A TRIGGER POINT IS NOT FORMATION OF FIBROCONNECTIVE TISSUE IN MUSCLES
A TRIGGER POINT IS NOT FORMATION OF FIBROCONNECTIVE TISSUE IN MUSCLES
by R. Turchaninov, B. Prilutsky
This article is a response to “Truthaches and Trigger Point Therapy” published in December 2005 issue of Massage Today by Dr. G. T. Lawton. Our article we would like to start from few statements
- Fibroconnective tissue formation in muscles is a myogelosis; uncurable muscular pathology.
- Myogelosis in many cases is the result of inadequate treatment of trigger points.
- A trigger point is a pinpoint localization of pain that can be found in muscles, connective tissue, and periosteum. The morphology of this point of pain is that the demand of blood supply is much higher than the actual blood supply.
- The theory of peripheral nerve pain at the motor end plate is not a new theory.
- Any theory must be supported by clinical output.
- Ischemic compression as a method of trigger point therapy has been proven by at least 4 decades of massive utilization as a safe and effective method.
- Ischemic compression techniques are performed in a manner of gradually increasing pressure, and thusly exclude the possibility of doing harm to the patient and the therapist.
For detailed descriptions of methods of trigger point discovery as well as application of ischemic compression techniques, please visit http://www.massagetoday.com/archives/2004/12/05.html
The body is a very complex and sophisticated system and truth lies in the integrative approach to the issue when all factors are considered. Unfortunately Dr. Lawton’s article does not offer this approach.
Thus we would like to present to the reader a short scientific review of the trigger point issue and trigger point therapy concept using statements from Dr. Lawton’s article as a guide.
1. Dr. Lawton: “The original theory of Travell and Simons was that a trigger point was a palpable nodule or taut band of fibro-connective tissue in muscle.”
2. Dr. Lawton: “There is, unfortunately, a lack of histological evidence that they (i.e., trigger points) actually exist, which led most established members of the research community to abandon that idea all together. Even Travell and Simons dropped the idea of applying ischemic compression on the trigger point and opted for cortisone and other “exciting” chemotherapeutic
There is a lot of published result of histological evaluation of the trigger point areas. Even in our short list of references they are under # 5, 6, 7, 13, 15. It will be nice to see precise references of “… most established members of the research community who abandon that idea.” Why did Dr. Lawton not include such publications in the list of references?
It is purely misleading to state that Dr. Travell and Dr. Simons recommended using ischemic compression for trigger point therapy. They advocated injection, stretch and spray techniques and muscle energy techniques for trigger point therapy. However, they did mention ischemic compression as an option based on the European medical sources. Thus, Dr. Simons never dropped the idea of applying ischemic compression for the one reason that he never recommended it as a treatment method.
3. Dr. Lawton: “The supporters of trigger point theory and trigger point therapists cite research that has been discredited as either inaccurate, having technical procedural flaws or that contains artifacts that have been caused by false positive readings in equipment such as electromyographic instruments (EMG). Needle biopsy of supposed trigger points identified by
trigger point “experts” has consistently failed to show any difference between the muscle tissue within the borders of an “identified” trigger point and any other normal muscle tissue.”
This is both a wrong statement and an unethical one.
What Dr. Lawton means “false positive reading in EMG studies”? According to Dr. Lawton, approach to the scientist and research probably following database also false statement. Awad (1973) examined biopsy tissues from trigger points using electron
microscope and detected significant increase in the number of plateles, which released serotonine and mast cells which released histamine. Both substances potent vasodilators and their increase is a clear sign that body tries to fight with local ischemia in the trigger point area”
In his now classical work, Fassbender (1975) conducted hystological
examination of the circulation in the area of the trigger point and
proved one and for all that “… the trigger point represents a region of local ischemia”. The same results were obtained by Popelansky et al., (1986) who used radioisotope evaluation of blood circulation in the area of the trigger point.
In order to dismiss the decades of international research and most important clinical results in one statement, Dr. Lawton should enlighten us with an answer to one very simple question: “Who exactly discredited all previous works and where is this new exciting information published?” An author can make such a “scientific” statement only under the condition that he or his team repeated the research and did not detect changes which were published. There are rules of mutual respect among scientists and if the author did not conduct scientific evaluation of other authors’ work it is unprofessional and unethical to dismiss them altogether in one groundless statement.
4. Dr. Lawton: “In an article titled, “Update of Myofascial Pain from Trigger Points,” Professor David Simons reviews many of the concepts of the last several decades and then ends the article by describing the newest hypothesis: the involvement of the motor endplate.”
