Buy Neuromidin solution intravenously and intramuscularly 5mg/ml 1ml No. 10 in pharmacies

The cholinesterase inhibitor Neuromidin is produced in tablets and in parenteral solution based on ipidacrine. The drug has a stimulating effect on the conduction of impulses along the fibers of the nervous system, its interneuronal and peripheral parts. The pharmacy market today provides a large selection of Neuromidin analogues, both in terms of active substance and therapeutic effect.

Neuromidin is used in the treatment of the following pathologies of the peripheral central nervous system:

• neuritis and polyneuritis;
• polyneuropathy of various etiologies;
• myelopolyradiculoneuritis;
• paresis and paralysis;
• myasthenia gravis;
• disturbance of blood microcirculation in parts of the brain;
• memory loss and delayed intellectual development in a child.

Neuromidin is also prescribed as part of combination therapy for multiple sclerosis and in the treatment of head and brain injuries, to stimulate the birth process in pregnant women.

Neuromidin is not used for:

• allergies to the medicinal composition;
• abnormal heart rhythm, angina pectoris;
• epileptic seizures;
• asthma;
• disturbances in the functioning of the vestibular apparatus;
• erosive and ulcerative processes in the gastrointestinal tract.

It is prohibited to use Neuromidin in the form of a solution in the treatment of children under 18 years of age, women with breastfeeding and pregnancy.

In the treatment of polyneuropathy and mononeuropathy of various etiologies, paralysis, paresis, the drug is administered subcutaneously at a dose of 5-15 mg once or twice a day. Myasthenia gravis – parenterally (under the skin) 1-3 times a day, with a single dosage of 5-30 mg. Therapy for multiple sclerosis – 1 tablet up to 5 times a day.

Side effects:

• dyspepsia;
• headache and dizziness;
• bronchospasms;
• disturbance of heart rhythm and blood pressure fluctuations;
• skin allergies - itching, rash, urticaria.

Nosological classification (ICD-10)

• F09 Organic or symptomatic mental disorder, unspecified
• G12.2 Motor neuron disease
• G37.9 Demyelinating disease of the central nervous system, unspecified
• G58 Other mononeuropathies
• G61 Inflammatory polyneuropathy
• G62 Other polyneuropathies
• G62.9 Polyneuropathy, unspecified
• G70 Myasthenia gravis and other neuromuscular junction disorders
• G92 Toxic encephalopathy
• G96.8 Other specified disorders of the central nervous system
• G96.9 Damage to the central nervous system, unspecified
• K59.8.0* Intestinal atony
• M79.2 Neuralgia and neuritis, unspecified

Compound

Axamon

Aksamon is a cheap analogue (synonym) of Neuromidin produced in Russia, which contains the same active substance (ipidacrine). Prescribed for neuritis, Alzheimer's disease, myasthenia gravis, central nervous system lesions and intestinal arrhythmia. The list of contraindications and side effects is the same.

Aksamon is produced in the following forms:

• pills;
• solution for intramuscular and subcutaneous administration (in ampoules);
• substance-powder.

The approximate price for this analogue is 596 – 1089 rubles.

Advantages are price and variety of dosage forms, disadvantage is a greater number of possible side effects.

Pharmacodynamics

Neuromidin® has a direct stimulating effect on the conduction of impulses along nerve fibers, interneuronal and neuromuscular synapses of the central nervous system and the peripheral nervous system. The pharmacological action of Neuromidin® is based on a combination of two mechanisms of action: blockade of potassium channels in the membrane of neurons and muscle cells; reversible inhibition of cholinesterase at synapses.

Neuromidin® enhances the effect on smooth muscles of not only acetylcholine, but also adrenaline, serotonin, histamine and oxytocin.

Neuromidin® has the following pharmacological effects:

– improves and stimulates impulse conduction in the nervous system and neuromuscular transmission;

- enhances the contractility of smooth muscle organs under the influence of agonists of acetylcholine, adrenaline, serotonin, histamine and oxytocin receptors, with the exception of potassium chloride;

- improves memory, inhibits the progressive course of dementia.

In preclinical studies, Neuromidin® did not have teratogenic, embryotoxic, mutagenic, carcinogenic or immunotoxic effects, and did not affect the endocrine system.

