Neurox

Neurox®

Intramuscularly (IM) or intravenously (IV) (stream or drip). When administered by infusion, the drug should be diluted in 0.9% sodium chloride solution.

Neurox® is injected slowly over 5-7 minutes, drip-wise at a rate of 40-60 drops per minute. The maximum daily dose should not exceed 1200 mg.

For acute cerebrovascular accidents

Neurox® is used in complex therapy in the first 10-14 days - 200-500 mg IV drip 2-4 times a day, then - 200-250 mg IM 2-3 times a day for 2 weeks.

For traumatic brain injury and consequences of traumatic brain injury

Neurox® is used for 10-15 days intravenously at a dose of 200-500 mg 2-4 times a day.

For dyscirculatory encephalopathy in the decompensation phase

Neurox® should be administered intravenously in a stream or drip at a dose of 200-500 mg 1-2 times a day for 14 days. Then - IM 100-250 mg/day over the next 2 weeks.

For course prophylaxis of dyscirculatory encephalopathy

Neurox® is administered intramuscularly at a dose of 200-250 mg 2 times a day for 10-14 days.

For neurocirculatory dystonia, neurotic and neurosis-like conditions

the drug is administered intramuscularly at 50-400 mg per day for 14 days.

For mild cognitive impairment

in elderly patients and
for anxiety disorders,
the drug is used intramuscularly at a dose of 100-300 mg per day for 14-30 days.

In acute myocardial infarction

as part of complex therapy, Neurox® is administered intravenously or intramuscularly for 14 days, against the background of traditional therapy for myocardial infarction (including nitrates, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, thrombolytics, anticoagulant and antiplatelet drugs, as well as symptomatic means according to indications).

In the first 5 days, to achieve maximum effect, Neurox® is administered intravenously; in the next 9 days, the drug can be administered intramuscularly.

Intravenous administration of the drug is carried out by drip infusion slowly (to avoid side effects) for 30-90 minutes (in 100-150 ml of 0.9% sodium chloride solution or 5% dextrose (glucose) solution), if necessary, a slow jet infusion is possible /in the administration of the drug, lasting at least 5 minutes.

The drug is administered (IV or IM) 3 times a day, every 8 hours. The daily dose is 6-9 mg/kg body weight, a single dose is 2-3 mg/kg body weight. The maximum daily dose should not exceed 800 mg, single dose - 250 mg.

For open-angle glaucoma

at various stages as part of complex therapy Neurox® is administered intramuscularly at 100-300 mg/day, 1-3 times a day for 14 days.

For alcohol withdrawal syndrome

Neurox® is administered intramuscularly or intravenously in a dose of 200-500 mg 2-3 times a day for 5-7 days.

In case of acute intoxication with antipsychotic drugs

the drug is administered intravenously at a dose of 200-500 mg/day for 7-14 days.

In case of acute purulent-inflammatory processes of the abdominal cavity (acute necrotizing pancreatitis, peritonitis), Neurox® is prescribed on the first day both in the preoperative and postoperative periods. The administered doses depend on the form and severity of the disease, the prevalence of the process, and variants of the clinical course. The drug should be discontinued gradually only after a stable positive clinical and laboratory effect.

For acute edematous (interstitial) pancreatitis, Neurox® is prescribed 200-500 mg 3 times a day, intravenously (in 0.9% sodium chloride solution) and intramuscularly. Mild severity of necrotizing pancreatitis - 100-200 mg 3 times a day by drip (in 0.9% sodium chloride solution) and intramuscularly. Moderate severity

- 200 mg 3 times a day, intravenously (in 0.9% sodium chloride solution).
Severe course
- in a pulse dosage of 800 mg on the first day, with a double dose regimen;
then 200-500 mg 2 times a day with a gradual reduction in the daily dose. Extremely severe course
- at an initial dosage of 800 mg/day until the manifestations of pancreatogenic shock are persistently relieved, after stabilization of the condition, 300-500 mg 2 times a day intravenously (in 0.9% sodium chloride solution) with a gradual decrease in the daily dosage.

Antioxidant drug. Ethylmethylhydroxypyridine succinate (EMHPS) is an inhibitor of free radical processes, a membrane protector with antihypoxic, stress-protective, nootropic, anticonvulsant and anxiolytic effects. Belongs to the class of 3-hydroxypyridines. The mechanism of action is due to antioxidant and membrane protective properties. Suppresses lipid peroxidation, increases superoxide oxidase activity, increases the lipid-protein ratio, improves the structure and function of the cell membrane. Modulates the activity of membrane-bound enzymes and receptor complexes, which promotes their binding to ligands, preservation of the structural and functional organization of biomembranes, transport of neurotransmitters and improvement of synaptic transmission. Increases the concentration of dopamine in the brain. It enhances the compensatory activation of aerobic glycolysis and reduces the degree of inhibition of oxidative processes in the Krebs cycle under hypoxic conditions with an increase in adenosine triphosphoric acid and creatine phosphate, and activates the energy-synthesizing function of mitochondria.

Increases the body's resistance to the effects of various damaging factors in pathological conditions (shock, hypoxia and ischemia, cerebrovascular accidents, intoxication with ethanol and antipsychotic drugs). Improves metabolism and blood supply to the brain, microcirculation and rheological properties of blood, reduces platelet aggregation. Stabilizes the membranes of blood cells (erythrocytes and platelets), reducing the likelihood of hemolysis. It has a lipid-lowering effect, reduces the content of total cholesterol and LDL. Normalizes metabolic processes in the ischemic myocardium, reduces the necrosis zone, restores and/or improves the electrical activity and contractility of the myocardium, and also increases coronary blood flow in the ischemic zone, increases the antianginal activity of nitro drugs, reduces the consequences of reperfusion syndrome in acute coronary insufficiency.

The stress-protective effect is manifested in the normalization of post-stress behavior, somatovegetative disorders, restoration of sleep-wake cycles, impaired learning and memory processes, and reduction of dystrophic changes in various brain structures.

EMGPS has a pronounced antitoxic effect during withdrawal syndrome, eliminates neurological and neurotoxic manifestations of acute alcohol intoxication, and corrects behavioral and cognitive disorders. Under the influence of ethylmethylhydroxypyridine succinate, the effect of tranquilizing, neuroleptic, antidepressant, hypnotics and anticonvulsants is enhanced, which makes it possible to reduce their doses and reduce side effects.

Pharmacokinetics

Suction

When administered intramuscularly, the drug is detected in the blood plasma for 4 hours after administration. With intramuscular administration, Tmax in plasma is 0.3-0.58 hours. With intramuscular administration at a dose of 400-500 mg, Cmax in plasma is 2.5-4 mcg/ml.

