Gabapentin: what is it, the effect of the drug, consequences

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Attention! The material contains information about substances, the use of which can cause serious harm to your health!

Pharmacy addicts are confident that the drugs sold at the pharmacy are less dangerous than drugs. In addition, they have a more favorable price, and it is possible to purchase without a prescription (for example, through friends or just like that, if the pharmacist practices this). All this makes pharmacy drug addiction accessible to teenagers and young people. This problem also includes the use of gabapentin, a pharmacological drug for epilepsy.

• Gabapentin as a drug
• What is gabapentin?
• Composition of gabapentin
• Photo of the drug: what it looks like
• Effect of gabapentin
• Duration of action of gabapentin
• Signs of Gabapentin Use
• Combination with other substances
• Gabapentin and Lyrica
• Gabapentin and coffee
• Gabapentin and alcohol
• Gabapentin and phenibut
• Consequences of using gabapentin
• Quick addiction from the drug effect
• The effect of gabapentin on the body
• Gabapentin addiction
• Overdose
• Gabapentin poisoning: first aid
• Withdrawal
• Treatment of Gabapentin Addiction

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Gabapentin as a drug

Although gabapentin is initially produced as a drug, its effects on the nervous system and psyche are actively used by drug addicts. The trouble is that using the drug for recreational (off-label) purposes quickly forms a persistent addiction.

What is gabapentin?

Gabapentin is a serious, potent pharmacological agent. A prescription is required to purchase it. Among the main indications for use are pathologies such as epilepsy and pain of neuropathic origin. It is also used as an anxiolytic – it reduces anxiety, improves mood, and normalizes sleep.

Gabapentin is the active ingredient of many drugs - analogues, for example, Neurontin, Convalis, Tebantin and others. If used incorrectly, these drugs have severe side effects. Many drug addicts, not knowing what kind of medicine it is, not understanding the meaning and danger of its effects on the body, purchase it to get a trip (altered mental state).

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Composition of gabapentin

Gabapentin is 1-(aminomethyl)cyclohexaneacetic acid. Its chemical formula as a compound is C9H17NO2. The drug Gabapentin contains the substance of the same name in an amount of 300 mg.

Photo of the drug: what it looks like

As a medicine, gabapentin comes in the form of tablets or capsules. Depending on the manufacturer, they can have different colors: green, white, yellowish.

Effect of gabapentin

At the moment, the exact mechanism of action of the substance is unknown. In terms of structural features, gabapentin is similar to gamma-aminobutyric acid, a neurotransmitter of the central nervous system. However, in the body it does not bind to molecules that interact with GABA.

Penetrating into the nervous tissue, the substance blocks the entry of calcium into the cells, as a result of which the inhibitory system is activated and the excitation system is suppressed. The content of serotonin in the blood increases. There is relief of pain and cessation of seizures.

Recreational use of gabapentin leads to changes in human consciousness. The surrounding reality changes dramatically, and hallucinations are possible.

Duration of action of gabapentin

The half-life of the substance in the body is approximately 5-7 hours. Elimination time does not depend on nutrition or dosage. Excreted by the kidneys or by hemodialysis.

Comparison of the effectiveness of Mydocalm and Sirdalud

The effectiveness of Mydocalm is quite similar to Sirdalud - this means that the ability of the medicinal substance to provide the maximum possible effect is similar.
For example, if the therapeutic effect of Mydocalm is more pronounced, then using Sirdalud even in large doses will not achieve this effect.

Also, the speed of therapy - an indicator of the speed of therapeutic action - is approximately the same for Mydocalm and Sirdalud. And bioavailability, that is, the amount of a drug reaching its site of action in the body, is similar. The higher the bioavailability, the less it will be lost during absorption and use by the body.

Signs of Gabapentin Use

You can suspect a drug addict using gabapentin based on the following signs:

• uncertain, shaky gait;
• confused speech;
• impaired coordination of movements, balance;
• excessive sociability;
• depression;
• insomnia combined with drowsiness;
• outbursts of aggression without reason;
• rave;
• hallucinations.

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Combination with other substances

Often, polydrug addicts, in order to reduce the symptoms of “withdrawal” or, on the contrary, enhance the narcotic effects of drugs, take different drugs at the same time. For example, it could be Amphetamine, Baclofen, Habana (aka Lyrica), ethyl alcohol and others. All combinations, without exception, increase the side effects of drugs, and some options end in coma or death.

