If the body experiences a decrease in bone mass, loses its ability to retain calcium, and excessively removes it from tissues, the person will be diagnosed with osteoporosis. Both young and old people are susceptible to the disease. The disease increases the likelihood of developing fractures and can significantly reduce the quality of life.

There are various ways to get rid of osteoporosis and relieve its symptoms. Doctors usually recommend comprehensive treatment to their patients. These can be in the form of injections, tablets, special vitamin complexes, and ointments can also be used.

This approach allows the affected bone to be affected, slowing down the rapid decay, and promotes the formation of new tissue. At the same time, the drugs can significantly increase bone density and reduce the likelihood of injuries and fractures.

If osteoporosis has developed in a woman due to a deficiency of the hormone estrogen, then replacement therapy will be based on the regular use of a product containing female sex hormones.

Treatment should be carried out over several years in a row. This is the only way to slow down bone loss and eliminate the symptoms of the disease.

Drugs for osteoporosis are usually divided into three groups depending on the mechanism of their effect on the body:

• slowing down bone destruction;
• stimulating bone formation;
• means of multifaceted influence.

Calcium and calcitonin

The basis of therapy for osteoporosis will be calcium and vitamin D. The effect of their correct combination will remain only with regular use and adequate dosage.

They are indicated for elderly people and those who lead a sedentary lifestyle, especially against the backdrop of poor nutrition.

In this case, calcium should be consumed at least 1200 g per day. You can get it from special preparations or food products rich in this mineral.

Calcium will help:

1. improve the absorption of vitamin D in the intestines;
2. restore the normal balance of minerals.

With systematic intake of these substances, after just a few years, you can reduce the risk of frequent limb fractures. The treatment will be especially effective if it is supplemented with recipes for products based on mumiyo.

Calcitonin can suppress bone resorption. Preparations with this substance can be prescribed both in the form of injections and a special spray. The nasal spray is more convenient to use, especially since it produces side effects several times less often.

Calcitonin is usually prescribed in combination with minerals, vitamin complexes and mumiyo. It works effectively, but is very quickly eliminated from the body. It is good to take these medications for osteoporosis:

• steroid;
• postmenopausal;
• senile

If there has been a compression fracture due to osteoporosis, then the drug has an analgesic effect, especially if the treatment is supported by the use of mumiyo.

The most popular drugs for osteoporosis are bisphosphonates. They can increase bone density and reduce the likelihood of fracture. These drugs are produced in the form of tablets, ampoules with liquid for intravenous and oral use.

Unpleasant side effects may occur after using the product:

1. vomit;
2. nausea;
3. headaches and muscle pain;
4. skin rashes;

Kidney damage may occur when administered intravenously. When used simultaneously with non-steroidal anti-inflammatory drugs, side effects are likely to worsen.

Bisphosphonates are taken under mandatory medical supervision.

Often, bisphosphonates are prescribed in advanced cases, when the symptoms of the pathology torment the patient even at night. In a similar way, the patient’s body will be affected by mumiyo, which is part of many folk recipes for the treatment of osteoporosis.

The selective effect is explained by the fact that bisphosphonates are similar in composition to bone tissue. Thanks to this, they can accumulate in places where new bone is formed, remaining there until it replaces the old one. These drugs help bone mass grow. The group includes funds:

• Xydiphone;
• Skelid;
• Bonefos;
• Actonel;
• Osteotab.

All of them are absorbed to a greater extent in the small intestine, and only partially in the stomach. As for contraindications, bisphosphonates cannot be used to treat pregnant women. These substances can cross the placental barrier and harm the fetus.

In order for the process of getting rid of osteoporosis to be successful and its symptoms not to appear, it is important to take calcium salts, mumiyo and vitamin D simultaneously with bisphosphonates. The interval between doses of these drugs should be at least 60 minutes.

Anabolics and hormones

Anabolic steroids have been used for long-term treatment of osteoporosis for many years. Such drugs stimulate bone formation and slow down their metabolism. Typically, the drugs are indicated for the treatment of men whose osteoporosis was provoked by the use of glucocorticosteroids.

If a patient is being treated with anabolic steroids, then he should be aware that such drugs have many side effects, especially in women. So, with a high probability the patient will suffer from:

• male pattern hair growth;
• changes in voice;
• changes in the volume of subcutaneous fat tissue.

For this reason, anabolic steroids are extremely rarely prescribed to young girls. In older women, the use of estrogens is indicated. Most often, they are recommended for use during menopause, when the symptoms of osteoporosis intensify, but hormonal therapy will not always be effective. It is more suitable for the prevention of pathology, just like mumiyo.

It is important to immediately note that hormone replacement therapy can have serious side effects, for example, the development of tumors in the uterine cavity and mammary glands. Therefore, treatment should be prescribed only to those women who are at risk of frequent limb fractures and only after consultation with a gynecologist.

If the patient’s body is suitable for such treatment, then with long-term use of estrogens the risks of compression fractures of the femoral neck are reduced. However, after the age of 70 years, the expected therapeutic effect will no longer occur.

To speed up recovery, you can take a piece of mumiyo every morning along with the main medications.

Fluorine and calcium salts

Fluoride preparations can increase skeletal mass. They help improve the bone tissue of the spine, but fluoride is not always adequately tolerated by the patient’s body, causing problems with the digestive tract.

Under the influence of drugs of this group, an inferior bone matrix is ​​formed that does not absorb minerals well. In view of this, the symptoms of pathology should also be relieved with calcium and vitamin D.

Calcium salts and mumiyo can improve metabolism. Pharmacology offers these drugs in the form of carbonates and citrates. It is better to take calcium citrates for osteoporosis, because carbonates cause the formation of stones in the urinary tract. Most often, calcium salts are indicated for senile osteoporosis in combination with:

• bisphosphonates;
• vitamin D;
• fluoride preparations;
• estrogen.

What to choose?

Drug treatment of osteoporosis has recently involved complex therapy with drugs from various groups. If we talk about men, the doctor will treat them with testosterone drugs, fluorides and bisphosphonates. Such therapy will primarily be aimed at eliminating the cause of osteoporosis and eliminating the pathological process.

Shilajit and biologically active supplements (dietary supplements) will help to cope with bone tissue problems. They usually include:

• glucosamine;
• collagen hydrolyzate;
• vitamin C;
• biotin;
• beta carotene;
• calcium.

Dietary supplements relieve symptoms of the disease, help tissues recover after injuries, fractures, and are effective for systemic bone lesions. Such drugs have an anti-inflammatory and analgesic effect, improve the functioning of the musculoskeletal system and eliminate the symptoms of osteoporosis.

One of the effective and popular supplements is Collagen Ultra. It can be a powder, ointment or gel. The drug will be an excellent assistant under the condition of complex therapy. To obtain greater results, all Collagen preparations should be used simultaneously.

Today there is no universal medicine that can reliably and quickly relieve a patient from osteoporosis. However, doctors have a lot of medicines in their hands that help prevent the disease and strengthen the bones of patients.

If a person is at risk or already suffers from an illness, then he should additionally take vitamin complexes, follow a diet, eat foods especially rich in calcium and practice traditional medicine recipes that include the use of mumiyo.

Under no circumstances should you self-medicate. It can cause unpredictable adverse reactions. Even ordinary ointment can be hazardous to health if it is used without a doctor’s permission.