Distribution

EMHPS quickly passes from the bloodstream into organs and tissues and is quickly eliminated from the body. The average retention time of the drug in the body with intramuscular administration is 0.7-1.3 hours.

Metabolism and excretion

Metabolized in the liver by glucuronidation.

It is rapidly excreted in the urine, mainly in the form of metabolites (50% in 12 hours) and in small quantities unchanged (0.3% in 12 hours). The most intensive elimination occurs during the first 4 hours after taking the drug. Urinary excretion rates of unchanged drug and metabolites have significant individual variability.

Neurox TB p/o 125 mg N 30

Dosage form:

Round, biconvex tablets, white film-coated. On a cross section, the kernel is white or white with a yellowish tint.

Compound:

For one tablet:

Active ingredient: ethylmethylhydroxypyridine succinate - 125 mg.

Excipients: lactose monohydrate, microcrystalline cellulose 102, potato starch, povidone-K90, croscarmellose sodium, magnesium stearate.

Film shell: Opadry II white 85F48105 (polyvinyl alcohol, macrogol, talc, titanium dioxide).

Pharmacotherapeutic group

antioxidant agent

Storage temperature

2℃ to 25℃

Special conditions:

Impact on the ability to drive vehicles and other mechanisms:

During the treatment period, care must be taken when driving vehicles and engaging in other potentially hazardous activities that require increased concentration and speed of psychomotor reactions.

Drug interactions:

Neurox® is combined with all drugs used to treat somatic diseases.

Enhances the effect of benzodiazepine drugs, antidepressants, anxiolytics, anticonvulsants and antiparkinsonian drugs.

Reduces the toxic effects of ethyl alcohol.

Pharmacodynamics:

Ethylmethylhydroxypyridine succinate is an inhibitor of free radical processes, a membrane protector with antihypoxic, stress-protective, nootropic, anticonvulsant and anxiolytic effects.

Ethylmethylhydroxypyridine succinate increases the body's resistance to various damaging factors (shock, hypoxia and ischemia, cerebrovascular accidents, intoxication with alcohol and antipsychotics (neuroleptics)).

The mechanism of action of ethylmethylhydroxypyridine succinate is due to its antioxidant, antihypoxic and membrane protective effects. It inhibits lipid peroxidation, increases the activity of superoxide dismutase, increases the lipid-protein ratio, reduces membrane viscosity, and increases its fluidity. Ethylmethylhydroxypyridine succinate modulates the activity of membrane-bound enzymes (calcium independent phosphodiesterase, adenylate cyclase, acetylcholinesterase), receptor complexes (benzodiazepine, gamma-aminobutyric acid, acetylcholine), which enhances their ability to bind to ligands, helps preserve the structural and functional organization of biomembranes, neurotransmitter transport and improve synaptic transmission . Ethylmethylhydroxypyridine succinate increases dopamine levels in the brain. Causes an increase in compensatory activation of aerobic glycolysis and a decrease in the degree of inhibition of oxidative processes in the Krebs cycle under hypoxic conditions with an increase in the content of adenosine triphosphate and creatine phosphate, activation of the energy-synthesizing functions of mitochondria, stabilization of cell membranes.

Improves metabolism and blood supply to the brain, improves microcirculation and rheological properties of blood, reduces platelet aggregation. Stabilizes the membrane structures of blood cells (erythrocytes and platelets) during hemolysis.

It has a lipid-lowering effect, reduces the content of total cholesterol and low-density lipoproteins.

The anti-stress effect is manifested in the normalization of post-stress behavior, somatovegetative disorders, restoration of sleep-wake cycles, impaired learning and memory processes, reduction of dystrophic and morphological changes in various structures of the brain.

Ethylmethylhydroxypyridine succinate has a pronounced antitoxic effect in withdrawal symptoms. Eliminates neurological and neurotoxic manifestations of acute alcohol intoxication, restores behavioral disorders, autonomic functions, and is also able to relieve cognitive impairment caused by long-term use of ethanol and its withdrawal.

Under the influence of ethylmethylhydroxypyridine succinate, the effect of tranquilizing, neuroleptic, antidepressant, hypnotics and anticonvulsants is enhanced, which makes it possible to reduce their doses and reduce side effects.

Ethylmethylhydroxypyridine succinate improves the functional state of ischemic myocardium. In conditions of coronary insufficiency, it increases collateral blood supply to the ischemic myocardium, helps maintain the integrity of cardiomyocytes and maintain their functional activity. Effectively restores myocardial contractility in reversible cardiac dysfunction.

Pharmacokinetics:

Rapidly absorbed when taken orally.

The maximum concentration at doses of 400-500 mg is 3.5-4.0 mcg/ml. Quickly distributed in organs and tissues. The average retention time of the drug in the body when taken orally is 4.9-5.2 hours.

Metabolized in the liver by glucuron conjugation. 5 metabolites have been identified: 3-hydroxypyridine phosphate - formed in the liver and, with the participation of alkaline phosphatase, breaks down into phosphoric acid and 3-hydroxypyridine; 2nd metabolite - pharmacologically active, formed in large quantities and found in urine 1-2 days after administration; 3rd - excreted in large quantities in the urine; 4th and 5th - glucuron conjugates.

T1/2 when taken orally - 2.0-2.6 hours. It is quickly excreted in the urine, mainly in the form of metabolites and in small quantities - unchanged. The most intensive elimination occurs during the first 4 hours after taking the drug. Rates of urinary excretion of unchanged drug and metabolites have individual variability.

Indications:

— Consequences of acute cerebrovascular accidents, including after transient ischemic attacks, in the subcompensation phase as preventive courses;

- mild traumatic brain injury, consequences of traumatic brain injury;

— encephalopathies of various origins (dyscirculatory, dysmetabolic, post-traumatic, mixed);

— vegetative dystonia syndrome;

— mild cognitive disorders of atherosclerotic origin;

- anxiety disorders in neurotic and neurosis-like conditions;

— coronary heart disease as part of complex therapy;

— relief of withdrawal syndrome in alcoholism with a predominance of neurosis-like and vegetative-vascular disorders, post-withdrawal disorders;

— conditions after acute intoxication with antipsychotic drugs;

— asthenic conditions, as well as for the prevention of the development of somatic diseases under the influence of extreme factors and stress;

— exposure to extreme (stress) factors.

Contraindications:

Acute liver and/or renal failure, increased individual sensitivity to the drug.