If Dr. Lawton read “Trigger Point Manual” carefully he will see that Travell and Simmons constantly emphasized the nervous system as a critical factor in the development of the trigger point and pointed out the importance of end-plate zones. They even name special types of trigger points called motor trigger points which are located in the middle of muscle belly where the motor nerve which innervates this muscle enters. Let us quote Dr. Travell and Dr. Simons again to defend the authors from the “scientific” claims of Dr. Lawton: “The functionally significant structure with regard to the innervation of muscle fibers is the myoneural junction (end-plate zone)…” and “Some trigger points are closely associated with myoneural junctions, others not.” (Travell and Simmons, 1983). In his article Dr. Lawton referred to the idea of the nervous system and the role of end-plate zones as a new concept. We would like to refer Dr. Lawton to works of Prof. Korr, who as early as 1947 addressed the same issues during his research. It is plain to see that this is not a new idea at all.
5. Dr. Lawton: “The question remains that if this is not muscle tissue pain, what kind of pain is it? Well, this question led to the discovery that what had erroneously been labeled as trigger point pain and attributed to pathological changes in muscle tissue, is most likely (new theory) peripheral nerve pain at the motor end plate. This bears repeating so this idea can replace all of the wrong information you previously have been taught in massage school and seminars, and keep reading about in massage magazines.”
Partially wrong statement
Dr. Latwon states that myofascial pain is originated in the motor end-plates and this is partially true. According to histologically conducted studies (Heine, 1997; Gogoleva, 2001) chronic pain and low grade tension in the skeletal muscles and fascia are responsible for the low grade inflammation around the terminal parts of the sensory and motor neurons which end in the soft tissues. This chronic inflammation activates the local fibroblasts, which deposit collagen around the nerve endings forming so-called “collagen cuffs”. This additional irritating factor triggers an afferent sensory flow to the central nervous system which is interpreted by the brain as pain. This mechanism is partially described generation of pain in the area of motor trigger points. However, it seems that Dr. Lawton considers that the terminal parts of the sensory and motor neurons are located somewhere but not in the soft tissues including skeletal muscles. In other words it will be very logical to assume that something must irritate the terminal parts of sensory and motor neurons and this something is a tension in the skeletal muscles; this includes trigger points which are not associated with motor trigger points because they are located in other parts of the skeletal muscle. Please consider that any inflammatory condition whether in motor end plates or muscular tissue means a decreased amount of blood supply to this inflamed tissue and gentle, gradual ischemic compression can be viewed as an anti-inflammatory effort.
There is no doubt that myofascial pain can be the result of peripheral nerve abnormalities. A great example is irritation of the sciatic nerve by overtensed piriformis muscles and formation of trigger points in muscles innervated by sciatic nerve. This list can be continued because any peripheral nerve’s entrapment in the key areas will cause formation of trigger points innervated by this nerve.
Here is another example showing Dr. Lawton looking at the problem from only one side. If one examines a patient with peripheral arterial disorder (e.g., Buerger’s disease) he will find a lot of active and sleeping trigger points in the leg and foot muscles. We think that readers will agree with us that insufficient arterial blood supply as a result vascular abnormality is responsible for the formation of the trigger points in the skeletal muscles rather than abnormalities of the motor end-plates. The same is true for trigger points in the skeletal muscles which are developed as a result of chronic visceral disorders (e.g., patients with cardiac disorders exhibit active trigger points in the trapezius, levator scapulae, rhomboideus muscles). In such cases the end-plate abnormalities do not have anything to do with formation of trigger points in the skeletal muscles. They are the result of the phenomenon of convergence of pain stimuli within the same segments of the spinal cord which are responsible for the innervation of both the affected inner organ and skeletal muscles. In 1955 Dr. Glezer and Dalicho concrete the theory that until today is clinically proven to be the right theory by developing and proposing maps of reflex zone abnormalities in skin, fascia and muscles, including trigger point development.
Finally, reading Dr. Lawton’s article, the reader gets wrong impression that the issue of trigger points is completely settled within medical and massage therapy communities and by accepting the end-plate theory as the only correct one. Dr. Lawton did not inform readers that there is another theory which links formation of trigger points with the shortage of ATP in the affected muscles as a result of insufficient arterial circulation. As known, ATP is the major energy source for the muscle contractions and relaxation. Authors of this theory, called Energy Crisis Theory, pointed out the formation of the trigger points in very healthy athletes who do not have signs of peripheral nerve abnormalities and still developed active trigger points. Gradual increase of the resting muscular tone in normal muscles triggers local vasoconstriction, interstitial edema and ATP exhaustion with following formation of active trigger points. Prof. D. Simons as a real scientist reviewed this theory as well and even extensively used works of his opponents Dr. D.R Hubbard and Dr. G.M. Berkoff in his own research. Thus we do not want readers to be misled by Dr. Lawton’s article. End-plate theory is not the only one, as it is plain to see.