Gabapentin and Lyrica

Gabapentin and Lyrica (Pregabalin, or Gabana) have almost similar properties in terms of both GABA and effects on the body. Both drugs are used in pharmacological practice for epilepsy.

However, there are also differences between them. For example, Gabapentin is absorbed only in the small intestine, partially, entering the bloodstream slowly and unevenly. Lyrica is absorbed completely, quickly, and penetrates the mucous membrane not only of the small intestine, but also beyond. The combined use of drugs leads to the receipt of the drug effect at different times, and also provokes an increase in the adverse reactions of both drugs.

Gabapentin and coffee

Scientific studies have not found an interaction between gabapentin and caffeine. The combined use of both substances has not been studied.

Gabapentin and alcohol

However, the body's reaction to the combination of gabapentin with ethyl alcohol has been studied quite well. These two substances are absolutely incompatible with each other. Their simultaneous use threatens with the following consequences:

• confusion;
• pain throughout the body;
• irritability, hostility;
• dryness of the oral mucosa;
• loss of coordination of movements;
• bruising (increased fragility of blood vessels);
• swelling of the face, limbs;
• convulsive muscle contraction.

Alcohol greatly increases the side effects of gabapentin, which can lead to coma and death.

Gabapentin and phenibut

Phenibut is a nootropic pharmacological agent, a stimulator of metabolism in the central nervous system. This is an antidepressant not prohibited in sports, which is used to treat anxiety, sleep disorders, restlessness, and irritability. According to reviews, it enhances the effect of gabapentin. At the same time, the likelihood of developing adverse reactions of both drugs increases.

Comparison of side effects of Mydocalm and Sirdalud

Side effects or adverse events are any adverse medical event that occurs in a subject after administration of a drug.

Sirdalud has more adverse effects than Mydocalm. This implies that the frequency of their occurrence is low in Sirdalud and low in Mydocalm. Frequency of manifestation is an indicator of how many cases of an undesirable effect from treatment are possible and registered. The undesirable effect on the body, the strength of influence and the toxic effect of drugs are different: how quickly the body recovers after taking it and whether it recovers at all. When using Sirdalud, the body's ability to recover faster is higher than that of Mydocalm.

Consequences of using gabapentin

The drug not only has a lot of side effects. In the case of recreational use, it causes a stable addiction, gradually depresses the nervous system, leading to the death of neurons, and provokes respiratory arrest.

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Quick addiction from the drug effect

Drug addiction to gabapentin develops very quickly. Among its signs are the following:

• loss of interest in what is happening around, in loved ones, in oneself;
• irresistible craving to use the drug;
• loss of ability to control the use of the drug;
• development of withdrawal syndrome, withdrawal symptoms;
• the emergence of resistance to the usual dose, the need to increase it;
• using a substance even when you feel very unwell.

The effect of gabapentin on the body

Long-term and excessive recreational use of the drug in violation of the instructions poisons the body, destroys the central nervous system, and reduces immunity. Among the most obvious consequences of using the drug as a drug are the following conditions and pathologies:

• disruption of the digestive system, abdominal pain, nausea to vomiting, stool disorders;
• the development of numerous infectious diseases due to low immunity;
• inflammatory processes in the lungs and nasopharynx;
• urinary tract infections, cystitis, pyelonephritis and so on;
• pathological changes in the central nervous system: impaired coordination of movements, depressive states;
• changes in the cardiovascular system - tachycardia, dizziness, noise or ringing in the ears;
• skin damage in the form of rashes, constant itching;
• swelling of soft tissues, face, limbs.

The addict constantly feels pain in the joints and/or muscles. The state of weakness and malaise is combined with drowsiness and irritability at the same time. Depression can lead to thoughts of suicide.

Possibility of using the drug tizanidine (Sirdalud®) in patients with post-stroke spasticity

Post-stroke spasticity significantly limits the motor capabilities of patients, complicates patient care, and contributes to the formation of pain syndromes. The article presents a modern view of the pathophysiology of post-stroke spasticity and discusses approaches to treatment. The mechanisms of action and capabilities of the drug tizanidine (Sirdalud®) for the correction of increased muscle tone in patients who have suffered a stroke are considered. The effect of tizanidine is compared with the effect of other muscle relaxants.