Due to insufficient knowledge of the effect of the drug - childhood, pregnancy, breastfeeding.

Lactose intolerance, lactase deficiency and glucose-galactose malabsorption syndrome.

Pregnancy and lactation:

The drug is contraindicated during pregnancy and breastfeeding due to insufficient data on the effectiveness and safety of the drug during these periods.

Overdose:

In case of overdose, drowsiness may develop.

Due to low toxicity, overdose is unlikely.

Treatment, as a rule, is not required - the symptoms disappear on their own within 24 hours. In case of severe manifestations, supportive and symptomatic treatment is carried out.

Side effects:

Individual adverse reactions may occur: dyspeptic or dyspeptic in nature, allergic reactions.

Neurox, 125 mg, film-coated tablets, 30 pcs.

Ethylmethylhydroxypyridine succinate is an inhibitor of free radical processes, a membrane protector with antihypoxic, stress-protective, nootropic, anticonvulsant and anxiolytic effects.

It has a lipid-lowering effect, reduces the content of total cholesterol and low-density lipoproteins.

Neurox solution for intravenous and intramuscular administration 50 mg/ml 2 ml ampoules 10 pcs. in Moscow

Ethylmethylhydroxypyridine succinate (EMHPS) is an inhibitor of free radical processes, a membrane protector with antihypoxic, stress-protective, nootropic, anticonvulsant and anxiolytic effects. Belongs to the class of 3-hydroxypyridines. The mechanism of action is due to antioxidant and membrane protective properties. Suppresses lipid peroxidation, increases superoxide dismutase activity, increases the lipid-protein ratio, improves the structure and function of the cell membrane.

Modulates the activity of membrane-bound enzymes and receptor complexes, which promotes their binding to ligands, preservation of the structural and functional organization of biomembranes and transport of neurotransmitters, and improvement of synaptic transmission. Increases the concentration of dopamine in the brain. It enhances the compensatory activation of aerobic glycolysis and reduces the degree of inhibition of oxidative processes in the Krebs cycle under hypoxic conditions with an increase in the level of ADP and creatine phosphate, and activates the energy-synthesizing function of mitochondria.

Increases the body's resistance to the effects of various damaging factors in pathological conditions (shock, hypoxia and ischemia, cerebrovascular accident, intoxication with ethanol and antipsychotic drugs). Improves metabolism and blood supply to the brain, microcirculation and rheological properties of blood, reduces platelet aggregation. Stabilizes the membranes of blood cells (erythrocytes and platelets), reducing the likelihood of hemolysis. It has a lipid-lowering effect, reduces the content of total cholesterol and LDL.

Normalizes metabolic processes in the ischemic myocardium, reduces the necrosis zone, restores and/or improves the electrical activity and contractility of the myocardium, and also increases coronary blood flow in the ischemic zone, increases the antianginal activity of nitro drugs, reduces the consequences of reperfusion syndrome in acute coronary insufficiency.

The stress-protective effect is manifested in the normalization of post-stress behavior, somatovegetative disorders, restoration of sleep-wake cycles, impaired learning and memory processes, and a reduction in dystrophic changes in various brain structures.

EMGPS has a pronounced antitoxic effect during withdrawal syndrome, eliminates neurological and neurotoxic manifestations of acute alcohol intoxication, and corrects behavioral and cognitive disorders. Under the influence of EMGPS, the effect of tranquilizing, neuroleptic, antidepressant, hypnotics and anticonvulsants is enhanced, which makes it possible to reduce their doses and reduce side effects.

Possibility of using Neurox in the complex treatment of chronic cerebral ischemia