Dr. Lawton constantly refers to his work as a medical massage educator. Both of us also have some experience in this matter, considering PhD degrees in medicine and physical rehabilitation on the topic of medical massage and manual therapy. Thus we think we are entitled to express our opinion as well: both theories are correct. Prof. D. Simons’ theory which Dr Lawton supports explains formation of the trigger points in areas of end-plates especially if peripheral nerve neuralgia is present. Energy-crisis theory (Hubbard and Berkoff, 1993) theory greatly justifies formation of trigger points in the areas of skeletal muscles where there are no end-plates and the individual does not have abnormalities of the peripheral nerves.
6. Dr. Lawton: “If trigger points are not a fibrotic alteration in muscle tissue, then what is with all of this ischemic compression, deep tissue break down of adhesions, knobbles, knuckles, rigid fingers, elbows and knees all about? If, as the current research’ strongly suggests, these pain sites are inflamed and abnormal nerve endings, then what in the world are we doing poking things into excited, painful nerves? Imagine you have a painful tooth. Do you want me to poke a fork into it? Does that sound therapeutic to you?” “This also is why there is a difference between medical massage instructors who teach nonphysiological theories and techniques and those teaching valid technique from the current research and scientific literature.”
Yes, Dr. Lawton, trigger point is not fibrotic alteration in muscle tissue. And you are right when you stated that trigger points are the result of inflammation in nerve endings. Given the fact that motor end plate located in the neuromuscular junction, we can assume that muscular tissue is inflamed as well. This means that these inflamed cells are suffering from ischemia. As we explained earlier, ischemic compression, effectively helps the body fight ischemia.
In regards to treatment options, Dr. Lawton is right when he mentioned vigorous deep tissue massage and similar techniques, as completely outdated, unscientific and even more important harmful for the patient. So, these methods are bad, but one important question is left unanswered: “Dr. Lawton what are your recommendations?” It is easy to critique without recommending alternative and/or better approaches. In any case we hope this new treatment method that Dr. Lawton developed was tested at least in clinical trial against placebo, the same way as ischemic compression was researched.
Dr. Lawton absolutely unfairly placed ischemic compression in very bad company with excessive and traumatic pressure. Therefore, we would like to make the record straight.
Ischemic compression is part of the trigger point therapy and when it is done correctly it is the most clinically effective tool for the elimination of trigger points. Thus we would like to share with readers and Dr. Lawton the clinical protocol of trigger point therapy which has been in use for more than 40 years since the time when Prof. R. Mezlack and Prof. P. Wall formulated their famous Gate-control therapy of pain which scientists in the medical massage and manual therapy fields adopted its principles. In our 50 years of combined personal clinical and research experience this protocol never failed us.
In overall the trigger point therapy has following goals:
2. Eliminate condition of the hyperirritability of the peripheral receptors
especially pain receptors
3. Block pain-analyzing system of the patient
4. Produce reflex vasodilation
5. Eliminate local ischemia
To effectively achieve these goals the practitioner should conduct trigger point therapy including several equally important components:
2. Detect pathway of the radiation of the pain and examine tissues along this pathway in case the satellite trigger points are formed
3. Detect entrance into the trigger point which is one angle of pressure’s application which causes the most uncomfortable sensation. When entrance into the trigger point is correctly detected the practitioner does not need to hurt his or her hands or patients because the amount of pressure is very moderate
4. To accomplish first three goals apply effleurage and kneading techniques on the affected muscles in the inhibitory regime for 5-7 minutes (comfortable gradual increase of pressure, same direction of the strokes).
5. Place finger in the trigger point. Slowly apply vertical compression of the tissues until the patient feels first sign of pain. As soon as he or she reports it stop application of pressure but maintain it on the same level. In 10 seconds of application of the pressure the pain which the patient initially felt will disappear. The patient should immediately report to you as soon as he or she feels the pain ceases. During the next 20 seconds the practitioner will be able to get to the “bottom” of the trigger point without unwanted activation of the pain analyzing system and generating protective muscular tension in the affected muscle or muscles of the region.
7. Exit the trigger point as fast as possible to produce quick and effective vasodilation and elimination of the local ischemia.
