Nervous trophism and dystrophic process. Additional research methods

Nervous trophism is the effect of nerves on tissue, causing a change in metabolism in it according to needs at a certain moment. The trophic action of nerves is closely related to their other functions (sensitive, motor, secretory) and together with them ensures the optimal function of each organ.

The first evidence that nerves have a trophic function was obtained back in 1824 by the French scientist F. Magendie. In experiments with transection of the trigeminal nerve in rabbits, he discovered the formation of ulcers in the zone of sensitive denervation (eye; Fig. 77).

In the future neurogenic ulcer model was reproduced many times when other nerves, such as the sciatic one, were cut. Trophic disorders occur in any organ if its innervation is disrupted through interference with nerves (afferent, efferent, autonomic) or nerve centers. Medical practice also shows that nerve damage (trauma, inflammation) threatens the formation of ulcers or other disorders (edema, erosion, necrosis) in the corresponding area.

Biochemical, structural and functional changes in denervated tissues. Experimental studies show that pathogenic influences on the peripheral nerve always cause changes in metabolism (carbohydrates, lipids, proteins, nucleic acids, etc.) in the corresponding organ. These changes are not only quantitative, but also qualitative. The general trend of changes in metabolism is that it becomes embryonic in nature, that is, glycolytic processes begin to predominate over oxidative ones. The power of the Krebs cycle weakens, the output of macroergs decreases, and the energy potential decreases.

When innervation is disrupted in tissues, characteristic morphological changes occur. If we are talking about the cornea, skin or mucous membrane, then all stages of inflammation sequentially develop in them. As a result, an ulcer forms that has no tendency to heal. Detailed studies have established changes in organelles, in particular a decrease in the number of mitochondria and lightening of their matrix. Obviously, this is associated with a violation of oxidative phosphorylation and Ca2+-accumulating ability of mitochondria, and at the same time - the energy capabilities of the cell. In denervated tissues, mitotic activity may decrease.

Denervated tissue reacts to many humoral factors differently than normal tissue. We are talking primarily about neurotransmitters of the nervous system. V. Cannon found that skeletal muscles, deprived in one case of sympathetic and in another of cholinergic nerves, react respectively to adrenaline and acetylcholine stronger than normal. So it was opened the law of denervation - increased sensitivity of denervated structures. In particular, this is due to the fact that cholinergic receptors, which are normally concentrated only in the area of ​​neuromuscular synapses, after denervation appear on the entire surface of the muscle fiber membrane. The unusual nature of the response of denervated structures may lie not only in its strengthening, but also in its distortion, when, for example, instead of relaxation of the vascular muscles, their contraction occurs, which can significantly affect the condition of the vessels, tissue circulation, etc.

An important question is the existence of special trophic nerves.

At one time, F. Magendie expressed the opinion that in addition to sensory, motor and secretory nerves, there are also special trophic ones that regulate tissue nutrition.

Later I.P. In an experiment on animals, Pavlov identified a branch among the nerves going to the heart that, without affecting blood circulation, increased the strength of its contractions. He called this nerve reinforcing and recognized it as purely trophic. Complete and harmonious innervation of the organ, according to I.P. Pavlov, provide three types of nerves: functional, vasomotor (regulating the supply of nutrients) and trophic (determining the final utilization of these substances).

L.A. shared the same opinion. Orbeli, who together with A.G. Ginetsinsky in 1924 proved that an isolated (without blood circulation) frog muscle, tired due to prolonged stimulation of the motor nerve, begins to contract again if the sympathetic nerve is stimulated. The trophic function of the sympathetic nerve is the influence on metabolism, preparation of the organ for action and its adaptation to future work, which is carried out thanks to the motor nerve.

At the same time, A.D. Speransky believed that all nerves influence tissue metabolism, there are no non-trophic nerves, “a nerve is functional only because it is trophic.”

Mechanisms of trophic influence of nerves. Nerve impulses, activating an organ (for example, a muscle), simultaneously change the metabolism in the cell according to the following scheme: mediator-activation of second messengers-activation of the genetic apparatus, enzymes. Metabolism in cells also changes under the influence of vasomotor nerves, which dilate or constrict blood vessels and thus change the flow of nutrients. In addition to these two (functional (impulse) and vascular) influences of the nervous system on the metabolism of a nerve cell, there is a third - non-impulse, or actually trophic. It is ensured by the movement of axoplasm both from the neuron to the effector cell (orthograde) and in the opposite direction (retrograde). With the help of orthograde axotok, innervated cells receive trophic substances produced by neurons, and through retrograde axotok, target cells (muscle, epithelial) supply such substances to neurons. These substances are called neurotrophic factors, or neurotrophins.

Currently, individual neurotrophins have been isolated from various nerve structures, satellite cells (glial cells, lemmocytes), as well as from target tissues and some organs, their structure has been deciphered, and their biological effect has been studied. These are nerve growth factor and related peptides such as brain-derived neurotrophic factor, neurotrophins-3, -4, -5, -6.