Pharmacokinetics

After oral administration, intramuscular and subcutaneous administration, it is rapidly absorbed. Cmax in blood plasma is achieved 1 hour after oral administration and 25–30 minutes after intramuscular or subcutaneous administration. Binding to blood plasma proteins is 40–50% of the active substance. It quickly enters the tissues, the half-life of distribution is 40 minutes. Metabolized in the liver. It is excreted through the kidneys (mainly by tubular secretion and only 1/3 by glomerular filtration) and extrarenally (through the gastrointestinal tract). T1/2 of Neuromidin® when administered parenterally is 2–3 hours. After parenteral administration, 34.8% of the drug dose is excreted unchanged in the urine.

Ensuring drug safety is a priority in modern medicine. It is associated with the creation of a large number of new drugs, the identification of new biological effects of previously synthesized drugs (drugs) that can modify the functional connections of organs and body systems, and the sensitization of patients due to polypharmacy. The results of pharmacoepidemiological studies indicate that underestimation of this problem is fraught with the development of serious consequences, an increase in the number of severe complications requiring hospitalization and often causing death [1-3].

The problem of drug safety is especially acute for patients with cerebrovascular diseases (CVD), since most of them have risk factors for the development of adverse effects of drugs: old age, comorbid pathology, the need to take two or more drugs, a burdened allergic history, etc. [ 4].

Neuroprotectors are widely used in the Russian Federation. Favorable pharmacokinetic parameters, low risk of drug interactions and side effects, and over-the-counter availability have led to their extremely widespread, often unsystematic and uncontrolled use. You should be aware that without taking into account pharmacodynamics and possible drug interactions, the prescription of any drug is associated with serious risks [5].

Neuroprotectors should be prescribed only for specific indications according to the instructions. It is necessary to strictly adhere to the course and daily dosage regimens. The possibility of adverse effects should be taken into account when taking several drugs simultaneously. In addition, it is necessary to keep in mind the patient’s age and the presence of concomitant pathology, predict the development of side effects and assess the risk-benefit ratio. Of the large number of neuroprotectors, only a few have demonstrated effectiveness in clinical studies [5]. The task of drug therapy is not only to find effective and safe drugs, but also to study the effectiveness of combinations that include drugs with different mechanisms of action [6].

Pathogenetic rationale for complex neuroprotection

In clinical practice, drugs that have a complex effect on various brain cells are most often used, since in case of cerebral circulation impairment, protection of not only neurons, but also astrocytes, oligodendrocytes, and microglia is required. Their use can increase the degree of brain adaptation to ischemia, increase cell viability, and ensure better recovery of impaired functions. The processes of neuroplasticity and neuroprotection are of primary importance [6].

Neuroplasticity includes the processes of regeneration of nervous tissue and is considered as the adaptation of a neuron to new functional conditions, reducing damage to brain tissue caused by ischemia.

Cell death occurs within a certain period of time after the development of ischemia and occurs through passive (necrosis) and active (apoptosis) pathways. Excitotoxic cell damage develops within minutes, with inflammation and apoptosis occurring in the following hours and days. The pathobiochemical cascade involves glutamate and calcium cation, the concentration of which is disrupted inside and outside the cell. Normally, apoptosis plays a positive role and, as a rule, does not activate inflammation, but the pathological processes associated with stroke are associated with excitotoxicity and inflammation. Extensive cell damage in the infarct area leads to neuronal swelling and lysis due to massive stimulation of NMDA receptors. Their moderate hyperactivity in the penumbra zone is a trigger for the formation of free radicals and processes leading to apoptotic damage.

Neurotrophic factors determine the processes of cell proliferation, migration, differentiation and survival. Understanding this mechanism is key to developing new treatment strategies. Defense processes can be natural or pharmacologically induced. They are interconnected and together cause a complex of processes of preservation and regeneration of nervous tissue. Pharmacotherapy for CVD should be combined and aimed not only at restoring blood flow in the affected area, but also at eliminating neurometabolic, neurotransmitter, neurotrophic and other reactions that determine the development of destructive changes in neurons. The therapeutic strategy should include correction of cerebral perfusion, systemic hemodynamics, energy metabolism and neurotransmitter metabolism. Adequate use of neurotrophic and neuroprotective drugs can slow down the formation of ischemic damage and increase the brain’s resistance to hypoxia [7].

The most common methods of combined neuroprotection

Most often, an antioxidant and a neurotransmitter drug are prescribed simultaneously [7]. Antioxidants are natural or synthetic substances that slow down or prevent the oxidation of organic compounds. Enzymatic antioxidants created on the basis of superoxide dismutase (SOD), isolated from natural materials (ontosein, oxodrol, peroxinorm), have significant disadvantages: they are unstable, quickly inactivated and have a number of side effects, as a result of which they have limitations for clinical use.

