Specific indicants of tissular circulation disorder
Among specific changes in soft tissues, which occur due to disorders of tissular circulation in skeletal muscles and connective tissue of healthy people and patients, there are such pathological formations as: muscular trigger dots (MTD), muscle contractures (indurations), myofibrilosis and myofascial pain syndrome (MPS).
Muscular trigger dot - a region of excessive irritability, mainly in bounds of strained (indurated) fascicle of skeletal muscles or muscular fascia. During compression MTD is painful and may project pain, increased sensibility and vegetative manifestations to definitive regions.
MTD can often be "undetected and inexplicable source of surprisingly ubiquitous muscle pains suffered by human" (Trevell, Simmons, 1989). There are active and latent MTDs. Active MTDs are painful even without irritability; latent ones are evident due to excessive irritability of a muscle (fascia) region and are painful only during palpation. In spite of that they may be the cause of restraint of movement and weakness of an affected muscle. Latent MTDs remain for many years, from time to time causing acute attacks of pain even after inconsiderable sprain, overuse or frigorism of muscle. Both active and latent MTDs cause muscle dysfunction without signs of atrophy.
It is important to note that muscular tissue normally does not contain MTD, there are not any indurated bands in it, it is painless during palpation, does not have any jerk responses and does not reflect pain during compression.
MTDs may be in the organism of a person of any sex and age. According to the data by J. Travel and D. Simmons (1989) among 200 examined people at the age of 17-35, who didn't have any clinical symptoms, 54% of women and 45% of men were reported to have latent MTDs in rotator cuffs. Examination of schoolchildren detected latent MTDs in skeletal musculature in 95.6% of cases (Ulsibat, 1998). This is the MTD region where muscle contractures are located.
Active MTDs are more frequently detected in muscles of neck, pectoral girdle, pelvic, masticator musculature and temporal muscle. Definitive locations for MTDs are cowl, scalene, clavisternomastoid, quadrate muscle of lumber and also the muscle which lifts spatula.
Modern ideas about the mechanisms of MTD occurrence are quite various. On the one hand the causes of MTD formation are considered to be microinjuries, overuse and long-lasting myospasms; on the other hand most researchers come to the conclusion that there is a local ischemia in the region of MTDs. This is indicated in the work by H.G. Fassbender and K. Wagner (1973), in which changes in endothelium of capillars and loci of cellular proliferation in connective tissues and MTD regions are described.
Muscular contracture - stable muscle contraction, caused by fibrous-dystrophic changes due to local ischemia. Microcirculation research (Chernukh, Esipova 1971) and detection of speed of egestion of radioiodine (Zaslavskiy, 1980) indicate about the presence of regional disorders of tissular circulation in the regions of local muscular indurations.
Myogelosis - formation in muscles of painful and painless loci of induration, caused by transformation of myofibril colloids into gel phase and by muscular homogenisation and myocerosis.
Myofibrilosis - a new term, suggested by V.B. Ulsibat (1990). It defines dystrophic processes progression in muscular and connective tissues quite clearly. Myofibrilosis is marked as self-sufficient pathology of muscular tissue, and the presence of disorders of organocirculation in muscles is called "ischemic disease of muscles and connective tissue". They consider that cowl, deltoid, gluteus maximus and calf muscles are afflicted with myofibrilosis more frequently.
III-1 Myofascial pain syndrome (MFPS)
Is the first manifestation which may be caused by initial evidences of disorders of the system of tissular hemo- and lymphocirculation. Clinically MFPS is evident due to weakness, constraint, increased fatigability of muscles, pain. V.B. Ulsibat (1990) suggested a hypothesis according to which dystrophic changes of myofibrils of muscle fibre (myofibrilosis) form the basis of MFPS.
Pathogenetic mechanisms of MFPS are defined with the following basic stages:
1. The impact on a muscle of pathogenic stress-factors of various nature (physical, chemical, biological etc.), which result in formation of disorders of microvasculature of tissues, which, in their turn, cause progression of dystrophic processes in skeletal musculature and connective tissue.