For many years, these diseases have been the leading cause of mortality in many economically developed countries, including Russia, and they account for up to 60% of total mortality [1]. Of all the individual risk factors for cardiovascular complications, the most powerful influence on life expectancy is arterial hypertension (AH), which is closely associated with various types of cerebral strokes (hemorrhagic, ischemic). In Russia, the incidence of stroke and mortality from it remain among the highest in the world; More than 400 thousand are registered annually, the mortality rate in which during the first month of the disease reaches 35% [2]. When determining the degree of risk of developing vascular complications, in addition to hypertension, risk factors such as cerebral atherosclerosis, smoking, alcohol consumption, atrial fibrillation, chronic heart failure, obesity, dyslipidemia, and stress are also taken into account, which, when acted simultaneously, enhance each other’s influence [3] . Preventing the development and progression of cerebral vascular disorders, as well as improving the quality of life of patients suffering from them, are among the key tasks of neurology. The most common cause of this pathology is hypertension, and if we take into account its complications, primarily myocardial infarction and stroke, then we can talk about this disease as one of the most significant for the adult population. The share of strokes in the structure of overall mortality is 21.4%, second to mortality from coronary heart disease, and disability after a stroke reaches 3.2 per 10 thousand population, ranking 1st among all causes of disability. However, disorders of cerebral hemodynamics can have not only an acute catastrophic, but also a chronic course. In this case, the so-called discirculatory encephalopathy (DE) gradually forms. Chronic cerebrovascular insufficiency (CCF) is the most common cerebrovascular pathology and is also one of the most common diseases leading to disability. Its most significant causes are considered to be atherosclerosis, hypertension and their combinations, diabetes mellitus, various diseases, including systemic ones, accompanied by vascular damage, blood diseases leading to an increase in its viscosity [Gusev E.I.]. Some authors distinguish the stages of CCI: initial manifestations of cerebrovascular insufficiency (CPF) and DE itself [Schmidt E.V., Maksudov G.A., 1971]. NPNMK are characterized by an intermittent feeling of heaviness in the head, sometimes short-term dizziness, and a feeling of instability when walking. The following symptoms are also pathognomonic: fatigue, decreased memory, speed of thinking, periodic headache, noise in the head, sleep disorders. Increasing manifestations of CNMC lead to the development of the next stage of CNMC – DE. Encephalopathy is a diffuse, multifocal lesion of the brain, in which, due to various factors (except for infectious and inflammatory processes in the brain), there are not only subjective complaints of headache, fatigue, depression of cognitive functions, etc., but also objective signs of multifocal or diffuse organic pathology of the brain, which are detected during a neurological and neuropsychological examination of the patient. DE is caused by chronic cerebral circulatory insufficiency, which causes diffuse changes in brain tissue and diffuse neurological microsymptoms, often in combination with emotional lability and a decrease in intellectual and mental functions. DE usually develops against the background of general vascular pathology. The symptoms of DE are formed as a result of disruption of connections between the cortex and subcortical structures (the “disconnection” phenomenon), which is caused by diffuse changes in the white matter of the brain, cortex, and basal ganglia [2]. DE is heterogeneous. Usually the following variants are distinguished: 1) atherosclerotic encephalopathy; 2) hypertensive DE; 3) venous; 4) mixed forms. Based on the severity of the clinical picture of DE, there are 3 stages of its development. With DE I, the ability to work is usually preserved, with DE II it is reduced to one degree or another, and in stage III, the patient is, as a rule, disabled. Among all DE, atherosclerotic discirculatory encephalopathy is the most common. According to the WHO definition, “atherosclerosis is a variable combination of changes in the inner lining (intima) of the arteries, including accumulation of lipids, complex carbohydrates, fibrous tissue, blood components, calcification and associated changes in the middle lining (media). Stage I of its development is characterized by mild cognitive impairment, which can be compensated for by initially high intelligence and stable professional skills. According to the figurative expression of Academician L.O. Badalyan, “brain lipids burn in the flame of thought.” In stage II, performance gradually decreases, bradypsychia occurs, and personal changes are possible - resentment, selfishness, narrowing of the circle of interests. In the neurological status, elements of akinetic-rigid syndrome are often observed. The ability to work is reduced, and usually these patients are disabled people of group III or II. In stage III of the development of atherosclerotic DE, there is a gradual worsening of the changes characteristic of DE II. Cognitive impairment reaches the level of moderate or severe dementia, there are significant diffuse focal neurological symptoms, manifestations of pyramidal insufficiency, extrapyramidal pathology, cerebellar disorders, pseudobulbar symptoms. Characterized by a decrease in criticism of one’s condition, loss of self-care opportunities; patients need outside care. This stage corresponds to disability group II, and then group I. Among the various manifestations of atherosclerotic DE, pollakihypnia (drowsiness after eating) and the so-called Winscheid triad are characteristic: a combination of headache, dizziness and memory disorders. In stage III of atherosclerotic DE, the appearance of a pseudo-Alzheimer's form of atherosclerosis of cerebral vessels, known as Hackebusch-Geyer-Heimanovich disease (described by domestic psychoneurologists in 1912), is possible. Dementia, accompanied by severe memory impairment, the appearance of confabulations, uncriticality, disorders of gnosis and praxis. Dystrophic processes in this form are most pronounced in the left temporo-parietal region. Chronic hypertensive encephalopathy (CHE) is a form of DE caused by various types of hypertension. The term “hypertensive encephalopathy” was proposed in 1928 by German neurologists BS Oppenheimer and AV Fishberg. The onset of the disease is usually 30–50 years. It is characterized by changes in cerebral vessels caused by hypertension. Changes in the brain matter take the form of small foci of destruction of various nature and duration. CGE also has 3 stages of development, the obligatory criterion for diagnosing hypertensive DE is hypertension (BP above 180/90 mm Hg) for 5–10 years; in this case, there must be other signs of hypertension: hypertensive retinal angiopathy, myocardial hypertrophy, etc. V.A. Karlov et al. (1987) believe that one of the leading factors in the pathogenesis of DE in patients with hypertension is total and uniform stagnation of blood in the venous system of the head; general phlebopathy is possible. The early stages of CGE are characterized by transient disorders in the form of occipital headache, neurosis-like syndrome, and noise in the head. Then bilateral pyramidal disorders, tremor, and manifestations of akinetic-rigid syndrome are possible. Over time, personality disorders, cowardice, and loss of former interests may arise. Loss of self-care skills and loss of control of pelvic functions develops. With CGE, more often than with atherosclerotic HE, disinhibition and a tendency to affective reactions are possible. It should be noted that in stage III CGE patients also have severe atherosclerosis, and the developed DE bears the features of atherosclerotic encephalopathy, in particular increasing manifestations of dementia. Some authors [V.A. Karlov et al., 1987] believe that it is more correct to talk about DE in patients with hypertension. One of the variants of DE, which has a mixed genesis (hypertension + atherosclerosis), but more often develops as a consequence of CGE, is Binswanger encephalopathy. This form is characterized by dysfunction of the perforating vessels of the brain and the development of multiple lacunar formations in the white matter of the cerebral hemispheres. In 1962, G. Olszewski proposed calling Binswanger encephalopathy subcortical atherosclerotic encephalopathy. The clinical picture is dominated by memory impairment and motor disorders of the subcortical type. Although patients with this form of DE are usually aware of the loss of their previous level of intellectual capabilities, the phenomena of dementia progress. CT scans usually reveal multiple lacunar lesions, which are low-density areas in the white matter of the brain, especially in the paraventricular areas. Venous encephalopathy usually occurs in patients with various forms of cardiac and cardiopulmonary pathology, arterial hypotension. Characteristic features include a dull, diffuse headache, aggravated by physical activity, non-systemic dizziness, fatigue, sleep disturbances, and signs of small-focal brain damage. Nausea, vomiting, and signs of intracranial hypertension are possible. The treatment strategy for chronic cerebrovascular insufficiency involves influencing the main pathological process, the basic links of which are hypertension and atherosclerosis. An adequate combination of antihypertensive drugs with diuretics, statins, adrenergic blockers, antioxidants, tranquilizers, and antidepressants leads in most cases to encouraging results. Also, reconstructive vascular surgery for stenotic processes of the brachiocephalic arteries usually gives a positive effect. In addition, at present, the concept of “quality of life” has also firmly entered our everyday life, suggesting, in