Brain-derived neurotrophic factor is formed directly in neurons, transported to the nerve endings and, released from there, maintains the normal state of the postsynaptic neuron.

Other neurotrophins bind to receptors on nerve endings, enter the neuroplasm and move retrogradely to the neuron body, where they activate the synthesis of substances necessary for the life of the nerve cell.

This family of neurotrophins to a certain extent includes epidermal growth factor, transforming growth factors (α and β), insulin-like growth factors I and II.

Neurotrophic factors include neuroleukin, ciliary and glial neurotrophic factors, platelet-derived growth factor, and acidic and basic fibroblast growth factors. Neurotrophic properties have been identified in substance P, opioid peptides, and atrial natriuretric peptide. In addition, glycolipids - gangliosides, as well as some hormones - thyroxine, testosterone, corticotropin, insulin, have a neurotrophic effect.

The most well studied factor is nerve growth factor. It is found in various tissues of animals and humans, but the largest amount is found in the salivary glands of male mice. This factor promotes the embryonic development and survival of sympathetic and some sensory neurons, as well as cholinergic neurons of the central nervous system responsible for memory. If you obtain antibodies to nerve growth factor and inject them into newborn animals, you can cause almost complete destruction of the sympathetic nodes (immunsympathectomy).

The main objects of action of the epidermal growth factor are glial cells (astrocytes), lemmocytes, cells of the central nervous system, which in turn produce such neurotrophic factors as glial, ciliary and nerve growth factors, etc.

Ciliary neurotrophic factor creates conditions for the survival of motor, sensory and sympathetic neurons. Neuroleukin affects both motor and sensory neurons and is produced by the salivary glands, skeletal muscles and stimulated T lymphocytes.

Experimental studies have shown that a deficiency of neurotrophins or their receptors can cause the development of neurodegenerative diseases. For example, deficiency of brain-derived neurotrophic factor in mice causes death of peripheral sensory neurons and degenerative changes in vestibular nerve neurons. In animals with a hereditary disorder in the formation of neurotrophin-3, death of skin mechanoreceptors is observed.

In pathogenesis In neurogenic dystrophy, the determining role is played by the disruption of the synthesis and axonal transport of neurotrophic factors. However, when analyzing the process, one should be guided by the fact that the trophic function is carried out according to the principle of a reflex and it is necessary to evaluate the significance of each of its links in the development of the dystrophic process.

The sensory nerve obviously plays a special role in this, since, firstly, the transmission of information to the nerve center from the denervation zone is interrupted, secondly, the damaged sensory nerve is a source of pathological impulses, including pain, and thirdly, From it come centrifugal (centrifugal) influences on the tissue. It has been proven, in particular, that substance P enters the tissue through sensory nerves from the axoplasm, which affects metabolism and microcirculation,

The importance of nerve centers in the development of dystrophy is evidenced by the experiments of A.D. Speransky with selective damage to the centers of the hypothalamus. The result of this is the formation of trophic ulcers in various organs on the periphery.

The role of efferent nerves in dystrophy is that their function (motor, secretory) is stopped or distorted. Impulse activity and the synthesis of mediators (adrenaline, serotonin, acetylcholine, etc.) cease, and the synthesis and axonal transport of neurotrophins change.

With the development of neurogenic dystrophy in cells, the processes of transcription and translation, the synthesis of enzymes are disrupted, the yield of macroergs decreases, and the exchange becomes more simplified. The transport functions of cell membranes undergo changes. An organ with impaired innervation can become a source of autoantigens. The process is complicated by the fact that in addition to purely neurotrophic changes, disturbances in blood and lymph circulation (microcirculation) with the development of hypoxia are added.

Thus, neurogenic dystrophy is a complex multifactorial process that begins with the fact that the nervous system ceases to adequately influence metabolism in tissues, and, as a consequence, complex disorders of metabolism, structure and function arise (Scheme 37).

1. When examining children, it is necessary to study the anamnesis data, important for the development of the musculoskeletal system in children, statics and motor skills (the state of the mother’s health during pregnancy, the nature of his nutrition, the state of the child’s health, his feeding and upbringing regime); as well as characteristic complaints (pain in bones, muscles and joints, changes in configuration, limited joint mobility, etc.).