The use of vasodilators for cervical osteochondrosis

Various groups of drugs are used to treat osteochondrosis. An important place among them is occupied by vasodilators. Let’s try to figure out why they are prescribed and which ones are used most often.

Why are vascular agents needed?

Vessels pass through the cervical spine. The most important of these are the vertebral arteries, which supply blood to the posterior parts of the brain. The cerebellum, which is responsible for balance and coordination of movements, is located here. The brain stem contains: the respiratory and vasomotor centers, the nuclei of the cranial nerves and other important structures that regulate various functions of the body.

The vertebral arteries supply the occipital lobe, which processes visual information, as well as part of the temporal lobes, which are responsible for the perception of sounds, taste and olfactory sensations. The inner ear, where the vestibular apparatus is located, which regulates the position of the body in space, receives blood from the same source. Therefore, when the blood supply to these parts of the brain is disrupted, characteristic clinical manifestations appear: headache, tinnitus, dizziness, impaired coordination of movement, nausea, vomiting, visual and auditory disorders. In severe cases, the appearance of an ischemic stroke clinic is possible.

With osteochondrosis, pain can lead to reflex vascular spasm. Bony spurs that form on the vertebrae can directly compress the vertebral artery or irritate the nerve plexus surrounding this vessel, which leads to its narrowing. Therefore, vasodilators are used to improve cerebral circulation.

Means to improve blood circulation

For cervical osteochondrosis, certain medications are used. The doctor prescribes therapy after making a diagnosis. Without consulting a specialist, treatment is not only harmful, but also dangerous to health.

Aminophylline

Its second name is better known – Eufillin. It has a direct relaxing effect on the smooth muscles of blood vessels. Prevents thrombus formation, improves microcirculation. Can be used intravenously, intramuscularly and in tablets.

Often, when changing the vertebrae and discs in the neck, electrophoresis with aminophylline is used, as a result the muscles relax, which is accompanied by a decrease in pain. Local blood circulation improves.

Pentoxifylline

Most often, Trental is used for pathology of the neck vessels. In addition to eliminating vascular spasm, pentoxifylline affects the coagulation function: it inhibits platelet aggregation and reduces blood viscosity. This leads to improved microcirculation in areas with poor circulation.

The medicine can be used intravenously, as well as in tablet form. The most common side effects are: hypotension, tachycardia, arrhythmias, heart pain, headaches, dizziness, dyspeptic disorders, changes in the cellular composition of the blood.

A nicotinic acid

Vitamin PP dilates mainly small vessels, including those of the brain, thereby improving blood circulation. Has an anticoagulant effect and reduces cholesterol levels. The drug is mainly administered intramuscularly, rarely intravenously.

Undesirable reactions appear almost immediately: redness of the face, upper body, feeling of a rush to the head. Dizziness and loss of sensitivity in the extremities are possible. These phenomena pass quickly.

Cinnarizine

The brand name is Stugeron. This medicine has a direct effect on the wall of blood vessels, which leads to an increase in their lumen. Regional blood flow improves and blood viscosity decreases. The drug has virtually no effect on the heart and blood pressure. Decreases the tone of the sympathetic nervous system.

Available only in tablets for oral administration. Usually well tolerated. Most often, dry mouth, dyspepsia, and possibly tremors of the extremities are noted.

Vascular agents with neuroprotective effects

Vinpocetine

Another well-known name is Cavinton. For osteochondrosis of the neck it is prescribed quite often. This drug helps reduce vascular tone, but does not have a significant effect on systemic blood pressure and heart function. Strengthens blood supply mainly to those parts of the brain where it is impaired.

The second important point is the improvement of the rheological properties of blood. Its viscosity and platelet aggregation ability decrease. It has a positive effect on red blood cells, which easily penetrate small capillaries and deliver oxygen to all cells of the body. Vinpocetine activates metabolic processes in the brain and increases resistance to hypoxia. It is an antioxidant and neuroprotector.

Used for intravenous infusions. The tablets are taken orally. Side effects are rare, but they do occur: dizziness, headache, fluctuations in blood pressure, arrhythmias.

Piracetam

This active substance is also found under other names: Lucetam, Nootropil. Refers to nootropics. But, in addition to improving thought processes, piracetam enhances microcirculation. By reducing the aggregation properties of platelets and increasing the elasticity of red blood cell membranes, blood circulation in small vessels increases, and this leads to an increase in blood flow in ischemic areas of the brain. Is a neuroprotector.

Available in the form of a solution for intramuscular and intravenous injections, capsules, and tablets. The dose of the medicine and the method of administration are chosen by the doctor. There are few side effects: dizziness, headache, drowsiness, changes in blood pressure, nausea, vomiting and some others.

Combined products

Such drugs are convenient to use, since the number of tablets taken is reduced, while the effectiveness of the drugs is maintained. The combination of cinnarizine with piracetam - Phezam and Omaron - has proven itself well. Both medications are available in capsules.

Thus, with pathological changes in the spine in the neck area, agents that dilate blood vessels and improve cerebral circulation play an important role in preventing quite serious complications. But treatment should be carried out for a long time under the supervision of a specialist. Otherwise, time and money will be wasted.

Drugs for the treatment of osteochondrosis are prescribed to eliminate the pathogenetic links of degenerative-dystrophic lesions of the spine: damage to the intervertebral discs, impaired blood supply, formation of bone osteophytes, normalization of skeletal muscle tone.

Against the background of the pathology, the nerve roots are pinched, which leads to pain in the lower back, inflammation in the surrounding tissues, and increased activity of the sympathetic nervous system. Against the background of pathology, blood vessels often spasm, which requires the prescription of vasodilating drugs (antispasmodics).

Chondroprotectors (chondroxide, structum, alflutop) are prescribed to restore the structure of intervertebral discs. When taking medications, the secretion of synovial fluid in the joints increases.

The basic basis for the treatment of degenerative-dystrophic diseases of the spine are anti-inflammatory drugs (diclofenac, voltaren, ketorolac).

Let's look at the above drugs in more detail.

Vasoconstrictor drugs for the treatment of cervical osteochondrosis:

• Pentoxifylline is a drug for normalizing blood supply in blood vessels and improving the rheological properties of blood. The action of the drug is based on vasodilation, improving blood supply and preventing cerebral hypoxia;
• aminophylline is a bronchodilator (expands the bronchial tree). This antispasmodic helps improve peripheral and cerebral blood supply. Eufillin is used for the treatment of neurological diseases associated with degenerative-dystrophic diseases of the spine;
• nicotinic acid and xanthinol nicotinate – improve microcirculation, increase aggregation activity and improve collateral blood supply and metabolic processes in tissues;
• lipoic acid (berlithion) – metabolic drugs that have the effect of enhancing collateral blood supply, restoring energy metabolism and improving nerve innervation. The product increases trophic properties and improves biochemical metabolism inside cells;
• Actovegin is a calf blood protein. It contains a large amount of nutrients (amino acids, nucleosides, fat metabolism products). The drug restores peripheral blood supply and increases vascular tone. It has a positive effect on patients with brain disorders. The positive effect of Actovegin is associated with the normalization of blood supply in internal organs and the development of collaterals.

Vasodilator drugs for osteochondrosis of the neck and thoracic spine help restore blood supply to the brain and reduce hypoxia in the tissues.

In practice, neurologists often prescribe medications such as vinpocetine and piracetam.

