Introduction
Medical massage therapy procedure consists of mobilization of skin, fascia and muscular tissue, trigger point therapy, and post-isometric relaxation techniques. Each of these modalities is equally important in order to reach rapid and sustained results. For decades, massive utilization of medical massage has proven to be a safe and very effective method of treatment for the support and movement system disorders, inner organ disorders, stress management, and more.
In the last few years, there have been numerous arguments in within the professional community about practitioners utilizing manual therapy and trigger point therapy. In recent professional publications many authors have been raising the following questions: Is a trigger point a formation of fibroconnective tissue in muscles? Have histological studies ever been done on trigger points? Is there a theory of peripheral nerve pain at the motor end plate a new theory and the only theory? Are ischemic compression techniques for trigger point therapy safe and effective?
The brief answers on aforementioned questions are:
1. Fibroconnective tissue formation in muscles is myogelosis, an incurable muscular pathology.
2. In many cases myogelosis is the result of inadequate treatment of trigger points.
3. 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 such that the demand of blood supply is much higher than the actual blood supply.
4. The theory of peripheral nerve pain at the motor end plate is not a new theory.
5. Any theory must be supported by clinical output.
6. 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.
7. Ischemic compression techniques are applied by gradually increasing pressure, thus excluding the possibility of doing harm to the patient and to the therapist.
In the search for true understanding of pathophysiology, the body’s sophistication and complexity requires us to take an integrative approach to any issue. Thus I would like to present to the reader a short scientific review of the trigger point issue and the trigger point therapy concept.
The Nature of Trigger Points
There is no statement in the modern scientific literature that calls a trigger point a “taut band of fibro-connective tissue.” However, it was once used in the late 19th/early 20th century until histological studies conducted by German scientists (Glogowski, and Wallraff, 1951; Miehlke et al., 1950) showed that there is no connective tissue proliferation (myogelosis) in the area of a trigger point in muscles. “In our opinion, fibrositis (in regard to trigger points) has become a hopelessly ambiguous diagnosis… is best avoided” (Travell, Simons, 1983). However, connective tissue will grow between muscle fibers when a core of the myogelosis is formed (Glogowski, and Wallraff, 1951). Myogelosis is a clinical outcome of years of reactivation of the active trigger point in the same area. At the same time, trigger point therapy is useless if the core of the myogelosis is already formed.
In 1843, for the first time, the German physician Dr. F. Froriep described trigger points as painful formation in skeletal muscles. In 1921 another German scientist, Dr. H. Schade, examined them histologically and formed the concept of myogelosis. In 1923 the British physician Dr. J. Mackenzie offered the first pathophysiological explanation of the trigger point formation mechanism and formulated the concept of the reflex zones in the skeletal muscles where the central and peripheral nervous system play a critical role. The reflex zones concept was further developed by the American scientist Prof. I. Korr in 1941 in a series of brilliantly designed experimental studies. Thus, the trigger point concept was developed long before the work of Travell and Simons, who based their publication (see references in “Trigger Point Manual” by Travell and Simons) on the works of the scientists mentioned.
There are numerous published results of histological evaluations of the trigger point areas. Even in the short list of references at the end of this article you can find ample evidence under references 5, 6, 7, 13, and 15.
It is 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. Although, Travell and Simons did mention ischemic compression as an option based on the European medical sources, they never recommended it as a treatment method.
The Role of Vasodilators in Local Ischemia
Awad (1973) examined biopsy tissues from trigger points using an electron microscope and detected a significant increase in the number of platelets, which caused the release of serotonin and mast cells, which in turn released histamine. Both serotonin and histamine are potent vasodilators and their increase is a clear sign that body is trying to fight the local ischemia in the trigger point area. In his now classical work, Fassbender (1975) conducted a histological examination of the circulation in the area of the trigger point and proved once 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.
The End Plate Theory
The end plate theory is not a new theory. Travell and Simmons constantly emphasize the nervous system as a critical factor in the development of the trigger point and point 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 the muscle belly at the neuromuscular junction. “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). The idea of the nervous system and the role of end-plate zones is not a new concept. As early as 1947 Prof. Korr addressed the same issues in his research.
According to histological 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 by the generation of pain in the area of motor trigger points. We have to consider that the terminal parts of the sensory and motor neurons are located in the soft tissues, including skeletal muscles. In other words, it would be logical to assume that something must irritate the terminal parts of sensory and motor neurons. This something is a tension in the skeletal muscles, including trigger points that are not associated with motor trigger points (since they are located in other parts of the skeletal muscle). Keep in mind that any inflammatory condition, whether in motor end plates or in muscular tissue, means that there is a decreased amount of blood supply to this inflamed tissue. From this it follows that 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. An example of this would be the irritation of the sciatic nerve by an over-tensed piriformis muscle resulting in the formation of trigger points in muscles innervated by the sciatic nerve. This list can be continued because any peripheral nerve’s entrapment in the key areas will cause formation of trigger points in muscles innervated by this nerve.
If one examines a patient with peripheral arterial disorder (e.g., Buerger’s disease) one will find numerous active and dormant trigger points in the leg and foot muscles. It would most certainly be agreeable that insufficient arterial blood supply as a result vascular abnormality is responsible for the formation of trigger points in the skeletal muscles rather than abnormalities in 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, and 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 the skeletal muscles. In 1955 Dr. Glezer and Dalicho formulated the theory that still stands clinically proven. They proposed and developed maps of reflex zone abnormalities of the skin, fascia and muscles, including trigger point development.
The Energy Crisis Theory
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. ATP is the energy source for cellular function, including muscles. Authors of this theory, called the Energy Crisis Theory, pointed out the formation of the trigger points in very healthy athletes who did 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 the subsequent formation of active trigger points. Prof. D. Simons reviewed this theory as well, and even used extensively works done by his colleagues, Dr. D.R Hubbard and Dr. G.M. Berkoff, in his own research.
Trigger Point Therapy Protocol
Ultimately trigger point therapy has the following goals:
1. Eliminate protective muscular tension in the muscles that harbor active trigger points.
2. Eliminate condition of the hyperirritability of the peripheral receptors, especially pain receptors.
3. Block the 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 utilizing several equally important components:
1. Detect location of the active trigger point.
2. Detect the pathway of pain radiation and examine tissues along this pathway in case satellite trigger points are formed.
3. Place finger in the trigger point. Slowly apply vertical compression of the tissues until the patient feels the first sign of pain. As soon as he or she reports it stop increasing pressure but maintain it at that same level. After 10 seconds of pressure application, the pain that the patient initially felt will disappear. The patient should immediately report to you as soon as he or she feels the pain cease. 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 in the region.
4. To accomplish the 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, in the same direction of the strokes).
5. Exit the trigger point as fast as possible to produce quick and effective vasodilation and elimination of the local ischemia.
The correct protocol of trigger point therapy does not have pitfalls. This protocol is equally effective for the motor trigger points, as well as for other trigger points. The applied pressure is 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 to normal, increases oxygenation of the tissues in the area of the trigger point, and gradually eliminates the trigger point.
References
1. Awad, E.A.: Interstitial myofibrositis: hypothesis of the mechanism, Arch. Phys. Med. Rehab, 54(10):449-453, 1973
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, Hippokrates, 1997.
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., 3:38-43, 1986.
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.
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