Introduction

Spasticity is one of the most common motor deficits in stroke patients. During the first year after a stroke, spasticity is observed in 17–43% of patients [1, 2]. As a rule, spasticity is accompanied by paresis of the corresponding muscles, but there is no strict relationship between these symptoms.

Hemiparesis, a classic clinical example of spastic paresis after a stroke, is characterized by the formation of the Wernicke-Mann position: the shoulder is adducted to the body, the forearm is flexed, the hand is pronated and bent, the thigh and lower leg are extended, the foot is in a plantar flexion position. Due to the “lengthening” of the leg, the patient is forced to move it across the side when walking, describing a semicircle. These changes occur due to an increase in tone mainly in anti-gravity muscle groups. However, in some cases, other variants of the distribution of increased muscle tone are observed, for example, hyperpronation of the forearm with extension of the fingers, bizarre placement of the hand and fingers, increased tone in the leg flexor muscles, hypersupination of the forearm and wrist extensors [3].

Most often, spasticity is detected simultaneously in the upper and lower extremities (68%), but an isolated appearance of this symptom in the arm (15%) or leg (18%) is also possible [4].

Pathophysiology of spasticity

To date, the question of the pathogenesis of post-stroke spasticity remains open. It is known that this symptom occurs due to structural and functional changes in the central nervous system and at the level of the peripheral neuromotor apparatus. Thus, with spasticity, along with the activation of the cortical zones involved in the organization of movement and the extrapyramidal pathways of the brain stem, a structural and functional reorganization of the segmental structures of the spinal cord occurs. In addition, changes in the neuronal control of the peripheral part of the motor system activate processes of transformation of the protein composition of soft tissues, primarily skeletal muscles.

In response to cerebrovascular accidents and the development of a structural and functional defect of the brain, the functional activity of the cortex changes on both the affected and clinically intact sides. In addition, new neuronal connections are formed, and the area of ​​representation of the affected part of the body in the motor and sensory cortex expands. In this case, an imbalance arises between intracortical excitation and inhibition towards the predominance of excitation [5–7]. In response to these changes, the extrapyramidal pathways of the brain stem are activated, which begin to generate spontaneous activity that is not associated with the motor activity of the cortex [6].

The main excitatory neurotransmitters of the nervous system involved in the regulation of muscle tone are glutamate and aspartate, the main inhibitory neurotransmitter is gamma-aminobutyric acid (GABA). A certain role in the implementation of muscle tone disorders is played by the serotonergic and noradrenergic systems of the brain stem, which can have both excitatory and inhibitory effects at the level of spinal neuronal networks [8].

A change in the functional interaction between different parts of the central nervous system leads to a reorganization of the segmental apparatus of the spinal cord. New contacts are formed between the neurons of the spinal cord and the descending pathways of the brain, which is accompanied by an increase in reflex excitability at the segmental level and is clinically realized by the formation of “dynamic” phenomena of spasticity in the form of clonus and synkinesis [6].

One of the methods for assessing the functional state of the segmental apparatus of the spinal cord is to study the parameters of the H-reflex (muscle response to irritation of sensory fibers of the peripheral nerve). It has been established that with spasticity, the zone of evocation of the H-reflex significantly expands [9].

Disruption of neuronal control of skeletal muscles leads to a transformation of their protein structure, primarily the myosin phenotype, as well as changes in the properties of the surrounding soft tissues (tendons and joint capsules). As a result, the proportion of “fast” but easily fatigued fibers in the muscle increases significantly, and tendon retraction leads to the formation of contractures [8, 10].

Spasticity of different muscle groups affects the patient's motor activity differently. For example, spasticity of the quadriceps femoris muscle in conditions of paresis can help maintain an upright posture by preserving the supporting function of the leg. At the same time, spasticity of the hand muscles always limits its functionality. In general, post-stroke spasticity has a negative impact on motor activity and is usually accompanied by a number of dynamic motor phenomena: involuntary movements, clonus or spasms, spastic synkinesis. In addition to the deterioration of motor functions, post-stroke spasticity can contribute to the development of post-stroke pain syndrome in the shoulder area, the prevalence of which varies from 16% in the early recovery period to 36% in the late recovery period [11].

The severity of clinical symptoms in post-stroke spasticity and its impact on the quality of life are assessed by the doctor, the patient, and caregivers. First of all, the degree of spasticity at rest is determined, for which the Ashworth scale is used, then the functional state of the limb during movement is assessed, as well as the presence of symptoms accompanying spasticity (pain, discomfort, pathological synkinesis). Taking into account all these factors, a treatment plan is developed.