For degenerative-dystrophic processes in the neck, these drugs are the most effective. They prevent spasm of the vertebral arteries, which are involved in the vertebrobasilar blood supply. While taking these antispasmodics, the following symptoms are eliminated:

1. headache;
2. dizziness;
3. movement disorders;
4. convulsions.

Antispasmodics are prescribed in combination with other drugs for the treatment of degenerative diseases of the spinal column.

Vinpocetine is a corrector of cerebral blood supply disorders. It is characterized by neuroprotective and vasodilating effects, enhances cerebral blood supply and increases blood delivery to brain tissues.

Piracetam – improves metabolic processes.

Each of these medications complements the previous one. To normalize the condition of the soft tissues of the spine, it is necessary to use chondroprotectors simultaneously with antispasmodics.

Action

Anti-inflammatory drugs act for osteochondrosis by blocking the enzyme cyclooxinase. This chemical triggers inflammatory reactions in the body. When it is blocked, inflammation does not appear. However, the drug has a temporary effect.

Anti-inflammatory drugs cannot be used for a long period of time, as they have side effects on the gastrointestinal tract.

The latest generation of drugs has a selective effect on cyclooxygenase receptors in bone tissue, but they do not affect intestinal receptors. Thus, it is possible to reduce the side effects of drugs.

The most effective remedy for the treatment of spinal diseases is diclofenac. This opinion, of course, will be disputed by some doctors. Today there are medications such as nimesulide and nise, which have minimal side effects on the intestines and prolonged action (allowing the dosage of the drug to be reduced). However, in terms of anti-inflammatory effectiveness, they are inferior to diclofenac and ketorolac.

Nonsteroidal anti-inflammatory drugs (NSAIDs) can be classified into 2 groups:

• selective;
• non-selective.

The first group is contraindicated in patients with ulcers, gastritis and children under 6 years of age (ibuprofen, diclofenac, indomethacin).

Selective anti-inflammatory drugs are contraindicated during lactation, pregnant women, adolescents and small children.

What side effects occur from taking NSAIDs:

1. drowsiness and fatigue;
2. hives;
3. fatigue;
4. stomach ache;
5. flatulence and constipation.

Treatment of degenerative changes in the thoracic and lumbar regions

For degeneration of the thoracic and lumbar spine, in addition to anti-inflammatory drugs, muscle relaxants are prescribed. They have an analgesic and sedative effect. Medicines provide relaxation of the skeletal muscles of the back, which eliminates the pain syndrome that occurs due to pinched nerve fibers in the thickness of the muscle tissue.

Before taking these medications, be aware of their side effects:

• dry mouth;
• paresthesia;
• vomiting and nausea;
• confusion;
• decreased performance;
• slower urination;
• constipation and diarrhea;
• drop in blood pressure;
• emotional disturbances (irritability, depression, euphoria).

Contraindications to taking muscle relaxants:

1. epilepsy;
2. myasthenia gravis;
3. chronic renal failure;
4. lactation and pregnancy;
5. increased sensitivity;
6. allergic reactions.

Narcotic medications for osteochondrosis are prescribed by psychiatrists if the patient has neuropsychiatric disorders. The following drugs are used to relieve pain: tempalgin, baralgin and pentalgin.

Attention! Narcotic anti-inflammatory drugs for osteochondrosis are used to eliminate pain only when other drugs do not have a positive effect.

Chondroprotectors

Chondroprotectors are drugs against spinal degeneration. They are prescribed for a long time to prevent further damage to the intervertebral discs.

What chondroprotective agents should be taken against degenerative-dystrophic diseases of the spine:

• injections to improve joint mobility and accumulation of cartilage cells in the spinal column;
• for oral administration (Teraflex, Dona and Structum) are prescribed for a long period of time (from 3 to 6 months). They bring the first results after six months, when the photographs show an increase in the height of the intervertebral spaces.

Treatment of degenerative diseases should begin in the early stages, when the destruction of cartilage tissue is insignificant.

Thus, drugs against degenerative-dystrophic diseases of the spine (antispasmodics, chondroprotectors, NSAIDs) are prescribed together with the initial stages of the pathological process. To increase their effectiveness, treatment is supplemented with steroids, biostimulants, psychotropics, and B vitamins. The choice of treatment regimen should remain with doctors.

Summary

The article substantiates the modern mechanisms of neurotrophicity, neuroprotection, neuroplasticity and their relationship with neurogenesis. For the first time in the literature, the use of nootropic drugs for various functional-organic diseases of the brain in adults and children is substantiated. A modern classification of nootropic drugs and neuroprotectors with mechanisms of neuroplasticity is presented. Neuropharmacological mechanisms of primary and secondary neuroprotection are considered. The difference between apoptosis and anoikis and their role in neurogenesis is substantiated.

The study is based on the current mechanisms of neurotrophicity, neuroprotection, neuroplasticity and their interactions with neurogenesis. The use of nootropic drugs for various functional-organic diseases of the brain in adults and children is strongly discussed in the literature. A current classification of nootropic drugs and neuroprotectors based on the mechanisms of neuroplasticity has been established. The neuropharmacological mechanisms of primary and secondary neuroprotection are considered. The role of apoptosis in anoikis and their role in neurogenesis is discussed.

In the article the modern mechanisms of neurotrophicity, neuroprotection, neuroplasticity and their correlation with neurogenesis are substantiated. For the first time in the literature the use of nootropic drugs in different functional organic brain disease in adults and children is proven. The current classification of nootropic drugs and neuroprotective agents with mechanisms of neuroplasticity is presented. Neuropharmacological mechanisms of primary and secondary neuroprotection are considered. The difference between apoptosis and anoikis and their role in neurogenesis are substantiated.

Keywords

nootropics, neuroprotectors, cerebrovascular diseases, neuropharmacology.

nootropics, neuroprotectors, cerebrovascular disease, neuropharmacology.

nootropics, neuroprotectors, cerebrovascular diseases, neuropharmacology.

The use of nootropics and neuroprotectors, especially in practical psychoneurology, is extremely important. According to the World Health Organization (WHO, 2010), 7 million strokes occur annually in the world (patients who survive need to take similar medications); due to increasing life expectancy, 157 million people suffer from vascular dementia; closed head injuries reached 2 million per year; over the past 5 years, the number of neurodegenerative diseases has increased by 17%; after severe forms of neuroinfections, a neuropsychiatric deficit is formed (up to 45% of cases); Every year, about 78 million children are born in the world with a pathology of the central nervous system (CNS), which often ends in the first years of life with psycho-speech-motor delay and dementia. Europe spends €75 billion annually on treating cognitive impairment.

In 2010, 3,186,686 people with various forms of cerebrovascular diseases and vascular lesions of the brain were recorded in Ukraine. And their number is higher than similar indicators in developed countries of the world.

Without a doubt, the need for the use of nootropic drugs (and their derivatives) in both pediatric and adult clinical practice is obvious.

Nootropics include medications that can have a direct activating effect on learning processes, memory, mental activity, increase the brain’s resistance to any aggressive influence and improve the quality of communication life of patients (WHO, 1991). More capacious in terms of nootropic effects on neurons and glia are represented by three mechanisms:

— neurotrophicity - a natural process involving cell proliferation and their migration, differentiation, survival;

— neuroprotection - this is an induced mechanism that counteracts damaging factors;

— neuroplasticity - a process of constant regeneration in the event of natural or pathological damage.