addition to physical longevity, also intellectual longevity. Therapeutic measures for CNM should be aimed at improving cerebral hemodynamics and increasing the functional capabilities of the brain. Recently, more and more attention has been paid to the study of free radical oxidation processes in health and disease. Being strong oxidizing agents, free radicals can cause irreversible changes in the structure of proteins and nucleic acids. With intensive formation of free radicals and insufficiency of the antioxidant system, oxidative stress occurs, which is the cause of numerous pathologies. The participation of free radical oxidation in the development of diseases such as atherosclerosis, coronary heart and brain disease, cerebral stroke, and dyscirculatory encephalopathy is most widely covered. In this regard, it seems important to search for new directions of influence on various parts of the pathogenesis of ischemic brain damage, as well as expand the understanding of the mechanisms of action of already known drugs [4]. Over the past decades, pharmaceutical companies have offered a large number of new drugs for the treatment of vascular diseases of the central nervous system and the correction of related disorders. Leading Russian scientific institutions have developed ethylmethylhydroxypyridine succinate. The drug, being a structural analogue of vitamin B6, has in its pharmacological formula a metabolite of the tricarboxylic acid cycle - succinate, which provides much more powerful antioxidant and antihypoxic properties compared to other antioxidant drugs, which has a positive effect on the main links in the pathogenesis of diseases associated with free radical processes. oxidation and oxygen-dependent pathological conditions. In addition, its chemical formula and mechanism of action account for extremely few side effects. The Russian company produces this drug under the name Neurox. It is multifunctional: it acts as an antioxidant, and on the other hand, due to the presence of succinic acid in its formula, it exhibits antihypoxic properties, improving energy metabolism in the cell. The transformation of succinic acid in the body is associated with energy production. Combining all the positive effects on metabolic processes and blood supply to the brain, Neurox also deserves attention due to its good tolerability, as well as a minimum of contraindications and side effects. It also has antiatherogenic, nootropic, GABA-protective effects. The feasibility of using the drug in the complex treatment of stroke and other diseases of the nervous system, in which there is an increase in the rate of lipid peroxidation, hypoxia, and cerebral metabolic disorders, has been proven. Thanks to the multifactorial mechanism of action, the pharmacological effects of the drug are realized at three levels - neuronal, vascular and metabolic. At the same time, it: • actively reacts with peroxide radicals of proteins and lipids; • has a modulating effect on some membrane-bound enzymes (phosphodiesterase, adenylate cyclase), ion channels; • has a hypolipidemic effect, reduces the level of peroxide modification of lipoproteins, reduces the viscosity of the lipid layer of cell membranes; • blocks the synthesis of some prostaglandins, thromboxane and leukotrienes; • optimizes the energy-synthesizing functions of mitochondria under hypoxic conditions, improves synaptic transmission; • optimizes the rheological properties of blood, suppresses platelet aggregation. Thus, Neurox improves the energy metabolism of the cell, activates the energy-synthesizing functions of mitochondria, affects the content of biogenic amines and improves synaptic transmission. Due to the presence of a succinate molecule in its composition, the drug affects the functioning of the respiratory chain, increasing its efficiency, inhibits free radical oxidation of membrane lipids by binding their peroxide radicals, and increases the activity of antioxidant enzymes responsible for the formation and consumption of reactive oxygen species, in particular superoxide dismutase. The anti-stress effect of the drug is expressed in the normalization of post-stress behavior, somato-vegetative indicators, restoration of sleep-wake cycles, as well as impaired learning and memory processes, reduction of dystrophic, morphological changes that occur after stress in various brain structures. Neurox has a geroprotective effect; has a clear corrective effect on learning and memory processes impaired during aging, improving the process of recording, storing and reproducing information; helps restore emotional and vegetative status; reduces manifestations of neurological deficits; reduces the levels of aging markers in the brain and blood - lipofuscin, malonaldehyde, cholesterol. The mechanism of the geroprotective effect of the drug is associated with its antioxidant properties, the ability to inhibit lipid peroxidation processes, direct membranotropic effect, the ability to restore ultrastructural changes in the granular endoplasmic reticulum and mitochondria, and modulate the functioning of receptors [5]. Its nootropic properties are expressed in the ability to improve learning and memory processes, and counteract the fading of acquired skills and reflexes [6,7]. The drug modulates receptor complexes of brain membranes, in particular benzodiazepine, GABAergic, and acetylcholine receptors. Neurox has an antiepileptic effect, influencing both primary generalized seizures caused primarily by the administration of GABAergic substances, and the epileptiform activity of the brain with a chronic epileptogenic focus [Badalyan O.L., 1998]. It has an antiatherogenic effect: it reduces hyperlipidemia, prevents the activation of lipid peroxidation, increases the activity of the antioxidant system, inhibits local vascular mechanisms of atherogenesis, and reduces the risk of developing pathological changes in the vascular wall. Neurox reduces the content of atherogenic lipoproteins and triglycerides, increases the level of high-density lipoproteins in the blood serum. In addition, it suppresses platelet aggregation and stabilizes biological membranes, in particular, the membranes of erythrocytes and platelets, inhibits the synthesis of thromboxane A, leukotrienes and enhances the synthesis of prostacyclin. The drug is capable of having a pronounced potentiating effect on the effects of neuropsychotropic drugs. Under its influence, the effect of tranquilizing, neuroleptic, hypnotic, anticonvulsant and analgesic drugs is enhanced, which makes it possible to reduce their doses and thus reduce side effects. The neurox turned out to be highly effective in acute cerebrovascular disorders, DE, vegeto -vascular dystonia, atherosclerotic disorders of the brain function and in other conditions accompanied by hypoxia of tissues [8]. Both the preventive and therapeutic effect of the drug in these diseases are shown [9]. So, its exchange rate at a dose of 300-400 mg/day. Parectarenly in patients DE on the background of hypertension and atherosclerosis had a pronounced positive effect. With DE in the phase of decompensation, neurox should be prescribed in a/in jet or drop at a dose of 100 mg 2-3 times/day. within 14 days. Then - in/m for 100 mg/day. over the next 2 weeks. For course prevention of discirculatory encephalopathy, the drug is administered in/m at a dose of 100 mg 2 times/day. For 10-14 days. The tolerance of the drug is good, which allows you to recommend neurox into the basic therapy of patients with hypertension with signs of chronic cerebrovascular insufficiency. Literature 1. Shevchenko O.P., Yakhno N.N. et al. Arterial hypertension and cerebral stroke. M., 2001. 2. Parfenov V.A. Secondary prevention of ischemic stroke as an unresolved problem // Remedium. 2006. No. 7. 3. Stampfer M, Ridker R. Risk Factor Criteria. Circulation 2004; 109: IV3 - IV5. 4. Smirnova I.N., Fedorova T.N., Tanashyan M.M. al. Clinical efficiency and antioxidant activity of Mexidol in chronic cerebrovascular diseases // Atmosphere. Nervous diseases. 2006. No. 1. P. 33–36. 5. Dumaev K.M., Voronina T.A., Smirnov L.D. Antioxidants in the prevention and treatment of pathologies of the central nervous system. M., 1995. 6. Voronina Ta. Pressent - Day Problems in Experimental Psychopharmacology of Nootropic Drugs. Harwood, 1992. Vol. 2. R. 51–108. 7. Voronina Ta. Nootropic Drugs in Alzheimer Disease Treatment. New Pharmacological Strategies. ALZHEIMER Disease: Therapeutic Strategies. Eds. Giacobini E, Becker R. Birkhauser; Boston, 1994. P. 265–269. 8. Nikiforov A.S., Konovalov A.N., Gusev E.I. // Clinical neurology. Medicine, 2002. 9. Smirnov L.D. Antioxidants of the heteroamatic series. Structure, activity, copper -zin application / collection. Theses of the 2nd Congress of Ross. scientific total pharmacologists. M., 2003. C. 171. 10. Suslina Z.A., Smirnova I.N., Fedorova T.N. et al. Assessment of the pharmacological effects of antioxidant of Mexidol in patients with vascular diseases of the brain / collection. Theses of the 2nd Congress of ROSC. scientific total pharmacologists. M., 2003. C. 209. 11. Lutskiy M.A., Nazarenko E.A., Razinkin K.A. The use of domestic antioxidant - the drug Mexidol in the complex treatment of ischemic stroke // Russ. honey. magazine. 2008. T. 16. 12. Yanishevsky S.N. The experience of using the drug Mexidol in the treatment of chronic cerebrovascular accident in patients with stenosis -oxing damage to the main brachycephalous vessels // Bull. let's experiment biol. honey. 2006. Appendix 1. 13. Voronina T.A., Smirnov L.D., Gorenova I.I. The mechanism of action and justification of the use of the drug Mexidol in neurology / mat. scientific and practical. conf. in neurology. M., 2000. S. 18. 14. Kraneva V.A. Features and mechanism of neuroprotective action of the drug Mexidol with a hemorarragic stroke in the experiment // Bull. let's experiment biol. honey. 2006. Appendix 1. 15. Seredenin S.B. The problem of individual sensitivity in pharmacology / Proceedings 7 Ross. national Congress "Man and Medicine". M., 2000. S. 96–124.