2. In the region of localization of muscle contractures there are progressive dystrophic and necrotic changes of myofibrils at levels of cells, fibre or fibre bundles, which are attached with appearance or progression of MPS.
3. During recurrent exacerbations, because of loss of regeneration ability by a muscle, lysis of necrotized myofibrils occurs and the process of substitution of these regions by connective-tissular elements begins. It results in formation of cicatrixes of linear shape in the form of bands, which have, as a rule, two points of fixation to bony prominences. Trigger dots progress. Progression of disease with involvement of new myofibrils is possible; there appear contractures on other regions of the same and other muscles.
4. Progression of cicatrical process in the thickness of muscle causes extravasate compression of blood-lymphovasculature. It leads first to chronic disorder of organocirculation and lymphoid outflow or, with acute progression of tension, to acute infarction of considerable region of muscular tissue, and it aggravates the course of a disease and causes pain. Acute infarction mainly progresses in gluteus maximus and deltoid muscles (Ulsibat, 1990).
Thus, the major cause of chronic and acute pain syndrome is the development of local disorder of tissular blood supply, which causes local dystrophic process of connective tissue and muscles and which leads to necrosis and formation of scar tissue on its location.
Comparative analysis of ischemic heart disease and diseases of soft tissues of locomotor system by some clinical evidences and structural morphological changes allows to find out similar pathological disorders both in cardiac muscle and skeletal muscles (table 4.1).
Based on the above, one can tell about fundamentally unite basis of detectable dislocations, which consists of common pathological mechanisms of stagnant ischemic origin, which combine a lot of diseases of different nature. According to its content and pathological nature, the phenomenon of CTI and microhemodynamics centralization can be related to evidences of common pathology as they are seen in very different disorders.
Table 4.1. Comparative features of main clinical morphological evidences of SIDST and IHD.
Head, neck, back, buttock, upper and lower limbs, joints
In the heart region, behind the breastbone with irradiation to the left arm, face, stomach
III-2 The syndrome of venous interstitial lymphoid stagnation and stagnant ischemic disease of soft tissues
The complex of detectable indicators, which reflect the mentioned disorders, let the writer form the concept of development of syndrome of venous interstitial lymphoid stagnation (VILS) in soft tissues of healthy and sick people. While executing regular monitoring we succeeded in detecting not only typical localization, degree of manifestation and the region of VILS syndrome extension but also in finding out the correlation of VILS syndrome manifestation and clinical symptoms of acute myofascial pain syndrome of various localization, osteochondrosis and concomitant neurological disorders, myofibrilloses, neurocirculatory dystonia, ischemic heart disease, chronic fatigue syndrome, depression, headache, stomach ulcer disease, peptic ulcer disease, vertebrobasilar insufficiency syndrome and other diseases.
As both patients with various diseases and healthy children and adults (including sportsmen) have the same nature of VILS syndrome manifestation, we can come to the conclusion that such morphofunctional status of tissues, taking into account their viscerosomatic and somatovisceral relations, can be considered to be the basis of diseases formation on the one hand, and the predictor of possible diseases on the other one.
On the academic level, detected indicators help differentiate VILS into:
• Mainly venous blood stagnation (extravasates).
• Venous lymphoid stagnation (extravasates with puffiness and local edemas)
Detected VILS regions in many cases coincide projectively with definitive localizations of myofascial pain syndrome, myofibrillosis (drawing 4.1), which can be quite a significant proof of congestive ischemic genesis of dystrophic processes in tissues. This is confirmed by the data which was used in the work of A.S. Zaychik et al (1999), according to which venous hyperemia may independently not only lead to dystrophic processes progression but also to tissular infarctions. Therefore with the disorder of venous outflow, progressing increase of venous and capillary movement happens, and it may even lead to vessel rupture, bloodstroke and postprimary twigs compression. As a rule this ends up with necrosis of regions of tissues – venous hemorrhagic infarction.