Thus, correct protocol of trigger point therapy does not have pitfalls Dr. Lawton mentioned when the practitioner hurts the patient. This protocol is equally effective in the area of motor trigger points Dr. Lawton addressed in his article because the applied pressure never strong enough to go over the patient’s threshold of pain, causing the pain and injury of motor nerve endings. Peripheral vasodilation restores local pH, increases oxygenation of the tissues in the area of trigger point and gradually eliminates trigger point.
Dear colleagues, 3 years ago we started incorporating in the treatment electrical vibration. Which in fact is a very effective modality that in most cases leads to rapid results. Therefore, using this opportunity, we would like to share with you the following recommendations.
Apply permanent fixed electric vibration in the area of
trigger point for one minute. Be sure that massager generates true vibration rather than vibration as a result of percussion. This is very important issue.
As numerous experimental and clinical studies are shown permanent fixed electric vibration with frequency around 100Hz blocks pain receptors (Wall and Crowly-Dillon, 1960), produces muscle relaxation and local vasodilation after at least one minute of application (Kreymer, 1987).
6. ——-Move massager to the side, expose trigger point and place
finger in it. Keep massager next to the finger. It will continue to block the patient’s pain analyzing
Apply ischemic compression techniques in the manner we recommended earlier.
In conclusion medical massage therapy procedure consists of mobilization of skin, fascia, muscular tissue, trigger point therapy, and post-isometric relaxation techniques. Each of the above mentioned modalities is equally important in order to reach sustained and rapid results. For many decades, massive utilization of medical massage has proven to be a safe and very effective method of treatment for support and movement system disorders, inner organ disorders, stress management, etc. Any new or old theory can become a fact only in the case that after a prolonged time it will be clinically proven to be safe and effective. To excite the massage community with “new ideas” may be possible for a short period of time but to discredit scientifically designed and decades-long clinically proven methods is clearly impossible.
Boris Prilutsky, MA – www.borismedmassage.com
Ross Turchaninov, MD, PhD – www.aesculapbooks.com
2. Fassbender H.G. Pathology of the Rheumatic Diseases.
Springer-Verlag, New York, 1975
3. Froriep, F. Ein Beitrag zur Pathologie und Therapie des
Rheumatismus. Weimar, 1843.
4. Glezer, O., Dalicho, V.A. Segmentmassage. Leipzig, 1955
5. Glogowski, G., Wallraff, J. “Ein beitrag zur Klinik und Histologie
der >Muskkelharten (Myogelosen)”, Z. Orthop., 80:237-268, 1951
6. Gogoleva, E.F. “New Approaches to Diagnosis and Therapy of
Fibromyalgia associated with Spondylosis.” Ther. Arch., 4:40-45, 2001.
7. Heine, H. Lehbruh der biologischen Medicine. Stuttgart,
8. Hubbard, D.R., Berkoff, G.M. “Myofascial trigger points show
spontaneous needle EMG activity”, Spine, 18:1803-1807, 1993.
9. Korr, I.M. “The Neural Basis of the Osteopathic Lesion.” JAOA,
47(4): 191-198, 1947.10. Kreymer, A.Y. Vibration Massage in Diseases of the Nervous System. Tomsk University, Tomsk, 1987.
11. Mackenzie, J. Angina Pectoris. Henry, Frowde & Hodder &
Stroughton, London, 1923.
12. Mezlack, R., Wall, P. “Pain Mechanism: A New Theory.” Science, 150 (Nov): 971-979, 1965.
13. Miehlke, K., Schulze, G., Eger, W. ” Klinische und experimentelle
Untersuchungen zum Fibrositis-syndrom. Z. Rheumaforsch, 19:310-330, 1960.
14. Popelansky, Y.Y., Zaslavsky, E.S., Veselovsky, V.P. Medicosocial
significance, etiology, pathogenesis, and diagnosis of non-articular
diseases of soft tissues of the lims and back. Vorpr. Rheumat.,
15. Schade, H. “Untersuchungen in der Erkaltungstrade: III. Uber den Rheumatismus, in besondere den Muskelrheumatismus (Myogelose).” Munch. Med. Wschr., 68, 95-99, 1921.
16. Travell, J.G., Simons, D.G. Myofascial Pain and Dysfunction. The
Trigger Points Manual. Williams & Wilkins, Baltimore, 1983.
17. Wall, P.D., Crowly-Dillon, J.R. “Pain, Itch and Vibration.” A.M.A.
Arch. Neurol., 2: 19-29, 1960.