce fibrosis and facilitate muscle regener-ation various techniques can be used to inhibit growthinvolved in the development of scar tissue. In this direction,some biologic approaches such as relaxin treatment (Negishiet al., 2005) or the use of antifibrosis substances such as

decorin (Fukushima et al., 2001), gammainterferon (gammaINF) (Foster et al., 2003) and others such as suramin (Chanet al., 2003) could inhibit TGF-b1, decrease myofibroblastproliferation, and promote proliferation and differentiationofmyoblasts, so improvingmuscle strength in vivo. However,clinical trials are required in order to safely include thistreatment in the standard management of muscle injuries.

Grinell (2008) has reported that: “physical manipulation offasciahas thepotential tochange thecell-matrix tension stateand also may influence localized release of cellular growthfactors. As demonstrated by our research on fibro-blastecollagen matrix interactions, such changes could leadtoprofoundandrapidmodulationof structural, functionalandmechanical interactions between fibroblasts and the extra-cellular matrix and, as a result, contribute to the reorgani-zation of fascia that results from bodywork practice”.

According to different authors, the relatively low levelof forces used by manual therapists would be insufficient tocause microfailure of the collagen, except perhaps in verythin or loose tissue (Chaudry et al., 2008). Thus it seemsprobable that a large part of the benefits of myofascialtherapies may be due to neurophysiological effects (Cantuand Grodin, 2001). In this sense, Schleip (2003) suggeststhat, in fascial techniques, the manual induction processwould be able to cause deep modulations, at differentlevels of the nervous system, through stimulation of inter-stitial receptors present in fascia, leading a global decreasein sympathetic tone that would produce a local vasomotorreaction, modifying, in short term the tissue viscoelasticity(thixotropic reaction).

Other authors suggest the possibility of causing structuralchanges in fibrosis and fascially restricted areas/ myofascialrestricted areas, through the decrease of cross-linksbetween collagen fibres, increasing gliding functionsbetween fascial layers, as well as inducing microfailure ofcollagen fibrils, as their tensile strength is exceeded. All ofthese changes might be associated with the transformationof ground substance, fromadensified state (gel) tomorefluid(sol) state (Simmonds et al., 2012; Tozzi, 2012) (Fig. 1).

With these concepts in mind, the authors of this paperhave developed a scar modelling technique (Table 1), thatattempts to reverse the matrix state from high to lowtension, with controlled mechanical stimuli through thecombined use of torsion, shear, traction, axial andcompressive vectors on scar tissue. All this is done in orderto generate a maintained tension, against a barrier, untila release of tension is perceived. (Pilat, 2003) (Fig. 2aec).We suggest that the pursuit of tensional homeostasis by thetherapist’s manual treatments, guided by the liberation of“jumps” of accumulated elastic energy in the interfaces,could cause the 3D reorganization of fascial interfaces ona macroscopic level (through junctions described above asfascial loops) (Passerieux et al., 2006), resulting intensional normalization on the microscopic level (tensionalreharmonization between the cytoskeleton and extracel-lular membrane through receptor integrins). This rehar-monization would act to normalize cell function andprovide medium-term remodelling of the extracellularmatrix. Obviously, further clinical trials are necessary totest this hypothesis.

Finally, in clinical practice, it is important to be alert tothe relationship development of hypertrophic scars andhigh-

Table 1 Brief description of the different stages of scar modelling technique.

1 Contact phase: this involves an initial vector compression, delivered by the second, third and fourth fingers of one hand.The applied pressure should be sufficient to reach the level of the scar, where the first resistance is met.

2 Stimulation phase: from this point, without losing the compression vector, an axial and/or spiral/circular component isadded, until a further resistance barrier is reached. In this way a combination of elastic barriers will have been engaged bythe fingers of the therapist. This combined compression and torsion is maintained for a variable time (30e90 s)

3 Release phase: at this point, depending on the tissue response to the initial stimulus, it is usual to perceive a release ofstored elastic energy in the form of “local unwinding.” This is followed by a progressive decrease of the initial tension, ascontact is maintained, and as reorganization of tissues in the scar area occurs, leading to a spontaneous repositioning of thefingers, as the barriers modify.

4 This process should be repeated as many times as needed (usually three to five) in order to perceive, finally, a normalizationof the initial feeling of tension.