Ethylmethylhydroxypyridine succinate (EMHPS) (Mexidol, Neurox, Mexiprim) has a wide range of pharmacological activity and has the ability to stabilize membranes. Unlike succinic acid preparations, pyridine and succinate residues facilitate the penetration of the molecule into the cell and have a minimal number of side effects. EMGPS, being an antioxidant, has antihypoxic, membrane-protective, nootropic, anticonvulsant and anxiolytic effects. EMGPS stimulate the oxidation of glucose through the pentose phosphate shunt, increasing the level of the pool of reduced nucleotides. Due to stabilization of the level of endogenous antioxidants, the succinate oxidase oxidation pathway is activated, which, under conditions of limited NAD-dependent oxidation in the early stages of hypoxia, allows maintaining a certain level of oxidative phosphorylation. Activation of the succinate oxygenase oxidation pathway during hypoxia increases cell resistance to oxygen deficiency and determines the antihypoxic effect of EMHPS. The drug also inhibits lipid peroxidation, increases SOD activity and the lipid-protein ratio, and reduces membrane viscosity, increasing its fluidity. Modulates the activity of membrane-bound calcium-independent phosphodiesterase, adenylate cyclase, acetylcholinesterase, benzodiazepine, GABA, acetylcholine receptor complexes, which increases their binding to ligands, helps maintain the functional organization of biomembranes, transport of neurotransmitters and improve synaptic transmission. EMGPS increases the content of dopamine in the brain, activates aerobic glycolysis and reduces the degree of inhibition of oxidative processes in the Krebs cycle with an increase in the formation of ATP and creatine phosphate. Pharmacological effects are realized at three levels: neuronal, vascular and metabolic. The combination of pyridine base and succinic acid ensures passage through the blood-brain barrier.

EMGPS is approved for the treatment of various CVD, encephalopathy (hypertensive, atherosclerotic, traumatic, etc.), neurotic and neurosis-like disorders with anxiety, for the relief of withdrawal symptoms in alcoholism, for the treatment of acute intoxication with neuroleptics, etc. EMGPS has a stress-protective effect, which manifests itself in normalization of post-stress behavior, somatovegetative disorders, restoration of the sleep-wake cycle, impaired learning and memory processes, reduction of dystrophic changes in brain structures [8].

The advantage of EMGPS is the low incidence of side effects. Enhances the effect of benzodiazepine anxiolytics, antiepileptic, antiparkinsonian drugs, nitrates, without affecting the state of systemic hemodynamics. The drug has no inhibitory or stimulating effects on spontaneous motor activity, coordination, exploratory behavior, rectal temperature, corneal reflex, does not cause drowsiness, the adequacy of the animal's response to provoking stimuli is maintained, simple reflexes are not impaired, even in high doses. Increasing the dosage by 4-5.5 times does not have a muscle relaxant effect; when used in ultra-high doses, an antiamnestic effect is manifested [8]. EMGPS does not cause hyperactivation, dyssomnia, or increased convulsive readiness. The range of therapeutic doses in the experiment ranges from 10 to 300 mg/kg. As the dose increases, the period of onset of the effect decreases and its severity increases. Stopping treatment does not cause withdrawal syndrome.

Four randomized studies of the use of EMGPS in patients with ischemic stroke (IS) were conducted, one of them was double-blind, placebo-controlled [9, 10]. EMGPS has been shown to be effective in the treatment of chronic cerebral ischemia (CCI) [11–16]. Of particular note is an open comparative controlled study lasting 15 days, which included 60 patients with stage 1–2 CCI aged 45–68 years [17]. Patients of the 1st group received Neurox, 2nd - Mexidol; There were no significant differences between groups by gender and age. A positive effect of both drugs on the oxidative potential of low-density lipoproteins, a decrease in their susceptibility to oxidative processes in vivo,

increased content of α-tocopherol and β-carotene. The therapeutic equivalence of the drugs was recorded.

Neurox (Sotex, Russia) has established itself as an effective, safe agent that improves metabolism and blood supply to the brain, microcirculation, metabolic processes in the ischemic myocardium, increases coronary blood flow in the ischemic zone, and reduces the consequences of reperfusion syndrome in acute coronary syndrome [18, 19 ]. Taking into account possible drug interactions, it can be recommended for the treatment of CVD [20].

Drugs with neurotransmitter and neurometabolic effects

Helps improve metabolic processes and eliminate mediator imbalance in the central nervous system. Of interest are drugs that affect acetylcholine metabolism.