2. When inspecting, pay attention to the following points: change in the size and shape of the head (micro- and macrocephaly, tower-shaped, sydney-shaped, saddle-shaped skull, scaphocephaly, oxycephaly, flattening of the occiput); development of the upper and lower jaws, characteristics of the bite, their nature (deciduous, permanent); the shape of the chest (conical, cylindrical, flat) and its changes (Harrison's groove, keel-shaped, funnel-shaped, barrel-shaped chest, cardiac hump, flattening of one half or unilateral protrusion of the chest); shape of the spine (presence of pathological kyphosis, lordosis, scoliotic distortions) and the child’s pelvis (flat rachitic pelvis); configuration of the limbs (acromegaly, brachydactyly, adactyly, aphalanxia, ​​etc.), shape of the joints (swelling, deformation), mobility in them and the condition of the skin and adjacent tissues (presence of rashes, nodules, etc.); muscle trophism (weak, medium and good degree of their development; atrophy, hypotrophy, hypertrophy), state of muscle tone (hypotonicity, hypertonicity).

3. musculoskeletal system in children, determine the density of the skull bones, the condition of the sutures and fontanelles (craniotabes, pliability of the edges of the fontanel, the size of the fontanelles); presence of fractures and deformations; signs of osteoid tissue hyperplasia (rachitic “rosary beads”, “bracelets”, “strings of pearls”); over ; muscle strength and tone, the presence of compactions in them.

4. Determination of trophism and muscle strength. Muscle trophism, which characterizes the level of metabolic processes, is assessed by the degree and symmetry of development of individual muscle groups. The assessment is carried out at rest and during muscle tension. There are three degrees of muscle development: weak, medium and good. With a weak degree of development, the muscles of the trunk and limbs at rest are insufficient; when tense, their volume changes quite little, the lower part of the abdomen hangs, the lower corners of the shoulder blades lag behind the chest. With an average degree of development, the mass of the muscles of the trunk at rest is moderately expressed, and the mass of the limbs is well expressed; when the muscles are tense, their shape and volume change. With a good stage of development, the soft muscles of the trunk and limbs are well developed, and with tension there is a clear increase in muscle relief.

Muscle strength in children is assessed using a special scale using a five-point system: 0 points - no movement; 1 - there are no active movements, but muscle tension is determined by palpation; 2 - passive movements are possible when overcoming minor resistance, 4 - passive movements are possible when overcoming moderate resistance, 5 - muscle strength is within normal limits.

5. Additional research methods:

a) determination of the content of calcium, phosphorus, alkaline phosphatase in blood serum;

b) x-ray examination of bones

c) electromyography

d) chronaximetry

e) dynamometry in older children;

f) muscle biopsy;

g) densitometry.

Signs of osteoid tissue hyperplasia

Signs of hyperplasia of osteoid tissue include costal “rosary beads”, “bracelets”, “strings of pearls”, enlargement of the frontal, parietal, occipital protuberances, “chicken breast”, square head.

Signs of osteomalacia

Signs of osteomalacia of osteoid tissue include craniotabes (softening of the temporal and occipital bones), flattening of the occiput, Harrison's groove, X-shaped and O-shaped shins.

Normal levels of calcium and phosphorus in blood serum (V. A. Doskin, 1997)

Total calcium - 2.5-2.87 mmol / l.

Ionized calcium - 1.25-1.37 mmol / l.

Inorganic phosphorus - 0.65-1.62 mmol / l.

Arthritis symptoms

Symptoms of arthritis include swelling, tenderness, swelling of the skin and tissues adjacent to the joints, limitation of joint mobility and range of active movements.

Types of muscle tone disorders

Hypotension- decreased muscle tone (with rickets, malnutrition, chorea, Down's disease, hypothyroidism, spinal muscular atrophy, peripheral paralysis).

Hypertension - increased muscle tone (in a healthy child during the first 3-4 months of life, with central paralysis, meningitis, tetanus).

Types of muscle trophism disorders

Atrophy- extreme degree of weak development and underdevelopment (simple form) or degeneration (degenerative form) of muscles.

A simple form occurs in cerebral palsy, diseases of the muscles (progressive muscular dystrophy, congenital myodystrophy) and joints (juvenile rheumatoid arthritis, tuberculous coxitis). The degenerative form occurs with peripheral paralysis, poliomyelitis, etc.

Hypertrophy is the thickening and increase in muscle mass. It is more often detected in children involved in sports and physical labor. In pseudohypertrophy, fat deposits simulate a picture of good muscle development.

Nervous trophism- This is the action of nerves on tissue, as a result of which the metabolism in it changes in accordance with the needs at any given moment. This means that the trophic action of the nerves is closely related to their other functions (sensitive, motor, secretory) and together with them ensures the optimal function of each organ.

The first evidence that nerves influence tissue trophism was obtained back in 1824 by the French scientist Magendie. In experiments on rabbits, he cut the trigeminal nerve and found an ulcer in the area of ​​​​sensitive denervation (eye, lip) ( rice. 25.5). Next this neurogenic ulcer model was reproduced many times, and not only in the trigeminal nerve area. Trophic disorders develop in any organ if its innervation is disrupted by intervention on nerves (afferent, efferent, autonomic) or nerve centers. Medical practice has provided a huge amount of evidence that also indicates that nerve damage (trauma, inflammation) threatens the occurrence of ulcers or other disorders in the corresponding area (edema, erosion, necrosis).