Nootropic functions are carried out by various mechanisms of brain activity. A person has a natural mechanism that performs this function and occurs with the help of neurotropism, neurotrophism, neuroplasticity, including sanitation mechanisms.

A variant of neuroplasticity is the following example: as is known, patients with congenital blindness have increased auditory spatial orientation due to additional activation of areas of the visual cortex during sound stimulation. At the same time, in patients with congenital deafness, when the visual analyzer is irritated, the auditory zone of the cortex is activated. Both blind and deaf patients have increased tactile sensitivity with excitation of the visual or auditory cortex, respectively, when performing somatosensory tasks. Such information can help predict the success of sensor implants. The use of cochlear implants in deaf patients with developed cross-modal neuroplasticity has proven effective. The dimensions of the left temporal lobe may serve as an anatomical marker of left hemisphere specialization for language abilities. The size of the medial temporal structures may correlate with the ability to recognize faces, and the periventricular region is responsible for spatial orientation. It is possible that after periventricular ischemia, this function suffers in a number of patients, especially in children.

Apoptosis - an active process that is under strict genetic control and requires the expenditure of ATP; usually, but not always, the process is associated with activation of caspases. As a rule, it occurs without inflammation.

Cell damage occurs through two main pathways: apoptosis and anoikis.

1. Internal genetic (natural) activation (mainly through mitochondria) caused by an increase in intracellular calcium, reactive oxygen molecules, glutamate, etc.

2. External activation (binding to cell death receptors), for example, TNF- binds to the Fas receptor.

Both pathways directly or indirectly lead to the activation of hierarchical caspases, of which at least 14 are cysteine-dependent and aspartate-specific proteases.

Anoikis - a process similar to apoptosis, but caused by an abnormal pathological effect on the cell matrix. In the body, these cell “damages” can occur simultaneously (necrosis, apoptosis, anoikis).

That is why therapeutic tactics for the same acute stroke are aimed at a number of dynamic processes accompanying a stroke: reperfusion, neuroprotection, neurotrophy, recovery and prevention.

Neurotrophicity, neuroprotection, neuroplasticity and neurogenesis are fundamental biological processes that constantly occur in the nervous system.

Many different etiological factors cause common pathophysiological mechanisms that are capable of depressing these basic processes, which leads to the development of a variety of neurological diseases that occur acutely, chronically and extremely slowly.

Impairments of cognitive and associative functions in conditions of cerebral pathologies occur against the background of pronounced structural changes in brain tissue and due to inhibition of bioenergy processes, the development of glutamate excitotoxicity, hyperproduction of reactive oxygen species (ROS), decreased activity of antioxidant systems, and activation of apoptosis.

The trigger for ischemic neuronal death is energy deficiency, which initiates the glutamate-calcium cascade - the release of excitatory aminoacidergic neurotransmitters - aspartate and glutamate and the intracellular accumulation of Ca 2+ ions.

The concept of neuroprotection allows us to distinguish two main directions. Primary neuroprotection is aimed at interrupting the rapid mechanisms of necrotic cell death - reactions of the glutamate-calcium cascade (antagonists of NMDA and AMPA receptors and calcium channel blockers: remacemide, rilutek, borisol, nimotop, etc.)). Implementation primary neuroprotection extremely difficult, since it is selective in nature and it is necessary to determine which receptors are involved.

Secondary neuroprotection aimed at reducing the severity of long-term consequences of ischemia - blocking pro-inflammatory cytokines, cell adhesion molecules, inhibition of oxidative stress, normalization of neurometabolic processes, inhibition of apoptosis, reduction of cognitive deficit: antioxidants, antihypoxants, metabolitotropic drugs and nootropics (emoxipine, thiotriazoline, glycine, piracetam, thiocetam , citicoline, cerebrolysin, cortexin, cerebrocurin, etc.). And yet, nootropics have the greatest practical importance among the means of secondary neuroprotection.

By chemical nature, nootropic drugs are derivatives of various compounds of amino and hydroxy acids, plant extracts, neuropeptides, proteins.

1. Pyrrolidine-2 derivatives (cyclic GABA, racetam): piracetam, nebracetam, isacetam, nefiracetam, detiracetam, etiracetam, aniracetam, oxiracetam, pramiracetam, dipracetam, phenotropil, etc.

2. GABA (-aminobutyric acid): aminalone, gammalon, nicotinoyl-GABA (picamilon), phenibut (noofen).

3. GHB (-hydroxybutyric acid): sodium hydroxybutyrate, sodium oxybate.

4. HOPA (hopantenic acid): calcium homopantothenate, pantogam.

5. Vitamin B 6 (pyridoxine): pyritinol (encephabol), pyriditol, enerbol, pyrithioxine.

6. Aminoacetic acid: glycine.

7. Chlorophenoxyacetic acid: meclofenoxate, deanol.

8. Tryptamine (N-acetyl-5-ethoxytryptamine): melatonin (melaxen, melapur, melaton).

9. Neuropeptides and neurotrophic cerebroprotectors: cerebrocurin, cortexin, semax, vasopressin, cerebrolysin, solcoseryl, synacthen depot, cerebrolecithin, lipocerebrin.

10. Dipeptides: noopept (N-phenylacetyl-L-prolylglycine ethyl ester).

11. Vinca alkaloids: cavinton, vincapane.

12. Other herbs: extract of ginkgo biloba (EGb761), Schisandra chinensis, ginseng, memoplant, bilobil, ginkyo.

13. Combined: thiocetam, diapiram, binotropil, apik, olatropil, orocetam, fezam, yucalin.

I. Nootropic drugs with a dominant mnestic effect (cognitive enhancers), or true nootropics

1. Pyrrolidone nootropics (racetams), predominantly of metabolite action: piracetam, oxiracetam, aniracetam, pramiracetam, etiracetam, dipracetam, rolisiracetam, nebracetam, isacetam, nefiracetam, detiracetam, phenotropil, combined racetams (thiocetam, diapiram, olatropil, orocetam, fezam).

2. Cholinergic substances: increased synthesis of acetylcholine and its release (choline chloride, phosphatidylserine, lecithin, acetyl-L-carnitine, citicoline, aminopyridine derivatives, etc.); cholinergic receptor agonists (oxotremorine, bethanechol, spiropiperidines, quinonucleotides); acetylcholinesterase (AcCh) inhibitors (donepezil, physostigmine, tacrine, amiridine, ertastigmine, galantamine, metrifonate, velnacrine maleate, etc.).

3. Neuropeptides and neurotrophic cerebroprotectors: Semax, Ebiratide, Cerebrolysin, Cortexin, Cerebrocurin, Noopept.

4. Modulators of the glutamatergic system:

a) low-affinity antagonists of the polyamine site of NMDA receptors and partial agonists of AMPA receptors (memantine, ademol);

b) AMPA receptor agonists (nooglutil);

c) partial agonists of the AMPA receptor, as well as those that enhance the release of norepinephrine and dopamine (Ritalin, modafinil, donepezil);

d) NMDA receptor coagonists (glycine);

e) NMDA mimetics (glutamic acid, milacemide, D-cycloserine).

5. Dopamine receptor agonists - pronoran.

6. GABA receptor agonists - baclofen.

If nootropics, by their mechanism of action, are often a “key in a lock,” then neuroprotectors are drugs that indirectly improve the same functions as true nootropics. Today there are no protocol recommendations on how to use them together, but clarifying the etiology that led to a decrease in cognitive functions is the key to prescribing neuroprotectors.

