How to treat muscle atrophy. Medicines to restore nerve tissue Symptoms of leg muscle atrophy

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. 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 fine. 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.

Trophic(Greek trophē nutrition) - a set of cellular nutrition processes that ensure the preservation of the structure and function of a tissue or organ.

The bulk of the tissues of vertebrate animals are endowed with indirect autonomic innervation, in which the trophic influences of the sympathetic part of the autonomic nervous system are carried out humorally - due to the mediator entering the effector cells through the bloodstream or by diffusion.

There are tissues whose trophism is provided by direct sympathetic innervation (heart muscle, uterus and other smooth muscle formations). It is carried out through mediators (acetylcholine, norepinephrine) secreted by nerve endings. Many researchers consider the trophic influences of the nervous system as impulseless, constant, associated with processes similar to neurosecretion. It is believed that various substances: mediators, oligopeptides and amino acids, enzymes, as well as particles of mitochondria, microsomes, nuclei and microtubules formed in the nerve cell reach the executive cells using axotok, i.e. continuous proximal-distal flow of axoplasm along the nerve fiber.

The sympathoadrenal and pituitary-adrenal hormonal systems are involved in the implementation of trophic influences. The first is capable of releasing an increased amount of adrenaline, which stimulates the mobilization of glycogen and fats from their depots, the production of cyclic AMP, etc.

The pituitary-adrenal system, by increasing the release of ACTH by the pituitary gland, stimulates the release of corticosteroids from the adrenal cortex, which in turn also enhance the mobilization of glycogen. The trophic function of many biologically active substances found in the tissues and fluids of the body - acetylcholine, histamine - has been proven.

The trophism of organs and tissues is directly dependent on the dynamics blood circulation: the magnitude of cardiac output and vascular tone located in front of the microcirculatory (see. Microcirculation ) the bed of this organ.

The amount of peripheral blood circulation is influenced by a variety of nervous, humoral and local chemical factors. Factors that cause cerebral vasodilation include a decrease in O 2 tension (hypoxia) and an increase in CO 2 tension (hypercapnia) in the intra- and extracellular spaces. A moderate increase in the content of potassium ions in the extracellular space and an increase in the content of adenosine in tissues have a similar effect. The influence of all these factors decreases or is completely eliminated with a decrease in the content of calcium ions in the perivascular space.

With increased load on the heart, trophic influences, expressed in increased blood supply to the myocardium, are ensured mainly due to the influence of local factors. Thus, a decrease in oxygen tension in tissues (hypoxia) is accompanied by an increase in the content of adenosine, a substance that has a vasodilating effect. In addition, an increase in blood supply to the myocardium, for example during intense work, is due to the stimulation of b-adrenergic receptors.

The mechanisms of trophic influences on skeletal muscles, associated, in particular, with increased blood flow, remain unclear. It is believed that the primary increase in muscle blood flow at the beginning of physical work is associated with the excitation of cholinergic sympathetic vasodilators. Blood flow in true (nutritive) capillaries during prolonged muscle work increases due to the action of a number of local chemical factors that reduce the basal tone of vascular muscles, independent of nervous influences. Such factors include an increase in the content of potassium ions in the extracellular fluid and an increase in osmotic pressure in it.

For the first time, the idea of ​​reflex mechanisms of trophic regulation (the so-called trophic reflexes) was expressed by I.P. Pavlov. Numerous experimental data obtained by the school of L.A. Orbeli, led, in particular, to the creation of the theory of the adaptive-trophic influence of the sympathetic nervous system (see. Autonomic nervous system ). A feature of the trophic reflex is its slower implementation than functional reflexes. Therefore, in some cases, overstrain of a function may be accompanied by depletion of its reserves, because the expended metabolic material does not have time to be replenished with new material. From the position of the theory of functional systems of the body P.K. Anokhin, trophic function is considered as an integral part of efferent synthesis (see. Functional systems ), providing the necessary level of metabolism for actuators that provide an adaptive result beneficial to the body. From a systemic point of view, the so-called pre-launch state becomes clear, i.e. a sharp increase in the metabolism of effectors, for example in skeletal muscles, occurring even before exposure to workload.

Assessing the trophic state of the body, organs, tissues and cells, they talk about eutrophy - optimal nutrition, i.e. about the normal structure, physicochemical properties and functions, the ability to grow, develop and differentiate tissues; hypertrophy - increased nutrition, expressed in an increase in the mass and (or) number of a certain group of cells, usually with an increase in their function; malnutrition - reduced nutrition, expressed in a decrease in the mass or number of a group of cells and a decrease in functional activity (its extreme degree is atrophy ), dystrophy - qualitatively altered, malnutrition, leading to pathological changes in the structure, physicochemical properties and function of cells, tissues and organs, their growth, development and differentiation (see. Dystrophy of cells and tissues ).

