Fascia is a sensory organ

A very good article on Fascia written by Dr Hammer. This article was published in April 2014, in the newsletter American Chiropractic Association.

The Fascial System Is a Sensory Organ
By Warren I. Hammer, DC

The knowledge that normal muscle function depends on the fascial system and between 30 and 40 percent of the force generated by muscle is due to its surrounding fascia can be compared in science to adding a new element to the periodic table of elements.

Science has dismissed the value of a connective tissue structure that encompasses our whole body both internally and externally. Carla Stecco, MD, elaborated this dismissal in her upcoming text entitled, Functional Atlas of the Human Fascial System (Elsevier 2015): “In anatomy text books, only local areas of fasciae are described and they are characterized by only one of their minor functions: as an opaque covering.” In her preface, she adds that most anatomists view connective tissue as something to remove so that joints, muscles, organs and tendons may be studied carefully. In fact, it has now been established that the basic function of joints, muscles, organs and tendons requires a normal, functioning fascial system.

Research demonstrates that more than 30 percent of the force generated from the muscle is transmitted not along a tendon, but rather by the connective tissue within the muscle and fascia contains mechanoreceptors and proprioceptors. In other words, every time we use a muscle, we stretch fascia that is connected to spindle cells, Ruffini and Paccini corpuscles and Golgi organs. The normal stretching of fascia thus communicates the force of the muscle contraction and the status of the muscle regarding its tone, movement, rate of change in muscle length and position of the associated body part to the central nervous system (CNS).

An important question now arises: What if the fascia, where these receptors are located, is restricted due to increased viscosity or is chronically overstretched? As receptors are activated by pressure or stretch, is it possible that the receptors, which must be free to function, are inhibited? Could inhibition of receptor function provide altered feedback to the CNS? The fascia is therefore much more than an “opaque covering.” It should probably be designated as another organ of the body. Something else to consider: The acupuncture system is within the fascial system. Langevin described the network of acupuncture points and meridians as a network formed by connective tissue (fascia). Practitioners must understand what causes fascia to become pathological and why it disrupts function. Ultimately, they need to know how to restore normality to the fascial system.

Anatomy and Physiology
This article is a very short introduction to the subject of fascia, but certain anatomical and physiological information has to be understood. Muscles are covered by specific types of deep fascia, designated as either epimysial or aponeurotic fascia. In the extremities, a thin layer of epimysial fascia called the epimysium envelops the surface of each muscle. It surrounds the entire surface of the muscle belly and separates it from adjoining muscles. It gives form to all of the extremity muscles. In the extremities, the epimysium is covered by aponeurotic fascia (AF). The fascia lata is aponeurotic fascia that covers the whole thigh and buttock like a stocking and slides over the epimysium of the muscles beneath it. AF is the “well-defined fibrous sheaths that cover and keep in place a group of muscles or serve for the insertion of broad muscles.”. Some examples of AF are the thoracolumbar fascia, the fascia lata and the fascia that covers all of the extremity muscles. A principal function of the AF is to transmit the force (myofascial continuity) of the muscle groups it covers by way of myofascial expansions or insertions. These expansions insert into the periosteum, the paratenons, neurovascular sheaths and the fibrous capsules of joints. During forward movement of the upper extremity for example, the clavicular fibers of the pectoralis major (epimysial fascia) upon contraction stretches the anterior brachial aponeurotic fascia. The biceps is contracting, thereby stretching the antebrachial (aponeurotic) fascia and by way of the lacertus fibrosus to the flexor carpi radialis and the thenar muscles. This sequence has been verified by dissection.

Similarly, the quadriceps muscle inserts into the tibia by way of its tendon and continues on to a myofascial expansion that passes anterior to the patella to the anterior knee retinaculum. The Achilles tendon connects from the calcaneus to fascial attachments to the plantar fascia over the back of the heel and to the heel fat pad. Every movement of the body will stretch particular patterns of intrafascial receptors, especially in the deep fascia. The firing of receptors embedded in the fascial network represents the perceptive continuity necessary for normal unimpeded movement and the transmission of information proximally and distally to adjoining muscles and to our CNS.

AF helps transmit the force of the muscles it covers and is innervated mostly in its superficial layer. Aponeurotic fascia in the extremities is separated from the epimysium by loose connective tissue, which allows normal glide between the two fascial layers. The AF is made up of two to three layers of parallel collagen fiber bundles, densely packed, separated by a thin layer of its own loose connective tissue. Each layer slides independently over its adjoining layer. The loose connective tissue with normal viscoelasticity allows normal tissue gliding. This gliding function becomes abnormal when the loose connective tissue viscosity increases.

Closely connected to the epimysium is an intramuscular fascial layer called the perimysium. The perimysium surrounds the muscle bundles (fascicles). Both the epimysium and perimysium are an organized framework that transmit the force produced in the locomotor system. Both the epi and peri are thickened in tendinosis and with immobilization. From a sensory point of view, the chief proprioceptors for muscles are muscle spindles that are localized in the perimysium. Their capsules connect to the epimysium and fascial septae. The chief sensory components of muscles, the spindle cells, reside in the fascia. Finally, there is the endomysium, which covers every muscle fiber and separates fibers from each other to allow individual fiber gliding.

The fact that spindle cells are in the fascia implies that if the fascia is altered — restricted or densified — the spindle cells may not function normally, depriving the CNS of necessary information about joint movement, muscle coordination and position. Spindle cells represent a common final pathway, since all proprioceptive input from fascia, ligaments, skin, etc., goes to the dorsal horn. The dorsal horn has collaterals that synapse on the gamma motor neurons causing reflex activation of spindle cells. Spindle cells are active even during sleep, and they must be stretched during muscle contraction or passive stretch to become activated. It is therefore probable that if the spindle cells are embedded in thickened, densified fascia, its ability to be stretched would be affected and normal spindle cell feedback to the CNS would be altered.