II. Neuroprotectors

1. Activators of brain metabolism: mildronate, phosphatidylserine, hopantenic acid esters, xanthine derivatives of pentoxifylline, propentofylline, tetrahydroquinolines, etc.

2. Cerebral vasodilators: vincamine, vinpocetine, nicergoline, vinconate, vindebumol, etc.

3. Calcium antagonists: nimodipine, cinnarizine, flunarizine, etc.

4. Antioxidants: mexidol, troloxate, -tocopherol acetate, -tocopherol succinate, exiphon, tirilazad, meclofenoxate, atherovit, ebselen, thiotriazoline, emoxypine, cytoflavin, glutoxim.

5. Substances affecting the GABA system: aminalon (gammalon), pantogam, picamilon, phenibut (noofen), sodium hydroxybutyrate.

6. Substances of different groups: etimil, orotic acid, methyl glucoorotate, oxomethacyl, gutimin, ginseng, lemongrass and ginkgo biloba, Elton.

In the mechanism of action of nootropic drugs, two main links can be distinguished: neurotransmitter and metabolic. Each of the mechanisms occurs in both groups of drugs, but one of the mechanisms is dominant.

Neurotransmitter mechanisms include the effect of the drug on the GABA, choline, glutamate, dopamine or glycinergic systems. In this regard, the most promising drugs are agonists of the NMDA and AMPA subtypes of glutamine receptors and GABA receptor agonists (nooglutil, memantine, modafinil), which are superior in potency to classical racetams (piracetam, pramiracetam, aniracetam).

It has been established that piracetam, oxiracetam and aniracetam activate the AMPA type of glutamate receptors (the endogenous ligand is amino-3-hydroxy-5-methylisoxazole-4-propionate), but do not affect the NMDA receptors of neurons. This leads to an increase in the release of calcium from the cell, resulting in a decrease in the concentration of intracellular calcium. Pramiracetam increases the rate of sodium-dependent choline uptake in the hippocampus. Its effects on cognitive function may occur through acceleration of the flow of impulses from cholinergic neurons in the hippocampal septum.

Racetams are characterized by an effect on energy-supplying metabolic reactions in neurons and glia, which consists of increasing the formation of ATP in anaerobic and aerobic reactions of glucose oxidation. They accelerate the conversion of ADP to ATP and contribute to a faster restoration of ATP concentration.

In addition, they can create conditions to facilitate the flow of synaptic mediator mechanisms, activation of protein synthesis, in particular the memory protein S-100 and RNA.

Recently, the issue of using nootropics, the dominant mechanism of action of which is the activation of glutamine AMPA receptors (ampakines) - nooglutil, memantine, ademol, modafinil and Ritalin, has been discussed. Under the influence of depolarization, another surface protein, the NMDA receptor, also reacts to glutamate.

Among the true nootropics, there are also drugs that activate cholinergic transmission - citicoline (ceraxon) and donepezil. Citicoline, also known as cytidine-5"-diphosphocholine (CDP-choline), is a mononucleotide consisting of ribose, cytosine, pyrophosphate and choline. Citicoline serves as a choline donor in the biosynthesis of acetylcholine and increases its release in cholinergic nerve endings, improves attention, learning and memory.

A central acetylcholinesterase inhibitor that modulates dopamine and glutamine transmission in the brain, donepezil (Aricept) is currently approved in the United States as a treatment for arresting progressive memory loss in Alzheimer's disease and narcolepsy. The discovery of neurotrophic peptide factors prompted the formation of a new pharmacotherapy strategy—peptidergic, or neurotrophic, therapy for CNS diseases.

Neurotrophic cerebroprotectors (Cortexin, Cerebrocurin and Cerebrolysin) reduce transmitter dysfunction by increasing the affinity of GABA receptors and limiting the hyperexcitability of NMDA receptors. Neurotrophic cerebroprotectors (cerebrocurin and cortexin) increase the binding affinity of BDNF to its receptors.

Thiocetam has a pronounced antioxidant effect - a decrease in markers of oxidative and nitrosating stress (aldehyde phenylhydrazones, carboxylphenylhydrazones, nitrotyrosine) and markers of endothelial dysfunction - homocysteine ​​and endothelin-1 against the background of an increase in the content of reduced equivalents of the thiol-disulfide system in patients with chronic cerebrovascular accident.

A similar mechanism of action on the neuronal-glial complex by nootropics is described in isolated reports regarding cerebrovascular accidents in infants. An increase in homocysteine ​​and endothelin-1 was reliably detected in the blood serum, which confirmed endothelial dysfunction not only of cerebral vessels, but also of the heart and kidneys. It is known that the cleavage of endothelin by metalloproteinase leads to the formation of active endothelin ET (1-12), a powerful vasoconstrictor. The relationship between possible endothelial dysfunction and high levels of antithrombin-3 has also been confirmed, and the latter correlates with hyperhomocysteinemia. The administration of vitamins B6, B12 and folic acid reduces homocysteine ​​levels. Nasal Semax (deltalicin) eliminates neurological deficits.

Endothelin-1 itself is found in the pituitary gland, brain parenchyma, kidneys, thyroid gland, and placenta. As is known, this peptide interacts with glial receptors, myocytes and cardiomyocytes. The prescription of cytoprotectors in combination with drugs that reduce homocysteine ​​is pathogenetically justified.

The molecular cascades triggered by pathophysiological mechanisms are practically the same, despite the diversity of etiology and clinical manifestations. The result of all processes is cell death such as necrosis, apoptosis or anoikis. Timely and complex blocking of these cascades reduces neuronal losses and is the goal of neuroprotection.

Subtle and timely stimulation of the mechanisms of neuroplasticity and natural neurogenesis leads to structural and functional neurorepair, which is the key to rapid and successful clinical rehabilitation.

Today, neuroprotection and neuroplasticity are no longer just theoretical concepts or the focus of experimental attention.

The main goal of neuroprotection is to prevent the death of neurons in the penumbra zone. The main mechanisms of neuronal death in the penumbra zone are: glutamate excitotoxicity; perifocal depolarization; inflammation, reperfusion injury and programmed cell death.

After all, the core of ischemia is dead tissue, and the penumbra itself is “anabiosis” brain tissue that is located around the core. Treatment measures are aimed at it, since bioenergetic processes in the penumbra are slowed down and neurons that have not yet died remain in it. Selective drug and non-drug therapy (oxybarotherapy, singlet oxygen, hypothermia), affecting the penumbra, is the essence of neuroprotection.

One of the most effective areas for the use of not only neuroprotectors, but also neurotrophics is the synthesis of peptides with potential metal ligand properties.

Several universal methods of transmembrane delivery of drugs have been patented using vitamin B12, low molecular weight peptides and lipid nanoparticles, ensuring penetration through the intestinal wall of those drugs that, in the absence of these systems, are not adsorbed at all.

Carnosine is one of the low molecular weight peptides that has the ability to bind zinc and copper and transport them to the brain, especially when administered intranasally. Carnosine may also prevent neuronal apoptosis caused by neurotoxic concentrations of zinc and copper. In particular, a sufficient amount of carnosine is contained in elcar (carniel), stimol, neotone, which determines their secondary neurotrophism.

