The main clinical SIDST evidence is acute or chronic myofascial pain syndrome.
Pain is the most significant signal of damage of tissues and constantly active regulator of homeostatic reactions, including their most extreme forms of behaviour. Pain is called “a watchdog of health”, “vigilant guard”, which gives a signal about danger. At the same time, pain must be regarded not only as an emergency signal but also as a stimulator, mobilizing protective-compensatory power of an organism to fight the existing danger. That is pain which triggers a whole range of nature-planned reparative mechanisms of damaged tissues and systems of an organism as a whole. Thus, on one hand, the presence of pain indicates about existing damage of tissues; on the other hand, it triggers activation of protective reparative processes, aimed to the elimination of the damage.
Sense of pain is assumed to be divided into two components. The first one is acute, clearly located pain, which appears immediately after the damage (cut, prick, hit, electric shock). The second one is delayed pain, which is able to increase and progress, sometimes becoming unbearable. Quick pain is activated directly by the damage of investing tissue of the body, just as deep structures normally do not have quick pain sensitivity. Gradually occurring pain is closely related to the process and the scope of destruction of tissues and may be felt not only after superficial damages but also in deep tissues and internals. As a rule, it is more difficult to locate than quick pain.
In the basis of any pain there is irritation of pain, or polymodal, receptors. As this feeling causes stimulation of different parts of neuroendocrine system, pain as an evidence includes emotional, vegetative and behavioral components. Pain, as a symptom of acute or chronic diseases, represents a complicated psychoemotional phenomenon, in formation of which higher parts of brain and systems of regulation of visceral functions take part.
In an organism, a special system of pain sensitivity (nociceptive system) is in functional balance with antonociceptive system of brain, which modulates ascending afferent flows of impulses, coming from nocireceptors. It consists of neurons of different parts and levels of CNS structure, which begin from the spinal cord and end with supersegmental structures of the brainstem. Neuromodulating function of antinociceptive system is executed by means of release of endorphins and enkephalins.
An important role in regulation of nociceptive reactions belongs to opioid neuropeptides. In regulation of motor and hemodynamic reactions this role belongs to noradrenalin, dopamine and GABA. Neuropeptides (endorphins, enkephalins, neurotensin, vasopressin, angiotensin, P substance) suppress transmissive nociceptive neurons and activate structures of antonociceptive system. Classic neuromediators suppress the activity of nociceptive neurons of posterior horns and cores of trifacial nerve. Analgesic effect of noradrenalin is connected with β-adrenoreceptors and following suppressing of pain at supersegmental and segmental levels of brain. GABA and serotonin change emotional colouring of pain syndromes.
Bradykinin, prostaglandins, leukotrienes, ions of kalium and hydrogen are released from cells in response to cells damage. The main stimulator of nocireceptors is bradykinin. Prostaglandins and leukotrienes sensitize nocireceptors to kinins, kalium and hydrogen facilitate their depolarization and appearance of electric afferent pain signal in them. Excitation is spread not only in afferent but also in antidromic way to neighbouring branches of terminal, causing secretion of so called P substance. This neuropeptide causes hyperemia, edema, degranulation of mast cells and thrombocytes around the terminal in paracrine way. Released at that histamine, serotonin, prostaglandins sensitize nocireceptors, and chymase and tryptase of mastocytes enhance the production of their direct agonist – bradykinin. Therefore in case of damage nocireceptors act as sensors and paracrine provokers of inflammation. As a rule, near pain receptors there are sympatic postanglionary nerve endings, which are capable of modulating nocireceptors sensitivity. It is necessary to note that, for example, depressions, caused by the decrease of production of opiates and serotonin, are often marked by exacerbation of pain sensitivity. Besides that, depression, as a rule, is attended with venous lymphoid stagnation of soft tissues of neck, back, shoulder joints and other parts of the body.
Pain receptors hold a unique position in the human organism. This is the only type of sensitive receptors, which does not show any signs of adaptation or desensitization under the influence of long-lasting and repeated signal. At that, nocireceptors do not increase their excitability threshold as it happens with other receptors, for example, cold receptors. It means that nocireceptor “does not get used” to pain (Zaychik, Churliov, 1999). On the contrary, at inflammation, damage of tissues, long-term and repeated pain irritants, one can see nocireceptors sensitization, their excitation threshold decreases.
Myofascial pain is a symptom complex of unpleasant feelings, which occurs in anatomic formations of soft tissues of locomotor system. Most pain receptors belong to skin, ligaments, fascial formations and muscle tendons, muscle tissue, cerebral sinuses, parietal layer of serous tunic, bronchi, bile passages, capsules of internals, periosteal coverage, blood vessels. All these structures, packed with nocireceptors, are the sources of pain. Ischemia and VILS syndrome, located in these formations, also muscle spasm and vasoconstriction may lead to pain syndrome. The areas of tissues, attached to bony structures, are the zones of the highest risk. In these areas dystrophic processes progress with the increase of years due to insufficient vascularisation.
At that, in such anatomical structures as osseous and cartilaginous tissues, in all nervous conductors (nerves, nerve-roots, spinal cord and brain), pain receptors are absent (Zharkov et al., 2001). That is why, they theoretically can not be the sources of pain.
