Neurotrophic disorders. Neurodystrophic vertebrogenic changes
LOCAL FACTORS
From the complex of local factors influencing the condition of periodontal tissues, the following should be highlighted: dental plaque, dental plaque microflora, uneven loads on periodontal tissue, malocclusion, traumatic occlusion, unsanitized oral cavity, defective fillings (supracontact, overhanging edge of a filling or artificial crown), defects in prosthetics, orthodontic appliances, bad habits, incorrect positioning of the frenulum of the lips and tongue, physical effects (burns, ionizing radiation), chemicals (acids, alkalis).
Dental deposits. The development of inflammatory changes in the periodontium is a consequence of the damaging effects of dental plaque.
There are soft non-mineralized– pellicle, dental plaque, white matter (soft plaque, food debris), dental plaque and hard mineralized- dental supra- and subgingival calculus, dental deposits.
Pellicle- This is an acquired thin organic film that replaces the cuticle. The pellicle is free of bacteria and is a derivative of salivary glycoproteins that selectively adsorb on the enamel surface. The pellicle is a membrane that gives the enamel selective permeability. The mechanism of pellicle formation is facilitated by electrostatic forces (van der Waals forces), which ensure strong bonding of the surface of hydroxyapatites of tooth enamel with positively charged components of saliva or gingival fluid.
Dental plaque It is a soft amorphous granular formation that accumulates on teeth, fillings, and dentures. It adheres tightly to their surface and is separated only by mechanical cleaning.
In small quantities the plaque is not visible, but when a lot of it accumulates, it takes on the appearance of a gray or yellow-gray mass. The plaque forms equally on the upper and lower jaws, more on the vestibular surfaces of the lateral teeth and the lingual surfaces of the lower frontal teeth.
Dental plaque consists mainly of proliferating microorganisms, epithelial cells, leukocytes and macrophages. It consists of 70% water, the dry residue is 70% microorganisms, the rest is the intercellular matrix. The matrix, in turn, consists of a complex of glycosaminoglycans, in which the main components are carbohydrates and proteins (about 30% each), lipids (15%), and the rest consists of waste products of plaque bacteria, remnants of their cytoplasm and cell membrane, food and salivary derivatives glycoproteins. The main inorganic components of the plaque matrix are calcium, phosphorus, magnesium, potassium and, in small quantities, sodium.
Dental plaque is basically a highly ordered bacterial formation, which is characterized by progressive growth and is quite firmly attached to the hard tissues of the teeth. Dental plaque begins to form within 2 hours after brushing your teeth. It forms and ripens within a short time - up to three weeks.
In the process of dental plaque formation, there are three main phases:
1st phase – formation of a pellicle that covers the surface of the tooth.
2nd phase – primary microbial contamination.
3rd phase – secondary microbial contamination and plaque preservation.
Primary microbial contamination occurs already in the first hours of pelicule formation. The primary layer covering the pellicle is Act. viscosus and Str. sanguis, due to the presence of special adhesive molecules, with the help of which these microorganisms selectively attach to similar adhesive foci on the pellicle. At Str. sanguis such adhesive sites are dextran molecules, in Act. viscosus are protein fimbriae that attach to proline proteins on the pellicle. First, microorganisms attach and adhere to the surface of the pellicle, then they begin to multiply and form colonies. With secondary microbial colonization, new periodontopathogenic microorganisms appear: Prevotella intermedia, Fusobacteria nucleatum, Porphyromonas gingivalis, Capnocytophaga saprofytum. Within a few days, there is an increase in cocci (their populations) and an increase in the number of gram-negative strains: cocci, rods, spindle-shaped bacteria (spirillum and spirochetes). Streptococci make up approximately 50% of the bacterial flora of the plaque. An important role in the occurrence of dental plaque is played by microorganisms that are capable of fermenting (synthesizing) carbohydrates with the formation of polysaccharides, dextrans, levans, characterized by adhesion to the hard tissues of teeth. These products form a mesh structure of dental plaque.
As dental plaque develops, its composition also changes. First prevail aerobic microorganisms, later - as the plaques mature - anaerobic.
In recent years, many scientists have considered dental plaque as a biofilm. The essence of the new approach is as follows: in accordance with the order of introduction of microorganisms into the plaque, the last to populate it are filamentous and spindle-shaped forms that secrete exopolysaccharides that form a viscous substance. Thus, all microbes included in the plaque are isolated from other microbial associations. In this state, this biofilm (or plaque) has direct access to nutrition, and therefore to reproduction and the realization of its damaging potential on adjacent soft tissue formations (in particular, on connective epithelial cells). Moreover, being part of biofilms, bacteria acquire new properties due to the exchange of genetic information between colonies, in particular, they acquire greater virulence and, at the same time, resistance to antibacterial influences.
The composition of dental plaque varies greatly among individuals. One of the reasons is the different intake of carbohydrates from food, which contribute to the accumulation of organic acids in the plaque.
As the plaque grows and organizes, the number of microorganisms in it increases to approximately 70-80% of its mass.
Mature plaque has a fairly organized structure and comprises: 1) acquired pellicle, which provides connection between the plaque and the enamel; 2) a layer of front garden-like fibrous microorganisms that settle on the pellicle; 3) a dense network of fibrous microorganisms in which there are colonies of other types of microbes; 4) the surface layer of coccus-like microorganisms. Depending on the location in relation to the gingival margin, supragingival (coronal and marginal) and subgingival plaques are distinguished. Subgingival plaque is divided into 2 parts: associated with the tooth and associated with the epithelium. Bacteria from subgingival plaque associated with the epithelium can easily penetrate the connective tissue of the gums and alveolar bone.
Plaque bacteria use nutrients (easily digestible carbohydrates - sucrose, glucose, and, to a lesser extent, starch) to form matrix components, consisting mainly of a polysaccharide-protein complex. The plaque contains inorganic substances in very small quantities, mainly calcium and phosphorus, traces of magnesium, potassium and sodium. The rate of plaque formation depends on the nature of the diet, the hygienic state of the oral cavity, the properties of saliva, but on average it takes about 30 days for the plaque to mature . As the plaque grows, it spreads under the gum, causing irritation of periodontal tissue, damage to the epithelium and the development of inflammation of the underlying tissues . Endo- and exotoxins secreted by plaque microorganisms have a toxic effect on periodontal tissue, disrupt cellular metabolism, cause vasomotor disorders, and sensitization of periodontal tissue and the body as a whole.
Plaque microorganisms, as a result of the active release of various enzymes (hyaluronidase, chondroitin sulfatase, proteases, glucuronidase, collagenase), have pronounced proteolytic activity). These enzymes cause depolymerization of glycosaminoglycans, periodontal tissue proteins, and primarily collagen, contributing to the development of microcirculatory disorders in the periodontium.
Advanced education Dental plaques are caused by mouth breathing, smoking, soft food consistency, excessive consumption of easily digestible carbohydrates, and poor oral hygiene.
White substance(soft plaque)- this is a superficial acquired formation on the teeth, covering the pellicle. It does not have a constant internal structure, which is observed in the plaque. Its irritating effect on the gums is associated with bacteria and their waste products. It is a yellow or grayish-white soft and sticky deposit that adheres less tightly to the tooth surface than plaque. The largest amount of plaque is located at the necks of the teeth, in the interdental spaces, on the contact surfaces and on the cheek surfaces of the molars. Plaque is quite easily removed with a cotton swab, a stream of water, a toothbrush, and is erased by chewing solid food.
Basically, plaque consists of a conglomerate of food debris (food debris), microorganisms, constantly exfoliating epithelial cells, leukocytes and a mixture of salivary proteins and lipids. Dental plaque contains inorganic substances - calcium, phosphorus, sodium, potassium, trace elements - iron, fluorine, zinc and organic components - proteins, carbohydrates, proteolytic enzymes. The bulk of dental plaque consists of microorganisms: 1 mg of plaque can contain up to several billion of them.
The intensity of formation and the amount of plaque depend on many factors: the quantity and quality of food, the viscosity of saliva, the nature of the microflora, the degree of tooth cleansing, and the condition of periodontal tissues. With increased carbohydrate consumption, the rate of plaque formation and its amount increase.
Mechanism of plaque formation:
1. stage – formation of a pellicle (thickness from 1 to 10 microns);
2. stage - adsorption of proteins, microorganisms and epithelial cells on the surface of the pellicle;
3. stage - mature dental plaque (thickness up to 200 microns);
Stage 4 - transition of soft plaque into tartar. This occurs when conditions of anaerobiosis are created in mature dental plaque, a change in the composition of microorganisms occurs (replacement of aerobes by anaerobes), a decrease in acid production and an increase in pH, accumulation of Ca and its deposition in the form of phosphate salts.
Food leftovers- This is the fourth layer of non-mineralized dental plaque. Food particles are located at retention points. When eating soft food, its remains undergo fermentation and rotting, and the resulting products contribute to the metabolic activity of dental plaque microorganisms.
Tartar. Over time, the concentration of inorganic substances in the dental plaque increases, and it becomes a matrix for the formation of tartar. The predominant calcium phosphate in the plaque impregnates its colloidal base, changing the ratio between glycosaminoglycans, microorganisms, desquamated epithelium, and leukocytes.
Tartar is predominantly localized in the cervical area of the teeth (vestibular, lingual surface), retention points, on the surface of the teeth adjacent to the excretory ducts of the salivary glands, under the marginal edge of the gums.
Depending on the location relative to the gingival margin, there are supragingival And subgingival tartar. They differ in the mechanism of formation, localization, hardness and influence on the development of pathological processes in the oral cavity. Mineral components (calcium, phosphorus, magnesium, carbonates, microelements) penetrate into the supragingival tartar from oral fluid, and in the subgingival region - from blood serum. About 75% of these are calcium phosphate, 3% calcium carbonate, the rest are magnesium phosphate and traces of various metals. The mostly inorganic part of tartar has a crystalline structure and is represented by hydroxyapatite. Depending on quantity minerals The consistency of tartar changes, with 50-60% of mineral compounds - soft, 70-80% - medium, more than 80% - hard.