Treatment

Patients with post-stroke spasticity are advised to undergo both non-drug and drug treatment.

Non-drug treatment includes physical exercise, positional therapy, the use of orthoses, massage, heat therapy, cryotherapy, electrical myostimulation, and biofeedback methods [3, 12]. Since these activities, as a rule, have a short-term effect, they should be carried out continuously, not limited to one or two courses per year. In this regard, it is necessary to train patients and their caregivers in techniques that can be used at home.

The optimal medical method for correcting local spasticity is considered to be local injections of botulinum toxin, which consists of neurotoxin type A and some other proteins. Botulinum toxin blocks the release of acetylcholine into the synaptic cleft. The most significant results of botulinum therapy include improved walking and increased self-care capabilities. The effect develops after four to seven days and lasts in most cases for 12–16 weeks [13]. However, the maximum effectiveness of the drug is achieved when it is administered under electromyography control, which is not always available. In addition, injections of the drug are not recommended for patients taking therapeutic doses of anticoagulants [13]. In general, despite the development of care for patients who have suffered a stroke, today the possibilities of botulinum therapy are limited.

Another method of local exposure is the use of alcoholic and phenolic neurolysis of the motor branches of nerves, which leads to their irreversible destruction and fibrosis of surrounding tissues. The procedure is carried out under the control of electromyography and/or ultrasound [13]. The disadvantage of this method is side effects such as dysesthesia, weakness and local swelling at the injection site [1]. Currently, neurolysis is rarely used (mainly in bedridden patients), usually in combination with botulinum therapy. The effect lasts from two to 36 months [13].

Of the first-line oral medications used for post-stroke spasticity, international recommendations indicate centrally acting muscle relaxants: tizanidine and baclofen. It is also possible to use tolperisone, diazepam, gabapentin [13]. In the treatment of cerebral spasticity, tizanidine is most often used; for spinal spasticity, tizanidine and baclofen are used [14].

Tizanidine in the treatment of post-stroke spasticity

Tizanidine (Sirdalud®) is a central agonist of imidazoline and alpha-2 adrenergic receptors at both the spinal and supraspinal levels [13, 15]. Tizanidine enhances presynaptic inhibition of motor neurons by reducing the release of excitatory amino acids (aspartate and glutamate) from spinal interneurons, as well as by inhibiting the activity of facilitatory cerebrospinal tracts. In addition, tizanidine prevents the release of substance P by thin sensory fibers, helps to reduce the functional activity of the locus coeruleus region in the brain stem and reduce the excitability of the segmental apparatus of the spinal cord [16].

Controlled clinical studies have shown the effectiveness of tizanidine in post-stroke spasticity. Thus, one study showed that tizanidine at a dose of 8 mg/day reduces the level of H-reflex facilitation in all patients (n = 14) with post-stroke spasticity. This does not happen when using a placebo. Decreased facilitation was observed on both the affected and clinically intact sides. At the same time, when taking tizanidine, there is no change in the Hmax/Mmax indicator and the threshold for evoking the H-reflex, which probably indicates the absence of the drug’s effect on the excitability of spinal motor neurons. There was a significant decrease in the degree of spasticity from 2.9 to 1.9 points on the Ashworth scale [17].

Several studies have shown a dose-dependent antispastic effect of tizanidine. In a group of patients with multiple sclerosis (n = 17) and a degree of spasticity in the lower extremities of two to three points on the Ashworth scale, a relationship was shown between the concentration of the drug in the blood and its antispastic effect. At the same time, no connection was found between certain values ​​of the drug concentration and the antispastic effect in the examined group, which indicates the need for individual dose selection. It was noted that the effect of 2 mg tizanidine was no different from that of placebo. Thus, the degree of spasticity two hours after taking 2 mg of the drug decreased by 29% (when taking placebo - by 28%), when taking 8 mg of tizanidine - by 38%. The antispastic effect was not accompanied by a decrease in muscle strength. In this study, data from a clinical assessment of the degree of spasticity were confirmed by the results of a quantitative study of muscle tone using an electrogoniometer (the device showed a high degree of sensitivity and reliability) [8].