Modern experience in the use of anticholinesterase drugs in neurology

Anticholinesterase drugs are used in neurological practice to activate regeneration and reinnervation processes in diseases of the peripheral and central nervous system.

For many years, the drug “Prozerin” has been widely used in medical practice, which has a pronounced effect on peripheral cholinergic synapses.

At the end of the 80s. In the 20th century, the drug “Amiridin” with a combined anticholinesterase effect was synthesized. Since 2002, the drug has been produced under the trade name Neuromidin.

The pharmacological effects of anticholinesterase drugs lead to increased action of acetylcholine. The choice of a drug from the group of anticholinesterase drugs is determined by its pharmacological properties, duration of action, activity, ability to penetrate tissue barriers, as well as side effects.

Proserin - N-(meta-dimethylcarbamoyloxyphenyl)-trimethylammonium methyl sulfate has strong reversible anticholinesterase activity. The basis of its mechanism of action is the inhibition of acetylcholinesterase, an enzyme that hydrolyzes the mediator acetylcholine, which is accompanied by a slowdown in the rate of its destruction, accumulation and enhancement of action in the area of cholinergic synapses with restoration of neuromuscular conduction.

Due to the presence of a quaternary ammonium group in the Proserin molecule, the drug poorly penetrates the blood-brain barrier and mainly affects peripheral cholinergic structures.

A significant difference between Neuromidin (ipidacrine) and Proserin is the ability of Neuromidin to block the potassium permeability of the membrane, which leads to an extension of the repolarization phase of its action potential and an increase in the activity of the presynaptic axon. This process is accompanied by an increase in the entry of calcium ions into the presynaptic terminal and, as a consequence, an increase in the release of the transmitter acetylcholine into the synaptic cleft in all synapses, contributing to increased stimulation of the postsynaptic cell.

In addition, Neuromidin has the effect of reversible inhibition of cholinesterase in cholinergic synapses, which further increases the accumulation of the neurotransmitter in the synaptic cleft and, accordingly, enhances the functional activity of the postsynaptic cell. However, the inhibition of the action of acetylcholinesterase in Neuromidin is less pronounced compared to Proserin.

Thus, Neuromidin stimulates the presynaptic nerve fiber, increases the release of the neurotransmitter into the synaptic cleft, reduces the destruction of the neurotransmitter acetylcholine by the enzyme, increases the activity of the postsynaptic cell by direct membrane and mediated mediator effects, that is, it acts on all parts of the conduction of excitation, in contrast to Proserin, which reduces metabolism mediator only at cholinergic synapses.

The M-cholinomimetic effects of Proserin and Neuromidin are similar, however, the activity of the effect on M-cholinergic receptors is higher in Proserin.

Neuromidin has the following pharmacological effects: restores and stimulates neuromuscular transmission, conducts impulses in the peripheral nervous system, disturbed due to the influence of various factors. Neuromidin increases muscle contractile activity under the influence of acetylcholine and other mediators: adrenaline, serotonin, histamine and oxytocin, having a direct effect on myofibrils, while Prozerin does not have this property.

Neuromidin, unlike Proserin, stimulates the conduction of nerve impulses not only in the neuromuscular synapse, but also in the central nervous system, which explains the positive effect of this drug on mnestic processes.

Attention should be paid to the extremely important, although moderately pronounced property of Neuromidin - the ability to block sodium permeability of the membrane. This effect is associated with its sedative and analgesic properties. In addition, the drug has an antiarrhythmic effect.

Prozerin and Neuromidin are metabolized in the liver and are excreted mainly through renal mechanisms. 50% of Proserin and 3.7% of Neuromidin are released unchanged, which indicates the accelerated metabolism of Neuromidin. The initial effect from the administration of Proserin is observed, on average, after 10–15 minutes, and from the administration of Neuromidin - after 15–20 minutes. The duration of action of Neuromidin is 3–5 hours, which is associated with a long-term blockade of potassium permeability of the membrane, and Prozerin ends its effect 2–3 hours after its administration.

Prozerin, as a result of its effect on H-cholinergic receptors, leads to a significant increase in the force of contraction of skeletal muscles and is therefore indicated for use primarily in patients with myasthenia and myasthenic crisis. The drug is also used in neurological practice for paralysis, paresis that occurs after mechanical injuries, residual effects of meningitis, polio, encephalitis and neuropathies.

Due to its muscarinic-like effects, Prozerin is used to eliminate postoperative atony of the intestines and bladder, occasionally with weakness of labor, and sometimes in ophthalmological practice with open-angle glaucoma.

Due to the fact that Prozerin facilitates the transmission of excitation in the autonomic ganglia, it is indicated for poisoning with ganglion blockers. In addition, Prozerin is effective in case of overdose of muscle relaxants with antidepolarizing action (muscle weakness, respiratory depression).