The organic basis of tartar is a conglomerate of protein-polysaccharide complex, desquamated epithelial cells, leukocytes and various types of microorganisms. A significant part consists of carbohydrates, represented by galactose, glucose, glucuronic acid, proteins and amino acids.
In the structure of dental stone there are a superficial zone of bacterial plaque without signs of mineralization, an intermediate zone with crystallization centers and a zone of dental calculus itself. The presence of a large number of bacteria (their enzymatic properties) in dental calculus explains its pronounced sensitizing, proteolytic and toxic effect, which contributes to the development of microcirculatory disorders in the periodontium and causes destruction of connective tissue.
Based on their structural characteristics, hard dental deposits are divided into into: crystalline-granular, concentric-shell-shaped and collomorphic.
Supragingival calculus(salivary) is more common and is formed due to the mineralization of soft dental deposits. It is usually white or whitish-yellow in color, hard or clay-like in consistency, and is easily detected upon inspection. The color is often affected by smoking or food pigments. There are several theories for the formation of supragingival tartar: salivary, colloid, microbial.
Subgingival calculus located under the marginal gum, in the gingival periodontal pockets, on the root cement. It is usually not visible during visual examination. Probing is necessary to detect it. It is dense and hard, dark brown in color and tightly attached to the surface of the tooth. Subgingival tartar is formed as a result of coagulation of protein and mineral substances of blood serum and inflammatory exudate in the periodontium.
Tartar (especially subgingival calculus) has a pronounced mechanical damaging effect on the periodontium and contributes to the development of local C-hypovitaminosis. It contains metal oxides (vanadium, lead, copper), which have a pronounced toxic effect on the periodontium. On the surface of tartar there is always a certain amount of non-mineralized plaques, which are the most important irritants of periodontal tissue and largely determine the nature of the pathogenic effect of tartar. The mechanism of the damaging effect of tartar on the periodontium is largely related to the action of the microflora contained in it.
Microflora. About 400 strains of various microorganisms constantly live in the oral cavity, but only about 30 of them can be considered opportunistic for periodontal tissues.
Microorganisms vary greatly in their ability to attach to different surfaces in the mouth. Thus, Streptococcus mutans, S. sanguis, Lastobacillus strains, Actinomyces viscosus readily attach to tooth enamel. Streptococcus salivarius, Actinomyces naeslundii inhabit the dorsum of the tongue, while Bacteroides and spirochetes are found in the gingival sulci and periodontal pockets. Such types of microorganisms as Streptococcus mutans, S.sanguis, S.mitis, S.salivarius, Lactobacillus strains have the ability to form extracellular polymers from dietary carbohydrates. These extracellular polysaccharides are insoluble in water and significantly enhance the adhesion of microorganisms, and therefore dental plaque, to the surface of the teeth. They stick to the surface of the pellicle and subsequently to each other, ensuring the growth of the plaque.
In addition to plaques tightly attached to the tooth, there are loose microbial accumulations on the walls inside the pocket. The role of dental plaque and loose microorganisms in the development of the pathological process is not the same: the influence of plaque dominates, but in some cases it is loosely attached microorganisms that play a significant role in the course of aggressive forms of periodontitis and in the onset of the exacerbation phase.
There are a significant number of different factors in the oral cavity that suppress the growth of microflora. First of all, this is saliva, which contains substances such as lysozyme, lactoperoxidase, lactoferrin. Immune components, such as IgA, are secreted by the salivary glands and enter the oral cavity, preventing the attachment of microorganisms to the surface of hard dental tissues and cell membranes.
The basement membrane is also considered as a fairly powerful barrier to the penetration of microorganisms, but if its integrity is damaged, bacteria relatively easily penetrate deep into the periodontal tissues. The entrance gate for microflora is a violation of the integrity (ulceration) of the attachment of the sulcus epithelium to the hard tissues of the teeth.
Periodontal tissues function fully when there is a balance between the resistance of the human body and the virulence of bacteria. Some types of microorganisms have the ability to overcome the host's defenses and penetrate the periodontal pocket and even the connective tissue of the gums. Bacteria can damage host tissue through direct action their toxins, enzymes, toxic metabolic products, or indirectly by stimulating host responses that cause damage to its own periodontal tissue.
The microbial population that forms on the surface of the teeth in the form of plaques is significantly different from the microorganisms found on the surface of the oral mucosa. Microorganisms entering the oral cavity first come into contact with saliva or saliva-coated surfaces. Therefore, they are easily washed off if they do not have the ability to adhere to the surface of the teeth. Consequently, adhesiveness is considered as an important property and the main factor in the opportunistic microflora of the oral cavity. If any changes occur in the host’s body or in the microorganisms themselves that are in symbiosis, this leads to a significant disruption of the habitat of microbes in the oral cavity. New conditions that have arisen require adaptation of the host organism and microbes, so the oral cavity is usually populated with new strains of microorganisms that are more adapted to the current conditions. This phenomenon is called bacterial heredity and occupies an important place in the pathogenesis of gingivitis and periodontitis.
There are a sufficient number of observations confirming the specificity of the complex of microorganisms that are associated with this disease or are most often isolated in various types of human periodontal diseases, various courses of generalized periodontitis. This occurs despite the rather different causes of the diseases and, apparently, reflects certain, more or less identical conditions that arise at this time in the periodontium
Microbiological research in this case, the complex of microorganisms most often sown from periodontal pockets is determined.
This made it possible to create a kind of classification of periodontal microbial complexes.
There are: red, green, yellow, purple, orange microbial complexes.
Red complex(P. gingivalis, B. forsitus, T. denticole). The combination of these microorganisms has a particularly aggressive effect on the periodontium.
The presence of this complex causes severe bleeding of the gums and the rapid course of destructive processes in the periodontium.
Green complex(E. corrodent, Capnocytophaga spp., A. actinomycetemcomitans). The main virulence factor of A. actinomycetemcomitans is a leukotoxin that causes neutrophil lysis. This combination of microbes can cause both periodontal diseases and other lesions of the oral mucosa and hard dental tissues.
Yellow complex(S. mitis, S. israilis, S. sanguis).
Purple complex(V. parvula, A. odontolyticus).
Orange complex(P. nigrescen, Prevotella intermedia, P. micros, C. rectus + Campylobacter spp.). Prevotella intermedia produces phospholipase A, disrupts the integrity of epithelial cell membranes, is an active producer of hydrolytic proteases that break down proteins of periodontal tissues and tissue fluid into polypeptides, produces proteolytic enzymes, and therefore plays a major role in the formation of periodontal abscesses.
These three complexes are also capable of causing periodontal lesions and other oral diseases.
The identification of these complexes does not mean that they include only the listed species of microorganisms, but these communities of species are the most stable.
A possible reason for the stability of just such microbial combinations is their existence in the form of viscous biofilms according to the principle of the above-mentioned “convenience” of their metabolism, when the products secreted by some are nutritional sources for other microbes or provide their increased stability and virulence.
The listed microbial associations are part of stable dental plaques attached to the surface of the tooth or to the walls of the periodontal pocket. Moreover, the composition free The location of microbial accumulations inside the periodontal pocket may be completely different.
Periodontal microorganisms identify a number of different pathogenic factors that cause the destruction of periodontal tissue, namely: leukotoxins, endotoxins (lipopolysaccharides), lipoic acid, resorbing factor, capsular material, various short-chain fatty acid. These bacteria also secrete enzymes: collagenase, trypsin proteases, keratinase, neuraminase, arylsulfatase. These enzymes are capable of lysing various components of periodontal tissue cells. Their effect is enhanced when combined with enzymes that release leukocytes accumulated on periodontal cells.
The primary reaction of the gums to the combined effect of these factors and, first of all, inflammatory mediators, is the development of gingivitis. Pathological changes in gingivitis are reversible, however, prolonged maintenance of inflammation leads to increased permeability of histohematic barriers, a significant increase in the migration of leukocytes and their infiltration of periodontal tissues, the interaction of bacterial antigens with antibodies, and increased secretion of lysosomal enzymes by leukocytes. Subsequent blast transformation of lymphocytes, leading to the formation of plasma cells and tissue basophils, stimulation of the secretion of lymphokines and activation of osteoclasts, determines the development of destructive processes in soft and hard periodontal tissues.
The development of periodontitis is directly dependent on the amount of plaque and general microbial contamination of the oral cavity and inversely on the effectiveness of hygiene measures.
Traumatic occlusion. Conditions in which the periodontium is exposed to loads that exceed its reserve compensatory capabilities and lead to its damage are called “functional traumatic overload”, “occlusal injury”, “trauma as a result of occlusion”, “traumatic occlusion”. There are various possible causes and mechanisms of development of traumatic occlusion. If excessive damaging chewing pressure acts on teeth with healthy periodontal disease not affected by the pathological process, then such traumatic occlusion is defined as primary. Primary traumatic occlusion can occur with traumatic overload of teeth due to increased bite (filling, crown, mouthguard, orthodontic appliance), malocclusion and individual teeth, loss of many teeth, pathological abrasion. Quite often, primary traumatic occlusion occurs as a result of parafunctions: bruxism, tonic reflexes of the masticatory muscles, compression of the tongue between the teeth. Traumatic overload occurs when the lower jaw is displaced due to loss of teeth or improper prosthetics. Thus, primary traumatic occlusion occurs as a result of the action of excessive (compared to normal, physiological) chewing load on the teeth or a change in its direction. It should be noted that primary traumatic occlusion is reversible pathological process.
On the other hand, against the background of a pathological process in periodontal tissues, the usual normal chewing load may exceed the reserve forces of the periodontium. As a result of resorption of alveolar bone and periodontal fibers, the tooth cannot resist the normal chewing pressure that it could withstand with intact periodontium. This habitual occlusal load begins to exceed the tolerance of its structures and turns from a physiological load into a factor that injures and destroys periodontal tissue. Wherein. the relationship between the height of the clinical crown and the length of the root changes, which causes significant overload of the bone walls of the alveoli. This leads to overload of the periodontium and accelerates resorption bone tissue holes. Such traumatic occlusion is defined as secondary. It most often occurs in generalized periodontitis. Formed vicious circle, pathological changes: traumatic occlusion occurs against the background of periodontal changes and subsequently it contributes to the further progression of destruction of the alveolar bone and other periodontal tissues. Typically, with secondary traumatic occlusion, resorption of periodontal tissue (periodontium, alveolar bone) and hard dental tissue (cement, dentin) occurs.