Biochemical, structural and functional changes in denervated tissues. Experience has shown that pathogenic effects on the peripheral nerve are always accompanied by changes in metabolism in the corresponding organ. This applies to carbohydrates, fats, proteins, nucleic acids, etc. Not only quantitative but also qualitative changes are observed. Thus, myosin in a denervated muscle loses its ATPase properties, and glycogen in its structure becomes simpler and more elementary. A restructuring of enzymatic processes is observed. Thus, the isoenzyme spectrum of lactate dehydrogenase changes in favor of LDH 4 and LDH5, i.e. those enzymes that are adapted to anaerobic conditions. The activity of an enzyme such as succindehydrogenase decreases. The general trend of changes in metabolism is that it acquires an “embryonic” character, i.e. Glycolytic processes begin to predominate in it, while oxidative ones decrease. The power of the Krebs cycle weakens, the output of macroergs decreases, and the energy potential decreases (V.S. Ilyin).

Significant morphological changes occur in tissues when innervation is disrupted. If we are talking about the cornea, skin or mucous membranes, then all stages of inflammation develop sequentially here. Eliminating infection, injury, or drying out does not prevent the process, but it slows down its development. As a result, an ulcer develops that has no tendency to heal. A study of the fine structure showed changes in organelles. Mitochondria decrease in number, their matrix becomes clearer. Obviously, this is associated with a violation of oxidative phosphorylation and Ca 2+ -accumulating ability of mitochondria, and along with this the energy capabilities of the cell. In denervated tissues, mitotic activity decreases.

As for functional disorders during the development of the neurodystrophic process, the consequences of denervation will be different depending on what tissue we are talking about. For example, when skeletal muscle is denervated, it loses its main function - the ability to contract. The heart muscle contracts even when all extracardiac nerves are cut. The salivary gland will secrete saliva, but its nature will no longer depend on the type of food. What was said is simple and clear. Much more interesting is the fact that denervated tissue reacts to many humoral factors differently than normal tissue. We are talking primarily about neurotransmitters of the nervous system. At one time, V. Cannon (1937) established that skeletal muscles, deprived of sympathetic nerves, react to adrenaline not less, but more than normal, the same muscles, disconnected from motor (cholinergic) nerves, react to acetylcholine more strongly than normal. So it was opened law of denervation, which means increased sensitivity of denervated structures. In particular, this is due to the fact that cholinergic receptors, which in normal muscles are concentrated only in the region of myoneural synapses, after denervation appear on the entire surface of the myocyte membrane. It is now known that the unusual response of denervated structures consists not only of an increase, but also of a perversion, when, for example, instead of relaxation of the vascular muscles, their contraction occurs. It is easy to imagine what this will mean, for example, for blood vessels and blood circulation.

An important question is: are there special trophic nerves?

At one time, Magendie admitted that, along with sensory, motor and secretory nerves, there are also special trophic ones that regulate tissue nutrition, i.e. absorption of nutritional material.

Later, I.P. Pavlov (1883), in an experiment on animals, among the nerves going to the heart, found a branch that, without affecting blood circulation, increased the strength of heart contractions. I. P. Pavlov called this nerve “strengthening” and recognized it as purely trophic. I. P. Pavlov saw complete and harmonious innervation of the heart in a triple nerve supply: functional nerves, vasomotor nerves that regulate the supply of nutrient material, and trophic nerves that determine the final utilization of these substances.

In principle, the same point of view was also held by L. A. Orbeli, who, together with A. G. Ginetsinsky in 1924, showed that an isolated (without blood circulation) frog muscle, tired to the limit by impulses along the motor nerve, begins to contract again if "throw" impulses at it along the sympathetic nerve. The trophic action of the sympathetic nerve is aimed at metabolism, preparation of the organ for action, its adaptation to the upcoming work, which is carried out by the action of the motor nerve.

From what has been said, however, it does not at all follow that trophic (sympathetic) nerves do not have other effects on tissue or that motor (secretory, sensitive) nerves do not have an effect on metabolism. A.D. Speransky (1935) said that all nerves influence metabolism, there are no non-trophic nerves - “a nerve is functional only because it is trophic.”

Mechanisms of trophic influence of nerves. Today no one doubts that nerves influence trophism, but how is this action carried out?

There are two points of view on this issue. Some believe that trophism is not an independent nervous function. A nerve impulse that activates an organ (for example, a muscle) thereby changes the metabolism in the cell (acetylcholine - permeability - enzyme activation). Others think that trophism cannot be reduced to the impulse (mediator) action of the nerve. New research has shown that the nerve has a second function, non-impulsive. Its essence is that in all nerves, without exception, axoplasm flow occurs in both directions. This current is needed to power the axons, but it turned out that substances moving along the processes of neurons penetrate through synapses and end up in innervated cells (muscle, etc.). Not only that, but it is now known that these substances have a specific effect on the effector cell. Surgery in which the nerve intended for the red muscle grows into the white muscle has shown that a radical change in its metabolism occurs. It switches from the glycolytic to the oxidative metabolic pathway.