Trophic disorders- disturbances in cellular nutrition processes responsible for maintaining the structure and function of a tissue or organ that are of neurogenic origin.

Most researchers associate trophic disorders with functional changes in the formations of the autonomic nervous system, mainly its sympathetic department; interstitial brain, borderline sympathetic trunk, peripheral nerves rich in sympathetic fibers, etc.

The close connection of the autonomic nervous system, higher autonomic centers with the endocrine system and centers for the regulation of humoral activity made it possible to consider trophic disorders as a complex of autonomic-endocrine-humoral disorders.

There are trophic disorders in primary lesions of the autonomic nervous system; trophic disorders with primary lesions of the vegetative-endocrine apparatus: trophic disorders with complex lesions of the vegetative-humoral apparatus. In addition, infectious dystrophies are distinguished (with e, tuberculosis, chronic dysentery, brucellosis, etc.); toxic dystrophies due to exogenous poisoning (chemical agents, industrial poisons); endogenous-trophic dystrophies (with vitamin deficiencies, protein metabolism disorders, malignant neoplasms).

Trophic disorders also occur with irritation of almost any part of the central nervous system, which may be due to the diverse connections of the limbic-reticular complex with various structures of the central nervous system. Wide representation of nonspecific brain formations, distribution of their regulatory function not only to vegetative,

The central nervous system (CNS) is a single mechanism that is responsible for the perception of the surrounding world and reflexes, as well as for controlling the system of internal organs and tissues. The last point is performed by the peripheral part of the central nervous system with the help of special cells called neurons. They make up the nervous tissue, which serves to transmit impulses.

The processes coming from the body of the neuron are surrounded by a protective layer that nourishes the nerve fibers and accelerates impulse transmission, and this protection is called the myelin sheath. Any signal transmitted along nerve fibers resembles a current discharge, and it is their outer layer that prevents its strength from decreasing.

If the myelin sheath is damaged, then full perception in this part of the body is lost, but the cell can survive and the damage will heal over time. If the injuries are quite serious, you will need drugs designed to restore nerve fibers like Milgamma, Copaxone and others. Otherwise, the nerve will die over time and perception will decrease. Diseases that are characterized by this problem include radiculopathy, polyneuropathy, etc., but doctors consider multiple sclerosis (MS) to be the most dangerous pathological process. Despite the strange name, the disease has nothing to do with the direct definition of these words and, when translated, means “multiple scars.” They arise on the myelin sheath in the spinal cord and brain due to immune failure, which is why MS is classified as an autoimmune disease. Instead of nerve fibers, a scar consisting of connective tissue appears at the site of the lesion, through which the impulse can no longer pass correctly.

Is it possible to somehow restore damaged nerve tissue or will it forever remain in a crippled state is a relevant question to this day. Doctors still cannot answer this question accurately and have not yet come up with a full-fledged drug to restore sensitivity to nerve endings. Instead, there are various medications that can reduce the process of demyelination, improve nutrition of damaged areas and activate the regeneration of the myelin sheath.

Milgamma is a neuroprotector for restoring metabolism inside cells, which allows you to slow down the process of myelin destruction and begin its regeneration. The drug is based on vitamins from group B, namely:

• Thiamine (B1). It is essential for the absorption of sugar in the body and the production of energy. With acute thiamine deficiency, a person's sleep is disturbed and memory deteriorates. He becomes nervous and sometimes depressed, as in depression. In some cases, symptoms of paresthesia are observed (goose bumps, decreased sensitivity and tingling in the fingertips);
• Pyridoxine (B6). This vitamin plays an important role in the production of amino acids, as well as some hormones (dopamine, serotonin, etc.). Despite rare cases of a lack of pyridoxine in the body, due to its deficiency, a decrease in mental abilities and a weakening of the immune defense are possible;
• Cyanocobalomin (B12). It serves to improve the conductivity of nerve fibers, resulting in improved sensitivity, as well as to improve blood synthesis. With a lack of cyanocobalamine, a person develops hallucinations, dementia (dementia), disturbances in heart rhythm and paresthesia are observed.

Thanks to this composition, Milgama is able to stop the oxidation of cells by free radicals (reactive substances), which will affect the restoration of sensitivity of tissues and nerve endings. After a course of taking pills, there is a decrease in symptoms and an improvement in general condition, and the drug must be taken in 2 stages. In the first, you will need to make at least 10 injections, and then switch to tablets (Milgamma compositum) and take them 3 times a day for 1.5 months.

Staphaglabrine sulfate has been used for quite a long time to restore the sensitivity of tissues and the nerve fibers themselves. The plant from whose roots this drug is extracted grows only in subtropical and tropical climates, for example, in Japan, India and Burma, and it is called smooth stephania. There are known cases of obtaining Stafaglabrine sulfate in laboratory conditions. Perhaps this is due to the fact that stephania smooth can be grown as a suspension culture, that is, suspended in glass flasks with liquid. The drug itself is a sulfate salt, which has a high melting point (more than 240 ° C). It refers to the alkaloid (nitrogen-containing compound) stepharine, which is considered the basis for proaporphine.