The adverse effects of traumatic occlusion increase with tooth extraction. When teeth are lost or removed, resistance from neighboring teeth disappears, which compensates for a certain horizontal component of the chewing load. Such teeth begin to take the load in isolation, and the dentition ceases to act as a single system. The resulting overload of such teeth leads to their inclination towards the defect in the dentition. This leads to atrophy of the alveolar bone at the site of application of excessive chewing pressure.
When a pathological situation exists for a long time, the reflex activity of the masticatory muscles changes, and this reflex is consolidated. Incorrect movements of the lower jaw, in which some areas of the dentition are not exposed to chewing load, while others, on the contrary, are overloaded, lead to changes in the temporomandibular joints.
Characterizing this pathological condition in general, it should be noted that traumatic occlusion is understood as such occlusal relationships separate groups teeth or dentition, which are characterized by premature and unstable closure, uneven distribution of chewing pressure with subsequent migration of overloaded teeth, pathological changes in the periodontium, dysfunction of the masticatory muscles and temporomandibular joints.
Sometimes like separate form combined traumatic occlusion is distinguished. In this case, signs of both primary and secondary traumatic occlusion are revealed.
Anomalies of bite and position of individual teeth have a significant damaging effect on periodontal tissue. Pronounced changes develop with a deep bite in the frontal area of the dentition, since these areas are overloaded during vertical and horizontal movements of the lower jaw. With a distal bite, this is aggravated by the resulting significant horizontal overload of the teeth, which subsequently manifests itself in a fan-shaped divergence of the upper frontal teeth. With medial, on the contrary, their displacement occurs to the palatal side. In the frontal area of the lower jaw, displacement of the teeth and their crowding are noted. In these areas there is a significant accumulation of food debris, microorganisms, and the formation of dental plaque and tartar.
The development of inflammatory processes in the periodontium with anomalies in the position of the teeth and occlusion pathology is associated with a violation normal functioning periodontal disease - overloading some of its areas and underloading others.
The severity of these pathological changes in the periodontium depends on the severity of the malocclusion and individual teeth.
Unsanitized oral cavity, in which there are many teeth affected by caries, represents a whole complex of periodontal damaging factors. Food debris accumulates in carious cavities, and the formation of a significant amount of dental plaque is observed in the area of these teeth.
Carious cavities located in the cervical region and on the contact surfaces of the lateral teeth have a particularly adverse effect on tissue. The damaging effect of the latter is enhanced by the absence of a contact point in these areas: food debris is pushed deeper during chewing, injuring the gums and other periodontal tissues. Approximately the same adverse effect on periodontal tissue is caused by improperly filled carious cavities on the contact surfaces of teeth, especially with edges overhanging the gingival papilla. Under them, food debris accumulates, dental deposits form and, thus, conditions are created for the emergence and progression of the pathological process in the periodontium.
Incorrectly manufactured artificial crowns, bridges and removable dentures have a similar effect on the periodontium. Fillings and fixed dentures that increase the bite additionally cause overload of the teeth during chewing movements of the lower jaw. This leads to the development of traumatic occlusion and the appearance of traumatic nodes in these areas.
Anomalies of the anatomical structure of gum tissue, mucous membrane and oral cavity as a whole also have an adverse effect on periodontal tissue. Thus, the high attachment of the frenulum of the lips or tongue leads to the fact that when they move, the gums are torn away from the necks of the teeth. In this case, a constant tension arises in the area of attachment of the gums to the necks of the teeth, or more precisely, the attachment of the epithelium of the gingival sulcus to the hard tissues of the teeth. Subsequently, in these areas the integrity of the epithelial attachment is disrupted, first a gap is formed, and then a periodontal pocket. Approximately the same mechanism of damaging action on the periodontium with a small vestibule of the oral cavity.
With prolonged mechanical overload of the teeth, swelling and destruction of collagen fibers occur, the mineralization of bone structures decreases, and then their resorption occurs.
The effect of microorganisms is significantly enhanced against the background of impaired trophism of periodontal tissue. This occurs when the structure of the soft tissues of the vestibule of the oral cavity is disrupted or when there are “pulling” strands of the mucous membrane.
Bad habits sucking or biting the tongue, soft tissues of the oral cavity, or any foreign objects have a damaging effect on periodontal tissue. Habitual biting of foreign objects creates a small but constant traumatic overload of the teeth in this area. Biting soft tissues, such as the cheek, causes additional tension on its tissues. Through the mucous membrane of the transitional fold, it is transmitted to the gum tissue and promotes its separation from the hard tissues of the teeth. This further leads to the accumulation of food residues in such areas and the formation of dental plaque.
Local irritants.
In addition to dental plaque, there are a number of different factors in the oral cavity that can cause mechanical trauma, chemical and physical damage to periodontal tissue.
Mechanical irritants There may be various foreign bodies that (especially in children) can easily injure the gums. Acute injury is possible due to careless use of hard objects (hard parts of food, toothpicks, toothbrushes, in children - parts of toys), injuries (bruise, blow) to the maxillofacial area.
A common cause of inflammatory periodontal diseases is chronic injury from the sharp edges of carious cavities (especially those localized in the cervical area or on contact surfaces), overhanging edges of defective fillings, and defective dentures.
Adolescents often experience acute periodontal trauma due to dental trauma, their dislocation or subluxation, or jaw contusion. In such cases, localized periodontitis usually develops.
Chemical damaging factors associated with the effect of various acids, bases (alkalis), chemical medications, and components of filling materials on the periodontium. Due to the expansion of the arsenal of household chemicals, chemical burns of the mucous membrane and periodontal tissue are observed, especially in children. Depending on the nature of the chemicals, their concentration and duration of contact with the oral mucosa, either catarrhal inflammation or gum necrosis develops, and in severe cases, deep periodontal lesions with necrosis of the alveolar bone. Typically, more severe lesions occur with burns caused by bases, which, unlike acids, cause the development of liquefaction necrosis of tissue.
Physical factors. These include damage to the periodontium when it is exposed to high or very low temperatures, electric current, or ionizing radiation. In domestic conditions, periodontal burns are possible hot water, food. Depending on the temperature, duration of action of the irritant, the age of the victim, the severity of changes in the periodontium may vary: from catarrh to deep destructive damage (ulcers, tissue necrosis).
When tissue is damaged by electric current, the integrity of the gum tissue is usually damaged, and in severe cases, necrosis of the superficial and deep periodontal tissues occurs. The cause of inflammatory changes in the gums may be microcurrents that occur between parts of dentures (metal fillings) made of different metals. In the latter case, a combination of electrothermal and electrochemical effects on periodontal tissue is possible.
The influence of ionizing radiation is possible when radioactive substances are incorporated into the oral cavity, accidental exposure of victims to areas of increased radiation, and during radiation therapy of neoplasms of the maxillofacial area. Depending on the type of ionizing radiation and its dose, various variants of the clinical course of the lesion are possible: from catarrhal inflammation to extensive erosive and ulcerative lesions and necrosis of periodontal tissue.
General factors:
Periodontal lesions are associated with a number of common factors: genetic predisposition, immunodeficiency, age-related changes, pregnancy, diabetes. The final result of their action is the strengthening of destruction processes and the weakening and slowing down of repair processes. Systemic diseases are more legitimately considered as aggravating the development of periodontal diseases or influencing their pathogenesis.
Neurotrophic disorders.
Periodontal disease as a neuro-dystrophic process was substantiated in his works in the 30-60s of the last century by D.A. Entin, E.E. Platonov, I.O. Novik, E.D. Bromberg, M.G. Bugaiova and modern scientists – N.F. Danilevsky, L.M. Tarasenko, L.A. Khomenko, T.A. Petrushanko.
In a number of works, D.A. Entin experimentally confirmed the role of the central nervous system in the occurrence of generalized periodontitis. By irritating the area of the gray tubercle, he for the first time received degenerative changes in the periodontal tissues, similar to generalized periodontitis in humans. These changes are based on organic and functional disorders of the central nervous system, which intensify under unfavorable environmental conditions (for example, hypovitaminosis C).
N.F. In experiments on monkeys, Danilevsky used a physiological stimulus - experimental neurosis caused by a violation of the sexual and herd reflexes.
- “...of particular interest are data on the neural organization of the hypothalamic-cortical relationship and the presence of bilateral communication of some neurons of the motor cortex with polyeffector, integral neurons of the hypothalamus. Reciprocal cortico-hypothalamic neural systems obviously play an important role in the corticofugal control of the mechanisms of the hypothalamus , and in the integration of somato and visceromotor components of emotional and behavioral reactions caused by the activation of certain structures of the hypothalamus."
Thus, there is every reason for mandatory consideration of the interdependence of mental and physiological homeostasis and mental and physiological maladaptation, respectively. It can manifest itself, in particular, in the fact that disturbances in mental homeostasis can interfere with the achievement of physiological homeostasis, which can manifest itself in the form of asthma, ulcerative colitis, psoriasis, stomach ulcers, etc.
The body's desire to achieve all types of adaptation, when mental maladjustment occurs, triggers mental adaptation reactions, the effectiveness of which depends on the reactivity of the entire cortico-hypothalamic neural system. Her hyporeactivity does not allow these reactions to be fully realized, so they are ineffective and frequent (i.e., they are chronic). S. Grof associates this course of the disease with an excess of perinatal energy, which, due to the presence of certain barriers, does not find a way out. With all the brightness of this image, it seems that it is more accurate and practically expedient to explain these data from the point of view of hyporeactivity or perverted reactivity of integrative brain structures that implement adaptive mental reactions. This point of view coincides with the well-known concept that interprets many frequently recurring mental manifestations as an outwardly unusual adaptive reaction of an individual to external social circumstances that are unacceptable to him. We can confidently assume that holotropic therapy is a type of homeopathic therapy that increases the reactivity of the corresponding regulatory structures and thereby helps the body develop adaptive reactions. Indeed, traditional homeopathic remedies enhance the manifestation of symptoms of physiological adaptation, and holotropic therapy - symptoms of mental adaptation ( external manifestation- increased mental disorders during therapy sessions).