The general conclusion from all that has been said is that the trophic action of the nervous system consists of two elements: pulse And non-impulse. The latter is carried out by “trophic substances”, the nature of which is being clarified.

Pathogenesis of neurogenic dystrophy. When analyzing the process, one should proceed from the fact that the trophic function is carried out according to the principle of a reflex. And from this it follows that when analyzing the dystrophic process, it is necessary to evaluate the significance of each link of the reflex, its “contribution” to the mechanism of development of the process.

Sensory nerve, apparently, plays a special role here. Firstly, information from the nerve center about events in the denervation zone is interrupted. Secondly, a damaged sensory nerve is a source of pathological information, including pain, and thirdly, centrifugal influences on the tissue emanate from it. It has been established that a special substance P is distributed through the sensory nerves with an axocurrent to the tissue, disrupting metabolism and microcirculation.

The importance of nerve centers is evidenced by many facts, including the experiments of A.D. Speransky with selective damage to the centers of the hypothalamus, which is accompanied by the appearance of trophic ulcers in a variety of organs on the periphery.

The role of efferent nerves in dystrophy is that some of their functions (normal) disappear, while others (pathological) appear. Impulse activity, production and action of mediators (adrenaline, serotonin, acetylcholine, etc.) stop, axonal transport of “trophic substances” is disrupted or stopped, function (motility, secretion) stops or is distorted. The genome is involved in the process, the synthesis of enzymes is disrupted, the exchange becomes more primitive, and the yield of macroergs decreases. Membranes and their transport functions suffer. An organ with impaired innervation can become a source of autoantigens. The pathogenesis of trophic disorders due to damage to peripheral nerves is presented schematically in rice. 25.6.

The process is complicated by the fact that, following purely neurotrophic changes, disturbances in blood and lymph circulation (microcirculation) occur, and this entails hypoxia.

Thus, the pathogenesis of neurogenic dystrophies today appears as a complex, multifactorial process, which begins with the fact that the nervous system ceases to “control metabolism” in tissues, and after this complex disorders of metabolism, structure and function arise.

Contents of the article:

Muscle atrophy is a pathological organic process in which gradual death of nerve fibers occurs. First, they become thinner, contractility decreases and tone decreases. Then the organic fibrous structure is replaced by connective tissue, which leads to impaired movement.

Description of the disease muscle atrophy

Hypotrophic processes begin with a malnutrition of muscle tissue. Dysfunctional disorders develop: the supply of oxygen and nutrients that ensure the vital activity of the organic structure does not correspond to the volume of utilization. The protein tissues that make up the muscles, without replenishment or due to intoxication, are destroyed and replaced by fibrin fibers.

Under the influence of external or internal factors, degenerative processes develop at the cellular level. Muscle fibers that do not receive nutrients or accumulate toxins slowly atrophy, that is, die. White muscle fibers are affected first, then red ones.

White muscle fibers have the second name “fast”, they are the first to contract under the influence of impulses and are turned on when it is necessary to reach maximum speed or react to danger.

Red fibers are called “slow”. To contract, they require more energy, and accordingly they contain a larger number of capillaries. That is why they perform their functions longer.

Signs of the development of muscle atrophy: first, the speed slows down and the amplitude of movements decreases, then it becomes impossible to change the position of the limb. Due to the decrease in the volume of muscle tissue, the popular name for the disease is “tabes.” The affected limbs become much thinner than healthy ones.

Main causes of muscle atrophy

Factors that cause muscle atrophy are classified into two types. The first includes genetic predisposition. Neurological disorders aggravate the condition, but are not a provoking factor. The secondary type of disease in most cases is caused by external causes: illness and injury. In adults, atrophic processes begin in the upper extremities; for children, the spread of diseases from the lower extremities is typical.

Causes of muscle atrophy in children

Muscle atrophy in children is genetic, but can appear later or be caused by external causes. It is noted that they are more likely to experience damage to nerve fibers, which disrupts impulse conduction and nutrition of muscle tissue.

Causes of the disease in children:

• Neurological disorders, including Guillain-Barré syndrome (an autoimmune disease that causes muscle paresis);
• Becker's myopathy (genetically determined) manifests itself in adolescents 14-15 years old and young people 20-30 years old; this mild form of atrophy extends to the calf muscles;
• Severe pregnancy, birth injuries;
• Poliomyelitis is a spinal paralysis of infectious etiology;
• Pediatric stroke - disruption of blood supply to cerebral vessels or cessation of blood flow due to thrombus formation;
• Back injuries with spinal cord damage;
• Disturbances in the formation of the pancreas, which affects the condition of the body;
• Chronic inflammatory processes of muscle tissue, myositis.

