Chart Above Shows Myofascial Trigger Points
Myofascia is a thin, almost translucent film that wraps around muscle tissue. It is the tissue that
holds all the other parts together. It gives shape to and supports all of the body’s musculatures.
You can see myofascia if you cut up a fresh chicken. It is the thin, sticky, somewhat filmy material that wraps around the muscle tissue. It wraps around muscle fibers, bundles of fibers, and the muscles themselves, and then goes on to form tendons and ligaments.
For people with Fibromyalgia syndrome (FMS) and/or myofascial pain syndrome (MPS), the myofascia takes on a new importance. Tightening and thickening of the myofascia occurs in many cases of FMS and/or MPS. If both of these conditions are present, this tightening causes more than double the trouble.
When the myofascial tissues become thickened and lose their elasticity, neurotransmitter ability to send and receive messages between the mind and body is damaged, and the communication between the mind and body is damaged. Myofascia, then, may well be the key to what goes wrong in FMS&MPS Complex.
In the myofascia there is a material called ground substance. This material can exist in a solid, semisolid, or fluid state.
When ground substance changes from a liquid to a gel, the myofascia tightens, and it is difficult to get it to reverse to a liquid state again without intervention.
FMS & MPS Complex
Fibromyalgia (FMS) and Myofascial Pain Syndrome (MPS) are very different syndromes. The majority of physicians lump the two conditions together, probably because they see many patients who have both FMS and MPS, which I call FMS&MPS Complex. Unless doctors have a thorough knowledge of and familiarity with individual TrPs, they don’t stand a chance of sorting out the different symptoms of the two different syndromes.
One interesting difference between the two conditions is that more women have FMS than men. Myofascial Pain Syndrome, however, affects men and women in equal numbers. One important difference is that in MPS, muscles located some distance from the trigger points have normal sensitivity, whereas in FMS, there is an overall flu-like achiness, and generalized sensitivity, but no trigger points.
There are many medical journal articles that explain why FMS and MPS are different, and why the difference is important. (See, for example, Borg-Stein and Stein (1996), Schneider (1995), Simons, Travell and Simons (1998.)
People with FMS & MPS Complex
face more than just the two sets of
symptoms of both conditions.
Fibromyalgia and MPS not only occur together, they reinforce and amplify the symptoms of both. Because of this, physical therapy and all other forms of treatment must proceed very carefully. Any treatment tried will be both more complicated and less successful than if the patient had only one of the two syndromes.
One study has already been done. Hong and Hsueh (1996) found that those with FMS and MPS experience more pain when they receive trigger point injections, that the trigger point injections have less effect, and that the effect often takes longer to develop and may not last as long than if the patients had MPS only. In FMS&MPS, chronic pain exists, which is characterized by the trigger points of MPS and many other symptoms.
All of these symptoms and trigger points are intensified by the pain amplification aspect of FMS. Furthermore, some of the treatments normally prescribed for FMS patients can damage MPS patients and the reverse is also true. In FMS, many different informational substances may be affected in different combinations interacting in different ways in different patients.
Other biochemicals in the body are affected to different degrees. For example, histamine (a neurotransmitter) is often an important factor when there are many allergic manifestations, but the possible combinations of biochemical dysfunction are endless. When the possible combinations of TrPs are calculated, it is easy to see why no two FMS&MPS Complex patients are alike. Fibromyalgia perpetuates MPS and the reverse is also true. The spiral of pain/contraction/pain/contraction continues until it is interrupted by relief in some form.
A lot can be done to relieve MPS and lighten the pain load. There are many things that help FMS, as well. It’s important for people with this combination of syndromes to take on the responsibility of managing their own treatment, seeing that the perpetuating factors are identified and dealt with as thoroughly as possible. It isn’t easy, and it takes concentrated focus to change the habits of a lifetime.
Getting as well as possible
~ optimizing your quality of life ~ takes commitment.
What is done to or for you can help a lot, but getting better is
primarily a function of what you do for yourself.
News in the World of Myofascial Pain
Life has been tough for those of us with myofascial pain syndrome. We have too often been met with doctors who “don’t believe in” MPS. We have been hampered by the lack of a scientifically credible and understandable cause for this condition and an officially recognized set of diagnostic criteria. This resulted in a lack of training of physicians and therapists. The insurance companies and the Social Security Administration made our lives even more difficult. This is about to change.
We now have facts that cannot be disputed. At last we have proof that myofascial pain caused by trigger points is a true disease. We know what creates a trigger point, what it is, and many of the ways it can cause us pain and other symptoms. We know what causes those taut bands that constrict our muscles, and we know why our muscles become so tight that they hurt.
A myofascial trigger point is a localized area starving for oxygen. It creates an increased local energy demand. This local energy crisis releases neuroreactive biochemicals which sensitize nearby nerves. The sensitized nerves initiate the motor, sensory, and autonomic effects of myofascial trigger points by acting on the central nervous system. Muscles with trigger points are muscles in a constant state of energy crisis.
Myofascial trigger points can be identified and documented electrophysiologically by characteristic spontaneous electrical activity (SEA). They may also be identified histologically (which means that the structure of the cells have changed) by contraction knots– the lumps and bumps we know only too well. Both of these phenomenon seem to result from excessive release of the neurotransmitter acetylcholine (ACh) from the nerve terminal of the motor endplate (the complex end formation of the nerve).