Together with that it is necessary to note that not in all cases there are coincidences between myofascial pain syndrome, localization of myofibrilloses and VILS syndrome as these disorders may be caused by also progressing local ischemia of regions of tissues.
Picture 4.1 Typical localizations of VILS and myofibrilloses:
I. The most typical regions of dystrophy foci formation (myofibrilloses): temporal, masticatory, epicranial muscles; trapezius, clavisternomastoid, splenius, scalenus; bladebone-lifting muscle, deltoid; greater pectoral muscle; lumbar quadrate muscle, gluteus maximus muscle; tender, gastrocnemius, flounder-like muscles; ligamentous apparatus of tarsal canal, pelmatic aponeurosis; brachioradial muscle, ligamentous apparatus of carpal canal;
II. Predominant localization of acute infarction regions in skeletal muscles: deltoid muscle; gluteus maximus muscle; myofibrilloses infarction.
Clinically ischemic evidences are marked with blanching of region of tissue, local decrease of temperature, disorder of sensibility as paresthesia (numbness, tingling, feeling of heaviness, creeping sensation), pain syndrome, and disorder of functional properties of tissues. With this in ischemized tissue one can see feebleness of circulation, decrease of arterial tension in the region of artery which is situated lower than hindrance, lowering of oxygen partial pressure in the region of ischemia, decrease of interstitial fluid formation, decrease of number of functioning capillars, arteriole and venule stenosis. Hypoxia, hypercapnia and acidosis formation appear in tissues (Drawing 4.2).
The most probable mechanisms of ischemic evidences are conditioned with:
• Microvessels vasoconstriction;
• Vessels endothelium dysfunction, which is connected with decrease of nitrogen oxide formation;
• Lesion and dystrophic changes of vascular wall.
Drawing 4.2. Pathogenesis of VILS and SIST:
1- sludge; 2 – regions of microcirculation disorder.
Chronic ischemia of tissues leads to atrophy, which typically starts with true capillars. Then it consequently spreads to main capillars, pre- and postcapillars and only then – to arteriolar and venular collaterals, arterioles and venules. Reduction of microvessels, which occurs in terms of long-lasting tissue ischemia, is a multiphase process. Thus, in capillars this process occurs first as anemia, then morphological evidences of atrophy of endothelium, pericytes and basal interseptum develop. Such transformations end up with obliteration and capillar sclerosis. Hyperplasia of collagenous fibrils with reducible microvessels is the pathological nature of the capillar sclerosis. For example, dismantling of hemomicrovasculature of bands during obliterating endarteritis and dismantling of pericardial sac during atherosclerotic cardiosclerosis start with decapillarisation, which occurs as atrophy of true capillars.
Decapillarisation is the basic indicant of pathology of hemomicrocirculation system. Such pathology greatly decreases its tissulartrophic function. That is why during long-lasting venous hyperemia in tissues and during long-lasting ischemia of tissues, pathological processes of the same type develop unavoidably: atrophic, dystrophic and destructive changes. The results of researches of N.E. Yarygin et al (2001) discovered three variants of pathological remodeling of hemomicrovasculature:
1. It starts with disorder of capillars, which is impossible to make up in necessary extent.
2. It starts with unregulated transformation of capillars into deposit microvessels (postcapillars, venules, small veins).
3. It occurs as the combination of the first two variants.
Decappillarisation comprises the basis of functional insufficiency of hemomicrocirculation system. As a result of this, pathological centralisation of microhemodynamics develops, intensity of transcapillary exchange decreases and tissulartrophic disorders occur. The phenomenon of centralisation of microhemodynamics and the syndrome of capillar trophic insufficiency of microcirculation system belongs to many diseases.