Indications for the use of Neuromidin are broader, since it is based on a biologically beneficial combination of two molecular effects (blockade of potassium permeability of the membrane and inhibition of cholinesterase) and it stimulates structural formations of the central nervous system. These are not only lesions of the peripheral nervous system: neuropathies, polyneuropathy, myelopolyradiculoneuritis, myasthenia gravis and myasthenic syndrome, multiple sclerosis and other forms of demyelinating diseases of the nervous system (in complex therapy), but also bulbar palsies and paresis with organic lesions of the central nervous system in the recovery period, as well as impairments of memory, attention, motivation and initiative of various origins, disorientation, emotional lability in senile dementia, Alzheimer's disease and other forms of late-life dementia, encephalopathy of traumatic, vascular and other origins, accompanied not only by memory impairment, but also by motor functions.

Neuromidin, like Proserin, is used for intestinal atony and intoxication with anticholinergic drugs.

A comparison of the clinical effect of Neuromidin and Proserin in myasthenia gravis showed that Proserin is significantly superior to Neuromidin in its anticholinesterase action. It is possible to achieve complete compensation of movement disorders in patients with myasthenia gravis only by using Proserin. However, its use is limited by a large number of side effects.

At the same time, the effectiveness of Neuromidin in the complex treatment of patients with myasthenia and myasthenic syndromes was noted, since it complements the action of Proserin. Both drugs improve the transmission of excitation at the neuromuscular synapse, and although Neuromidin is weaker in anticholesterase activity, it has a longer duration of action.

Neuromidin leads to a decrease in myasthenic crises, a faster onset and increase in the duration of remissions, an increase in muscle contractile activity, and an improvement in the general condition of patients.

According to the Russian Myasthenic Center, Neuromidin demonstrated maximum effectiveness in patients with Lambert-Eaton myasthenic syndrome, in contrast to Proserin, while a relative decrease in the severity of autonomic-trophic disorders was noted.

And yet, a reliable differential diagnostic test in the diagnosis of acute conditions in myasthenia gravis, namely myasthenic and cholinergic crises, is the administration of Proserin. A test with Proserin in a myasthenic crisis is positive and manifests itself in an increase in muscle strength or its complete restoration, and in a cholinergic crisis it is negative.

Clinical studies have shown the advantages of Neuromidin compared to Proserin in the complex treatment of facial nerve neuropathy, traumatic neuropathies and plexopathies. Treatment with Neuromidin can be started at the onset of the disease, and Proserin is prescribed 10 days later, taking into account the risk of post-paralytic contracture. Restoration of muscle function occurs faster when using Neuromidin. A clear positive effect was achieved in 89.5% of patients with damage to the facial muscles, in 80% of patients with traumatic neuropathies and plexopathies. Complete restoration of lost limb function was recorded in 40% of patients. Moreover, the activation of reinnervation of patients is confirmed by the positive dynamics of electromyography (EMG) indicators. It should be emphasized that there were no signs of contracture of the limbs or facial muscles in any of the observed patients. Despite the late administration of Proserin, several patients still experienced the appearance of pathological synkinesis on days 16–22 of the disease.

Neuromidin in the treatment of patients with demyelinating diseases of the nervous system (multiple sclerosis, amyotrophic lateral sclerosis) demonstrated a positive effect in the early stages of the disease in 40% of patients. Of course, the therapeutic effect of Neuromidin is less pronounced, but it is longer than that of Proserin. Under the influence of Neuromidin, the conduction of excitation in the spinal cord and peripheral nervous system is restored, which is manifested by a decrease in the severity of paresis and paralysis, sensitivity disorders, and an increase in strength in the affected muscle groups.

Effective treatment of sensory symptoms, regardless of the pathogenesis of peripheral nerve damage, is due to the blocking of ion channels of the axolemma and neuronal membranes, mainly potassium and partially sodium, which distinguishes Neuromidin from Proserin.

The analgesic effect of Neuromidin, which blocks ion channels, is achieved by inhibiting ectopic discharges and ephaptic transmission of excitation in the damaged nerve, in regenerating axonal branches as a result of collateral sprouting, as well as reducing the excitability of central neurons.

Neuromidin is part of a group of drugs used as a pathogenetic treatment of diabetic chronic distal symmetric sensorimotor polyneuropathy. The pathogenetic mechanisms of diabetic polyneuropathy lead to the progressive loss of myelinated fibers, as a result of which the conduction of the nerve impulse slows down, and in the “new” synapses newly formed as a result of regenerative sprouting, neuromuscular transmission is not effective. A study of Neuromidin in the treatment of diabetic polyneuropathy demonstrated a decrease in the severity of sensory symptoms, especially paresthesia, cramps, shooting pain, confirmed by EMG results (increased amplitude of the M-response).

Neuromidin, unlike Proserin, which does not actually penetrate the blood-brain barrier, has the ability to stimulate structural formations of the central nervous system, in particular cognitive processes.

Cognitive disorders are the leading clinical manifestations of chronic cerebrovascular insufficiency. There is an opinion that mnestic disorders are associated with central cholinergic deficiency, and the glutamate excitotoxicity that occurs in this case is secondary.

In older people, both the presynaptic and postsynaptic components of the central cholinergic synapses located in the cerebral cortex and hippocampus are impaired, resulting in decreased acetylcholine release and reduced sensitivity to it in old age.

After a course of Neuromidin in patients with progressive vascular leukoencephalopathy, short-term memory improved, manifestations of asthenic syndrome decreased, and cognitive function indicators improved.

In patients with senile dementia of the Alzheimer's type and multi-infarct dementia who received Neuromidin, a decrease in behavioral disorders, improvement in cognitive functions, speech and social adaptation were detected.

An independent factor in cognitive impairment and the development of dementia is diabetes mellitus. Conducted clinical studies allow us to consider Neuromidin as a first-line drug for the treatment of patients with diabetes mellitus with moderate cognitive impairment and dementia.

In patients with the consequences of moderate or mild cerebral stroke, during treatment with Neuromidin, physical activity, intellectual functions, and memory capacity increased. During the recovery period of moderate ischemic stroke, patients experienced a significant decrease in the degree of paresis of the limbs without an increase in muscle tone, bulbar paralysis and paresis, regression of sensory disorders, and vegetative-trophic disorders. In 70–80% of patients with vascular and other organic lesions of the brain in the acute and long-term periods, there was a rapid regression of impairments in memory, attention, praxis, unsteadiness when walking, a decrease in asthenic phenomena, improved sleep, and an increase in the patient’s intellectual capabilities and performance. Almost all patients with aphasia showed improvement in speech functions.