The dependence of the antispastic effect on the dose of tizanidine in patients with post-stroke spasticity was studied in a multicenter study that included 47 patients, the degree of spasticity was two to three points on the Ashworth scale, the time since stroke was six months [16]. The dose of the drug was titrated to 36 mg (reaching the maximum dosage in 21% of patients). As a result of taking tizanidine over 16 weeks, the degree of spasticity decreased without changing muscle strength, the intensity of pain syndrome and, as a result, the quality of life of patients improved [16].

Thus, studies have confirmed the dose-dependent clinical effect of the drug; the treatment of spasticity requires the use of higher doses of tizanidine than the treatment of pain syndromes. The lack of effect in some cases may be due to an insufficient dose of the drug [8, 18].

An analysis of the results of several studies examining the antispastic effect of tizanidine compared with placebo and other oral muscle relaxants showed a reduction in spasticity with tizanidine of 21-37%, while for placebo this figure ranged from 4 to 9%. At the same time, muscle tone decreased in 60–80% of patients in the tizanidine group, in 60–65% in the baclofen group, and in 60–83% in the diazepam group. Tolerability of the drug was assessed as very good in 44–100% of patients in the tizanidine group, 38–90% in the baclofen group and 20–54% in the diazepam group. However, in the tizanidine group, patients did not experience an increase in muscle weakness, unlike patients taking baclofen. All drugs caused drowsiness [19]. Based on a combination of efficacy and tolerability indicators, tizanidine demonstrated significant advantages in the treatment of post-stroke spasticity compared to other oral muscle relaxants [16, 19, 20].

Studies comparing the treatment effects of tizanidine and botulinum toxin for post-stroke spasticity in the upper extremity have shown that both drugs are effective. At the same time, to achieve optimal results, it is necessary to accurately follow the dosage and determine the injection sites of botulinum toxin [18]. Another study examined the combined use of botulinum toxin with oral antispasticity drugs in a group of children with cerebral palsy. The combination of botulinum toxin with tizanidine has been found to be more effective than the combination of botulinum toxin and baclofen [21].

When taken orally, tizanidine is rapidly absorbed, with maximum plasma concentrations achieved within one to two hours. The optimal therapeutic effect, as a rule, develops when the drug is prescribed in a daily dose of 12–24 mg, divided into three doses; the effective dose range is 2–36 mg [22]. The maximum daily dose is 36 mg. Increasing and decreasing the dosage should be done gradually. Tizanidine is metabolized in the liver mainly by the CYP1A2 isoenzyme. It should be remembered: drugs such as ciprofloxacin and fluvoxamine inhibit this enzyme, as a result of which the hypotensive effect of tizanidine can be significantly enhanced. Particular caution should be exercised when combining the drug with antihypertensive drugs. Abrupt discontinuation of tizanidine may lead to withdrawal syndrome, especially with long-term treatment in conjunction with antihypertensive drugs.

The most common side effects observed while taking tizanidine are drowsiness, dizziness, and decreased blood pressure. General weakness, dry mouth, sleep disturbances, and hallucinations are also possible [8, 17]. It should be noted that all side effects are dose-related and can be minimized with proper dose titration. If they appear, the dosage should be reduced to the previous level for several days, and then the dose increase should be resumed [8]. As a rule, with poor tolerability, side effects appear even at minimal dosages of the drug [8, 22].

Currently, tizanidine is also available in a 6 mg dose in the form of modified-release capsules (Sirdalud® MP). For most patients, the optimal dose is 12 mg/day, in rare cases – 24 mg/day [22]. Treatment begins with one capsule per day, if necessary, the dose is increased every seven days. It should be noted that Sirdalud® MR has shown high effectiveness against central sensitization in the development of post-stroke pain syndrome in the shoulder area [11].

Other muscle relaxants

Another first-line drug for the treatment of post-stroke spasticity is baclofen, an agonist of B-type GABA receptors located in the area of ​​the endings of the primary sensory afferents of the spinal cord. By enhancing the polarization of interneuron membranes, baclofen prevents the flow of calcium into presynaptic terminals and the release of endogenous transmitters, resulting in inhibition of mono- and polysynaptic reflexes of the spinal cord [13].

The maximum dosage is 120 mg/day, changing the dose up or down should be done once a week and by no more than 15 mg. Side effects of baclofen are also dose-dependent: general weakness and drowsiness are most often noted. Experimental studies in animals have shown that GABAergic drugs may reduce brain plasticity in the early recovery period after stroke, and therefore it is not advisable to prescribe them at this time. The drug is also not recommended for elderly patients due to the development of severe drowsiness [13].