It is quite obvious that the mechanisms of repression of full-fledged mental and physiological adaptive reactions are similar, which is quite natural, since in both cases they are associated with a violation of the organization of neural structures of the brain, i.e. with the presence of a pathological combination according to A. D. Speransky, which can decay under a certain excitation.
This small difference between our interpretation and the interpretation of S. Grof could not be discussed, but... Recognition of the possibility of both physiological and mental hyporeactivity and, accordingly, physiological and mental maladjustment, as well as the quite naturally assumed possibility of their interaction (mutually reinforcing and mutual weakening) leads to important practical assumptions.
It is possible to normalize the reactivity of certain parts of the cerebral cortex by transferring to them excitation from the hypothalamus. This probably explains the good therapeutic effect against neuroses, early forms of epilepsy, schizophrenia and other psychosomatic diseases achieved when using Gravidan. It is probably optimal to eliminate both physiological and mental maladjustment through simultaneous (or close in time) stimulation of the cortex and hypothalamus (i.e., the organization of “counter” flows of excitation of nervous structures that are in reciprocal relationships). If the latter is true, then one can expect brilliant results from the combined (close in time) use of injection urine therapy or similar therapy, for example, implemented using the Majkov-Trunecek drug (section 3.2.1) and holotropic therapy, giving good results and when used in isolation. A wide range of diseases and disorders, conventionally classified as either somatic or mental (but in fact often or always containing a second component, i.e., essentially psychosomatic) may be subject to the specified complex treatment. First of all, this technique should be tested in the treatment of neuroses, early psychopathy, stomach ulcers, psoriasis, ulcerative colitis, and alcoholism. It is possible that holotropic therapy can also be used as an antitumor polyvalent agent, which, on the one hand, normalizes nervous trophism, and on the other, causes hypoxia of the body, which negatively affects the growth of malignant tumors and metastasis. Indirect confirmation of this assumption are the results of work that takes into account the achievements of psychology and psychotherapy necessary to introduce a person into special states of consciousness. Its authors believe that in these states a person gains access to the body's reserve capabilities; using them, he can correct functional and morphological disorders. Introducing cancer patients into special states of consciousness gave the following results:
It was possible to completely stop or significantly reduce the severity of side effects after chemotherapy and radiation therapy (nausea, vomiting, pain, asthenia, etc.);
With targeted exposure, there is a rapid restoration of the number of leukocytes in patients undergoing chemotherapy and radiation therapy, without the use of hemostimulating drugs;
There is a faster regression of tumor formations when combining traditional methods of antitumor treatment and psychotherapy;
Persistent positive emotional states are developed, which significantly affects the entire course of treatment.
Of course, introducing cancer patients into special states of consciousness is easily combined with gravidatherapy and urine enemas (in particular for colon tumors).
Concluding the topic of treatment of mental disorders and diseases, it should be recalled that their old forms are the development of incorrectly or poorly treated initial forms. Misunderstanding of the maladaptive nature of these diseases has led in many cases to a fundamentally incorrect approach to treatment initial stages. It is very easy to classify gravidan injections and holotropic therapy as elements of paramedicine. But it is not easy to be responsible for the transformation of initial forms of diseases into persistent chronic, often incurable ones. Maybe we should stop putting labels on everything that is incomprehensible or forgotten?
Let's return to holotropic therapy. It is possible that its nonspecific nature is a prerequisite for enhancing its therapeutic effectiveness through the additional use of specific homeotherapy, both classical and according to R. Voll. The compatibility of the latter with holotropic therapy can be illustrated by the following two typical examples from the book by S. Grof and N. L. Lupichev:
- "Norbert, a psychologist and priest, suffered for many years from severe pain in his shoulder and pectoral muscles. Repeated medical examinations, including x-rays, revealed no organic changes and all therapeutic attempts remained unsuccessful. During a holonomic integration session, he had great difficulty managed to bear the music and had to be persuaded to remain in the process, overcoming the acute discomfort he experienced. For about an hour and a half he experienced severe pain in his chest and shoulder, fought furiously as if his life was threatened, choked and coughed, uttering loud cries. Later "He calmed down, relaxed and became quiet. With noticeable surprise, he reported that this experience released tension in his shoulder and he got rid of pain. The relief was permanent, more than five years have passed since the session, and the symptoms have not recurred."
- “Patient K., 60 years old. Causalgic syndrome. Ten years ago, after injury to the skin of the right shoulder, severe burning pain in the right arm arose. In connection with this, he underwent a sympathectomy - without effect. Six years ago he underwent amputation of the arm to the upper third of the shoulder - without effect . Phantom pains appeared, spreading from the shoulder to the hand. Other treatment methods - drugs, acupuncture, electrical stimulation did not produce an effect. Electropuncture testing showed that with the help of Botticelli's painting "Spring" the indicator of the point of the central nervous system is normalized. After seven sessions (15 minutes each daily) the pain, according to the patient, decreased by 80%. After seven additional sessions, the pain disappeared (according to the patient, by 95%) and did not reappear for eight months."
Continuing the theme of holotropic therapy, we need to add the following.
S. Grof’s position seems insufficiently substantiated, according to which part of the memory patterns (namely eating feces, drinking urine, menstrual blood, kissing the devil on the anus, scatological pleasure from uncleanness) projected into the consciousness of patients during holotropic therapy sessions relates to perinatal memory about spontaneous defecation and diuresis of both mother and child during labor. Of course, S. Grof appropriately recalls the Latin proverb “We are born among feces and urine,” but the short duration of the child’s contacts with these excrements during the birth act allows us to doubt that the memory of these events is manifested in holotropic therapy sessions. It seems that the stability and frequency of these manifestations during its implementation is due to their belonging to more natural and ancient patterns related to the depths of phylogenesis. In other words, not to perinatal, but to transpersonal memory of calorie eating, drinking and licking urine by animals, i.e. to phylogenetic (stable and natural) elements of behavior. The rest of these patterns also have a natural, predominantly sexual, character and relate to the usual, biologically natural manifestations of male courtship of females during the period of estrus. Thus, M.L. Butovskaya and her co-author present the main indicators of reproductive behavior of primates. In particular, tamarins initiate mating through the following techniques: mutual following posturing, piloerection, mutual marking, sniffing and licking the partners' genitals. It is not difficult to notice the similarity of these behavioral elements with cunnilingus, which is not so rarely used in human sexual practice.
The foregoing allows us to assume that mental disorders are revealed in the process of holotropic therapy in a person’s memory in the form of phylogenetically ancient behavioral patterns, naturally, with one or another distortion of their external expression.
It seems that the proposed interpretation, on the one hand, is more biological, on the other hand, it indicates the difficulty of accurately attributing patterns to a specific type of unconscious memory (perinatal or transpersonal). It may not be worthwhile to go into a discussion on this issue, but the theme of this book makes it necessary to emphasize the naturalness of animals’ consumption of urine and feces and, accordingly, the biological validity of the classical versions of urine and coprotherapy.
To summarize, it is logical to assume that preliminary manual or other therapy of the spine, subsequent holotropic therapy and injection urine therapy can eliminate local and general neurophysiological disorders and, therefore, significantly increase the speed and completeness of all types of adaptive reactions, and ultimately lead to recovery. Such a “clean” and cheap equipment-free and, most likely, harmless, complex therapy is logical, has an extremely physiological nature and can well be considered as a serious alternative to many harsh and harmless methods of treatment.
Let's look at other combinations.
We must be careful to assume that there is more contained in a word than in a trivial sound or written medium of information. Much amazing information has been accumulated about the power of the word and human will. Among them is the ability to lift stones by pronouncing a magic phrase, and the impact of some mantras on masses of people with an alleged effect comparable to the effect of nuclear weapons, and much more, very interesting, but which is almost impossible to rely on in a serious discussion. Therefore, we will use only modern data that seems quite reliable. Taking them into account, the following treatment methods can be developed, including urine therapy.
The therapeutic effectiveness of certain texts has been established long ago and quite reliably; their modern practical application is the merit of G. N. Sytin. Recently, Harvard University conducted a study on the healing effects of prayers and reliably established their healing effectiveness; At the same time, it turned out that prayers do not necessarily have to be of a religious nature. Psychotherapy and self-hypnosis increase the life expectancy of patients with malignant tumors, which is due to the fact that the neuroendocrine and immune systems are the most likely mediators between the mental state and the course of cancer.
The mechanism of word treatment probably lies in the fact that the patient’s repetition of texts that evoke positive emotions leads to increased production of opioid neuropeptides by certain parts of his brain, which have a positive regulatory effect on the hypothalamus. The resulting correction of the regulatory function of the hypothalamus, in turn, leads to the elimination of maladaptation and, accordingly, to the normalization of disturbed homeostasis, and ultimately to recovery.
We believe that these psychocorrection techniques can be supplemented by any of the urine therapy options, especially injections and drinking. The latter option is far from new - reciting mantras while taking urine is probably a very ancient tradition.
The possibility of using another technique follows from the following data.
"Moscow News" published very interesting interviews with Moscow psychiatrists who developed a new method of psychocorrection. As can be understood from these materials, which for quite natural reasons are limited in information content, the experimental subject is first asked questions regarding the most significant, including the qualities and life circumstances he is hiding. Questions are hidden in indifferent sound information and are not realized by the patient. His correct answers, which he, as well as the questions, are unaware of, are received using contact sensors and processed using a special program. Processing the information received allows us to identify verbal individual methods effective impact on the consciousness of the experimental subject. The subsequent suggestion of behavioral “advice” (instructions), unnoticed by him, is also carried out unnoticed against an indifferent sound background. Judging by the interview texts, the effectiveness of psychocorrection is very high.