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risk reinjury, and poor treatment outcomes (Engebretsenet al., 2010). Eventually, the scar will have its own charac-teristics determined by its degree of resistance and elas-ticity. These characteristics contribute to the quality of thescar, which is key in maintaining the integrity of forcetransmission. Itmust be strong enough to transmit forces andto sustain the loads of contraction, and elastic enough toabsorb forces and to prevent tearing under externallyapplied strains (Purslow, 2002). At this point, Heiderscheitet al. (2010) suggest the relevance of fascial stiffnessincrease as an etiological factor in muscle injuries, since it isknown that fascia demonstrates viscoelastic behavior (Yahiaet al., 1993; Chaudry et al., 2008) andplays an important rolein transmitting and deforming mechanical forces betweenmuscles (Huijing, 2009). So, in this context, could thepretension states related to hypertrophic scar and fascialstiffness, be modified by fascial therapy to decrease risk ofreinjury, while improving myofascial force transmission? Ifso, how might we measure local chronic fibrotic scars?

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Real-time sonoelastography andsonoelastographic evolution control

We propose the use of real-time sonoelastography (RTSE) asan image test to evaluate our hypotheses. Ophir et al.(1991) described the principle of strain imaging (elastog-raphy). In order to reduce time consuming calculationsPesavento et al. (2000) developed a fast cross sectionaltechnique based on real-time elastographical imaging thatcan provide very rough information about the assessment ofelasticity of biological tissues. Palpation is a well-knownsubjective method used by physicians to assess organsstiffness (Garra, 2007). In our context, ultrasound elasticityimaging can be considered as an extension of the ancientart of body palpation that can provide very valuableobjective data in prevention and treatment of myofascialinjury in order to: (a) measure local fascial pretension asa relevant etiological factor of increasing fibrotic phase inmyofascial wound healing; (b) measure the mechanicaldose we apply to the tissues and their reaction to themyofascial therapy, before and after treatment and (c)measure fascial stiffness by hypertrophic scars, as a rele-vant etiological factor of muscle injury and relapse.

RTSE is based on Young’s, or shear elasticity modulusmeasurements, and the principle that each biological tissuehas its own elastic characteristics, quantified according to

the formula for the Young’s modulus, which relates thecompression of a material when an external pressure isapplied, to its deformation (Sarvazyan, 2001).

In recent years, elasticity imaging has attracted attentionas a technique that directly reveals the physical property oftissue, making it possible to determine the change of tissuehardness caused by pathology (Frey, 2003). The originalapplication of RTSE was to detect and classify tumors, basedon the fact that these are significantly harder thansurrounding tissues. Thus, when a mechanical compressionor vibration is applied, the tumor (hard tissue) deforms lessthan the surrounding tissues (Bercoff et al., 2003).

This information is represented on amonitor as a chromaticspectrum called an elastography image (elastogram) over theconventional ultrasound image: areas in red represent themost elastic areas (fluids), areas in blue reproduce the mostrigid ones (bone),while areas in green can represent firmareaswith intermediate consistency/stiffness (Lalitha and Balaji,2011). In addition, it is possible to compile an elastographyscore, basedona5point scale according to thedifferent colorsdisplayed in the elastogram (minimal scoree 1e for scarswithelasticity similar to the surrounding myofascial tissue andmaximal score e 5 e for hypertrophic scars with no deform-ability). In this way it is possible to achieve a subjectiveassessment of elasticity tissue (Wang et al., 2010). In brief:sonoelastography is an echogram that is colored according tothe elasticity of the depicted tissue (see Figs. 3 and 4).

Some elastography equipment allows calculation of thestrain ratio. For example, by choosing a selected damagedarea, a region of interest (ROI), a comparative relationship isestablished, based on a constant hardness numerical value(bone to lesion strain ratio) or constant soft numerical value(fat to lesion strain ratio). In this way, it is possible to obtainobjective numerical relative elasticity databyevaluating thecompliance difference between the local lesion and thesurrounding tissues (Cho et al., 2010) (see Fig. 5).

Although RTSE is not yet usually used in routine clinicalphysical therapypractice, it hasbeenshowntobeuseful in thedifferential diagnosis of breast cancer, showing a high sensi-tivity, specificity and histopathological correlation in charac-terizingmalignant lesions of the breast (Andreea et al., 2011).However, variability in specificity between sites andobserversis possibly due to individual technique differences in per-forming elastography and measuring lesions (Barr et al.,2012). In addition RTSE has also been used to diagnosedifferent pathologies, including thyroid (Lim et al., 2012),cervical (Thomas et al., 2007) and prostate (Walz et al., 2011)

Figure 3 Elastography evaluates the deformation produced

Figure 2 (a) Scar modelling technique based in axial andcompressive vectors. (b) Contact phase: initial vectorcompression maintained by the finger flexor tone of thesecond, third and fourth fingers. (c) Stimulation phase usingspiroid/circular vector to generate a maintained tensionagainst a sense of resistance.