The analysis of clinical observations indicates that VILS syndrome is being formed in almost everyone; children, adults (not only those who lead sedentary lifestyle but also sportsmen) in clinically healthy people and patients with various pathologies. At that the question seems quite important: what must be considered to appear earlier – VILS or the disease which leads to the stagnation? The strategy and tactics of preventive measures and treatment greatly depend on this. Clinicians usually regard many diseases (chronic cardiopulmonary decompensation, lungs and heart diseases, angiopathy etc.) as states which contribute the progression of venous blood stagnation in tissues because of capillar trophic insufficiency and angiospastic ischemia and angioparetic hyperemia, which combine with venous spastic moderation or stasis, venous capillary hyperemia and blood sludging. In this case preventive measures and preventive treatment may seem irrelevant.
However, by taking into account laws of VILS syndrome formation and data about congenital deficiency of nutritious capillars (Korablev, Nikolaeva, 1999) one can consider that VILS syndrome is of the initial pathogenetic components of microvasculature disorders (congenital or acquired), which cause pathology progression. This hypothesis, of course, helps optimize the process of treatment and, even at the early stages, carry out active preventive measures and therapy of wide range of diseases with the use of developed highly effective method of VILS correction and ischemia – VGT.
Writer’s personal observations and literature data give significant ground to think that in pathogenesis of many human diseases the key role belongs to microcirculatory disorders of fluid internal environments with the formation of their integral indicant – VILS syndrome. VILS syndrome leads to functional and pathological changes of visceral organs and systems, which aggravate disorders of microcirculation system on the feedback principle. Conducted with the help of vacuum test examination of patients and healthy people, children and adults, of those who regularly did medical gymnastics, sports, physical training, had good nutrition, practiced periodic abstinence from food and lived in safe Switzerland and of those who lead ascetic way of life, don’t do any sports and live in Russia revealed the same tissulartrophic disorders such as VILS syndrome and other clinical indicants.
Summarizing everything written above, it is necessary to emphasize some key statements about VILS syndrome as the leading pathogenetic component of many diseases:
• Almost all people may have VILS, healthy people and patients, irrespective of sex, age, level of physical training, applied traditional treatment and preventive measures.
• VILS is a basis on which, to considerable extent, dystrophy, atrophy, sclerosis of tissues, connected with them diseases and aging occur and develop.
• Diagnostics, preventive measures and treatment of VILS syndrome are possible with the help of using measured VGT which at the same time leads to curing a lot of diseases and regeneration of tissular structures – reconstruction of damaged structures.
Thus, the presented spectrum of non-specific evidences of disorders of tissular hemodynamics can be very useful information about formed and progressing morphofunctional disorders of soft tissues.
The complex of morphofunctional changes, which are detected in tissues of patients and healthy people (VILS syndrome, ischemia, myofibrilloses etc.), is the basis of formation of development concept of stagnant ischemic disease of soft tissues (SIDST) in almost every person. SIDST is seen in the wide range of diseases of skeletal muscles and connective tissue, which are known, for example, as myositis, osteochondrosis and connected with them neurological disorders, of tunnel syndrome of compression-ischemic nature, vertebrobasilar insufficiency, neurocirculatory dystonia etc. As a rule, they are combined with various visceral pathology, which goes together with stagnant-ischemic evidences in tissues. SIDST appears more frequently in back tissues, in neck, face, gluteal region, lower and upper limbs, juxta-articular tissues and other organs and parts of the body. There one can see most frequently MFPS, MTD, myofibrillosis, VILS syndrome, ischemia and other changes, which are considered to be clinical and pathomorphological substrates of SIDST.
Clinical progression of SIDST develops with different speed in every person: in some people it develops gradually, latently, in others it is attended with severe clinical symptoms (SFMP, scoliosis, chronic fatigue syndrome and other diseases). It is also certain that with aging functional evidences of SIDST increase greatly. They are aggravated with repeated stresses, hypodynamia or extreme physical training, unfavourable influence of the environment, wrong nutrition and other factors.
From the point of common pathology SIDST concept may be very significant in strategy and tactics of therapeutic measure not only in case of diseases of locomotor system but also in case of various visceral pathology. SIDST has inducing influence on formation of pathological foci in different organs; therefore, it predetermines their readiness for the emergence of diseases.
