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Luigi Stecco, physiotherapist and author of the Fascial Manipulation® method (Stecco L 2004, Stecco L & Stecco A 2017), has focused on the relationship between muscles, deep fascia and its components (epimysium, perimysium and endomysium – see Ch. 1 ) to develop a new approach to musculoskeletal dysfunctions that takes into account movement limitation, weakness and distribution of pain. Based on the idea of fascia as the uniting element between the various body segments, this author also considers fascia, with its innervation, relationship with muscle spindles and Golgi tendon organs and the presence of conspicuous myotendinous expansions that link adjacent segments together, as having a potential role as a coordinating component for motor units of unidirectional muscle chains.

Fascial Manipulation ® aims at interpreting the passage of tensional compensation from one segment to another and the evolution from an initial, segmental disturbance to a more generalized dysfunction . ‘Manus sapiens potens est’ ( Fig. 9.1 ), the logo coined for this method, means ‘A knowledgeable hand is powerful’, suggesting that only by understanding the origin of a problem can manual therapies resolve them rapidly and efficiently. Numerous histological, biomechanical, and functional studies have been undertaken to verify some of the hypotheses proposed by Stecco, focusing on the anatomy of the superficial (Lancerotto et al. 2011) and deep fascia (Stecco C et al. 2009), innervation (Stecco C et al. 2007), and the possible mechanisms of action of the manual technique itself.

The thoracolumbar fascia (TLF) region is one area of fascia that has been closely examined and its implications in low back pain have been considered (Langevin et al. 2009, Schilder et al. 2014). The TLF is a large, diamond-shaped sheet that forms part of the deep fascia. While descriptions vary amongst different authors, according to C. Stecco (2015), the TLF consists of two macroscopic layers, anterior and posterior, the latter having three sublayers, a feature of aponeurotic-type deep fascia (Benetazzo et al. 2011). These three sublayers have different fiber characteristics, thickness and innervation, with the outermost layer being the most innervated. The multilayer posterior lamina connects latissimus dorsi and the contralateral gluteus maximus and joins with part of the external oblique and trapezius, via their fasciae. This lamina also fuses with the serrati posterior fascia and the erector spinae aponeurosis. Distally, it attaches to the posterior superior iliac spine, the iliac crests and the long dorsal sacroiliac ligament, as well as to the supraspinal ligament and spinous processes to the L4 level. The anterior layer of the TLF attaches medially to the transverse processes of the lumbar vertebrae and laterally to the internal oblique and transversus abdominis muscles. The different fiber directions give the TLF a crosshatched appearance.

Thus, different vectors act on each segment. Between the two principal vectors of every MFU (monoarticular fibers and biarticular fibers), there are many smaller vectors formed by single muscle fibers situated some distance apart. If we analyze all of these fibers, we can see how the monoarticular fibers are deeper and more voluminous than the biarticular ones. Partially free to slide in their fascial sheaths, the deep monoarticular muscle fibers transfer their tension to the superficial fascial layers via the continuity of the endomysium, perimysium and epimysium. The monoarticular fibers can exert strength and stability during movement while the biarticular fibers transmit tension between adjoining segments. While regional specializations in fascial structures do exist (Stecco A et al. 2009a), the same ‘architecture’ can be found in every MFU.

Each MFU has two functionally different areas. The first is on the deep fascia covering the muscle belly and can be considered as the active component of the MFU. Known as the center of coordination (CC), according to the Fascial Manipulation ® model, the forces involved in muscle fiber contraction converge in this small area. The second area is a passive component. It is situated around the joint that is moved by MFU muscle fiber contraction. Called the center of perception (CP), this is where the patient feels the movement resulting from MFU activity (in a physiological situation) or pain (in a pathological situation).

According to Stecco A et al. (2013b), impeded sliding between collagen fiber layers within the fascia of a malfunctioning MFU could produce atypical afferent information from mechanoreceptors embedded within the fascial component of the MFU. Furthermore, given that the connective tissue capsule of muscle spindles is embedded in endomysium and it is continuous with the perimysium, altered sliding of these fascial tissues could affect correct muscle spindle firing (Stecco L 2016). Consequent anomalies in motor unit recruitment result in unaligned joint movement. Over time, joint conflict, inflammation of periarticular soft tissues, pain or joint instability can develop, with symptoms arising in the corresponding CP.

