Traditionally, fascial tissue wasn’t given as much attention as muscle by researchers and clinicians. This began to change in the early 1980s. From that time, a variety of practitioners have stimulated a great deal of interest in fascia. For the most part, the practitioners who’ve done so have been massage therapists and myofascial trigger point therapists. However, some physical therapists and osteopathic, medical, and chiropractic physicians have also made notable contributions. I’ll refer to all clinicians who’ve contributed as "myofascial practitioners."

Health care consumers have benefited from this new interest in fascia. They’ve benefited because myofascial practitioners have provided relief from pain and dysfunction that result from abnormalities of fascial tissues. Patients and practitioners have often asked me about the factors that induce abnormalities of fascia. Because of this interest, I’m publishing here part of a presentation I delivered on audiotape in 1989 (The Purpose and Practice of Myofascial Therapy, Houston, McDowell Publishing Co). So what I’ll talk about here are the three main factors that induce fascial abnormalities. They are (1) trauma, (2) chronic strain, and (3) immobility of fascial tissues.

"Dr. Ida Rolf first began to promote her view in the 1950's that fascial tissues bind muscles and thereby impede adaptive, fluid motion of the body. Dr. Ray Nimmo, the chiropractor who championed trigger point therapy in the middle of the 20^th century, didn't agree with her: ‘I could not agree,’ he wrote, ‘with her explanation that the muscles were bound down by connective tissue and had to be broken loose. Connective tissue is too strong to be broken loose.’ He also mentioned taking a class from D.C. McIntosh who taught a fascial release method. Nimmo wrote, ‘We would palpate for tensed fascia (so we thought), then release it. Fascia got snagged up, [McIntosh] said, and we would release it. I couldn't figure how anything as slick as fascia could get hung up. What it was, of course, was tensed musculature.’

"When Nimmo made those comments, no one could do much more than conjecture about fascia. But today we have data that show Ida Rolf was right. Fascia does bind together, and it can be broken loose. Most of these data come from studies of either connective tissue injury or peripheral joint stiffness after periods of immobility. The studies aren't tantamount in depth nor breadth to the advanced and voluminous research that's been done on muscle. However, they do show that fascia can contribute in at least three ways to the woes of the myofascial patient. It can do this by becoming fibrotic when traumatized and when subjected to chronic strain. And it can do so by webbing together after periods of immobility. Any of these conditions can restrict mobility and pull myofascial attachments. The pulling can cause compression that impedes blood flow, produces energy-deficient contractures and trigger points, and sets off the adverse neurological ramifications I've talked about on other tapes in this series. I’ll now describe how each of these factors—trauma, chronic strain, and immobility—can adversely affect fascia.

If the fibers are allowed to remain irregularly webbed, however, they’ll contract and draw the tissue together toward its center. The contracted fibers will reduce the mobility of the myofascial tissue they’re attached to. As the collagen fibers shorten, the pressure within the myofascial tissue will increase. The increased pressure will compress the arteries, veins, and lymphatics that course through the contracting tissue. This will create ischemia and, again, will induce energy-deficient contractures and trigger points.

Most myofascial practitioners have palpated the effect of this stretch-hypertrophy. They’ve done so when they’ve palpated the hard, fibrous cords that run longitudinally along each side of the thoracic spine in the erector spinae muscles. Some practitioners call these cords "linear fibrosis." The fibrosis is especially prominent in the patient who projects his head out in front of the gravity line, as though leading his body with it when he walks. The upper thoracic erectors have to guy-wire the patient's head and neck---sometimes more, other times less. And this intermittent overloading stimulates the fibroblasts to synthesize and deposit so much collagen in the fascial layers that the erector muscles in some patients feel like steel cables.

I've found referring trigger points in these muscles in many patients. The trigger points are usually highly resistant to specific myofascial therapy. The treatment resistance suggests that the trigger points aren't just in contractured muscle. Contractured muscle is usually capable of releasing its tension, elongating, and thereby allowing inactivation of the trigger point. The treatment resistance of the trigger points instead implies that fibrous (or what some call "dystrophic") tissue is involved. We can induce fibrous, dystrophic tissue to release its pressure on hypersensitized nerves, and I'll explain how when I talk about treatment procedures and techniques on sides 9, 10, and 11 in this tape series.

When connective tissue stays immobile, changes in the ground substance are perhaps more clinically important than the effects on collagen fibers. Protein-carbohydrate complexes in the ground substance bind water and give it its amorphous gel quality. (Researchers formerly called these water-binding complexes mucopolysaccharides, but they’ve changed the name to glycosaminoglycans.)