Let's dream a little about the possibility of humanely using this method and not only for the psychocorrection of people with deviations that are dangerous for them and others. Let us imagine that an old man at will undergoes complex therapy, including injections of gravidan and the described correction to remove senile layers on the psyche: apathy, irritability, suspiciousness, etc. Rejuvenated in soul and body by 10-20 years, a wise, kind, full of strength person returns to active life. Not necessarily the father of the nation, but also a musician, teacher, doctor, engineer, agronomist. Yes, just any person who knows like an old man and can like a young man. Unfortunately, when current state peace, this method should be guarded under two headings and more jealously than nuclear weapons. However, the inability to use it as a component of a therapeutic, in particular, geriatric complex, is not fundamental. Judging by S. Grof's data, holotropic therapy may turn out to be an almost complete replacement for this method.
It would be possible to finish this section already, if not for one very significant thing. Let's return to the topic of karma and the biofield, using materials from the acclaimed work of S. N. Lazarev.
Its author, based on his own research, “noticed that character, fate and illness are somehow interconnected, but this connection is multivariate... health, character and even fate are determined by karmic structures... there is a dialectical connection between field and physical structures with mutual influence on each other. The fate and character of a person are also encoded in field structures and, if they are influenced, much can be gradually improved...
I have the opinion that the cause of diseases is a violation of field structures and it is not the diseased organ that needs to be treated, but the field.”
He argues that the violation of karmic structures is caused both by the misdeeds of the person himself and by the evil being done now or committed previously by his relatives, acquaintances, or even strangers. A grandmother's misconduct or a grandfather's grave sin may be the cause of a grandson's illness. These negative impacts can also spread in the opposite direction - both children and parents pay with illnesses and even early death for the sins (evil) of each other. In general, evil done is always punished in one way or another. Since retribution for it is realized slowly, misfortunes that occur in human health are almost never associated with the causes that gave rise to them, which are very separated from them in time.
Based on this, he believes that a radical cure achieved by conventional means modern medicine and bioenergy, is impossible for the following reasons.
- “...having cured the body, we can harm the soul, that illness is a protective blocking of incorrect behavior and incorrect understanding of the world around us... The main protection against illness is the implementation of the highest ethical laws.”
Therefore, treatment carried out without taking into account these provisions is ineffective, since as a result of it the disease is transformed into another or transferred to another person. Complete healing is achieved only by eliminating violations of karmic structures and eliminating the causes that caused them initially or can cause them to be violated again. Using his unique abilities, S. N. Lazarev discovers and eliminates these causes, corrects karmic structures, and also gives recommendations to patients and their loved ones on how to change thoughts and behavior in order to prevent the occurrence of new diseases. He believes that the most important means of amateur treatment and prevention are the renunciation of evil and envy, the cultivation of repentance and forgiveness. The practical achievements of this man, a talented psychic and psychologist, in the correction of karmic structures and, accordingly, treatment and prevention are beyond doubt.
We believe that even if we do not use S. N. Lazarev’s technique in practice, there is no reason not to analyze and not take into account its capabilities just because the therapeutic techniques of its author have not been subjected to serious and thorough research, in particular by means of electropuncture or electroencephalography diagnosing patients. And this must be done, if only because the presence of this technique calls into question the need to use many fundamental principles and practical means of modern medicine. And urine therapy, which at first glance makes writing this book unnecessary. To eliminate this situation, let us analyze the provisions of the above work, for which we first answer the following questions.
Is its author right in denying the effectiveness, and therefore the need, of treating somatic disorders and diseases using known methods of traditional or alternative medicine? Does his method have any limitations in the treatment of many, including tumor and severe infectious diseases? Regarding S. N. Lazarev’s unique ability to correct karmic structures, it should be assumed that there are few unique people like him, and there are so many sick people that the demand for his services far exceeds his capabilities. And even if there were many people like him, there is no guarantee that they will always be there in case of urgent need. Therefore, it is appropriate to ask the question: is it possible to obtain the same treatment results, but with means available to any doctor?
Further:
Effect of the nervous system on metabolic reactions (and through them on the nature and intensity of functioning and plastic processes) of various organs and tissues (including the nerve formations themselves) is carried out either by the very fact of innervation (regulation of functional activity and blood supply to innervated structures), or through the mechanisms of neurotrophic control .
Antinociceptive system
Concept of neurotrophic control consists in postulating the mutual regulation of the functional state of both the elements of the nervous system (neural pathways and networks) and the non-nervous structures innervated by them (for example, muscle). This is realized through influences that differ from the standard mechanisms inherent in the nervous system (propagation of AP along axons → secretion of a neurotransmitter into the synaptic cleft → interaction of a neurotransmitter with its receptors on the postsynaptic membrane → postsynaptic electrogenesis).
Mechanisms of neurotrophic control. Neurodystrophic process.
Within concepts of neurotrophic control Several possible mechanisms for its implementation are considered.
Changes in impulse activity in axons(frequency of APs, intervals between them). It is assumed that patterns (from the English pattern - sample) of impulses have informational value and change the permeability of cell membranes for ions.
Education special neurotrophic factors(“trophogens”), transported along the processes of nerve cells, secreted into the synaptic cleft and interacting with postsynaptic partners.
Changes in the value of PP, PD and, as a consequence, the level functioning of the postsynaptic partner(the old idea of organ atrophy from disuse).
Preservation of intact synaptic transmission - states of innervation. The development of denervation syndrome after damage to a nerve or blockade of axonal transport in it is a serious consequence of a violation of this mechanism.
Possible mechanisms of influence of the nervous system on metabolism in cells.
Neurodystrophic process
Disturbance of the trophic function of the nervous system forms the pathogenetic basis of the neurodystrophic process. The neurodystrophic process can occur both in peripheral organs and tissues and in the nervous system itself. Typically, the neurodystrophic process develops with denervation syndrome.
Denervation syndrome.
Manifestations of denervation syndrome(using the example of skeletal muscle denervation) are presented in the figure.
Dysfermentosis. Changes occur in the normal spectrum of enzymes in the cell, their expression, activity, appearance or disappearance of isoenzymes.
- “Embryonization” of metabolism. Metabolic reactions acquire properties and characteristics characteristic of the early stages of organism development (for example, a decrease in the activity of oxidation processes, the dominance of anaerobic glycolysis reactions, activation of the pentose cycle).
- Ultrastructural changes in cellular elements (primarily membranes). Electron microscopic studies reveal signs of swelling and destruction of mitochondrial cristae, labilization of lysosome membranes, and disruption of the selective permeability of the plasmalemma.
Dystrophies and dysplasias of various types due to disturbances in the expression of individual genes and metabolic disorders.
Action of autoaggressive AT, T cells, macrophages.
Hypersensitization of denervated structures to the missing neurotransmitter. Thus, in skeletal muscle fibers the synthesis of acetylcholine receptors is increased. Receptors are embedded not only in the plasma membrane of the postsynaptic membrane region, but also throughout the entire surface of the muscle fiber.
Typical disorders in postsynaptic structures due to impaired axonal transport.
Disturbances in the neurotrophic regulation of other organs during their denervation are less pronounced. At the same time, inertia of the mechanisms of humoral control is noted. This narrows the range of compensatory capabilities of the denervated organ, especially under conditions of its functional load or damage. The same features are observed in transplanted organs (heart, kidneys, liver).
It is important that during denervation the resistance of the denervated organ or tissue to damaging factors decreases: infection, mechanical trauma, temperature and other influences.
Deafferentation.
Neutrophic disorders occur not only with denervation syndrome. They develop when the afferent structures of the nervous system are damaged. Thus, deafferentation caused by transection of the sensory nerve can lead to no less pronounced trophic disorders in the organ than its efferent denervation.
Neurodystrophic processes are a component of almost all forms of human pathology, caused by both functional disorders and organic damage to the nervous system. They are manifested not only by changes in the functional activity of organs, but also by gross deviations in their structure (atrophy, erosion, ulceration, malignancy).
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Neurodystrophic process
Neurodystrophic process occurs in various organs and tissues (including the nervous system itself) as a result of loss or disruption of various nervous influences from the side of afferent, associative and efferent neurons (their bodies and processes) of the somatic and autonomic nervous system.
The neurodystrophic process is based on the following changes.
Disorders of the synthesis, secretion and/or action of neurotransmitters, comediators (substances released together with neurotransmitters and playing the role of neuromodulators that provide regulation of receptor and membrane effects and are involved in the regulation of metabolic processes) and trophogens (macromolecular substances, mainly peptides, which carry out their own trophic influences on nerve cells and tissues innervated by them). Trophogens(trophins, neurotrophic factors) are formed mainly in neurons (enter target cells, move in an anterograde manner with the axoplasmic current of the neuron), glial and Schwann cells, as well as in target cells of tissues and organs (move in a retrograde manner). Trophogens can be formed from blood proteins and cells of the immune system. They provide not only a variety of synaptic, but also non-synaptic intercellular interactions, induce trophic-plastic and structural processes, differentiation, growth, development of both neurons and various cell-tissue structures innervated by them.
May form pathotrophogens ( substances formed both in neurons and in peripheral tissues of various effector structures). Pathotrophogens induce stable pathological changes in executive cell-tissue structures regulated by neurons. They usually occur with significant, severe damage not only to neurons, but also to the tissues they regulate, accompanied by disturbances in their structural, metabolic and physiological processes. The neurodystrophic process intensifies with the occurrence of disorders of hemo- and lymphatic circulation, energy and plastic types of metabolism and various trophic disorders that occur as with organic (irreversible) damage different structures neurons and nerve centers, as well as during their functional (reversible) changes (for example, with neuroses).
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Neurodystrophic process is a complex of trophic disorders in organs and tissues that occurs when peripheral nerves or other structures of the nervous system are damaged. Particularly severe disorders develop when afferent fibers and nerves are damaged.