To simplify the interpretation of myofascial dysfunctions, Stecco describes movement in terms of directions on the three spatial planes. In classical terminology, the hip joint flexes when the femur moves forward but at the knee, the same direction of movement is called extension. In Fascial Manipulation® terminology, all forward movements on a sagittal (medial) plane are called antemotion and all backward movements retromotion. Adduction and abduction are substituted by lateromotion (outwards from the center) and mediomotion (inwards from the periphery), and intrarotation and extrarotation are used every time a segment moves on the horizontal plane. Thus, movements on the sagittal plane are governed by the MFUs of ante- and retromotion, movements on the frontal (coronal) plane by the MFUs of latero- and mediomotion and movements on the horizontal plane by the MFUs of intra- and extrarotation (Table 9.1 ).

Agonists are a group of muscles that contract to provide the force required to produce a particular movement. Antagonists are the muscles that oppose the action of the agonists. In Stecco’s model, agonist and antagonist MFU interaction is important for myofascial force transmission and the coordination of movement, as also demonstrated by other studies (Huijing & Baan 2003). As the agonist MFU is activated during movement (albeit forwards, backwards or sideways), the antagonist MFU adapts according to the angle of inclination of the body part (reciprocal inhibition).

For example, the MFU for elbow extension has its own antagonist myofascial unit that coordinates elbow flexion ( Fig. 9.3 ). When the elbow extends, the monoarticular fibers contract and the intermuscular septum (where they insert) is stretched. The monoarticular fibers of the antagonist MFU (elbow flexion) insert on the other side of this same septum meaning that during extension, its monoarticular components are stretched a little too, causing embedded stretch receptors to fire. Therefore, fascia can be considered as an active component in agonist–antagonist activity.

Stabilization by monoarticular vectors and synchronization between adjacent segments by biarticular muscular fibers allows for precision and stability of each segment during movement. The biarticular muscle fibers composing each MFU connect unidirectional MFUs responsible for movement in only one direction to form myofascial sequences (MFS). Part of the biarticular fibers from each MFU also insert onto the deep fascia of adjacent segments forming myotendinous expansions that link one segment to the next (Stecco C et al. 2008, Stecco A et al. 2009b) and providing the anatomical substratum of the MFS.

For example, the anatomical continuity of the MFS on the sagittal plane in the lower limb can be traced from antemotion talus (dorsiflexion of the foot), which is carried out by tibialis anterior, extensor digitorum longus and extensor hallucis longus muscles. These muscles originate from the condyles of the tibia and the fibula, from the intermuscular septa and the overlying fascia. The tendinous expansion of the quadriceps tensions the anterior fascia of the leg proximally, whereas the previously listed muscles traction it distally. The fascia lata connects with the anterior fascia of the leg, and is tensioned distally by its insertions into the intermuscular septa of the vastus medialis and lateralis. Moreover, it is continuous with the ileopsoas fascia, which inserts onto the vastus medialis that tensions it distally, together with the sartorius. Ileopsoas fascia continues above over the fascia of the iliacus and psoas minor muscles. The iliacus fascia is involved in antemotion of the pelvis (retroversion of the pelvis) together with the inferior rectus abdominis, which is surrounded by the lateral raphe. This weave of connective tissue joins the abdominal muscles and the anterior and posterior layers of the TLF.

The contraction of the triceps surae stretches the popliteal fascia and the fibers of the gastrocnemius inserted into it. A few fibers of the biceps femoris, as well as some fibers of the semitendinosus and semimembranosus, tension the popliteal fascia and the fascia of the leg proximally. These latter muscles participate both in retromotion genu (knee flexion) and retromotion coxa (hip extension); therefore, they not only tension the popliteal fascia but also the sacrotuberous ligament. This myofascial concatenation is tensioned during the push-off phase of each step. The sacrotuberous ligament continues proximally with the TLF. The erector spinae muscles originate from the TLF and during retromotion lumbi (extension of the spine) they become tensors of the retromotion sequence of the lower limb.