Both drugs are produced in tablet form (Prozerin 15 mg, Neuromidin 20 mg) and ampoule form 1 ml (Prozerin 0.05%, 0.5% solution is used in ophthalmic practice, Neuromidin 1.5% and 0.5% solution ). Prozerin is also available in powder and granule form (for children). It is used orally and subcutaneously. For adults, Proserin is prescribed orally 30 minutes before meals in powders or tablets 10–15 mg 2–3 times a day, 0.5 mg (1 ml of 0.05% solution) is administered subcutaneously 1–2 times a day, into the eyes 1-2 drops of 0.5% solution 1-4 times a day.

With the development of myasthenic crisis in adults, Proserin is administered intravenously - 0.5–1 ml of a 0.05% solution, then subcutaneously in a dose of 1.5–2.5 ml, depending on the patient’s weight. Treatment of myasthenia gravis with Proserin is carried out for a long time. For other diseases, the course of treatment lasts 25–30 days; if necessary, it is repeated after a 3-4 week break.

Neuromidin is used orally, regardless of food intake, subcutaneously and intramuscularly. For lesions of the peripheral nervous system - 20 mg 2-3 times a day for 30-40 days. Courses of treatment are repeated with a break of 1–2 months. For acute neuritis, use 10–20 mg per day for 10–15 days; for chronic neuropathies, the duration of treatment is increased to 20–30 days. If necessary, courses are repeated 2-3 times with an interval of 2-4 weeks until maximum effect is achieved.

For myasthenia gravis, myasthenic syndromes, and demyelinating lesions of the nervous system, the dose of Neuromidin can be increased to 20–40 mg 5–6 times a day. The maximum daily dose is 180–200 mg. Relief of myasthenic crisis - 5-15 mg 1-2 times a day subcutaneously or intramuscularly.

The greatest effect for stimulating cognitive processes was obtained when using medium (50–60 mg/day) and high doses (80–120 mg/day) of Neuromidin.

For Alzheimer's disease and other forms of dementia, individual selection of the Neuromidin dosage regimen is required. The maximum daily dose can reach 200 mg; The duration of the course of therapy is from 4 months to 1 year. If it is necessary to use high doses, it is advisable to use 4-5 times a day with an interval of 2-3 hours.

In the recovery period of mild to moderate ischemic stroke, use a 1.5% solution of Neuromidin intramuscularly for 14 days, 1 ml per day.

For traumatic brain injury, Neuromidin is prescribed from 40 mg to 120–160 mg per day. The course of treatment is 30–40 days, 4 times a year with an interval of a month.

For the treatment and prevention of intestinal atony - 15–20 mg 2–3 times a day for 1–2 weeks.

Contraindications to the use of Proserin and Neuromidin are: hypersensitivity, epilepsy, extrapyramidal disorders with hyperkinesis, bronchial asthma, angina pectoris, severe bradycardia, pregnancy and lactation.

The number of contraindications and side effects for Proserin is greater compared to Neuromidin, which is associated with its strong anticholinesterase activity. Prozerin should not be used in cases of severe atherosclerosis, organic diseases of the heart and blood vessels, thyrotoxicosis, peptic ulcer of the stomach and duodenum, peritonitis, inflammatory processes in the abdominal cavity, mechanical obstruction of the gastrointestinal tract and urinary tract, prostate adenoma, period of acute illness, intoxication.

Caution should be exercised when using Neuromidin in patients with diseases of the cardiovascular system, thyrotoxicosis, and gastric ulcers, however, these conditions are not contraindications to its use.

When using Proserin, hypersalivation, profuse sweating, spastic contractions and increased intestinal motility, nausea, vomiting, flatulence, diarrhea, and frequent urination may occur. In addition, headache, dizziness, weakness, loss of consciousness, drowsiness, miosis, visual disturbances, arthralgia, allergic reactions including anaphylaxis may develop. From the cardiovascular system: slow heart rate, arrhythmias, AV block, nonspecific changes on the ECG, decreased blood pressure, cardiac arrest. From the respiratory system: shortness of breath, bronchospasm, respiratory depression to the point of stopping. Due to nicotine-like effects, Prozerin can cause tremors, spasms and twitching of skeletal muscles, including fasciculations of the tongue muscles, dysarthria, and convulsions.

To relieve side effects, reduce the dose of Proserin or stop taking it, and, if necessary, administer anticholinergic drugs.

When parenterally administering large doses of Prozerin, preliminary or simultaneous administration of atropine is necessary to neutralize the side effects of muscarinic. For developed convulsions, Sibazon is used.

Neuromidin, in comparison with Proserin, is well tolerated, side effects occur rarely, are mild and, as a rule, do not require discontinuation of the drug, due to weak anticholesterase activity and rapid elimination, which prevents accumulation and the occurrence of side effects.

In addition, when taking Neuromidin, unlike Proserin, there are no side effects caused by the effect on N-cholinergic synapses - fasciculations, cramps. Side effects of Neuromidin are associated with activation of M-cholinergic synapses. These are mainly dyspeptic symptoms (nausea, increased peristalsis, increased stool frequency without diarrhea), which regress on their own and do not require cessation of treatment.

The appearance of other side effects, such as dizziness, hypersalivation and bradycardia, skin allergic reactions, requires dose adjustment or a short 1-2-day break in treatment.

To prevent side effects, it is necessary to titrate the drug to a therapeutic dose so that the body adapts to increased cholinergic activity.

Due to the fact that Neuromidin can have a sedative effect, during treatment it is necessary to refrain from engaging in potentially hazardous activities that require increased concentration, including driving. During treatment, you should avoid taking ethanol, as adverse side effects may increase.

Neuromidin and proserin, despite the general anticholinesterase effect, are drugs with heterogeneous pharmacological properties, which determines their range of use. Due to its high anticholinesterase activity, Prozerin has a number of significant side effects and remains the drug of choice for myasthenia gravis, myasthenic crises and demyelinating diseases. Neuromidin has a wider spectrum of pharmacological activity, including a stimulating effect on the structural formations of the central nervous system, therefore it is successfully used both in the treatment of diseases of the peripheral nervous system and organic lesions of the central nervous system. The undoubted advantage is its good tolerability and the absence of pronounced side effects, which allows its long-term use in elderly patients suffering from numerous concomitant diseases.

For questions regarding literature, please contact the editor.

Z. A. Suslina , Doctor of Medical Sciences, Professor, Academician of the Russian Academy of Medical Sciences M. N. Sharov , Doctor of Medical Sciences, Professor O. A. Stepanchenko , Candidate of Medical Sciences MGMSU , Moscow