The neurodystrophic process is characterized by the following signs:
1) structural disorders - the development of ulcers on the skin and mucous membranes, muscle atrophy, dystrophic changes in tissue, phenomena of degeneration and cell death; 588
2) functional changes - increased sensitivity of denervated structures to the action of humoral factors (Cannon’s law);
3) metabolic disorders - inhibition of the activity of some enzymes and increased activity of others, activation of biochemical processes characteristic of the embryonic period of development.
The following factors play a major role in the pathogenesis of neurogenic dystrophy that develops as a result of peripheral nerve injury: (according to N.N. Zaiko).
1. Stopping the flow of information from the denervated organ to the nerve center (regional node, spinal cord or brain) and the absence of corrective trophic influences along the remaining nerves.
2. Stopping the production of neurohormones by the nerve, including those brought to the cell through axoplasmic current.
3. Pathological impulses from the central stump of the cut nerve, aggravating the dysfunction of the nerve centers and metabolic disorders that have arisen on the periphery.
4. Carrying out pathological impulses with the cut sensory nerve in the opposite direction (antidromically).
5. Changes in the genetic apparatus of the cell in a denervated organ and disruption of protein synthesis, leading to the appearance of substances of an antigenic nature. The immune system at the same time responds with a reaction of rejection.
6. Inappropriate reactions, most often elevated, to biologically active substances, medications and other humoral influences (Cannon’s law of denervation). For example, after cutting the vagus nerve, the muscular lining of the stomach becomes more sensitive to the influence of nerve mediators. In addition, it exhibits unusual metabolic changes in response to the action of certain hormones.
7. Traumatic environmental influences (mechanical trauma, infection), contributing to a more rapid development of trophic disorders in denervated tissues.
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Cell trophism– a set of processes that ensure the vital activity of the cell and the maintenance of genetically inherent properties. A trophic disorder is a dystrophy, and developing dystrophic changes constitute a dystrophic process.
Neurodystrophic process - This developing disorder trophism, which is caused by loss or change in nervous influences. It can occur both in peripheral tissues and in the nervous system itself.
The loss of nervous influences consists of:
In the cessation of stimulation of the innervated structure due to a violation of the release or action of the neurotransmitter;
In violation of the secretion or action of comediators - substances that are released together with neurotransmitters and play the role of neuromodulators that provide regulation of receptor, membrane and metabolic processes;
In violation of the release and action of trophogens.
Trophogens(trophins) are substances of various, mainly protein nature, which carry out the actual trophic effects of maintaining the vital functions and genetically inherent properties of the cell.
Sources of trophogens:
Neurons from which trophogens enter with an anterograde (orthograde) axoplasmic current into recipient cells (other neurons or innervated tissues in the periphery);
Cells of peripheral tissues, from which trophogens enter the nerves with a retrograde axoplasmic current into neurons (Fig. 5);
Glial and Schwann cells that exchange trophic substances with neurons and their processes.
Substances that play the role of trophogens are also formed from serum and immune proteins. Some hormones can have a trophic effect. Peptides, gangliosides, and some neurotransmitters take part in the regulation of trophic processes.
TO normotrophogens include various types of proteins that promote the growth, differentiation and survival of neurons and somatic cells, maintaining their structural homeostasis (for example, nerve growth factor).
Under pathological conditions, trophic substances are produced in the nervous system, causing stable pathological changes in recipient cells - pathotrophogens(according to G.N. Kryzhanovsky).
Pathotrophogens are synthesized, for example, in epileptic neurons; when they enter other neurons with an axoplasmic current, they can induce epileptic properties in these recipient neurons.
Pathotrophogens can spread throughout the nervous system as food web, which is one of the mechanisms of spread of the pathological process.
Pathotrophogens are also formed in other tissues.
Dystrophic process in denervated muscle. Substances synthesized in the neuron body and transported to the terminal with axoplasmic current are released nerve ending and enter muscle fibers (see Fig. 4), performing the function of trophogens.
Effects of neurotrophogens visible from experiments with motor nerve transection: the higher the cut is made, i.e. the more trophogens preserved in the peripheral segment of the nerve, the later the onset of denervation syndrome.
A neuron, together with the structure it innervates (for example, a muscle fiber), forms regional trophic contour (or regional trophic system, see Fig. 4). For example, if you implement cross reinnervation of muscles with different initial structural and functional characteristics (reinnervation of “slow” muscles by fibers from neurons that innervated “fast” muscles, or vice versa), then the reinnervated muscle acquires significantly new dynamic characteristics: “slow” becomes “fast”, and “fast” - “slow”.
Rice. 4. Trophic connections between motor neuron and muscle. Substances from the body of the motor neuron (MN), its membrane 1, perikaryon 2, nucleus 3 are transported with anterograde axoplasmic current 4 to terminal 5. From here they, as well as substances synthesized in terminal 6 itself, enter transsynaptically through the synaptic cleft (SC) to the terminal plate (LP) and into muscle fiber (MF). Part of the unused material flows back from the terminal into the neuron body with a retrograde axoplasmic current 7. Substances formed in the muscle fiber and end plate enter transsynaptically in the opposite direction to the terminal and then with a retrograde axoplasmic current 7 into the neuron body - to the nucleus 8, into the perikaryon 9, to the membrane of dendrites 10. Some of these substances can come from dendrites (D) transsynaptically to another neuron through its presynaptic ending (PO) and from this neuron further to other neurons.
Between the neuron and the muscle there is a constant exchange of substances that maintain trophism, structural integrity and normal activity of both formations. Glial cells (G) take part in this exchange. All of these formations create regional trophic system(trophic circuit)
New trophogens appear in the denervated muscle fiber, which activate the proliferation of nerve fibers ( sprouting). These phenomena disappear after reinnervation.
Neurodystrophic process in other tissues. Mutual trophic influences exist between each tissue and its nervous system.
When afferent nerves are cut, dystrophic changes in the skin occur. Transection of the sciatic nerve (mixed nerve, contains sensory and motor fibers), causes the formation dystrophic ulcer in the area of the hock joint in the rat.
Classic experiment of F. Magendie(1824), served the beginning of the development of the entire problem of nervous trophism, consists of cutting the first branch of the trigeminal nerve in a rabbit. As a result of the operation, ulcerative keratitis develops, inflammation occurs around the ulcer, and vessels that are normally absent in it grow into the cornea from the limbus. Ingrowth of blood vessels is an expression of pathological disinhibition of vascular elements - in a dystrophically altered cornea, the factor that normally inhibits the growth of blood vessels into it disappears, and a factor appears that activates this growth.
The conclusion about the existence of trophic nerves led to the idea of nervous trophism, and the results of transection of these nerves led to the idea of neurogenic (denervation) dystrophies.
Subsequently, the opinion about the existence of the trophic function of nerves was confirmed in the works of I.P. Pavlova. A huge credit goes to I.P. Pavlov is that he extended the doctrine of the reflex activity of the nervous system to neurotrophic processes, putting forward and developing the problem of trophic reflexes.
Subsequent studies by K.M. Bykova (1954) and A.D. Speransky (1955) deepened and expanded ideas about trophic disorders and their connection with the nervous system.
K.M. Bykov obtained data indicating the functional connection of the cerebral cortex and internal organs, ensuring the constancy of the internal environment and the normal course of trophic processes in the body. Disorders of the cortical control of visceral functions of various origins can lead to neurodystrophic processes in tissues, for example, the appearance of ulcers in the gastrointestinal tract.
HELL. Speransky found that disruption of neurotrophic processes in the body can occur under the influence of stimuli of different nature and damage to any part of the peripheral or central nervous system.
Dystrophic processes in various organs appear when peripheral nerves, nerve ganglia, and the brain itself are irritated. The localization of the primary damage to the nervous system only made differences in the picture of neurogenic dystrophies, but the mechanisms of their development turned out to be the same. Therefore, the process that develops after damage to any part of the nervous system, A.D. Speransky named standard neurodystrophic process. These facts served as the basis for the formation of an important position for pathology about the existence of a stereotypical form of neurogenic trophic disorders - neurodystrophy.
I.V. Davydovsky (1969) considered neurotrophic disorders responsible for the occurrence of dystrophy, necrosis and inflammation in vitamin deficiencies, leprosy, foot ulcers, Raynaud's disease, bedsores, frostbite and many other pathological processes and diseases.
Clinical manifestations neurodystrophic process. Clinicians have described neurogenic atrophies during denervation of organs, especially striated muscles, and neurogenic trophic ulcers that appear with various types of damage to the nervous system. A connection has been established with the nervous system of trophic skin disorders in the form of altered keratinization, hair growth, epidermal regeneration, depigmentation, as well as disorders in fat deposition - lipomatosis.
Trophic disorders identified nervous origin and in diseases such as scleroderma, syringomyelia, tabes dorsalis, etc. Trophic disorders are found not only in cases of violations of the integrity of nerves, plexuses or brain damage, but also in so-called functional disorders of the nervous system, for example, neuroses.
Additional factors of the neurodystrophic process. Factors involved in the development of the neurodystrophic process include: vascular changes in tissues, disorders of hemo- and lymph microcirculation, pathological permeability vascular wall, disruption of transport of nutrients and plastic substances into the cell.
An important pathogenetic link is the emergence of new antigens in dystrophic tissue as a result of changes in the genetic apparatus and protein synthesis, antibodies to tissue antigens are formed, autoimmune and inflammatory processes. This complex of pathological processes also includes secondary infection of the ulcer, the development of infectious lesions and inflammation. In general, neurodystrophic tissue lesions have a complex multifactorial pathogenesis.
At damage cervical region spinal cord Complete conduction disorder syndrome first manifests itself as flaccid tetraplegia with loss of tendon and periosteal reflexes in the arms and legs, loss of abdominal and cremasteric reflexes, absence of all types of sensitivity downward from the level of spinal cord damage and dysfunction of the pelvic organs in the form of persistent urinary and fecal retention.
In the syndrome of partial conduction disturbance of the cervical spinal cord, neurological disorders are less severely expressed; there is a dissociation between the degree of loss of movements, sensitivity and dysfunction of the pelvic organs, as well as reflex disorders.