Syndrome of myofascial pains (SMFP) was called “a great imitator and potentiator of many diseases” (Rosen, 1993). According to modern ideas, dystrophic processes in skeletal muscles, caused by microcirculatory disorders, are the cause of SMFP progression.
Nowadays, there are a lot of suggested ways of treatment of SMFP. Medicinal treatment is treated negatively by specialists due to insufficient and unstable analgesic effect, side effect, risk of intoxication development, the increase of dose or usage of more effective medications up to synthetic narcotic substances with the development of drug dependence.
Application of some physiotherapeutic methods, including acupuncture, electric acupuncture, pressopuncture, lasero- and magnitopuncture, did not take firm anesthetic effect. Moreover, conducted by D. Dawson comparative clinical tests showed that acupuncture methods resulted in decrease of pains in 20% of cases whereas placebo-effect was seen with the frequency of 26-60%. According to the data by A. Kernbicher, acupuncture leads only to temporary decrease of pains and only in easily convinced patients.
At the VIII world congress of International Association of Rehabilitation Medicine (Kyoto, 1997) with the aim of SMFP blocking the following methods were suggested: intrathectal analgesia with the help of subcutaneously implanted automatic system of injection; stimulation of posterior funiculuses of spinal cord; stimulation of spinal cord with the help of epidural electrodes; epidural morphine injection; lumbar sympathectomy; therapy with the help of low-intensive laser.
The method of gradual fibrothomy by V.B. Ulsibat (1990), used on masticatory, temporal, cowl, greater pectoral, salens and other muscles, and the method of fasciotomy (Khabirov et al., 1995) showed high effectiveness at muscle pains. VGT application led to pain syndrome elimination and restoration of damaged functions (Korobkov, 1974; Velhover, Radysh, 1983; Mikhailichenko, 2000). Application of method of microincisures in a painful region led to the decrease and complete elimination of pain syndrome (Mikhailichenko, 2000).
The existence of many, sometimes mutually exclusive, approaches in SMFP treatment indicates about complexity of processes of tissular pathology and at the same time about the absence of an appropriate instrument of pathogenetic therapy. It is necessary to emphasize that not only effectiveness of an approach in elimination of pain is essentially important, but also important is the appropriate influence on conditions, causing its formation (circulation disorder, dystrophic changes etc.), though in practice the main goal is pursued, which is the decrease and elimination of pain syndrome, i.e. nearly always palliative therapy is executed. That is why only the combination of analgesic effect and abilities of restorative-reparative influence on structures of tissues gives ground to talk about pathogenetic influence of any method.
Writer’s long clinical practice and literature data allow to assume that this is VGT method which has such properties. Its influence leads to release of encephalin-like peptides, which favour analgesic effect, elimination of microvessels spasm, normalization of microcirculation system in the area of damage, dispersion of fibrous cicatrical contractures and reconstructive restoration of dystrophically damaged tissues.
Main clinical evidence of SMFP is pain and pathological statuses, connected with it. For example, according to the data by E.V. Tsoi (2001), clinical features of SMFP include necessary symptoms, which are marked by chronic muscle pain (100%), increased fatigability of muscles (about 90%), morning constraint, lasting more than 15 minutes (about 90%), sleep disorders (75-80%), depression (50-80%), astheny (95-100%), qualms (30-50%). At that, the combination of pain syndrome, morning constraint, astheny, sleep disorders is seen in more than 75 % of patients with SMFP. Besides this, SMFP is often attended with general fatigability (75%), headache (30-70%), paresthesia (40-90%), irritated intestinal tract syndrome (20-90%), dysmenorrhea (10-40%), Reino syndrome (3-30%) and other evidences.
According to the progress of the process and the number of damaged muscles, SMFP is nominally divided into local and progressive. Clinical course of a disease may be acute or chronic.
The second most important necessary SMFP evidence is restriction of movements or function disorder in the region of pain and in some neighbouring areas.
Unfortunately, nowadays, there is no such a laboratory-instrumental research which may be used for authoritative diagnostics of SMFP. That is the reason why diagnostics is based upon clinical evidences, to which we can refer: the analysis of the patient’s complaints, finding out the unbiased status of muscles at examination and with the help of palpation (the degree of development, presence of asymmetry, trophic changes, fibrillations; the amount of movements, configuration; consistence, tonus, muscle strength), localization and intensity of pain syndrome, irradiation in certain directions, the presence of vegetative and other concomitant disorders.
At the present time, the main method of clinical examination at SMFP in children and adults is palpation. Muscles are normally painless at palpation, do not contain indurations, do not react with jerk responses and do not reveal pain at pressuring. Palpation is done on symmetrical areas in the direction transverse to the axis of muscle fascicles, then interfacially, then with the use of special techniques (deep sliding, pincer, pinching palpation). The condition of the examined muscle is assumed in the status of rest (relaxation) and movement (active and passive stretching).
The application of vacuum test at SMFP is able in most cases to detect the zones of VILS syndrome with the presence of venous lymphoid stagnation in tissues quite accurately. As a rule, muscle pain syndrome occurs in the region of tissues with marked VILS syndrome. At the same time at pain syndrome, caused only by ischemic evidences, vacuum test may fail to reflect tissular changes in dermato-vascular response.