Myopathy (a hereditary degenerative disease) can be provoked by paresis of the nerves of the limbs, anomalies in the formation of large and peripheral vessels.

Causes of muscle atrophy in adults

Muscle atrophy in adults can develop against the background of degenerative-dystrophic changes that arose in childhood, and appear against the background of spinal and cerebral pathologies, with the introduction of infections.

The causes of the disease in adults can be:

1. Professional activity that requires constant increased physical stress.
2. Illiterate training if physical activity is not designed for muscle mass.
3. Injuries of various types with damage to nerve fibers, muscle tissue and the spine with damage to the spinal cord.
4. Diseases of the endocrine system, such as diabetes, and hormonal dysfunction. These conditions disrupt metabolic processes. Diabetes mellitus causes polyneuropathy, which leads to limited movement.
5. Poliomyelitis and other inflammatory infectious processes in which motor functions are impaired.
6. Neoplasms of the spine and spinal cord causing compression. Innervation of trophism and conductivity appears.
7. Paralysis after injury or cerebral infarction.
8. Dysfunction of the peripheral circulatory and nervous systems, resulting in the development of oxygen starvation of muscle fibers.
9. Chronic intoxication caused by occupational hazards (contacts with toxic substances, chemicals), alcohol abuse and drug use.
10. Age-related changes - as the body ages, thinning of muscle tissue is a natural process.

Adults can provoke muscle atrophy with illiterate diets. Prolonged fasting, during which the body does not receive useful substances that restore protein structures, causes the breakdown of muscle fibers.

In children and adults, degenerative-dystrophic changes in muscles can develop after surgical operations with a protracted rehabilitation process and during serious illnesses against the background of forced immobility.

Symptoms of muscle atrophy

The first signs of the development of the disease are weakness and mild pain that does not correspond to physical activity. Then the discomfort intensifies, spasms or tremors periodically appear. Atrophy of the limb muscles can be unilateral or symmetrical.

Symptoms of leg muscle atrophy

The lesion begins in the proximal muscle groups of the lower extremities.

Symptoms develop gradually:

• It is difficult to continue moving after a forced stop; one gets the feeling that “your legs are cast iron.”
• It is difficult to get up from a horizontal position.
• The gait changes, the feet begin to go numb and sag when walking. You have to raise your legs higher and “march.” Foot sagging is a characteristic symptom of damage to the tibial nerve (which runs along the outer surface of the lower leg).
• To compensate for hypotrophy, the ankle muscles first sharply increase in size, and then, when the lesion begins to spread higher, the calf loses weight. The skin loses turgor and sags.

If treatment is not started on time, the damage spreads to the thigh muscles.

Symptoms of thigh muscle atrophy

Thigh muscle atrophy may occur without involvement of the calf muscles. The most dangerous symptoms are caused by Duchenne myopathy.

The symptoms are characteristic: the thigh muscles are replaced by adipose tissue, weakness increases, the ability to move is limited, and knee reflexes are lost. The lesion spreads throughout the body and in severe cases causes mental impairment. Boys 1-2 years of age are most often affected.

If hip atrophy appears against the background of general dystrophic changes in the muscles of the limbs, then the symptoms develop gradually:

1. There is a feeling that goosebumps are running under the skin.
2. After prolonged immobility, spasms occur, and when moving, painful sensations occur.
3. There is a feeling of heaviness and aching in the limb.
4. The volume of the thigh decreases.

In the future, severe pain is already felt while walking, it radiates to the buttocks and lower back, to the lower back.

Symptoms of gluteal muscle atrophy

The clinical picture of this type of lesion depends on the cause of the disease.

If the cause is hereditary factors, then the same characteristic symptoms are noted as with myopathies of the lower extremities:

• Muscle weakness;
• Difficulties when it is necessary to move from a horizontal position to a vertical position and vice versa;
• Change in gait to a waddling, duck-like one;
• Loss of tone, pale skin;
• Numbness or the appearance of pins and needles in the area of ​​the buttocks during forced immobility.

Atrophy develops gradually and takes several years to worsen.

If the cause of the disease is damage to the gluteal nerve or spine, then the main symptom is pain spreading to the upper part of the buttock and radiating to the thigh. The clinical picture at the initial stage of myopathy resembles radiculitis. Muscle weakness and limited movement are pronounced; the disease progresses rapidly and can lead to disability of the patient within 1-2 years.

Symptoms of arm muscle atrophy

With muscular atrophy of the upper extremities, the clinical picture depends on the type of fibers affected.