Cervical spinal cord injuries are accompanied by paralysis of the striated muscles of the chest, which leads to severe respiratory impairment, often requiring a tracheostomy and the use of artificial mechanical ventilation. Damage at the level of the IV cervical segment also leads to paralysis of the diaphragm and, if the patient is not urgently transferred to mechanical breathing, to his death.
The severity of the condition of a victim with damage to the cervical spinal cord is often aggravated by ascending edema of the medulla oblongata and the appearance bulbar symptoms- swallowing disorders, bradycardia followed by tachycardia, nystagmus and, if the therapy is ineffective, respiratory arrest due to paralysis of the respiratory center. The occurrence of bulbar symptoms immediately after injury indicates combined damage to both the cervical spinal cord and brainstem, which is an unfavorable sign.
In the absence of an anatomical break in the spinal cord, its conductive functions are gradually restored, active movements appear in the paralyzed limbs, sensitivity improves, and the function of the pelvic organs is normalized.
At thoracic injury spinal cord, flaccid paralysis occurs (with less severe damage - paresis) of the leg muscles with loss of abdominal reflexes, as well as tendon reflexes in the lower extremities. Sensory disturbances are usually conductive in nature (corresponding to the level of damage to the spinal cord), dysfunction of the pelvic organs consists of urinary and fecal retention.
At damage to the upper thoracic region spinal cord paralysis and paresis of the respiratory muscles occurs, which leads to a sharp weakening of breathing. Damage at the level of III-V thoracic segments of the spinal cord is often accompanied by impaired cardiac activity.
At damage to the lumbosacral region spinal cord, flaccid paralysis of the leg muscles along their entire length or the muscles of the distal sections is observed, and all types of sensitivity below the site of injury are also impaired. At the same time, the cremasteric, plantar, and Achilles reflexes are lost, and with higher lesions, the knee reflexes as well. At the same time, abdominal reflexes are preserved. Retention of urine and feces is often replaced by a paralytic state of the bladder and rectum, resulting in fecal and urinary incontinence.
In the absence of an anatomical break of the spinal cord, as well as in the syndrome of partial disruption of its conductivity, a gradual restoration of impaired functions is observed.
Clinically progressive traumatic disease can manifest itself:
- myelopathy syndromes (syringo-myelitic syndrome, lateral amyotrophic sclerosis, spastic paraplegia, spinal circulatory disorders);
- spinal arachnoiditis, characterized by polyradicular pain syndrome, aggravation of existing conduction disorders;
- dystrophic process in the form of osteochondrosis, deforming spondylosis with persistent pain syndrome.
Complications and consequences of injuries to the spine and spinal cord are divided as follows:
- infectious and inflammatory complications;
- neurotrophic and vascular disorders;
- dysfunction of the pelvic organs;
- orthopedic consequences.
Infectious and inflammatory complications can be early (develop in the acute and early periods of PSCI) and late. In the acute and early period, purulent-inflammatory complications are primarily associated with infection of the respiratory and urinary systems, as well as with the bedsore process, which occurs like a purulent wound. With open SCI, the development of such serious complications as purulent epiduritis, purulent meningomyelitis, spinal cord abscess, and osteomyelitis of the spinal bones is also possible. Late infectious and inflammatory complications include chronic epiduritis and arachnoiditis.
Bedsores- one of the main complications that occurs in patients with spinal injuries, which are accompanied by damage to the spinal cord. According to various sources, they occur in 40-90% of patients with injuries of the spine and spinal cord. Quite often, the course of deep and extensive bedsores in the necrotic-inflammatory stage is accompanied by severe intoxication, a septic state and in 20% of cases ends in death. In many works concerning spinal patients, bedsores are defined as trophic disorders. Without disruption of tissue trophism, bedsores cannot occur, and their development is caused by spinal cord injury. With this interpretation, the appearance of bedsores in spinal patients becomes inevitable. However, in a number of spinal patients, bedsores do not form. Some authors associate the formation of pressure ulcers with factors of compression, displacement force and friction, the long-term impact of which on the tissue between the skeletal bones and the surface of the bed causes ischemia and the development of necrosis. Poor circulation (ischemia) with prolonged compression of soft tissues ultimately leads to local trophic disorders and necrosis of varying degrees depending on the depth of tissue damage. Ischemia of soft tissues, which turns into necrosis during long-term exposure, in combination with infection and other unfavorable factors, leads to impaired immunity of the patient, causes the development of a severe septic condition, accompanied by intoxication, anemia, hypoproteinemia. Long purulent process often leads to amyloidosis of internal organs, which results in renal and liver failure.
Bedsores in the sacral area they occupy first place in frequency (up to 70% of cases) and usually appear in the initial period of traumatic disease of the spinal cord, which prevents early rehabilitation measures and in some cases does not allow timely reconstructive interventions on the spine and spinal cord.
When assessing the condition of bedsores, you can use the classification proposed by A.V. Garkavi, in which six stages are distinguished: 1) primary reaction; 2) necrotic; 3) necrotic-inflammatory; 4) inflammatory-regenerative; 5) regenerative-scar; 6) trophic ulcers. Clinically, bedsores in the primary reaction stage (reversible stage) were characterized by limited skin erythema and the formation of blisters in the sacral area.
Neurotrophic and vascular disorders arise due to denervation of tissues and organs. In the soft tissues of patients with SCI, bedsores and poorly healing trophic ulcers develop very quickly. Bedsores and ulcers become entry points for infection and sources of septic complications, leading to death in 20-25% of cases. Anatomical interruption of the spinal cord is characterized by the occurrence of so-called solid edema lower limbs. Metabolic disorders (hypoproteinemia, hypercalcemia, hyperglycemia), osteoporosis, anemia are typical. Disruption of the autonomic innervation of internal organs leads to the development of purulent-necrotic ulcerative colitis, enterocolitis, gastritis, acute gastrointestinal bleeding, and dysfunction of the liver, kidneys, and pancreas. There is a tendency to stone formation in the biliary and urinary tracts. Violation of the sympathetic innervation of the myocardium (with injuries of the cervical and thoracic spinal cord) is manifested by bradycardia, arrhythmia, and orthostatic hypotension. Coronary heart disease may develop or worsen, while patients may not feel pain as a result of disruption of noceptive afferent impulses from the heart. From the pulmonary system, more than 60% of patients develop pneumonia in the early period, which is one of the most common reasons death of victims.
One of the complications is also vegetative dysreflexia. Autonomic dysreflexia is a powerful sympathetic reaction that occurs in response to painful or other stimuli in patients with spinal cord lesions above Th6. In patients with tetraplegia, this syndrome is observed, according to various authors, in 48-83% of cases, usually two or more months after the injury. The cause is pain or proprioceptive impulses caused by bladder distension, catheterization, gynecological or rectal examination, as well as other intense influences. Normally, proprioceptive and pain impulses travel to the cerebral cortex along the posterior columns of the spinal cord and the spinothalamic tract. It is believed that when these pathways are interrupted, impulses circulate at the spinal level, causing excitation of sympathetic neurons and a powerful “explosion” of sympathetic activity; at the same time, descending supraspinal inhibitory signals, which normally modulate the autonomic response, do not have the proper inhibitory effect due to damage to the spinal cord. As a result, spasm of peripheral vessels and vessels of internal organs develops, which leads to a sharp rise in blood pressure. Uncorrected hypertension can lead to loss of consciousness, the development of intracerebral hemorrhage, and acute heart failure.
Another serious complication, often leading to death, is deep vein thrombosis, which, according to various sources, occurs in 47-100% of patients with PSCI. The risk of deep vein thrombosis is highest in the first two weeks after injury. The consequence of deep vein thrombosis can be pulmonary embolism, which occurs on average in 5% of patients and is the leading cause of death in post-traumatic brain injury. In this case, as a result of damage to the spinal cord, typical clinical symptoms of embolism (chest pain, dyspnea, hemoptysis) may be absent; the first signs may be heart rhythm disturbances .
Pelvic organ dysfunction appear urinary disorders And defecation. In the stage of spinal shock, acute urinary retention is observed, associated with deep depression of the reflex activity of the spinal cord. As we emerge from shock, the form neurogenic dysfunction bladder depends on the level of spinal cord damage. When the suprasegmental sections are affected (the bladder receives parasympathetic and somatic innervation from segments S2-S4), a conduction-type urination disorder develops. Initially, there is urinary retention associated with an increase in the tone of the external sphincter of the bladder. Paradoxical ischuria may occur: when the bladder is full, urine is released drop by drop as a result of passive stretching of the bladder neck and vesical sphincters. As the automaticity of the parts of the spinal cord located distal to the level of the lesion develops (two to three weeks after the injury, and sometimes at a later date), a “reflex” (sometimes called “hyperreflex”) bladder is formed: the spinal center of urination begins to work , localized in the conus of the spinal cord, and urination occurs reflexively, according to the type of automatism, in response to the filling of the bladder and irritation of the receptors of its walls, while there is no voluntary (cortical) regulation of urination. There is urinary incontinence. Urine is released suddenly, in small portions. Paradoxical interruption of urination may occur due to involuntary transient inhibition of urinary flow during reflex voiding. In this case, the imperative urge to empty the bladder indicates an incomplete disruption of spinal cord conduction (preservation of afferent pathways from the bladder to the cerebral cortex), while spontaneous sudden emptying of the bladder without urge indicates a complete disruption of spinal cord conduction. Incomplete damage to the pathways is also indicated by the feeling of the process of urination itself and the feeling of relief after urination (preservation of the paths of temperature, pain and proprioceptive sensitivity from the urethra to the cerebral cortex). With a suprasegmental lesion, the “cold water” test is positive: a few seconds after 60 ml of cold water is introduced through the urethra into the bladder, water, and sometimes the catheter, are forcefully pushed out. The tone of the external rectal sphincter is also increased. Over time, dystrophic and cicatricial changes may occur in the walls of the bladder, leading to the death of the detrusor and the formation of a secondary wrinkled bladder (“organic areflex bladder”). In this case, there is an absence of the bladder reflex, and true urinary incontinence develops.