One potential route for administering neurotrophics is their convective delivery to peripheral nerves using microcannulas. The use of neuropeptides in the form of aromatic compositions and solutions for intranasal drip administration is being studied.

Until recently, all explanations for the effects of the drug were based on the content of amino acids in it as a specific nutritional substrate for the brain. Modern neurochemistry has proven that neuropeptides carry the main neurotrophic pharmacological load. The presence of a low molecular weight peptide fraction makes it relatively easy to overcome the blood-brain barrier (BBB) ​​and reach directly nerve cells under conditions of peripheral administration.

Modulation of microelement homeostasis can be one of the essential components of the neuroprotective effect of a number of drugs.

A priority direction of modern neuropharmacotherapy is the creation of new effective methods of drug delivery. Galantamine is a competitive and reversible selective cholinesterase inhibitor (50 times or more active against anticholinesterase drugs - AChE). In addition to its AChE inhibitory properties, galantamine acts as a modulator of nicotinic anticholine receptors.

Almer has a unique dual mechanism of action. This is a new drug for the treatment of lost cognitive functions, dementia, and has a dual mechanism of action in relation to the cholinergic system:

A. Increases the concentration of AcCh in the synaptic cleft due to reversible inhibition of the enzyme that destroys AcCh, acetylcholinesterase.

B. Changes the spatial structure of H-cholinergic receptors. Almer interacts with both presynaptic and postsynaptic H-cholinergic receptors.

In patients with dementia and psychospeech delay after 5 years, there is a decrease in other neurotransmitters (GABA, glutamate, serotonin), which can lead to serious consequences:

1. Decreased glutamate levels worsen learning and memory impairments.

2. A decrease in serotonin causes disturbances in the emotional sphere, such as depression and anxiety.

3. A decrease in GABA leads to instability of behavior - sexual disorders and aggression. Therefore, modulation of H-cholinergic receptors has effects not only on cognitive functions such as learning and memory, but also on the psychological and behavioral components of dementia.

4. Substances that enhance acetylcholine synthesis and its release: ceraxon (gliatilin), pramiracetam (pramistar), vasopressin, almer - a selective acetylcholinesterase inhibitor contains the active substance donepezil.

The main mechanism of action of Ceraxon, which determines its neuroprotective properties, is to ensure the safety of external and internal (cytoplasmic and mitochondrial) neuronal membranes, namely:

a) maintaining normal levels of cardiolipin (the main component of mitochondrial membranes) and sphingomyelin;

b) activation of phosphatidylcholine biosynthesis;

c) stimulation of glutathione synthesis and weakening of lipid peroxidation processes (antioxidant effect);

d) normalization of Na + /K + -ATPase activity.

Indications for use in children: psycho-speech-motor delay of various etiologies; hypoxic-ischemic encephalopathy (acute period) and its consequences; consequences of severe forms of neuroinfections and injuries (including apallic syndrome); syndromes of periventricular leukomalacia, subcortical necrosis, ischemia and hemorrhage in infants; correction of cognitive functions in children with epilepsy receiving anticonvulsants; progressive muscular dystrophy; demyelinating diseases (multiple sclerosis and polyneuropathies); consequences of toxic brain damage (poisoning).

Directions for use in children: infants - 1.0-2.0 ml 1 r/day orally; children under 3 years of age - 2.0-4.0 ml 2 times / day orally, 250 mg intravenously (i.m.). In adults, 500, 1000 or 2000 mg orally per day for up to 6 weeks (including acute stroke). Parenteral: 500-1000-2000 mg IV - up to 10 days.

Diseases of the nervous system and psyche in adults for which the use of Ceraxon is effective: all types of hemorrhagic and ischemic (8 subtypes) stroke; traumatic brain injuries; hereditary degenerative diseases; discirculatory (atherosclerotic, toxic and hypertensive) encephalopathy; Alzheimer's disease; multiple sclerosis (when recovering from an exacerbation); Guillain-Barré polyneuropathy in the subacute period; parkinsonism and Parkinson's disease; poisoning with carbon monoxide, methanol, alcohol, etc.; glaucoma, optic nerve atrophy; neuroAIDS (HIV encephalopathy, meningovascular neuroAIDS with stroke, multifocal polyneuropathy); amyotrophic lateral sclerosis; consequences of severe forms of neuroinfections (botulism, etc.).

Cerebrocurin is a domestic bionootropic, an active neuropeptide obtained from the brain of cattle embryos. The drug was first tested at the Donetsk Regional Children's Clinical Center for Neurorehabilitation (2001-2002). It is used for organic diseases of the nervous system in children and adults.

What unites seemingly different diseases, but similar therapeutic measures?

To a lesser extent, the material in the article is based on specific psychoneurological diseases, and to a greater extent on the final manifestation of the destructive process in the brain, which led to intellectual, speech and motor disorders. Examples of this:

1. Vascular pathology of the brain.

2. Demyelinating diseases of the nervous system.

3. Delayed mental development and speech.

4. Chronic pain syndromes (fibromyalgia).

5. Chronic fatigue syndrome.

6. Cerebrocardial and cardiocerebral syndromes.

Stages of the glutamate cascade in ischemic stroke:

1. Decreased cerebral blood flow.

2. Glutamate excitotoxicity.

3. Intracellular accumulation of calcium.

4. Activation of intracellular enzymes.

5. Increased nitric oxide synthesis and development of oxidative stress.

6. Gene expression.

7. Damage to the BBB, local inflammation, impaired microcirculation, depletion of cholinergic neuromediation.

8. Apoptosis - necrosis of neurons and glia.

In contrast to the negative effects of overstimulation of NMDA receptors, physiological processes at synaptic NMDA receptors promote neuronal survival.

Suppression of NMDA receptor activity in vivo causes widespread apoptosis in the developing central nervous system, intensifying neurodegenerative processes preceding the final death of the cell.

A key mechanism for survival is the phosphoinositide 3-kinase-Akt cascade (activated in many, but not all, types of neurons). This also applies to multiple sclerosis. It is axonal damage that is the basis for the formation of neurological deficits at the early stage of this disease. Axonal damage is diagnosed by a decrease in the synthesis of N-acetyl aspartate. This process is exacerbated by depression of cholinergic (acetylcholine) activation.

As a result of the inflammatory-degenerative process, “naked” axons become a target for long-term glutamate-mediated cytotoxicity, which first forms a motor and then a cognitive defect. Irreversible clinical symptoms in multiple sclerosis develop due to increasing excitotoxicity and depletion of cholinergic activity. Similar mechanisms of development of pathology are characteristic of other neurodegenerative diseases (amyotrophic lateral sclerosis, olivopontocerebellar degenerations, Strumpel's disease, adrenoleukodystrophy).

The evidence obtained explains the more subtle mechanisms of damage to neuronal-glial complexes. This allows for timely correction of emerging pathology using pharmacological agents.

Prescribing neuroprotectors is advisable for the following diseases:

Children:

1. Consequences of hypoxic-ischemic postnatal encephalopathy with psycho-speechmotor delay.

2. Motor alalia and decreased cognitive functions.

3. Mental retardation (F71.0).

4. Consequences of apallic syndrome without frequent epileptic seizures.

5. Stroke in children and their consequences.

6. Cerebral palsy (F70.0).

7. Enuresis (dysontogenetic)

8. Guillain-Barre syndrome.

Adults:

1. Acute period and consequences of strokes with hemiparesis, aphasia, mnestic disorders.

2. Binswanger's disease (periventricular leukoaraiosis and leukomalacia due to hypertension) without critical blood pressure values.