Long clinical writer’s observations and literature data show clearly that in the first place SIDST releaser is chronic influence of psychoemotional distress and also other forms of stress (physical, chemical, biological etc.). It is necessary to note that hypodynamia, inappropriate nutrition and other factors may undoubtedly deteriorate the course of SIDST but they should be regarded as secondary factors.
In terms of pathogenic stress, capillars of tissular microcirculation system, which are functionally triune (metabolic, transport, morphogenetic) elements, are quite sensitive, vulnerable, easily damaged structures. That is why true capillars are the first to be subjected to destruction, atrophy and reduction during long-lasting local, regional and systematic ischemia of tissues. In the same way in terms of long venous stagnation they are the first to be involved in the process of pathologic transformation into deposit vessels, which necessarily leads to inevitable progression of atrophic, dystrophic, destructive and sclerotic changes. It is important to note the fact of existence of processes of decapillarisation of tissue regions, which lead to SIDST formation in terms of either ischemia or venous stagnation.
In terms of many common diseases the whole hemomicrovasculature of an organism responds to pathogenic influence of stress as integral system. So, vessels status at arterial hypertension, atherosclerosis, IHD and other widespread diseases is marked by severe microvessels dysfunction (arterioles, precapillars, muscle venules). At that unstriated muscles spasm develops in some vascular terminals and muscle paresis – in others. It leads to peripheral hemodynamics disorder with the appearance in tissues of angiospastic ischemia and angioparetic hyperemia foci. Both pathophysiological phenomena go together with venous spastic feebleness of circulation and blood stagnation, venous capillary hyperemia and blood sludging. Aggregation of blood corpuscles is one of the earliest disorders, which appears as a result of influence of stress. Such rheological disorders in considerable extent favour following progression of dislocations in microcirculation system. At that the increase of blood and plasma viscosity is seen as well as decrease of blood flow, decrease of erythrocytes deflectivity, increase of penetrance of venular microvessels walls. At the same time A.M. Chernukh et al (1982) emphasize that systemacity of microcirculation disorders at this or that disease does not exclude but, on the contrary, suggests dissimilar degree of their manifestation in different organs and tissues. One can do nothing but agree with this statement, however, it is essential to emphasize that at various disorders and in conditions of clinical health similar disorders of investing tissues microvasculature are seen, especially in stress-dependent regions of a human body. This can indicate about the primary dislocations in microcirculation system even at early stages of life of a person. These dislocations later determine SIDST occurrence and other evidences of various disorders.
A large number of facts, which indicate about the main role of SIDST in progression of locomotor system and internals disorders, help regard stagnant-ischemic disease as an independent pathology of the whole complex of skeletal muscles and connective tissue structures.
The value of SIDST concept, first of all, is in the possibility of using a unique (according to the range of influence) instrument of reconstructive, reparative influence on tissues of an organism – VGT.
One can see from long clinical observations that VGT does not only favour diagnostics and elimination of clinical evidences of various disorders but it also has considerable reconstructive, reparative influence on pathomorphological substrates (VILS syndrome, ischemia, MTD, fibrous-cicatrical bands, myofibrilloses and other disorders of structure and function of tissues), which are not easily subjected to traditional treatment. Vacuum-gradient therapy helps simultaneously have influence on a number of key mechanisms of formed disorders and take active preventive measures of their treatment. Detected key mechanisms of formation and course of SIDST and other pathological processes, which are connected with it, give sufficient ground to reconsideration of long-existing traditional approaches of pathogenesis, treatment and preventive treatment of many diseases.
Comparative analysis of treatment effectiveness of SIDST with traditional therapeutic methods showed that they altogether, in contrast to VGT, do not make it possible to influence considerably the key pathogenetic mechanism of formation of pathological disorders in tissues.