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cancers, as well as degrees of hepatic fibrosis in patients withchronic liver disease (Rath et al., 2011) (see Fig 6).

In recent years, RTSE has emerged as a way of charac-terizing the mechanical properties of the tissues of themusculoskeletal system, for example showing good feasi-bility and reproductibility in assessment of lateral epy-condilitis (De Zordo et al., 2009a, b). Other authors suggestthe relevance of RTSE in measurement of elasticity inhealthy achilles tendon (De Zordo et al., 2009a, b;Drakonaki et al., 2009) as well as in achilles tendinopathy(De Zordo et al., 2010; Sconfienza et al., 2010) and myo-fascial trigger points (Sikdar et al., 2009).

The authors of this paper propose the use of fascialtherapy (scar modelling technique) and RTSE, in combina-tion, for appropriate assessment, treatment and monitoringof myofascial injuries. Therefore, in fascial therapy, whenwe manually evaluate the status and fascial tonicity of theaffected tissues, we usually do a “fascial quick scan”. Inother words, we generate a mechanical wave manually,with the intention of spreading it through tissues. Thewavelike elastic rebound is palpated and evaluated by thetherapist’s hand. This provides a subjective evaluation,based on the individual’s years of clinical experience andstudy. When performing an assessment with RTSE we usea similar approach by generating a controlled deformationthrough the probe, to study the elastic behavior based onits transmission through tissues. This information isana-lyzed by the equipment software, which then providesa color-coded elasticity map containing objective andstorable information (elastogram). Moreover, as describedabove, with a strain ratio, we can quantitatively objectifythe elastic behavior of myofascial tissue during the repairprocess, thereby evaluating the effects of manual therapyduring the treatment process (see Figs. 7 and 8).

We believe that the elasticity measurement procedurethat we have developed, named sonoelastographic evolu-tion control (SEEC), is highly applicable for clinical use. Wepropose the following steps.

Palpatory identification

Through palpation, the therapist finds a possible scar orhypomobile area by attempting to relate it to the infor-mation that obtained when taking the case history.

Ultrasound location

Although we utilize ultrasonography (US) preferentially inthe transverse and longitudinal cuts, we can also use some

by an injury. Tissue hardness is indicated by a color scale.

Figure 4 Sonoelastography in real-time is a non-invasive method that utilizes a system to obtain images using an ultrasounddevice combined with a pressure sensor. This allows identification of the elasticity of a tissue region that has a different elasticity,compared with the surrounding tissues. Tissue hardness is indicated by a color scale.


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dynamic applications to study movement behavior. Oncewe have localized the area of interest, we draw a mark onthe skin framing the probe’s margins, and then collect theultrasound images. Additionally, based on the work ofLangevin et al. (2009), using ultrasound we assess not only

Figure 5 Strain ratio study in different regions of interest of th(0.01). (A) 61.71; (B) 39.99; (C) 8.60.

inflammation and fibrosis, but also fascial thickness. Itseems that repetitive motion and mechanical stress overhyperfibrotic scars, following myofascial injury, may resultin excessive deposition of collagen, increasing fibrosis andadhesions between fascial interfaces. In order to assess the

e same elastogram with regard to a constant reference value

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Figure 6 Images of the degrees of liver fibrosis compared with fibrosis stages Images become more uniform, and hard zonesincrease, as the disease progresses.


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dynamic performance and force transmission of the myo-fascial system, we suggest the use of dynamic ultrasound asan image test. This is capable of providing valuable infor-mation regarding myofascial interface sliding capacity,when subjected to active or passive movement, movementagainst resistance, or manual treatment by the therapist.