During IS and CCI, the content of phospholipids in the brain sharply decreases due to slower biosynthesis and increased degradation of phosphatidylcholine [21]. The role of phospholipids in hemocoagulation has been studied. Intravascular fibrin formation is characterized by disorders of the blood coagulation system with a violation of the ratio between neutral (NPL) and acidic phospholipids (APL) [22]. The process of transformation of fibrinogen into fibrin, accompanied by a decrease in the content of CPL and an increase in the level of NFL, changes this ratio. It is characterized in each specific case by their pro- and anticoagulant activity. This may be manifested by the stimulating or inhibitory effect of these compounds on prothrombin time values, thromboplastic activity, blood clotting time, fibrinogen concentration and fibrinolytic activity [23]. Under ischemic conditions, the synthesis of phosphatidylcholine decreases, which is an important factor in brain aging and neuronal damage in CVD [24]. In this situation, it is important to prescribe drugs that affect phospholipid metabolism. The use of natural metabolites makes it possible to slow down the progression of the process already in the early stages of the disease.

Citicoline

Of undoubted interest are data on the use of citicoline (cytidine 5'-diphosphocholine; trade names - Ceraxon, Neipilept, Recognan). Its effectiveness over the past 30 years has been studied in detail for CVD in Europe, the USA and Japan [25]. Information was obtained about its pleiotropic effect, impact on the consequences of cerebral ischemia, processes of restoration of the structure and functions of nervous tissue. There is an extensive evidence base for the drug; about 12,000 patients were included in studies of its effectiveness. Citicoline is normally present in all cells of the human body and is a natural product of biochemical processes. Consists of cytidine and choline linked by a diphosphate bridge and is a necessary intermediate in the synthesis of phosphatidylcholine, the main brain phospholipid (Kennedy pathway), reduces the loss of phosphatidylcholine, which is part of the cell membrane. Being a source of choline, it participates in the synthesis of acetylcholine, stimulates the activity of tyrosine hydroxylase and the secretion of dopamine.

In an experiment, citicoline reduced the degeneration of hippocampal neurons caused by the administration of beta-amyloid (BA) [26]. BA is a protein formed as a result of proteolytic processing from the BA precursor (PBA), which is expressed in virtually all animal cells. The severity of cognitive impairment (CD) is directly proportional to its accumulation. Choline in combination with cytidine stimulates the secretion of normal neurotrophic PBA by rat neurons [27]. Citicoline reduces the deposition of BA in the brain, which is clinically manifested by an improvement in cognitive function.

A large number of clinical studies have been conducted on the effectiveness of citicoline in the treatment of CR associated with brain aging and CVD [27]. In addition to its effect on AD, the neuroprotective effect of citicoline is due to the redistribution of the main glutamate transporter EAAT2 and an increase in its uptake [28]. Citicoline leads to the mobilization of bone marrow endothelial progenitor cells, improving functional recovery after acute IS [29].

Citicoline has high bioavailability both orally and intravenously. After absorption, the drug breaks down into choline and cytidine, which easily penetrate the blood-brain barrier, from which citicoline is synthesized in the brain. Its content in blood plasma after oral administration has two peaks - after 1 hour and 24 hours.

Studies have shown the safety and effectiveness of long-term (6 months) administration of citicoline to prevent post-stroke CR [30-32]. The use of citicoline within 24 hours from the onset of IS symptoms and subsequent continuous use for 6 months is an effective means of preventing post-stroke CR compared with placebo. Improvements were observed in time orientation, attention, and executive function. The use of citicoline in patients who underwent stroke for 12 months demonstrated good tolerability and effectiveness in preventing post-stroke CR [33].

The drug citicoline neipilept (Sotex, Russia) is produced from a substance manufactured in Italy and is available in the form of solutions for intravenous and intramuscular administration, as well as a dosage form for oral administration.

An open comparative multicenter randomized study of the effectiveness and safety of the use of Neipilept and Ceraxon in patients with acute carotid IS showed their safety and high efficiency [32], a minimal number of side effects and compatibility with other drugs, which gives grounds to recommend it for use in clinical practice.

Choline alphoscerate

Choline alphoscerate (gliatilin, cereton, cerepro) contains 40% choline, which in the body is converted into a metabolically active form - phosphorylcholine, which penetrates the blood-brain barrier and activates the synthesis of acetylcholine in the presynaptic terminals of neurons [34]. Glycerophosphate is involved in the synthesis of the membrane phospholipid phosphatidylcholine [35].

Choline alfoscerate is a centrally acting parasympathomimetic drug. Three main mechanisms of its action have been established. As a donor of acetylcholine, it helps restore interneuron connections and improve neurotransmission. Participates in the repair of neuronal membranes, reducing the severity of degeneration of free fatty acids [36].