Siegfried Mense, MD, one of the world’s leading experts on muscle pain and neurophysiology, when questioned about fascial adhesions having an adverse effect on spindle cells, answered: “Structural disorders of the fascia can surely distort the information sent by the spindles to the CNS and thus can interfere with a proper coordinated movement,” and “the primary spindle afferents (Ia fibers) are so sensitive that even slight distortions of the perimysium will change their discharge frequency.” When our patients complain that the last thing they did was the cause of their pain (i.e., “must have gotten out of bed wrong”), they are already in an uncoordinated situation.

What is the actual mechanism of fascial disruption creating abnormal sensory afferentation? One of the chief causes of fascial restriction is related to a substance called hyaluronic acid (HA). HA is a high molecular weight glycosaminoglycan polymer of the extracellular matrix. Among its many functions, HA is a lubricant that allows normal gliding between joints and between connective tissue. The concept of gliding within the fascial system is crucial for normal fascial function. Normal gliding between the layers of fascia surrounding the muscle and within the muscle depends on the normal hydration provided principally by HA. HA is already proving successful when it is injected into osteoarthritic knees or frozen shoulders. A major location of HA is in the loose connective tissue between the deep aponeurotic fascia and muscle (where aponeurotic fascia slides on the epimysium), the loose connective tissue between the two or three layers of the aponeurotic fascia and between the intramuscular fascia. Loose connective tissue appears as an irregular gelatinous mesh containing mainly HA, some fibroblasts, collagen and elastic fibers. “If the HA assumes a more packed conformation, or more generally, if the loose connective tissue inside the fascia alters its density, the behavior of the entire deep fascia and the underlying muscle would be compromised. This, we predict, may be the basis of the common phenomenon known as ‘myofascial pain.’ There is evidence that if the loose connective tissue within the fascia has increased viscosity, the receptors will not be activated properly. Densified HA also alters the distribution of the lines of force within the fascia. In this environment, pain and stiffness may be created with stretching, even within the physiological ranges. When the HA chains become concentrated, their viscoelastic properties are altered, and this contributes to myofascial pain and the myofascial pain syndrome.

There are corroborating studies that demonstrate the relationship between HA and myofascial pain. Under tissue stress, like tissue injury, hyaluronan becomes depolymerized and lower molecular mass polymers of hyaluronan fragments appear. These smaller HA fragments signal to the host that normal homeostasis has been profoundly disturbed. Smaller HA fragments contribute to scar formation. With overuse and trauma, HA becomes fragmented and proinflammatory. “By increasing the concentration of HA, HA chains begin to entangle, conferring to the solution distinctive hydrodynamic properties: the viscoelasticity is dramatically increased.” Other studies show that thoracolumbar fascia shear strain was approximately 20 percent lower in human subjects with chronic low-back pain. This reduction of shear plane motion may be due to abnormal trunk movement patterns and/or intrinsic connective tissue pathology. Fascial thickening has been held responsible for chronic pain in both the neck and lower back. In the neck study, the thickness was found in the loose connective tissue, rather than the collagen fibers. In the lowerback study, the chronic low-back pain group had approximately 25 percent greater perimuscular thickness and echogenicity, compared with the non-low-back pain group. In the chronic neck-pain study, the variation of thickness of the fascia correlated with the increase in quantity of the loose connective tissue, but not with dense connective tissue. The value of 0.15 cm thickness of the sternocleidomastoid (SCM) fascia was considered as a cut-off value that allows the clinician to make a diagnosis of myofascial disease in a subject with chronic neck pain.

Restoring deep fascial glide requires a method of reaching the deep fascia, especially since this is the principal location of the spindle cells and the HA. In a study where the tissue was sensitized equally from the skin to the deep fascia in the erector spinae muscles, longtime sensitization to mechanical pressure and chemical stimulation remained in the deep fascia rather than the superficial areas. Another study compared the methods of manual effects on restoring HA fluidity. They compared perpendicular vibration and tangential oscillation with constant sliding motions. The perpendicular and tangential motions caused a greater HA lubrication than the sliding method. This demonstrates why it is important to treat an area long enough. The treatment area is less than 2 cm2 and usually requires between 2 to 4 minutes until palpation reveals a gliding sensation rather than a densification. As we treat the HA fragments, which are proinflammatory, they finally reach a size where they become anti-inflammatory. This resultant reduction in inflammation takes about 48 hours. This may explain the possible side effects of continued pain after treatment. It is recommended that the same area should not be treated for at least four days or more. Vertical-type pressure using elbows, knuckles and Graston Technique® is necessary to effect this change.

Much of the information in this article is derived from the research of Luigi Stecco, PT; Carla Stecco, MD, and Antonio Stecco, MD. They have created a modality called Fascial Manipulation® (FM), which is now being taught on almost every continent. Some basic principles of FM that readers might apply to their own methods of fascial treatment are:

• The fascia is a sensory organ.

• Normal muscular function requires that its surrounding fascia be hydrated to allow normal tissue gliding.

• Improper tissue gliding is directly related to mechanoreceptive and proprioceptive insufficiency and muscle incoordination.

• Dysfunction follows along myofascial kinetic chains, especially those that relate to both the anatomical myofascial and acupuncture meridian fascial planes.

• A thorough case history that considers areas of previous trauma or surgery may reveal fascial densities responsible for present complaints.

• Functional testing and palpation of fascial planes are a primary diagnostic method.

• Treatment of affected points should be continued until normal density is palpated and negative functional testing improves.

Much of the research regarding these questions can be found in the U.S. National Library of Medicine, National Institutes of Health.

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