3. Vascular (atherosclerotic) dementia.

4. Atherosclerotic discirculatory encephalopathy caused by stenosis of the great vessels (memory impairment, statics, etc.).

5. Multiple sclerosis - 4-5 points according to EDDS with tetraparesis, ataxia, depression and increasing dementia.

6. Amyotrophic lateral sclerosis.

7. Creutzfeldt-Jakob disease.

8. Parkinsonism + atrophic tetraparesis + dementia.

9. Primary neuroAIDS (HIV encephalopathy, sensorimotor polyneuropathy, neurovascular cerebral syndrome).

10. Chronic fatigue syndrome (as a manifestation of confirmed persistent herpes infection type HVS-6) with depression.

11. Chronic generalized fibromyalgia with myofascial pain syndrome and depression.

12. Vegetovascular dystonia, migraine, neurocirculatory dystonia.

Yet future restoration of lost or reduced neuronal and glial function depends on the use of neurotrophic agents and stimulation of postnatal neurogenesis. Neuroplasticity is the process of remodeling synaptic connections aimed at optimizing the functioning of neuronal networks. It plays a decisive role in the processes of phylogenesis and ontogenesis (in the establishment of new synaptic connections that arise during learning), as well as in maintaining the functioning of already formed neuronal networks - primary (natural) neuroplasticity after damage to the structures of the nervous system, during the restoration of lost functions - post-traumatic or post-stroke neuroplasticity.

The most significant result of the last period of development of neurobiology was the discovery of neuronal stem cells (NSCs), which provide homeostatic, adaptive regeneration of neurons in the central nervous system. NSCs are concentrated in two neurogenic zones - in the lateral walls of the lateral ventricles (subventricular zone) and in the dentate gyrus of the hippocampus (subgranular zone). In addition, new neurons can arise from other poorly differentiated cells of several types scattered throughout different parts of the central nervous system.

Neurogenesis in the brain of adult mammals is an intensive process that leads to the renewal of the population of interneurons in such brain regions as the olfactory bulbs and the hippocampus. Achievements in regenerative neurobiology have made it possible to begin the development of fundamentally new technologies for the treatment of diseases and injuries of the brain and spinal cord, based on stimulating the processes of reparative regeneration of neurons, creating conditions for the regeneration of nerve and glial cells, the growth of nerve fibers and the development of technologies aimed at blocking factors that inhibit the above processes.

But reparative neurogenesis can be enhanced by the administration of drugs, cytokines or growth factors, as well as through rehabilitation measures or cell transplantation.

New directions in clinical neuropharmacology are promoting the development of neuroprotection. In terms of the neuroprotective effect, substances with potential effects on different parts of the ischemic cascade are being studied: beta-interferon, magnesium preparations, iron chelates (DFO, desferal, a new iron chelator code-named DP-b99), AMPA receptor antagonists (zonanpanel), serotonin agonists (repinontan, piclozotan), membrane modulators (ceraxon), lithium preparations, selenium (ebselen).

A new target for neuroprotection is the impact on the chain of reactions dependent on the activity of superoxide dismutase. The drug phosphatidylinositol 3-kinase (PI3-K)/Akt (protein kinase B) targets neuronal survival.

Calcium antagonists and magnesium ions block slow calcium channels and reduce the proportion of patients with adverse outcomes and neurological deficits due to hemorrhagic stroke in the middle cerebral artery caused by ruptured aneurysms and dissection of pre- or intracerebral vessels.

Thus, using subtle psychological tests to study cortical function, it is possible to calculate the nootropic or neurotrophic that the patient needs.

And yet, the main thing in the choice of these funds is the professionalism and clinical thinking of the doctor. The search for the causes of the disease takes a long time, but it is necessary, since the end result is adequate and acceptable treatment for the patient!

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To correct metabolic disorders in diseases of the retina and optic nerve, drugs belonging to various groups are used. V. N. Alekseev and E. A. Egorov (2001) distinguish direct neuroprotectors: enzyme antioxidant - superoxide dismutase, selective adrenergic blocker with calcium channel blocker properties - betaxolol [INN], peptide bioregulators (cymedins) - retinalamin, cortexin, epithalon [INN]. Indirect neuroprotective effects have non-enzymatic antioxidants- emoxipine and histochrome, vitamins, antihypoxants - cytochrome C, synthetic analogue of ACTH - Semax [INN]. Features of the use of some drugs that have a neuroprotective effect were described in previous sections. This section will describe the pharmacological properties of neuropeptides.

Peptide bioregulators(cymedins) are substances of a polypeptide nature obtained from various organs and tissues of the body (brain, hypothalamus, bone marrow, spleen, lymph nodes, blood vessels, lungs, liver, thymus, retina and others).

Pharmacodynamics: cymedins have the ability to induce specific differentiation processes in the population of cells that are the starting material for their production.

Cymedines are obtained from various tissues using the acid extraction method followed by purification from ballast substances. According to their chemical structure, they are alkaline polypeptides with a molecular weight from 1000 to 10,000 Da.

In humans and animals, regulatory polypeptides are located on the cell surface and are part of cell membranes. They are absent from the nuclear, mitochondrial and lysosomal fractions. As a result of the physiological destruction of membranes, they appear in the intercellular spaces and have a gambling effect.

The biological effects of cytomedins are carried out through specific receptors located on the cell surface.

After exogenous administration of polypeptides, the effect of a peptide cascade develops, as a result of which, even after complete removal of exogenous polypeptides from the body, their biological effect is preserved.

Cytomedins affect cellular and humoral immunity, the state of the homeostasis system, lipid peroxidation and other protective reactions of the body.

The following cymedines are used in ophthalmology:

• Cortexin is a complex of peptides isolated from the cerebral cortex of cattle and pigs;
• Retinalamine is a complex of peptides isolated from the retina of cattle.

Cortexin has a triple effect on nervous tissue, regulates the metabolism of neurotransmitters and peroxidation in the cerebral cortex, optic nerve and retinal neurons.

Retinalamine reduces destructive changes in the retinal pigment epithelium in various forms of degeneration, modulates the activity of cellular elements of the retina, improves the efficiency of the functional interaction of the pigment epithelium and the outer segments of photoreceptors, stimulates the fibrinolytic activity of the blood, has an immunomodulatory effect (the expression of receptors on T- and B-lymphocytes increases, phagocytic activity of neutrophils).

Pharmacokinetics: There are no data on ocular pharmacokinetics.

Indications for use: Cortexin is used to treat patients with chorioretinal dystrophies and optic nerve atrophies of various origins.

Retinalamine is used in the treatment of the following conditions:

• diabetic retinopathy;
• retinal pigment abiotrophy;
• involutional central chorioretinal dystrophies;
• thrombosis of the central vascular system and its branches;
• in complex therapy of eyeball injuries;
• in complex therapy of glaucoma.

Contraindications: individual intolerance to the components of the drug, pregnancy.

If necessary, use during lactation should stop breastfeeding.

Side effects: allergic reactions, moderate pain at the injection site.

Directions for use and doses: retinalamin is administered parabulbarly or intramuscularly at 0.5-1.0 ml daily or every other day. The course of treatment is 5-10 injections. The course of treatment is repeated after 3-6 months.

Cortexin is injected into the sub-Tenon's space 1 ml once.