In cases of low back pain, clinicians apply Stecco’s biomechanical model to interpret the spread of tensional compensations from one segment to another. A tensile alteration in any given MFU causes a counter tension in another MFU along the same sequence, as a means of preserving the fascia’s basal tension. Such tensile adjustments are a remedy that often creates acute pain because the free nerve endings, or mechanoreceptors, in this segment of fascia are subjected to excessive, abnormal traction. The body then compensates this tension as a means of re-establishing equilibrium. Compensatory tension can be symmetrical (in the antagonist sequence) but, with reference to the MFU where the compensation originated, it could be localized in a proximal or distal segment. In the trunk, each MFU of antemotion and retromotion can act with the contralateral side of the body. For example, it is possible to find that a hypertonic left-sided component of the antemotion MFU in the lumbar region is compensated by a right-sided component of retromotion.

Key Point

Silent CCs are asymptomatic areas of deep fascia that can be deduced from the patient’s symptoms and located by using knowledge of the continuity of the sequences on the three planes.

Application of the Fascial Manipulation® method involves compilation of a specific assessment chart that assists the selection of CCs to treat, and provides concise documentation of treatment sessions. Patient’s personal data and history, an abbreviated description of the presenting symptoms, including pain location, characteristics, and chronicity, and identifiable painful movements are all noted.

Patients are encouraged to report any concomitant pain because even minor painful areas are useful in indicating the disturbed sequence or plane.

The following questions are taken into consideration:

In which plane have the various tensional compensations developed?

What could have been the initial trauma that determined these compensations?

Are they ascending or descending compensations?

Are there any hidden compensatory strategies ( silent CCs )?

Multisegmental problems are approached through the analysis of chronological events involved in each individual case. Asymptomatic previous disturbances are frequently the cause of presenting pain because fascia often repairs a trauma initially with densification and, subsequently, with a buildup of an excess of collagen fibers, neutralizing the lack of elasticity due to established densifications by extending tension along the same sequence. While heat applied to an initial densification can resolve changes in the extracellular matrix of the muscular fascia, any excess fibers will not be spontaneously removed by the body’s physiological reparative mechanisms because they are normal collagen fibers and are not recognized as being inappropriate.

• Elasticity: fascia is an elastic tissue with established limits, which permits involvement in motor coordination and perception of motion. Different studies do suggest that fascia is richly innervated. Nerves passing through the deep fascia are surrounded by loose connective tissue. Therefore, they are subjected to traction when the fascia lengthens. However, when these nerves terminate in neuroreceptors (e.g. free nerve endings) they insert directly into the collagen fibers. The abundance of free and encapsulated nerve endings could activate specific patterns of proprioceptors, potentially providing directional and spatial afferent information.

In general, if a traumatic stimulus causes local inflammation, rest and physiological movement induce reorganization of collagen fibers along the lines of traction and a normal healing process of the damaged area ensues. Repeated inflammation (overuse, repetitive strains) can affect the extracellular matrix, or ground substance, of the loose connective tissue layer interposed between the multilayers of collagen fibers present in the deep fascia (Table 9.2 ). In chronic situations, this can lead to increases in the number of collagen fibers resulting in a chaotic redistribution of these fibers at the CCs. Trauma, disuse with consequent diminished circulation, repetitive motion and poor posture can cause the ground substance to transform from a sol to gel state, resulting in lack of sliding.

Key Point

In Fascial Manipulation® treatment of deep muscular fascia, the term friction refers to the force required to modify the increased viscosity of the extracellular matrix in the loose connective tissue located between intrafascial collagen fiber layers. The manual technique is referred to as a deep friction because it involves a perpendicular pressure together with a tangential oscillation applied to densified tissue. This technique is a potentially effective method for influencing flow characteristics of hyaluronan (HA) in the extracellular matrix (Roman et al. 2013). Furthermore, deep friction applied to such tissue causes an increase in local temperature, setting off a chain reaction that modifies HA viscosity (Cowman et al. 2015).