Choline alfoscerate replenishes the biochemical and functional deficiency of the cholinergic system affected by ischemia, which justifies its use in IS [37]. In addition, it has an anabolic effect, manifested in the stimulation of glycerolipid synthesis due to the formation of membrane phospholipid precursors from its breakdown products [38].

Experiments have shown that drugs of this series prevent induced cholinergic deficiency, prevent the development of dementia, and facilitate learning and memory processes by increasing the synthesis and release of acetylcholine in brain structures [39]. The neuroprotective effect of exogenous choline sources during ischemia has been proven in both preclinical and clinical studies [40].

The largest study of the effectiveness of gliatilin in patients with IS was conducted in Italy (2058 patients in 176 clinical centers) [41]. Treatment began no later than 10 days after the development of IS or transient ischemic attack and lasted for at least 6 months. A significant decrease in cognitive and motor impairment was observed after the first month of injection therapy with the drug (1000 mg IM). The results obtained confirm the effectiveness of choline alfoscerate in restoring neurological and cognitive functions. The most significant effect was recorded by the 3rd month of observation. A subsequent meta-analysis studying the use of choline alfoscerate showed its effectiveness against CR, exceeding that of other acetylcholine precursors [42].

Mechanisms of the neuroprotective effect of citicoline and choline alfoscerate

The drugs have different mechanisms of action - the main effect of citicoline is associated with the effect on membranes, the effect on neurotransmission is less pronounced, the dominant effect of choline alfoscerate is an improvement in neurotransmission with a weaker membrane protective effect. Thus, the main mechanisms of citicoline are the repair of neuronal membranes, reducing the degeneration of free fatty acids, and choline alfoscerate is increasing the production and release of acetylcholine from the terminals [43]. The difference between choline alfoscerate is its ability to restore acetylcholine levels, while the main neuroprotective properties of citicoline lie in the preservation of both external and internal neuronal membranes [44-46]. Citicoline helps stabilize protein synthetic processes in the vascular wall and neurons. If therapy is not started in a timely manner, correction of the destruction of these membranes will no longer be possible, therefore, to enhance the effects of these drugs, it is advisable to use them in combination as early as possible in the disease [47, 48]. The choice of cholinergic drugs for patients with CVD should be pathogenetically justified, taking into account the dysfunction of modulating subsystems of brain activation, the predictors of which are the patient’s age, level of consciousness, the presence of somatic pathology, a history of cerebrovascular accidents, and CR.

Disturbances in metabolic processes in the vascular wall and neurons underlie the development of subsequent neurodegenerative lesions. Neurological diseases often occur against the background of severe somatic pathology and are often accompanied by decompensation of an existing brain lesion, especially in elderly patients [49]. Therefore, it is important to prescribe drugs that affect the metabolism of phospholipids, since they are a structural component of all cell membranes, and from them Numerous cell functions are directly dependent. The more pronounced the hypoxia, the higher the consumption of phosphatidylcholine. Depletion of its pool exceeding 20% ​​is accompanied by membrane destruction [50]. Replenishment of phosphatidylcholine deficiency is not able to eliminate the cause of the disease, therefore citicoline should be considered as a universal membrane protector capable of preserving the basic properties of biological membranes in patients with severe somatic pathology, in acute and recovery periods of IS and traumatic brain injury, in patients with Parkinson's disease, hypertensive encephalopathy with severe CR.

Over a certain period of time, choline reserves for acetylcholine synthesis can be provided by hydrolysis of phosphatidylcholine by phospholipases. A decrease in its concentration leads to the death of cholinergic neurons [51]. This biochemical phenomenon is called phosphotidylcholine autocannibalism [52]. Therefore, it is necessary to enhance the cholinergic effect through the use of a choline donor - choline alfoscerate.

Another form of use of drugs in young and middle-aged patients with minimal clinical manifestations is initial therapy with choline alfoscerate, since the leading clinical picture is mild CR due to acetylcholine deficiency. Also, choline alfoscerate should be considered as a drug that stimulates cholinergic neurotransmission in patients with acute, including severe IS [53].

Thus, when treating patients with CVD, it is necessary to use rational combination therapy with the use of neuroprotectors, taking into account information about their possible positive and negative effects.

Contraindications

hypersensitivity to any of the components of the drug;

epilepsy;

extrapyramidal diseases with hyperkinesis;

angina pectoris;

severe bradycardia;

bronchial asthma;

mechanical obstruction of the intestine or urinary tract;

vestibular disorders;

peptic ulcer of the stomach or duodenum in the acute stage;

pregnancy (the drug increases the tone of the uterus);

lactation period;

children under 18 years of age (no systematic data on use).