In case of spinal cord injury with direct damage to the spinal micturition centers (sacral segments S2-S4), loss of bladder emptying reflex in response to its filling. A hypo-reflex form of the bladder develops (“functional are-reflex bladder”), characterized by low intravesical pressure, decreased detrusor strength and a sharply inhibited micturition reflex. Preservation of the elasticity of the bladder neck leads to overstretching of the bladder and a large number residual urine. Strained urination is typical (to empty the bladder, the patient strains or performs manual squeezing). If the patient stops straining, emptying stops (passive intermittent urination). The “cold water” test is negative (the reflex response in the form of expulsion of water introduced into the bladder is not observed within 60 seconds). The anal sphincter is relaxed. Sometimes the bladder empties automatically, but not due to the spinal reflex arc, but due to the preservation of the function of the intramural ganglia. It should be noted that the sensation of distension of the bladder (the appearance of equivalents) is sometimes preserved with incomplete damage to the spinal cord, often in the lower thoracic and lumbar region due to preserved sympathetic innervation (sympathetic innervation of the bladder is associated with segments TH1, TH2, LI, L2). As dystrophic processes develop in the bladder and the neck of the bladder loses elasticity, an organic areflex bladder and true incontinence are formed with the constant release of urine as it enters the bladder.
When identifying clinical syndromes, the main importance is given to the tone of the detrusor and sphincter and their relationship. Detrusor tone or the force of its contraction is measured by the increase in intravesical pressure in response to the introduction of an always constant amount of liquid - 50 ml. If this increase is 103+13 mm aq. Art., the tone of the detrusor of the bladder is considered normal, with a smaller increase - reduced, with a larger increase - increased. Normal sphincterometry values are considered to be 70-11 mmHg. Art.
Depending on the relationship between the detrusor and sphincter states, several syndromes are distinguished.
Atonic syndrome It is observed more often with damage to the conus of the spinal cord, that is, the spinal centers for the regulation of urination. In a cystometric study, the introduction of 100-450 ml of liquid into the bladder does not change the zero bladder pressure. The introduction of large volumes (up to 750 ml) is accompanied by a slow increase in intravesical pressure, but it does not exceed 80-90 mm aq. Art. Sphincterometry in atonic syndrome reveals low levels of sphincter tone - 25-30 mm Hg. Art. Clinically, this is combined with atony and areflexia of skeletal muscles.
Detrusor hypotonia syndrome- also the result of segmental dysfunctions of the bladder, while due to a decrease in detrusor tone, the bladder capacity increases to 500-700 ml. Sphincter tone can be decreased, normal, or even increased.
Predominant sphincter hypotension syndrome observed with injuries at the level of S2-S4 segments; it is characterized by frequent involuntary separation of urine without urge. Sphincterometry reveals a clear decrease in sphincter tone and a cystogram shows slightly reduced or normal detrusor tone. Palpation examination of the rectal sphincter and perineal muscles reveals low tone.
Detrusor sphincter hypertension syndrome observed in patients with conduction type bladder dysfunction. Cystometrically, when 50-80 ml of liquid is introduced into the bladder, a sharp jump in intravesical pressure to 500 mm aq is observed. Art. During sphincterometry, its tone is high - from 100 to 150 mm Hg. Art. Sharp contractions of the perineal muscles are observed in response to palpation.
The syndrome of predominant detrusor hypertension during cystometry is characterized by an increase in detrusor tone with a small bladder capacity (50-150 ml), there is a high jump in intravesical pressure in response to the introduction of 50 ml of fluid, and the sphincter tone can be normal, increased or decreased.
To determine the electrical excitability of the bladder, transrectal electrical stimulation is also used. During severe degenerative processes in the bladder, the detrusor loses its excitability, which is manifested by the absence of an increase in intravesical pressure in response to electrical stimulation. The degree of degenerative processes is determined by the number of collagen fibers using the cystic biopsy method (in case of infection urinary tract or significant trophic disorders in the wall of the bladder, biopsy is not indicated).
Often, spinal injury is combined with urinary disorders and the development of urinary tract infections(Profit center). Urinary tract infections (UTIs) currently represent a leading cause of morbidity and mortality in patients with spinal cord injury. About 40% of infections in this category of patients are of nosocomial origin and most of them are associated with bladder catheterization. UTIs in 2-4% of cases are the cause of bacteremia, while the probability of death in patients with urosepsis using modern management tactics for this category of patients ranges from 10 to 15%, and this figure is three times higher than in patients without bacteremia.
UTI infection depends not only on risk factors caused by both bladder denervation and the chosen catheterization method. The overall incidence of UTI in spinal patients is 0.68 per 100 people. The most dangerous methods from the point of view of infection are the methods of constant drainage and the use of open systems. The probability of developing an infection is 2.72 cases per 100 patients, while when using intermittent catheterization and closed systems catheterization, this figure is 0.41 and 0.36 cases per 100 people per day, respectively. Spinal patients are characterized by an atypical and minimally symptomatic course of UTI.
Violation of the act of defecation with PSCI also depends on the level of spinal cord damage. With a supra-segmental lesion, the patient ceases to feel the urge to defecate and fill the rectum, the external and internal sphincters of the rectum are in a state of spasm, and persistent stool retention occurs. When the spinal centers are damaged, flaccid paralysis of the sphincters and disruption of reflex intestinal motility develop, which is manifested by true fecal incontinence with its discharge in small portions when entering the rectum. In a more distant period, automatic emptying of the rectum may occur due to the functioning of the intramural plexus. With SCI, hypotonic constipation may also occur due to the patient's hypomobility, weakness of the abdominal muscles, and intestinal paresis. Hemorrhoidal bleeding is often observed.
Orthopedic consequences SCI can be conditionally divided according to their localization into vertebral, that is, associated with changes in the shape and structure of the spine itself, and extravertebral, that is, caused by changes in the shape and structure of other elements of the musculoskeletal system (pathological settings of limb segments, joint contractures, etc.) . The nature functional disorders, arising from SCI, orthopedic consequences can also be divided into static, that is, accompanied by a violation of the statics of the body, and dynamic, that is, associated with a violation of dynamic functions (locomotion, manual manipulation, etc.). Orthopedic consequences may be as follows: instability of the injured spine; scoliosis and kyphosis of the spine (kyphotic deformities with a kyphosis angle exceeding 18-20° progress especially often); secondary dislocations, subluxations and pathological fractures; degenerative changes in intervertebral discs, joints and ligaments of the spine; deformation and narrowing of the spinal canal with compression of the spinal cord. These consequences are usually accompanied by persistent pain, limited mobility of the injured spine and its functional failure, and in cases of spinal cord compression - progressive dysfunction of the spinal cord. Orthopedic disorders that arise in the absence of timely treatment often progress and lead the patient to disability.
A large group of orthopedic consequences consists of secondary deformations of the limbs, joints, false joints and contractures, which form in the absence of orthopedic prophylaxis within a few weeks after the primary injury.
A fairly common complication of PSCI is heterotopic ossification, usually developing in the first six months after injury, according to various sources, in 16-53% of patients. Ectopic ossifications appear only in areas located below the neurological level of the lesion. The areas of large joints of the extremities (hip, knee, elbow, shoulder) are usually affected.
Considering the concept of G. Selye (1974) about “stress” and “distress” in clinical, psychological and social aspects, we can assume in the clinic of complicated injuries of the spine and spinal cord the presence, in addition to biological ones, also general nonspecific and private specific personal, psychological and social adaptive reactions, currently studied only in general terms, which significantly affects the degree of rehabilitation of patients.
Analysis of the identified neuropsychic disorders showed that among the factors determining the state of the neuropsychic sphere, the leading role is played by traumatic, associated with damage to the cervical spinal cord, which is largely involved in the regulation of higher-level mental functions.
It should be noted that injuries to the cervical spinal cord do not exclude the presence of combined traumatic brain injury and development state of shock, which also contributes to mental disorders in the long term. This manifests itself as a violation spatial orientation, body diagrams, visual, auditory and speech disorders, decreased attention and memory, general exhaustion of mental processes.
Another factor that determines the degree of mental disorders is the severity of the consequences of injury to the cervical spinal cord in the form of severe motor and sensory disorders, dysfunction of the pelvic organs, disorders of the respiratory and of cardio-vascular system and metabolism.
The third significant factor in the formation of mental disorders in patients in the late period of traumatic spinal cord disease is social. Limitations of movement, dependence of a patient with a cervical spine injury on outside care Everyday life, social maladaptation - all this determines a depressed state of mind, aggravates functional and somatic disorders. It must be emphasized that the social factor, being complex, includes both purely social and personal components. Social components include such as the establishment of disability, the inability to perform work, a decrease in the level of material support, isolation, a narrowing of the circle of friends and restrictions on types of activities. Personal - relationships in the family, difficulties in sexual life, problems of giving birth and raising children, dependence on outside care, etc.
As a result of studying all the data on the condition of the patient with TBSM, it is necessary to formulate a complete functional diagnosis, which should include the following sections:
1. Diagnosis according to ICD 10 (T 91.3) - consequences of spinal cord injury or post-traumatic myelopathy.
2. Nature of the injury (traumatic dislocation, fracture-dislocation, fracture, wound, etc.), level of injury, date of injury. For example: complicated compression fracture-dislocation of C6-T2. ASIA type of spinal cord injury.
3. Level of complete and incomplete damage to the spinal cord (sensory, motor on both sides of the patient’s body).
4. Existing spinal cord lesion syndromes.
5. Existing complications.
6. Concomitant diseases.
7. The degree of limitation of functional activity and life.
Ivanova G.E., Tsykunov M.B., Dutikova E.M. Clinical picture traumatic disease of the spinal cord // Rehabilitation of patients with traumatic disease of the spinal cord; Under general ed. G.E. Ivanova, V.V. Krylova, M.B. Tsykunova, B.A. Polyaeva. - M.: OJSC "Moscow Textbooks and Cartolithography", 2010. - 640 p. pp. 74-86.