With immobility, the complexes gradually disappear from the ground substance. As a result, progressively less water is bound, and the bulk of the ground substance diminishes. As this happens, the collagen fibers come closer together. When the distance from one collagen molecule to another diminishes beyond some critical threshold, the molecules begin forming cross-bindings. As more and more molecules cross-bind, the involved connective tissue become less and less elastic. The tissue becomes less elastic because the collagen fibers and fascial sheets lose the ability to slide freely along one another. The effect is as though the tissue has lost some lubricating factor. But it appears that the collagen molecules of fascial sheets are actually tethered together.

Reduced mobility, or virtually immobility, of myofascial tissues is part of the problem with the patient who has heavy fibrosis of the upper thoracic erector spinae myofascia. As I said before, sustained guy-wiring of a forward-projecting head and neck chronically overloads these paraspinal myofascial tissues. This stimulates fibrosis. To worsen the problem, the upper thoracic spine has minimal mobility compared to the spine in the lower thoracic, lumbar, and cervical areas. And unless a person works at it, the paraspinal myofascia in the upper thoracic area is seldom stretched, torqued, or laterally bent. It just sits there. As fibroblasts deposit more and more collagen in response to the guy-wiring, the collagen appears to cross-link to form the thick cords we myofascial practitioners are so familiar with.

Most of us myofascial practitioners have patients who keep some—maybe even most—of their body parts practically immobile. That is, they use certain parts of their bodies in a guarded, tightly restricted range of motion. This is especially true of elderly patients. Many of these people have trigger points in these relatively immobile tissues, although most of the trigger points are "latent." This means, of course, that the trigger points aren’t actively referring pain.

Travell and Simons (the authors of the famous Trigger Point Manuals) have pointed out that many elderly people have latent trigger points. They say these people seem to automatically restrict their range of motion to avoid activating and suffering from their trigger points. Based o principle, these elderly people’s myofascial tissues are more likely to be fibrotic. This is likely because their reduced mobility permits type I collagen fibers to cross-link extensively throughout their bodies. The cross-linked collagen will exhibit physiological creep—that is, a steady pulling in on itself. At some critical point, the creep will cause the pressure within the tissues to increase to a critical point. At this point, blood flow will diminished, perhaps to the level of ischemia, and pain-mediating mechanoreceptors will be activated. At this time, the people will begin experiencing pain although they restricted their motion to avoid it. This is consistent with the view that the amount of collagen in connective tissues increases with age, making old animal meat tough. While the amount of collagen increases, the collagen fibers also develop extensive type I cross-linking.

As the years pass, many people restrict their body movements more and more. Eventually, their capacity for mobility becomes markedly reduced and they generally perceive stiffness. Mobility is important to tissue fluid exchange, and so their limited mobility seriously reduces blood flow. Blood flow in some circumscribed areas becomes so sluggish that the tissues become distinctly ischemic. At that stage, real trouble begins. First, energy-deficiency contractures can form and create trigger points. Far worse, though, the ischemia can cause muscle fibers to deteriorate. At the same time, fibroblasts become active and increase their output of collagen, bringing about some degree of myofascial fibrosis. The collagen fibers of this fibrotic area are likely to form cross-bonds that will tighten the tissue even more.

If the receptors of type C and type A delta nerves are trapped in this squeezing fibrotic tissue, the patient is likely to experience local tenderness and referred pain. These nerve responses are also likely to facilitate the segments of the spinal cord they enter. (Facilitation refers to a lowered threshold for neuronal firing.) This will stimulate motor fibers at the same level and cause hypertonicity of the associated paraspinal muscles. The nerve signals will also ascend to the brain stem and stimulate their reticular activating formations. The signals will also reach the thalamus. From there, relayed signals will stimulate cortical centers, disturbing thought and perception. The signals will also reach the basal (limbic) areas of the brain beneath the thalamus, which can produce disturbed emotions and interfere with the body's general homeostasis.

When relatively immobile myofascia lead to pain, freeing the patient from it may be difficult. Patients with fibrotic tissue aren't as responsive to therapy as patients whose source of pain is muscle contractures. There are at least two reasons for this.

First, fibrotic tissue can only be softened or stretched, and its cross-binds broken. First, in between therapy sessions, the tissue can shorten again unless the patient works diligently to keep it elastic. Diligence is required to counter the "physiological creep" I mentioned before. Second, many people who’ve minimized their movements to avoid myofascial pain have lost mobility and become generally stiff. They may lack the flexibility to cooperate in stretching muscles that house painful contractures and trigger points. For some of these people, relief can come only from therapies such as ultrasound and cross-friction massage that soften fibrotic tissues. Stretching the involved tissues, however, is fundamental to long-term improvement. If the patient isn’t able to effectively stretch because of severe inflexibility, he may require clinical care at frequent intervals.