With caution: for gastric and duodenal ulcers, thyrotoxicosis, cardiovascular diseases, as well as for patients with a history of obstructive diseases of the respiratory system or acute respiratory diseases.

Additionally for tablets

With caution: with lactase deficiency, lactose intolerance, lactose/isomaltose malabsorption syndrome, because the drug contains lactose.

"Amiridin"

The drug is available in the form of tablets with ipidacrine as the main component.

The medicine is prescribed to patients for:

• moderate or mild dementia of the Alzheimer's type;
• cerebral palsy;
• disorders of neuromuscular transmission (muscular dystrophy, myasthenia gravis);
• diseases of the peripheral nervous system (including neuritis, polyneuritis, polyneuropathy, radiculoneuritis);
• damage to the anterior horns of the spinal cord after spinal muscular atrophy, poliomyelitis.

There are also quite a few contraindications for use. Among them:

• presence of allergies to the components of the drug;
• childhood;
• bradycardia;
• bronchial asthma;
• heart failure;
• angina pectoris;
• hyperkinesis;
• epilepsy;
• mechanical intestinal obstruction;
• severe renal and liver dysfunction.

Treatment with Amiridin is also not recommended during pregnancy and lactation.

Side effects

Caused by stimulation of m-cholinergic receptors: salivation, increased sweating, palpitations, nausea, diarrhea, jaundice, bradycardia, epigastric pain, increased secretion of bronchial secretions, bronchospasm, convulsions. Salivation and bradycardia can be reduced with m-anticholinergic drugs (atropine, etc.). Increased uterine tone, allergic skin reactions.

Rarely (after using higher doses), dizziness, headache, chest pain, vomiting, general weakness, drowsiness, and skin reactions (itching, rash) were observed. In these cases, reduce the dose or interrupt the drug for a short time (for 1–2 days). These side effects are observed in less than 10% of patients.

Cheap analogues of Neuromedin in tablet form

There are analogues on the pharmacological market that are cheaper than Neuromidin. These medications are made in tablets and have a similar effect on the human body.

Kalimin 60N

Kalimin based on pyridostigmine bromide is a reversible cholinesterase inhibitor. Prescribe medication for:

• myasthenia gravis and myasthenic syndrome;
• impaired motor ability after injury;
• paralysis and encephalitis.

Also prescribed during the rehabilitation period after polio.

Not prescribed for:

• epileptic seizures;
• hyperkinesis;
• bronchial asthma;
• sclerosis of the coronary and intracardiac arteries, angina pectoris.

Tablets should be taken 1-3 times a day, 60 mg each, the solution is administered by injection at 0.4 g/1 ml.

Negative manifestations:

• dyspepsia with abdominal pain and defecation disorders;
• dizziness and headache;
• cardiac disorders and pressure fluctuations;
• skin itching;
• urticaria and bronchospasms.

This analogue differs from the original drug in composition and cost.

Amiridine

Amiridin contains the active ingredient ipidacrine. In addition to its effect on cholinesterase, it has a blocking effect on calcium channels, which differs from other inhibitors of this enzyme.

The main indicators for use are the following pathologies:

• polyneuritis and mononeuritis;
• myasthenia gravis;
• paresis and atony;
• bulbar palsy.

A medication is also prescribed to stimulate labor as the baby passes through the birth canal, as well as to reduce the severe symptoms of dementia in Alzheimer's disease.

The medication is not prescribed for:

• epileptic seizures;
• hyperkinesis;
• bradycardia, tachycardia, angina pectoris and arrhythmias;
• pathologies of a cardiac and systemic nature;
• vestibular disorders;
• bronchial asthma.

It is also not prescribed in pediatrics, in case of allergies to the medicinal composition, during lactation and during pregnancy.

The medicine is taken orally and parenterally. Orally – 1-3 doses per day, 10-20 mg. Subcutaneously or inside muscle fibers - 5-15 mg once or twice a day. The therapeutic course lasts 30-60 days. To relieve an attack of myasthenia gravis, 15-30 mg or 1-2 tablets up to 6 doses per day.

To stimulate the approach of labor, a pregnant woman should take 1 tablet, and if the therapeutic effect is insufficient, after 1 hour, repeat the dose in the same amount.

Side effects:

• bronchospasms;
• bradycardia;
• diarrhea and dyspepsia;
• jaundice and loss of appetite;
• ataxia and dizziness;
• skin rash and itching.

The composition of this drug is no different from Neuromidin, but the list of its indications is slightly narrower.