The following symptoms may appear:

1. Muscle weakness, decreased range of motion;
2. Feeling of “goosebumps” under the skin, numbness, tingling, often in the hands, less often in the muscles of the shoulders;
3. Tactile sensitivity increases and painful sensitivity decreases, mechanical irritation causes discomfort;
4. The color of the skin changes: tissue pallor occurs, turning into cyanosis, due to a violation of tissue trophism.

First, atrophy of the hand muscles occurs, then the forearms and shoulders are affected, and pathological changes spread to the shoulder blades. There is a medical name for hand muscle atrophy - “monkey hand”. When the appearance of the joint changes, tendon reflexes disappear.

Features of the treatment of muscle atrophy

Treatment of limb muscle atrophy is complex. To bring the disease into remission, pharmaceuticals, diet therapy, massage, physical therapy, and physiotherapy are used. It is possible to connect funds from the arsenal of traditional medicine.

Medications for the treatment of muscle atrophy

The purpose of prescribing pharmaceuticals is to restore trophism of muscle tissue.

For this we use:

• Vascular drugs that improve blood circulation and accelerate blood flow in peripheral vessels. This group includes: angioprotectors (Pentoxifylline, Trental, Curantil), prostaglandin E1 preparations (Vasaprostan), Dextran based on low molecular weight dextran.
• Antispasmodics for vasodilation: No-spa, Papaverine.
• B vitamins, normalizing metabolic processes and impulse conductivity: Thiamine, Pyridoxine, Cyanocobalamin.
• Biostimulants that stimulate the regeneration of muscle fibers to restore muscle volume: Aloe, Plazmol, Actovegin.
• Preparations for restoring muscle conduction: Proserin, Armin, Oxazil.

All pharmaceuticals are prescribed by a doctor based on the clinical picture and severity of the disease. Self-medication can worsen the condition.

Diet for the treatment of muscle atrophy

To restore the volume of muscle tissue, you need to switch to a special diet. The diet must include foods with vitamins B, A and D, proteins and foods that alkalize physiological fluids.

Enter into the menu:

1. Fresh vegetables: bell pepper, broccoli, carrots, cucumbers;
2. Fresh fruits and berries: pomegranate, sea buckthorn, apples, viburnum, cherries, oranges, bananas, grapes, melons;
3. Eggs, lean meat of all types, except pork, fish, preferably sea;
4. Porridge (necessarily boiled in water) from cereals: buckwheat, couscous, oatmeal, barley;
5. Legumes;
6. Nuts of all types and flax seeds;
7. Greens and spices: parsley, celery, lettuce, onion and garlic.

A separate requirement for dairy products: everything is fresh. Unpasteurized milk, cheese with at least 45% fat content, cottage cheese and sour cream made from natural milk.

The frequency of food consumption does not matter. Weakened patients with low vital activity are recommended to eat small portions up to 5 times a day to avoid obesity.

When introducing protein shakes into your daily menu, you should consult your doctor. Sports nutrition may not be combined with medications.

Massage to restore trophic tissue of the limbs

Massage treatments for limb atrophy help restore conductivity and increase blood flow.

Massage technique:

• They start from the peripheral zones (from the hand and foot) and rise to the body.
• They use kneading techniques, in particular transverse kneading, and mechanical vibration techniques.
• Be sure to include the area of ​​the buttocks and shoulder girdle.
• Additional selective targeting of the gastrocnemius and quadriceps muscles may be required.
• Large joints are massaged with a spherical rubber vibrator.

In most cases, already at the onset of malnutrition, a massage of the whole body is prescribed, regardless of the affected area.

Physical therapy against muscle atrophy

A sharp limitation of motor function leads to atrophy of the muscles of the limbs, therefore, without regular training, it is impossible to restore the amplitude of movements and increase the volume of muscle mass.

Principles of therapeutic exercises:

1. The exercises are performed first in a lying position, then sitting.
2. The load is increased gradually.
3. Cardio exercises must be included in the training complex.
4. After training, the patient should feel muscle fatigue.
5. If painful sensations appear, reduce the load.

The treatment complex is tailored to each patient individually. Physical therapy exercises should be combined with a specially designed diet. If the body does not have enough nutrients, muscle tissue does not build.

Physiotherapy for the treatment of muscle atrophy

Physiotherapeutic procedures for muscle wasting are prescribed to patients on an individual basis.

The following procedures are used:

• Exposure to a directed flow of ultrasonic waves;
• Magnetotherapy;
• Treatment with low voltage currents;
• Electrophoresis with biostimulants.

If muscle atrophy occurs, laser therapy may be required.

All procedures are performed on an outpatient basis. If you plan to use home appliances, for example, Viton and the like, you must inform your doctor.

Folk remedies against muscle atrophy

Traditional medicine offers its own methods of treating muscle atrophy.