The drugs are produced in the form of lyophilized powders in bottles. Before use, the powder is diluted in 1 ml of physiological solution.

Drugs

• Cortexin (Geropharm LLC, Russia) - lyophilized powder in 10 mg bottles;
• Retinalamin (Retinalamin) (Geropharm LLC, Russia) lyophilized powder in bottles. Each bottle contains 5 mg of active substance and 17 mg of glycine.

Semax - a synthetic analogue of corticotropin (ACTH).

Pharmacodynamics: nootropic agent. The drug improves energy processes and increases adaptation capabilities, increasing resistance to damage and hypoxia of nervous tissue, including the brain.

Pharmacokinetics: when instilled into the nose, the drug is well absorbed into the vessels of the mucous membrane. About 60-70% of the administered dose enters the systemic circulation.

Indications for use: optic nerve atrophy of various etiologies.

Contraindications: individual intolerance to the components of the drug, acute mental disorders accompanied by anxiety, pregnancy, lactation, endocrine diseases.

There are no data on the safety of use in pediatrics.

Side effects: not identified.

Directions for use and doses: Semake is used intranasally. One drop contains 50 mcg of active substance. A single dose is 200-2000 mcg (at the rate of 3-30 mcg/kg). Usually 2-3 drops of the drug are injected into each nostril. The course of treatment is 5-14 days.

In addition, the drug can be administered in the form of endonasal electrophoresis. In this case, the drug is administered from the anode once a day. The dose of the drug is 400-600 mcg/day.

A drug

• Semax (Company Institute of Molecular Genetics RAI. Russia) - 0.1% solution in 3 ml bottles.

… significantly improve the prognosis and outcomes of ischemic stroke.

Neuroprotectors(syn. cerebroprotectors) are drugs that stop and limit damage to brain tissue that develops as a result of acute ischemia (hypoxia).

Neuroprotective therapy is most effective when the following basic principles are observed::

№ 1 - prescription of neuroprotective drugs, the effectiveness of which has been proven as a result of large RCTs (randomized controlled trials) or fundamental meta-analyses of a large number of RCTs;

№ 2 - the earliest possible prescription of neuroprotective drugs - within the first hours after the development of ischemic stroke;

№ 3 - ensuring an optimal level of cerebral blood flow, ensuring the “transport” of the neuroprotector to the infarction zone and adjacent brain compartments, to a certain extent compensating for the emerging neurological deficit (to normalize cerebral blood flow, sometimes the administration of neuroprotectors is combined with simultaneous or long-term reperfusion therapy).

Neuroprotectors that meet the criterion specified in paragraph No. 1(list of basic principles of neuroprotective therapy) - are neuroprotectors (1) first class (“class” means “level of evidence” according to the generally accepted gradation of neuroprotectors accepted in world practice).

Unlike neuroprotectors (1) of the first class, neuroprotectors:

(2) second class the level of evidence of their effectiveness corresponds to at least “one well-designed RCT”;

(3) third class the level of evidence of their effectiveness corresponds to “observation of a few patients”;

(4) fourth grade the level of evidence of their effectiveness corresponds to “opinions, expert assessments, single clinical observations of authoritative researchers.”

First class neuroprotectors (1), registered in Russia:

Cerebrolysin(26 RCTs) - hydrolyzate of the brain of young pigs, containing 85% amino acids and 15% peptides; the molecular weight of the peptides that make up this drug does not exceed 10,000 Daltons, which ensures rapid penetration of Cerebrolysin through the blood-brain barrier (BBB), active inclusion in the correction of metabolic disorders of brain neurons, and also eliminates the possibility of anaphylactic reactions in response to the administration of the drug; the optimal daily intravenous dosage of Cerebrolysin for moderate ischemic stroke is 10 ml, for severe ischemic stroke - 20 ml intravenously, the administration of Cerebrolysin in daily dosages of 30 and 50 ml does not increase the clinical effect;

Gliatilin(choline alfoscerate) - a centrally acting cholinomimetic, contains 49.5% choline, which can penetrate the BBB and be released in the brain; participates in the synthesis and maintenance of the physiological level of acetylcholine (one of the main mediators of nervous excitation), activates the structures of the reticular formation, ensures plasticity, density and survival of neurons, and also improves regional blood flow, causes a quickly manifested awakening effect (after the development of severe ischemic stroke); regimen for prescribing gliatilin for moderate ischemic stroke: during the first 5 days. IV 1 g in the morning and evening, and subsequently orally, depending on body weight, 400–1200 mg (1–3 capsules) per day: first dose in the morning 1–2 capsules, daily dose 1 capsule; for severe forms of ischemic stroke, accompanied by a sharp depression of consciousness and disruption of vital functions - 1 g IV 4 times a day; The duration of administration is determined by the clinical effect.

Cortexin– a domestic preparation containing a complex of left-handed amino acids and polypeptides with a molecular weight from 1 to 10 kDa and a balanced vitamin and mineral composition, extracted from the cerebral cortex of calves (pigs), has an organ-specific effect, and freely penetrates the BBB; regulates the ratio of inhibitory and excitatory amino acids, the level of serotonin and dopamine, has antioxidant activity, reduces the content of antibodies to total myelin protein and helps normalize the bioelectrical activity of the brain; Prescription regimen: IV 20 mg/day. within 10 days;

Citicoline- a natural metabolite of processes in the body, which is not a foreign chemical compound, like most drugs, consists of two biologically active substances - natural metabolites cytidine and choline, which are normally present in all cells of the body and stabilize neuromediation and neurometabolic function; the leading mechanism of the neuroprotective activity of the drug is the interruption of the leading links of the “ischemic cascade” and the preservation of the penumbra, that is, the blockade of the main mechanism of cell death and the formation of neurological deficit; The optimal dose of Cytocoline orally is 2000 mg/day.

Semax– a neuropeptide with a pronounced nootropic effect; increases the adaptive capabilities of the brain, increases its resistance to stress damage, hypoxia and ischemia, and has a pronounced antioxidant, antihypoxic, angioprotective and neurotrophic effect. When administered intranasally, Semax (12–18 mg/day) after 4 minutes. penetrates the BBB. The therapeutic effect with a single injection lasts 20–24 hours;

Glycine- amino acid, a natural brain metabolite, has a positive effect on the functional state of specialized (motor and sensory) systems and nonspecific brain structures and thereby significantly prevents or minimizes the formation of neurological deficits; in addition, glycine creates certain conditions for the implementation of the reperfusion phenomenon; The results of RCTs, by comparison with data in placebo control groups, established that for ischemic stroke in the carotid system, sublingual administration of Glycine (1–2 g/day) significantly reduces the incidence of deaths and significantly improves functional outcomes. In contrast, in ischemic stroke in the vertebrobasilar region, Glycine does not affect the incidence of deaths, but accelerates the regression of neurological deficit;

Emoxipin- has a broad antihypoxic effect; according to the results of 2 extensive RCTs, a significantly more rapid and complete regression of the extensive neurological deficit observed in severe forms of ischemic stroke, in particular, caused by extensive thrombosis of the internal carotid artery, was achieved;

Ebselen- a broad-spectrum antioxidant, it has been proven that oral administration of the drug (150–300 mg) during the first 12–18 hours after the development of ischemic stroke significantly, in a short period of time, sharply reduces the severity of neurological deficit and limits the volume of the infarction zone detected during repeated MRI.