Interaction

Neuromidin® enhances the sedative effect in combination with CNS depressants.

The action and side effects are enhanced when used together with other cholinesterase inhibitors and m-cholinomimetic drugs. In patients with myasthenia gravis, the risk of developing a cholinergic crisis increases if Neuromidin® is used simultaneously with other cholinergic drugs.

The risk of developing bradycardia increases if β-blockers were used before starting treatment with Neuromidin®.

Neuromidin® can be used in combination with nootropic drugs.

Alcohol increases the side effects of the drug.

Reduces the inhibitory effect on neuromuscular transmission and the conduction of excitation along peripheral nerves by local anesthetics, aminoglycosides, and potassium chloride.

Modern spinal neurosurgery

Only modern minimally invasive surgical intervention (for example, video endoscopic microdiscectomy, or laser vaporization and nucleoplasty) can remove the hernia defect itself, or prevent its appearance in the case of protrusion. However, the Russian patient knows very well what surgery is. It hurts. This takes you out of normal life for a long time. It may be dangerous. There are so many such “buts” that surgery is considered the last type of treatment, when massage therapists, carboxytherapy sessions, manual therapists and kinesiotherapists stop helping.

Fortunately, in European countries, Israel, and the USA, the approach is completely different. If there are indications, the patient is operated on without pain, and often leaves the hospital on his own feet on the same day or the next. His quality of life is preserved. He is not prohibited from sitting for many days, and he is not forced to relieve himself while standing. Therefore, modern surgery is considered the best, fastest and most effective means of radical treatment. By the way, doctors in many Eastern European countries, for example, the Czech Republic, show excellent results in treating hernias surgically at fairly modest costs.

In Russia, they prefer not to immediately remove the hernial protrusion, but for many years to deal with its consequences and complications - to periodically treat inflammation, pain and swelling of the roots, which persistently arise again and again. And in this respect, the domestic patient resembles an unfortunate driver who, instead of finally changing a punctured tire, is forced to pump it up every half hour of driving. Only, unlike the driver, a patient who has been “treating” a hernia for a long time sometimes spends several times more money than the operation would cost.

Cervical hernia on MRI.

But even among the drugs for relieving swelling, back pain, and excess muscle tension, Neuromidin is not “listed.” However, it is sometimes prescribed for hernias, and is completely unjustified. The situation is aggravated by an unimaginably large number of sites that are written with stunning medical illiteracy. Because if there is a request “How to take Neuromidin for hernias,” then a helpful but illiterate article will immediately appear, which can even harm your health. How to take Neuromidin for hernias? Don't accept it at all. But first things first….

Directions for use and doses

Inside, s/c or i/m. Doses and duration of treatment are determined individually, depending on the severity of the disease.

Pills

Diseases of the peripheral nervous system:

- mono- and polyneuropathy, polyradiculopathy, myasthenia gravis and myasthenic syndrome of various etiologies - 10-20 mg (0.5-1 tablet) 1-3 times a day. The course of treatment is from 1 to 2 months. If necessary, the course of treatment can be repeated several times with a break between courses of 1–2 months;

— to prevent myasthenic crises, in case of severe disorders of neuromuscular conduction, 1–2 ml (15–30 mg) Neuromidin® 1.5% solution for injection is administered parenterally for a short time, then treatment is continued with Neuromidin® tablets, the dose can be increased to 20–40 mg (1–2 tablets) 5 times a day.

Diseases of the central nervous system: bulbar paralysis and paresis, the recovery period of organic lesions of the central nervous system (traumatic, vascular and other origins), accompanied by motor and/or cognitive impairment - 10–20 mg (0.5–1 tablet) 2–3 times a day day. The course of treatment is from 2 to 6 months. If necessary, the course of treatment is repeated.

Treatment and prevention of intestinal atony - 20 mg (1 tablet) 2-3 times a day for 1-2 weeks.

Solution for intramuscular and subcutaneous administration

Diseases of the peripheral nervous system:

- mono- and polyneuropathy of various origins - subcutaneously or intramuscularly 5-15 mg 1-2 times a day, course - 10-15 days (in severe cases - up to 30 days); then treatment is continued with the tablet form of the drug;

- myasthenia gravis and myasthenic syndrome - subcutaneous or intramuscular 15-30 mg 1-3 times a day with further transition to the tablet form. The general course of treatment is 1–2 months. If necessary, treatment can be repeated several times with a break between courses of 1–2 months.