Home Recipes:

1. Calcium tincture. White homemade eggs (3 pieces) are washed from dirt, blotted with a towel and placed in a glass jar, poured with the juice of 5 fresh lemons. The container is placed in the dark and kept at room temperature for a week. The eggshell should be completely dissolved. After a week, the remaining eggs are removed, and 150 g of warm honey and 100 g of cognac are poured into the jar. Mix and drink a tablespoon after meals. Store in the refrigerator. The course of treatment is 3 weeks.
2. Herbal infusion. Mix equal amounts of flaxseed, calamus, corn silk and sage. Infuse in a thermos: 3 tablespoons pour 3 cups of boiling water. In the morning, strain and drink the infusion after meals in equal portions throughout the day. Duration of treatment - 2 months.
3. Oat kvass. 0.5 liters of washed oat seeds in a shell without husks are poured into 3 liters of boiled cooled water. Add 3 tablespoons of sugar and a teaspoon of citric acid. After a day you can already drink. The course of treatment is not limited.
4. Warming baths for feet and hands. Boil peelings of carrots, beets, potato peels, and onion peels. When steaming, add a teaspoon of iodine and table salt to each liter of water. Under water, the hands and feet are vigorously massaged for 10 minutes. Treatment - 2 weeks.

Traditional medicine methods must be combined with drug therapy.

How to treat muscle atrophy - watch the video:

Muscle atrophy caused by chronic diseases or injuries can be eliminated with the help of complex therapy. Hereditary myopathy cannot be completely cured. The disease is dangerous because it does not appear immediately. The sooner treatment begins, the greater the chance of bringing the disease into remission and stopping muscle damage.

• TROPHY in the Encyclopedic Dictionary:
  and, pl. no, w. In combination: tr o f i c a n e r v a n ...
• TROPHY in the Complete Accented Paradigm according to Zaliznyak:
  tro"fika, tro"fiki, tro"fiki, tro"fic, tro"fike, tro"fikam, tro"fika, tro"fiki, tro"fika, tro"fika, tro"fika, tro"fike, ...
• TROPHY in the Complete Spelling Dictionary of the Russian Language:
  trophism...
• TROPHY in the Spelling Dictionary:
  traffic, ...
• TROPHY in the Large Modern Explanatory Dictionary of the Russian Language:
  and. The influence of the nervous system on metabolism, on the nutrition of individual organs and tissues (in medicine) ...
• NERVOUS TROPHIC in Medical terms:
  regulation of tissue trophism carried out by the nervous...
• NERVOUS TROPHIC
  nervous (from the Greek trophe - food, nutrition), the regulating influence of the nervous system on the structural and chemical organization of organs and tissues, their growth and ...
• NERVOUS TROPHIC in the New Dictionary of Foreign Words:
  (gr. trophi nutrition) physiol. effects of the nervous system that directly affect the metabolism in the tissues and organs of the animal...
• NERVOUS TROPHIC in the Dictionary of Foreign Expressions:
  [physiol. effects of the nervous system that directly affect the metabolism in the tissues and organs of the animal...
• BALINT THEORY in Medical terms:
  (historical; balint) theory of the pathogenesis of peptic ulcer disease, according to which peptic ulcer of the stomach occurs as a result of the development of acidosis, as a result of which trophism is disrupted...
• CYTOPHOTOMETRY in the Great Soviet Encyclopedia, TSB:
  (from cyto..., photo... and...metry), one of the methods of quantitative cytochemistry that allows you to determine the chemical composition of cells in ...
• HEAT TREATMENT in the Great Soviet Encyclopedia, TSB:
  thermotherapy, a set of physiotherapeutic methods using heat from natural and artificial sources. At home, water and electric heating pads, poultices and...
• SPERANSKY ALEXEY DMITRIEVICH in the Great Soviet Encyclopedia, TSB:
  Alexey Dmitrievich, Soviet pathologist, academician of the USSR Academy of Medical Sciences (1939) and the USSR Academy of Medical Sciences (1944). ...
• SYRINGOMYELIA in the Great Soviet Encyclopedia, TSB:
  (from Greek syrinx, genitive syringos - tube, canal and myelos - spinal cord), a chronic progressive disease of the human nervous system, ...
• SECRETION in the Great Soviet Encyclopedia, TSB:
  (from Latin secretio - separation), the production and secretion of secretions by glandular cells. Essentially, in every cell of the body during...
• NERVOUS REGULATION in the Great Soviet Encyclopedia, TSB:
  regulation, coordinating the influence of the nervous system (NS) on cells, tissues and organs, bringing their activities into line with the needs of the body and ...
• CELL in the Great Soviet Encyclopedia, TSB:
  an elementary living system capable of independent existence, self-reproduction and development; the basis of the structure and life activity of all animals and plants. K. exist...
• DARSONVALIZATION in the Great Soviet Encyclopedia, TSB.
• HISTOLOGY in the Great Soviet Encyclopedia, TSB:
  (from the Greek histos - tissue and...logy), the science of tissues of multicellular animals and humans. Anatomy is the study of plant tissue...