Elastography mode

The elastography mode is used to define the elasticbehavior of the intrinsic elastic characteristics of thetissues in the studied area. What is being searched for iscontinuity or, if this is not observed for the loss of homo-geneity in the tissue’s color scale, relative to surroundingtissues that are histologically identical (see Figs. 9 and 10).In current clinical practice, it is sometimes difficult, oreven impossible, to distinguish pathological tissue fromsurrounding healthy tissue on conventional ultrasound.Damaged inflamed or fibrotic areas often present the sameechogenicity. Moreover, it is well known that inflammationand fibrosis lead to changes in tissue elasticity. Therefore,because distinct tissue softening, linked to musculoskeletaldisorders, can be detected in real-time strain imaging (DeZordo et al., 2009a, b), we propose the use of RTSE as anideal method for objectifying the type of injury, and thestate of repair. Further, according with our hypothesis, wethink RTSE could be an ideal method for objectifying thestatus changes produced in soft tissues, after fascialmanipulation, providing information regarding the dailyevolution of muscle injuries, and the responses to manual

Figure 7 Images of the sonoelastography state before and after fscale evaluation, elasticity was quantitatively measured in the zonafter fascial therapy.

therapy. As explained below, this might allow application,in an effective manner, of the type of treatment required.This proposes that, depending on the tension degree in thedamaged area (based on the elasticity curve concept),progress can be judged as the matrix returns from a high-tension state to a low-tension one, or vice versa.

Measurement

It is possible to obtain an elastography score and/or a strainratio of a studied area e a numerical value of the relativeelasticity of a region of local lesion (scar), relative tosurrounding tissues. Additionally, histograms can providegraphical representations, showing a visual impression ofthe distribution of numerical data.

The next step is treatment. Scar modelling technique isapplied, according to the application principles describedabove, until the therapist produces a “change of status”.

In our clinical practice we then repeat the process, orstart from the elastography mode, where we obtain newrecordings. We compare the new results to those obtainedinitially. In this way, we can study elastic behavior oftissues over time with respect to the reference values wehave accumulated.

Discussion

In this article, we describe our clinical experience in thetreatment of muscle injuries with manual therapy and,specifically, with scar modelling techniques. To assess the

ascial therapy in the L5eS1 interspace. In addition to the colore of interest and local elasticity demonstrated a 10� increase

Figure 8 Changes in the elasticity of a previously repairedscar over a 3 weeks evolution in the soleus-medial head of thegastrocnemius union after scar modelling techniques takenafter 30 min of scar modelling techniques. Measurements weretaken in the most inelastic area (blue 1.26 cm2) and are shownto diminish considerably after therapeutic intervention(0.26 cm2).

Figure 9 RTS Real-time sonoelastographic and dynamicecography.

Figure 10 Sonoelastographic control images of a muscle injurtreatment. Note the large change in local elasticity as indicated b


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type of muscle injury, in clinical practice different imagetechniques are used, such as ultrasonography (US) andmagnetic resonance (MR). Sometimes, ultrasound cannotdistinguish pathological tissue from healthy tissue becauseinjured areas, involving inflammation or fibrosis, presentthe same echogenicity. While some authors suggest theimportant role of MR to evaluate the risk of recurrentmuscle injury (Koulouris et al., 2007), others have foundthat the MR use is limited in identifying individuals at riskfor reinjury (Heiderscheit et al., 2010). In this article, wepropose the use of RTSE and, in addition, dynamic ultra-sound, not only to improve the clinical use of diagnosticimaging techniques in muscle injuries, but also to direct ina very accurate way, the kind of treatment required inrelation to the mechanical properties of the injured area,as well as to measure the mechanical response of myofas-cial tissue following fascial therapy. In addition, the use ofRTSE can offer relevant clinical information, facilitatingcontrol and decreasing the high risk of relapse, secondaryto a hyperfibrotic dense scar.

It is known that differences in extracellular matrixelasticity can be a determinant of healing processes inmuscle regeneration and during the fibrotic phase ofmuscle repair. In an initial phase there is a need to main-tain the initial reflex contracture as an ideal tensionhabitat to increase biosynthetic activity, and movement offibroblasts to the scar region. Additionally, the use of bio-logical agents such as autologous growth factors (platelet-rich plasma) can accelerate the healing process, releasinghigh doses of growth factors to damaged tissue (Creaneyand Hamilton, 2008). Recent findings suggest the impor-tant therapeutic potential of intramuscular injection ofmuscle-derived stem cells that can improve and accelerateskeletal muscle healing, by increasing angiogenesis anddecreasing scar tissue formation (Ota et al., 2011;Gharaibeh et al., 2012). In the physical therapy context,with a focus on muscle remodelling, different authors(Valero et al., 2012) suggest that eccentric strengthtraining can stimulate the activation and proliferation ofsatellite stem cells that participate in the skeletal muscleregeneration. In order to obtain complete restoration ofthe pre-injury status of damaged tissue, excessive collagenproliferation should be avoided, in order to prevent