Diseases of the central nervous system:

— bulbar paralysis and paresis — subcutaneous or intramuscular 5–15 mg 1–2 times a day for 10–15 days; if possible, switch to tablet form;

- rehabilitation for organic lesions of the central nervous system - 10-15 mg intramuscularly 1-2 times a day, course - up to 15 days, then, if possible, switch to tablet form.

If the next dose was not taken on time, then it is not taken additionally.

The maximum daily dose is 200 mg.

How does Neuromidin work?

The active substance Neuromidin was developed in the late 80s and replaced Prozerin, which had been used in neurology for many years. Unlike a conventional inhibitor, Ipidacrine simultaneously combines several mechanisms of action and is capable of stimulating structural formations of the central nervous system, which significantly expands the range of indications for its use. In modern medical practice, both drugs are used, and they are often compared.

Only the attending physician can determine whether Neuromidin or Proserin is better, separately for each specific patient and clinical case.

It has been established that the chemical structure of Proserin makes it difficult for its molecules to penetrate biological membranes, so the drug mainly affects only cholinergic (transmitting excitation using acetylcholine) peripheral synapses located on the border between nerve endings and working organs.

1. The therapeutic effect of Proserin is more pronounced and appears within 10-15 minutes after administration, but ends after 2-3 hours.
2. The effect of Neuromidin is felt after 15-20 minutes and lasts for 3-5 hours. In addition, Ipidacrine affects all parts of the distribution of excitation, which additionally determines its analgesic and sedative properties, and antiarrhythmic effect.

How Neuromidin acts on the body and what it helps with:

• changes the excitability of the cell, provides the ability to adequately respond to a stimulus;
• normalizes the transmission of nerve impulses and their transformation into mechanical movement, improves the ability of muscle tissue to express contractions;
• enhances the effect of mediator substances on nerve ganglia, smooth and striated muscles;
• stimulates the autonomic nervous system, maintaining homeostasis;
• increases muscle tone, strength in the affected muscles, prevents the occurrence of attacks, reduces the severity of paralysis, paresis, sensitivity disorders in the innervation zone;
• improves concentration, prevents memory loss, decreased cognitive function, behavioral disorders and other signs of dementia.

Information about: anti-inflammatory drug Diaflex may be useful.

The instructions provide the main pharmacokinetic parameters of Neuromidin:

• Absorption: when taken orally or parenterally, the active substance is quickly absorbed, the peak concentration in the blood is recorded after 1 hour (from the gastrointestinal tract) and 25-30 minutes (from the injection site), respectively.
• Distribution: in the systemic circulation, Ipidacrine circulates half in free form, 40-50% of the incoming dose is bound to plasma proteins. 50% equilibrium concentration in target tissues is achieved after 40 minutes.
• Metabolism: under the influence of liver enzymes, the substance is partially biotransformed.
• Excretion: leaves the body in the urine and through extrarenal excretory organs. The concentration of Ipidacrine in the bloodstream decreases by 50% 2-3 hours after the injection.

Overdose

Symptoms: decreased appetite, bronchospasm, lacrimation, increased sweating, constriction of the pupils, nystagmus, increased gastrointestinal peristalsis, spontaneous bowel movements and urination, vomiting, jaundice, bradycardia, intracardiac conduction disturbances, arrhythmias, decreased blood pressure, restlessness, anxiety, agitation, feelings of fear, ataxia, convulsions, coma, speech impairment, drowsiness, general weakness.

Treatment: symptomatic therapy is used, m-anticholinergic blockers are prescribed (atropine, cyclodol, metacin, etc.).

special instructions

There are no systematic data on the use of Neuromidin® in children.

Alcohol should be avoided during treatment (it increases the side effects of the drug).

Impact on the ability to drive a car or perform work that requires increased speed of physical and mental reactions. During treatment, you should refrain from driving a car, as well as engaging in potentially hazardous activities that require increased concentration and speed of psychomotor reactions.

Release form

Tablets, 20 mg. 10 tablets each in blister packs made of PVC film and aluminum foil. 5 blister packs per cardboard pack.

Solution for intramuscular and subcutaneous administration, 5 mg/ml and 15 mg/ml. 1 ml of the drug in neutral glass ampoules (type I). 5 amp. in blister packs made of PVC film. 2 blister packs in a cardboard pack.

For the drug produced at SOPHARMA JSC, Bulgaria: 10 amp. in blister packs made of PVC film. 1 blister pack in a cardboard pack.

Cost of Neuromidin and its analogues

Prices for Neuromidin are in the high price segment. The cost of foreign analogues of the drug is also quite high. The price of domestic Neuromidin substitutes is significantly lower than the original and its foreign generics.