Attention should be paid to the possibility of intrathecal administration of baclofen using a pump. This is a highly effective treatment method for severe spasticity, including in patients who have suffered a stroke, which significantly reduces the incidence of side effects. However, this method is used relatively rarely, which is associated with the high cost of equipment [13].

In our country, tolperisone is widely used - a centrally acting muscle relaxant, similar in structure to lidocaine. The drug stabilizes nerve cell membranes. The use of tolperisone has shown high efficacy and safety in reducing muscle tone in spasticity in several controlled studies [23, 24].

In Russia, a comparative study was conducted on the effectiveness of various muscle relaxants in patients with post-stroke spasticity, the results of which showed a decrease in the degree of spasticity and an improvement in everyday adaptation in patients taking tolperisone and tizanidine. In this case, tolperisone was prescribed at a dose of up to 900 mg/day. During the study, no significant side effects were identified when taking tolperisone [23]. However, there have been no large international studies of this drug in post-stroke spasticity. It is advisable to start treatment with tolperisone with a daily dose of 300 mg, which, if necessary, can be increased to 900 mg.

Other oral medications used to reduce muscle tone in spasticity are benzodiazepines, gabapentin and dantrolene (not registered in Russia). However, no data have been obtained on their effectiveness in post-stroke spasticity [13].

The literature discusses the possibility of combining various muscle relaxants in order to achieve maximum effect. To date, there is no evidence base for recommending any combinations of drugs; however, the likelihood of additive side effects increases, and therefore attempts to combine oral muscle relaxants seem irrational [13].

Conclusion

Regardless of the severity of post-stroke spasticity, it should be remembered that spasticity increases significantly in the presence of pain syndromes, bedsores, constipation, and urinary tract infections. Treatment of these conditions, as well as providing a comfortable environment, are necessary conditions for correcting spasticity and improving the patient’s quality of life. Pharmacological treatment should be individualized and carried out over a long period of time. The dose of the selected drug should be increased gradually until a clinical effect is achieved. In the absence of significant effect from oral medications, it is necessary to consider a combination of pharmacotherapy and surgical methods for the treatment of post-stroke spasticity.

Gabapentin addiction

The rapid development of dependence on gabapentin is explained by the rapid emergence of body resistance to a certain dosage of the drug. The desired effect is not achieved, and the withdrawal syndrome makes itself felt fully, which forces the drug addict to increase the dosage.

Overdose

As with any drug, using too much gabapentin can lead to an overdose. The reaction depends on the dose, and it will be individual for everyone: the gastrointestinal tract will react more strongly in some, the heart and blood vessels in others, and others may fall into a coma. In general terms, the symptoms of an overdose are as follows:

• depressed state, drowsiness;
• speech problems;
• double vision;
• breathing problems;
• vomiting and/or diarrhea.

If the dose is very large, death is possible, especially in combination with alcoholic beverages.

Gabapentin poisoning: first aid

In case of overdose, first of all, it is necessary to keep vital functions under control. You should definitely call an ambulance. Primary measures include gastric lavage and taking sorbent medications. There are no antidotes for gabapentin. Treatment is mainly symptomatic, but if necessary, hemodialysis can be performed in a hospital setting. In some cases, resuscitation measures may be required.

Withdrawal

Drug withdrawal, or withdrawal syndrome, can occur even in people who take gabapentin for therapeutic purposes, not to mention pharmaceutical drug addicts. Withdrawal syndrome is characterized by such phenomena as: changes in blood pressure and body temperature, severe pain in joints, muscles, and head. A depressive state reaches its peak, irritability and aggressiveness arise, sleep is disturbed, and appetite disappears.

This condition may last up to 10 days after stopping the drug. Moreover, in a more or less mild version, these manifestations will persist for another 1-1.5 months.

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Comparison of ease of use of Mydocalm and Sirdalud

This includes dose selection taking into account various conditions and frequency of doses. At the same time, it is important not to forget about the release form of the drug; it is also important to take it into account when making an assessment.

The ease of use of Mydocalm is approximately the same as Sirdalud. However, they are not convenient enough to use.

The drug ratings were compiled by experienced pharmacists who studied international research. The report is generated automatically.

Last update date: 2020-12-04 13:48:04