y over a 3-week evolution taken after 50 min of myofascialy the color scale. F

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Figure 11 Schematic relationship between the physiologicalprocess of cicatrization and the elastography chromatic scale.Elasticity curve that shows the ideal moment to choose scarmodelling to prevent fibrosis. The green line represents cica-trization with restitution of local elasticity after manual“modelling” of the scar, and the blue line shows cicatrizationwith elasticity loss and a high risk of relapse. (For interpreta-tion of the references to colour in this figure legend, the readeris referred to the web version of this article.)


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formation of hyperfibrotic scarring, with high risk of relapse(Desmouliere et al., 1993). Since scar tissue is stiffer thanthe contractile tissue it replaces and can alter themechanical environment of muscle fibres, evaluation of themechanical properties of the extracellular matrix is sug-gested. It is known that activation of TGF-b1 and excessiveextracellular matrix secreting and remodelling activities ofmyofibroblasts can, decisively, increase skeletal muscle

Figure 12 Elasticity curve with strain ratio measurements taken aof evolution.

fibrosis (Li et al., 2004) e processes that are partlycontrolled by the mechanical properties of the microenvi-ronment cells, and tissue stiffness (Wipff and Hinz, 2009;Hinz, 2009).

The authors propose the need of modifying what we call“elasticity curve” that registers the myofascial tissueduring the repair and fibrosis processes (see Fig. 11). Inthose cases in which a scar shows significantly higherstiffness rates than surrounding tissues, it would benecessary to control the use of treatment protocols such aseccentric exercise, that can potentially increase localpretension in the injured area, and favor an increase ofTGF-b1, related not only to muscle repair but also tofibrosis increase. Also those techniques based on biologicalagents such as autologous growth factors (platelet-richplasma) that, as cited previously, can be related to localrelease of growth factors that lead to significant collagenproliferation. On the contrary, it is proposed, in thiscontext (high-tension matrix) the use of scar modellingtechniques that encourage the extracellular matrix muscleto return from high-tension state to low-tension one. Toconfirm this proposal we suggest the use of RTSE and SEEC,including strain ratio and elastography imaging (elasto-gram) as clinical tools that allows the evaluation of changesin local elasticity, secondary to treatment.

During the evolution of the healing process, followinga muscular injury, the use of RTSE can offer valuableinformation, allowing adaptation of the treatment plan tothe recovery process e from the outset until the return tophysical activity. In other words, early mobilization (exer-cises with appropriate loading starting at 3e6 days post-injury) is needed to optimize the regeneration process, andto recover the extensibility and strength of the injured

fter 10 min of scar modelling technique of a scar after one year



skeletal muscle to pre-injury levels. In contrast, a minimumperiod is required to produce a scar of sufficient strengthand elasticity to bear the forces induced by remobilisation,without re-rupture (Jarvinen et al., 2007). Thus, theparameters usually used to assess treatment advice inrelation to evolution of the patient, image diagnosis withMRI, or ultrasound tests, of strength and extensibility, andthe manual therapist’s perceptions, and the sensationsdescribed by the patient, could be usefully supplementedwith RTSE and SEEC, including strain ratio and elastographyimaging.

Moreover, the high rate of recurrent injuries suggeststhat our current understanding of myofascial injury andreinjury risk may be incomplete (Opar et al., 2012).

The multifactorial origin of myofascial injuries is relatedto different risk factors including, among others, anatomicalfactors, such as biarticular organization, fiber-type distri-bution, muscle atrophy, strength imbalances and fatigue(Opar et al., 2012). Further, previous injury and formation ofdense fibrotic scar tissue can be a significant injury andreinjury risk. In this way dense scar tissue can be formedwithin the damaged muscle, hindering muscle regenerationand, potentially, provoking a decrease of contractile func-tion and muscle extensibility, as well as alteration of thetransmission of forces from the myofascial tissue to the

Figure 13 Elasticity curve with strain ratio measurements of a scbetween pre-treatment and immediate effects in elasticity changnique. Interestingly, structural changes in long-run elasticity can bscar modelling technique.