Stephaglabrin sulfate serves to reduce the activity of enzymes from the class of hydrolases (cholinesterase) and to improve the tone of smooth muscles that are present in the walls of blood vessels, organs (hollow inside) and lymph nodes. It is also known that the drug is slightly toxic and can reduce blood pressure. In the old days, the medicine was used as an anticholinesterase agent, but then scientists came to the conclusion that Stefaglabrin sulfate is an inhibitor of connective tissue growth activity. From this it turns out that it delays its development and scars do not form on the nerve fibers. That is why the drug began to be actively used for injuries to the PNS.

During the research, specialists were able to see the growth of Schwann cells, which produce myelin in the peripheral nervous system. This phenomenon means that under the influence of the medication the patient noticeably improves the conduction of impulses along the axon, since the myelin sheath begins to form around it again. Since the results were obtained, the drug has become hope for many people diagnosed with incurable demyelinating pathologies.

It will not be possible to solve the problem of autoimmune pathology only by restoring nerve fibers. After all, no matter how many lesions have to be eliminated, the problem will return, since the immune system reacts to myelin as a foreign body and destroys it. Today it is impossible to eliminate such a pathological process, but you no longer have to wonder whether the nerve fibers are being restored or not. People are left to maintain their condition by suppressing the immune system and using drugs like Stefaglabrin sulfate to maintain their health.

The drug can only be used parenterally, that is, past the intestines, for example, by injection. The dosage should not exceed 7-8 ml of 0.25% solution per day for 2 injections. Judging by time, usually the myelin sheath and nerve endings are restored to some extent after 20 days, and then a break is needed and you can understand how long it will last by asking your doctor about it. The best result, according to doctors, can be achieved through low doses, since side effects develop much less frequently, and the effectiveness of treatment increases.

In laboratory conditions, during experiments on rats, it was found that with a concentration of the drug Stefaglabrin sulfate of 0.1-1 mg/kg, treatment proceeds faster than without it. The course of therapy ended earlier when compared with animals that did not take this medicine. After 2-3 months, the rodents’ nerve fibers were almost completely restored and the impulse was transmitted along the nerve without delay. In the experimental subjects who were treated without this medication, recovery lasted about six months and not all nerve endings returned to normal.

Copaxone

There is no cure for multiple sclerosis, but there are drugs that can reduce the effect of the immune system on the myelin sheath, and these include Copaxone. The essence of autoimmune diseases is that the immune system destroys the myelin located on nerve fibers. Because of this, the conductivity of impulses deteriorates, and Copaxone is able to change the target of the body’s defense system to itself. The nerve fibers remain untouched, but if the body’s cells have already begun to corrode the myelin sheath, then the drug will be able to push them aside. This phenomenon occurs because the drug is very similar in structure to myelin, so the immune system switches its attention to it.

The drug is capable of not only attacking the body’s defense system, but also producing special cells of the immune system to reduce the intensity of the disease, called Th2 lymphocytes. The mechanism of their influence and formation has not yet been thoroughly studied, but there are various theories. There is an opinion among experts that dendritic cells of the epidermis are involved in the synthesis of Th2 lymphocytes.

The produced suppressor (mutated) lymphocytes, entering the blood, quickly penetrate into the part of the nervous system where the source of inflammation is located. Here, Th2 lymphocytes, due to the influence of myelin, produce cytokines, that is, anti-inflammatory molecules. They begin to gradually relieve inflammation in this area of ​​the brain, thereby improving the sensitivity of nerve endings.

The drug has benefits not only for the treatment of the disease itself, but also for the nerve cells themselves, since Copaxone is a neuroprotector. The protective effect is manifested in stimulating the growth of brain cells and improving lipid metabolism. The myelin sheath mainly consists of lipids, and in many pathological processes associated with damage to nerve fibers, they are oxidized, so the myelin is damaged. The drug Copaxone can eliminate this problem, as it increases the body's natural antioxidant (uric acid). It is not known why the level of uric acid increases, but this fact has been proven in numerous experiments.

The drug serves to protect nerve cells and reduce the severity and frequency of exacerbations. It can be combined with medications Stefaglabrin sulfate and Milgamma.

The myelin sheath will begin to recover due to the increased growth of Schwann cells, and Milgamma will improve intracellular metabolism and enhance the effect of both drugs. Using them yourself or changing the dosage yourself is strictly prohibited.

Whether it is possible to restore nerve cells and how long it will take only a specialist can answer, based on the results of the examination. It is prohibited to take any medications on your own to improve tissue sensitivity, since most of them are hormonal and therefore difficult to tolerate by the body.