Under physiological conditions, CCs are not hypersensitive nor do they produce referred pain when stimulated. Normally, the elasticity of the fascia allows it to adapt to compression without straining embedded nerve endings. Densified CCs increase overall tension, lowering the pain threshold of the free nerve endings, and minimal compression can then be sufficient to set off local as well as referred pain. This process can also involve the CP of the implicated MFU, the CP of the antagonist MFU, or the entire MFS, which can explain the irradiation of pain along this structure. These stresses can apparently resolve spontaneously through tensional compensations and a densified CC often becomes silent (similar to latent trigger points) and pain is no longer felt at the CP. This seemingly balanced condition is unstable and, whenever the body is no longer capable of maintaining these compensations, chronic fascial densifications become active, and pain presents again.

The alteration of a CC can cause joint pain (in the CP) as well as a joint blockage. In the latter case, if it is a recent lesion then it is possible to intervene directly with joint mobilizations. Freeing the articulation reduces the painful afferent and eliminates MFU hypertonicity. However, if the chronicity of the problem has created a true ‘densification’ of the CC or, in more chronic conditions, a fibrotic state with collagen fiber dysplasia, then manipulation applied directly to the CC is required (Pedrelli et al. 2009, Pavan et al. 2014).

Considerable amounts of hyaluronan (HA), previously referred to as hyaluronic acid, are found in the ground substance of the loose connective tissue layer between the deep fascia and the surface of muscle and in the intrafascial layers (Stecco C et al. 2011). HA normally acts as a lubricant but, under pathological conditions, it aggregates, increasing ground substance viscoelasticity, resulting in densification (Stecco A et al. 2013b). Manipulation is required to act on a densified CC for a sufficient amount of time for the friction against the fascia to produce heat (Borgini et al. 2010). This heat is needed to modify the consistency of the ground substance and to initiate the inflammatory process required for healing.

Case Example Fascial Manipulation® applied to low back pain

LR is a 50-year-old male who has been suffering from low back pain for 1 year. Symptoms were resistant to treatment of any kind.

He had never suffered from backache prior to this and a CAT scan has excluded a prolapsed disc. Pain, localized along the right posterior side of the lumbar region and pelvis, had begun 1 year ago after a tennis match and since then it has never completely disappeared but it has varied in intensity. Symptoms are accentuated with running and bending forward.

Two segments (LU, PV) are indicated as the site of pain distributed in the posterior part (RE) of both segments. This could indicate the sequence of retromotion but this would mean considering only the present situation without considering other potential causes. Certainly, by treating the CC of RE-LU and RE-PV it is likely that the patient will have some relief but at the first attempt at running it may well recur. When asked ‘Have you ever had pain in the past in any part of your body? Did you ever suffer from fractures or ankle sprains? Did something happen to your knees in the past?’ the patient recalls having a right first metatarsal fracture when aged 40 (10 years ago) and he remembers rupturing his right Achilles tendon 1 year later (9 years ago).

From this data it was possible to hypothesize that the spasm in the retromotion sequence (RE-TA, RE-LU, RE-PV) may have been determined by a compensation created by the antagonist antemotion sequence (AN-PE) that had not caused any problems for 10 years. It required an intense physical stress, such as a long tennis match, to decompensate the tensile equilibrium.

Movement assessment revealed pain along the posterior leg during the test for antemotion talus (ankle) and pes (foot). Palpation assessment revealed densification of five CCs (RE-LU, AN-PV, RE-TA, AN-TA and AN-PE).

The AN-PE and RE-TA CCs were treated first. Post-treatment movement assessment demonstrated that the pain in the lumbar region had decreased from 8 to 3 on the VAS scale. The other three CCs were treated in order to complete the tensile balance (Fig. 9.7 ).

The patient was pain-free after the first treatment; therefore, the following advice was given: ‘When the treated points are no longer tender you can recommence running. The first run should be brief and you should stop if any pain reappears. Try again after 2 days and if the pain is felt again then ask for a second appointment.’

The athlete called after 10 days to say that he had some pain during the first run but during the following run, no disturbance had been felt.

Sagittal plane	Frontal plane	Horizontal plane
Antemotion (AN)	Mediomotion (ME)	Intrarotation (IR)
Retromotion (RE)	Lateromotion (LA)	Extrarotation (ER)

Repeated mechanical stimuli	Chronic dysfunction
Inflammation	Repeated inflammation
Repair	Ground substance densification
Reorganization of collagen fibers	Collagen fiber dysplasia
Healing	Fibrosis