tendon (Ciciliot and Schiaffino, 2010). In this context, rec-ognising the secondary myofascial stiffness of hypertrophicscars as a relevant etiological factor of muscle injury andrelapse, we propose the use of RTSE and SEEC, includingstrain ratio and elastograms, to control the resistance andelasticity degree of the scar tissue. We also propose thata direct relationship must exist between local elasticity inthe scar and physiological force transmission, which meansthat when there is higher sonoelastographic similaritybetween the local elasticity of the scar and the elasticity ofthe surrounding tissues with identical histological charac-teristics, there will be better physiological transmission ofmechanical forces. Thus, when we find higher similaritybetween local elasticity and the surrounding tissues, thechances of relapse can decrease proportionately.

In connection with the ability of the RTSE to assessmechanical changes, before and after treatment, in ourinitial experience we have found that short-term changesmay be related to an important secondary vasomotorresponse to treatment (thixotropic reaction). Subse-quently, in the short term, a normalization of the degreeof elasticity is commonly observed (see Fig. 12). In clinicalsettings, in relation to chronic scarring, we have observedthat the greater the mechanical response that a scar hasto treatment, the better prognosis there will be,

ar after 3 months of evolution. It is possible to see differenceses (thixotropic reaction) after 50 min of scar modelling tech-e seen after 4 days, particularly after a second treatment with

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regardless of the adjustment of the elasticity index in theshort term. It is important that we develop protocols toevaluate elasticity long-term. The use of RTSE, secondaryto treatment, allows the assessment of structural changesin the medium and long term, unrelated to the immediatethixotropic reaction (short-term effect), involving stiff-ness decrease and tension normalization in the scar envi-ronment (i.e. the long-term effect) (see Fig. 13). In ourclinical experience an interesting correlation is commonlyobserved between the structural changes noted aftertreatment in the medium term (4e8 days), and theperceived self-improvement of the patient, regardingincreased extensibility, feeling of strength and functionalcapacity (Fig. 13).

Several limitations need to be addressed. A numberof studies have investigated the sensitivity and specifityof RTSE in assessing the mechanical properties of RTSEinvolving various tumor types, such as breast tumor(Andreea et al., 2011). In parallel, the evaluation andtreatment of musculoskeletal injury, for example, lateralepycondilitis, has shown a high reproductibility (De Zordoet al., 2009a, b). Furthermore, in the clinical context ofmyofascial injury it has been demonstrated that the strainratio is signally lower in the regeneration-fibrotic phase,and in hyperfibrotic scars in relation to surrounding tissues.Moreover, in clinical contexts we have observed a directrelationship between elastographic changes after fascialtherapy and improvements in clinical symptomatology,expressed by patients. However, high-quality clinical trials,with larger samples, are required to prove the sensitivity,reproductibility, intra-interobserver reliability, accuracyand validity of use of RTSE in assessment, treatment andmonitoring of myofascial injury. Additionally, in clinicalpractice, in a grade I (mild) muscle strain there may havecertain limitations in specifically characterizing and gradingthe elasticity of small scars with similar elasticity to thesurrounding myofascial tissue. In contrast, the greater thedegree of injury and subsequent repair process (densehyperfibrotic scarring), the more efficient is the ability ofRTSE to detect differences in elasticity between the scarand peripheral tissue. Further, because in our currentclinical practice we use manual compression this techniquecan be seen to be operator-dependant. However, newequipment, with controlled tissue compression systems andimage segmentation, could improve elasticity image capa-bility. Also, in our clinical experience it is sometimesdifficult to visualize the region of interest (ROI) after fascialtechniques. This may be because of the 3D tissue reorga-nization related to small “landslides” involving the releaseof accumulated elastic energy in the fascial interfaces.

Conclusion

Skeletal muscle injuries cause loss of activity and increasedrisk of recurrent injury. We propose the use of RTSE andfascial therapy (scar modelling technique), in combination,for appropriate assessment, treatment and monitoring ofmyofascial injury. The use of RTSE allows objectifying of thetype of injury, and the state of repair. Further, we think RTSEcould be an idealmethod for objectifying the status changes,produced in soft tissues after scar modelling technique,

allowing treatment to be directly linked to the degree oftension in thedamagedarea. In addition, randomizedclinicaltrials are required to check the potential of RTSE to evaluateand monitor myofascial injury.

Acknowledgments

We gratefully acknowledge Leon Chaitow for his assistanceand contribution to this article.

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