Clinically interesting are the groups of patients with various diseases who got multimodality therapy with various kinds of massage, manual therapy, oxygenbarotherapy, hirudotherapy, pharmacological medications (analgetics, spasmolysants, anti-inflammatory agents), physioprocedures (UHF, laser, magnetotherapy etc.). In most cases, as a rule, decrease of acute clinical symptoms was seen. However, even in these cases vacuum testing detected in tissues evident VILS syndrome, MTD, deep muscular-connective-tissular formations such as contractures, cicatrixes etc. Without mentioning the possible side effects of the listed methods, we can assume that such complex treatment favours elimination of symptoms of diseases, but not their causes.
It is now evident that listed treatment measures do not have enough (according to effectiveness and intensity of influence) therapeutic influence on fundamental processes in tissues such as microvasculature normalization and adequate tissulartrophic function regeneration.
It is acknowledged that mechanisms of therapeutic effect of massage, cupping massage, manual therapy, hirudotherapy, oxygenbarotherapy, aspirin and other medicines, which normalize rheological blood properties, are directly or indirectly aimed for improvement of tissular circulation. Long clinical author’s observations showed that, in spite of general positive effects of listed-above procedures, they had almost no influence on main part of SIDST pathogenesis. After their use clinical evidences of a disease decrease and disappear, however, together with that, venous interstitial lymphoid stagnation, myofibrillosis, cicatrical-fibrous conglomerates chronically remain in deep layers of soft tissues. Patients and healthy people have similar results after undergoing regular courses of apitherapy, phytotherapy, osteopathy, acupuncture, yoga, Chi Kung gymnastics, evacuation of bowels and other methods of health improvement.
In the list of therapeutic treatment of SIDST we should mark the application of cupping massage with the use of regular cupping glasses or some glasses of various capacity and linear sizes. Sometimes, because of impossibility to measure the intensity of influence, this method causes extreme microtraumatism of skin capillars but, as a rule, the intensity of influence of such cupping glasses is quite insufficient. At the same time there is no possibility of controllable influence on deep structures. Application of such an unintensive and uncontrollable cupping massage allows to some extent to detect and decrease the degree of manifestation of VILS syndrome but in general this decrease occurs in interfacial layers of tissues. Ischemia and venous blood stagnation foci, which are situated in deep layers, are not appropriately influenced and later on become bigger. It favours their transit into chronic stage and dystrophic changes progression. This is clinically proved with occasional exacerbations of evidences of VILS syndrome. Conducted, after the course of regular cupping massage, control tests with the help of measured vacuum of high intensity (VGT) constantly detected venous blood stagnation in deep layers of tissues, local edema, deep muscular-connective-tissular indurations and other evidences of SIDST.
Considering the effectiveness of traditional approaches of treatment and preventive measures of problems of soft tissues from the point of view of common pathology, it is necessary to acknowledge that, firstly, since Hippocrates and Avicenna there have not been a lot of changes in this field and, secondly, application of traditional methods makes both doctors and patients indulge in illusion of recovery. In spite of the fact that till present there have been accumulated a lot of theoretical and clinical experimental data about the major role of disorders of tissular circulation in progression of various diseases of skeletal muscles and visceral pathology the effectiveness of modern methods of therapy is still far from excellence. It is connected with the fact that till present pathogenetic mechanisms of these disorders have not been worked out and, what is more important, an appropriate instrument of direct influence on microcirculation system of interfacial and deep layers of tissues has not been found. With the appearance of new technological abilities of reparative medicine, in particular, the method of noninvasive reconstructive reparative therapy, which was worked out by the writer, for the first time it became possible to find out the most physiologic way of direct therapeutic influence on pathologically changed regions of tissular microcirculation system with simultaneous inclusion of personal resources of processes of autoregulation and active autoregeneration of tissular structures of an organism. Besides, such a way appeared to be quite effective not only in conditions of pathology but also at prenosological stages of progression of various diseases. It gives ground to consider that the appropriate instrument of direct therapeutic influence on SIDST and mechanisms of occurrence of many diseases, which are connected with SIDST, has been discovered.