Antidepressants without a prescription: what they are, how they differ from tranquilizers. The use of selective serotonin reuptake inhibitors in neurological practice Selective serotonin agonists

For quotation: Yavorskaya S.A. The use of selective serotonin reuptake inhibitors in neurological practice // RMJ. 2007. No. 5. P. 429

In modern medicine, the problem of depression is considered one of the most important. The relevance of the problem is determined by the widespread prevalence of depressive disorders in the general population, their tendency to be protracted and chronic, as well as the often high risk of suicide. The increase in the number of patients with depressive disorders has an increasing impact on the socio-psychological and economic aspects of life and health of society. Depressive conditions are currently one of the most common mental disorders - its prevalence by the 90s of the twentieth century in the population of European countries and the United States was 5-10%. According to WHO forecasts, by 2020 depression will become one of the main causes of disability. Depressive disorders that develop in somatic and neurological diseases reduce the quality of life of patients and affect the course and prognosis of the disease. Depression often occurs under the guise of dementia and conversion disorders, which can make it difficult to recognize. Late diagnosis of depressive and depressive-anxiety disorders and untimely initiation of treatment contribute to the chronic course of the disease and aggravation of the severity of the condition and often lead to difficulties in further therapy. However, the prevalence of depression in patients with somatic and neurological pathologies has not been sufficiently studied, and the literature provides rather heterogeneous information regarding its frequency and severity.

The development of depression can be situationally determined, but in neurological patients it is usually caused by organic brain damage or an imbalance of neurotransmitter systems. Patients with chronic neurological diseases are more susceptible to depression than patients with somatic pathology. Neurological diseases that can cause depression are numerous. This disorder is one of the common symptoms in Parkinson's disease, parkinsonism syndrome, acute and chronic cerebrovascular diseases, degenerative dementias, pain syndromes, multiple sclerosis, and brain tumors. Encephalopathy, which develops in the late stages of liver and kidney failure, a number of endocrine, hematological and systemic disorders, and alcoholism, is also often accompanied by the development of depression, which is associated with hypoxic, dysmetabolic and toxic damage to the brain. Depressive disorders can be caused by long-term use of medications. The list of these drugs is quite large, and many are widely used. These are b-blockers, calcium channel blockers, corticosteroids, anabolic steroids, oral contraceptives, cardiac glycosides, barbiturates, clonazepam. Neuroleptic depression occurs against the background of long-term use of large doses of antipsychotics (buterophenones, fluphenazine, chlorpromazine, risperidone) and is accompanied by extrapyramidal disorders. Depressive disorders can occur under the guise of dementia and may accompany its development. At the same time, depression is often observed in vascular dementia and less often in Alzheimer's disease.
The modern pathomorphosis of depression has led to a change in its clinical picture, an increase in the frequency of atypical, hidden, erased forms. Currently, the proportion of typical cases is only 10%, and the bulk of depression occurs atypically. In the practice of a neurologist, depression most often appears under the guise of vegetative dystonia syndrome, chronic pain syndromes, insomnia, and neuroendocrine disorders. The most striking manifestations of vegetative dystonia syndrome include vegetative crises (panic attacks). Another very common mask for depression is chronic pain syndromes, including in children. Depression accompanies and can intensify conversion disorders within psychogenic and psychoorganic diseases.
The mechanisms underlying depression are currently being actively studied. It has been shown that not only the limbic system, but also cortical structures are involved in emotional reactions. Particular importance is attached to the frontal lobes of the brain. In a number of mental disorders that have traditionally been considered “functional,” morphological changes in the nervous tissue have been identified, not only at the microstructural level (in the form of atrophy of synapses, shortening of dendrites and death of some neurons), but also at the macrostructural level (in the form of a decrease in the volume of the hippocampus and some other parts of the brain). Moreover, in recent years it has been shown that pathological processes in the brain can be partially reversible under the influence of therapy with drugs that have neurotrophic and neuroprotective properties. According to some data, with depression, signs of hyperreactivity of the hypothalamic-pituitary-adrenal system are found; there is also information about an increase in the number of neurons secreting corticotropin-releasing factor. 33-66% of patients with depression have adrenal hyperplasia, and cortisol levels are elevated and positively correlate with the severity of the condition. Chronic hypercortisolemia contributes to the formation of insulin resistance, arterial hypertension, overproduction of steroids, hyperglycemia, hypercholesterolemia, which increase the risk of cardiovascular complications. According to experimental data, in situations of chronic pain, emotional or social stress (which are models of depression), the volume of the hippocampus statistically significantly decreases (up to 10%, as in patients with depression), the number of granular cells in the dentate gyrus decreases, and in the CA1 and CA3 fields of the hippocampus the size of the bodies of pyramidal cells decreases and atrophy of their dendrites develops (up to 50% of the length), which leads to disruption of the normal functioning of the limbic system and its connections with other parts of the brain. Thus, the effects of chronic stress and affective disorders in humans, as well as behavior disorders similar to depression in animals, are associated with damage and death of brain cells. These findings are consistent with the idea that anxiety disorders caused by stressors may not only precede, but also cause, at least some forms of depressive disorders. The predominant localization of morphological changes primarily in the limbic system, basal ganglia and rostral cortex may explain the disorders of both emotional, motor and cognitive functions that develop with depression. It is assumed that these morphological changes are a consequence of the cytotoxic action of a number of agents, primarily excitatory amino acids and possibly calcium. The development of excitotoxicity is greatly facilitated by the increased levels of corticosteroids (mainly cortisol) noted in depression and the deficiency of g-aminobutyric acid. It is possible that a number of disorders are based on neurotransmitter dysfunctions, most likely associated with a deficiency of central serotonergic and noradrenergic structures. Some authors also mention the role of hypoglycemia and a possible decrease in cerebral blood flow in the pathogenesis of depression. Of particular importance in the pathogenesis of depression in the elderly is given to vascular damage to the subcortical-frontal connections with the occurrence, in addition to depression, of impaired executive functions, psychomotor retardation, and apathy. Currently, several pathophysiological mechanisms of the influence of depression on the state of the cardiovascular system in the elderly are being considered. One of the main pathological processes in depressive disorders is an imbalance of the autonomic nervous system with activation of the sympathetic department. Increased release of catecholamines leads to an increase in myocardial oxygen demand due to an increase in heart rate, blood pressure and the force of myocardial contraction. It has been established that the appearance of depression in patients with diseases of the cardiovascular system is accompanied by a significant decrease in heart rate variability, reflecting a deterioration in regulatory mechanisms and a decrease in the body’s adaptive capabilities in response to stress.
An achievement of neuroscience in recent years has been evidence that the destructive processes occurring in affective disorders are partially reversible under the influence of successful therapy with drugs that exhibit neurotrophic and neuroprotective properties. The restoration of brain tissue and its functions is associated with the reorganization and formation of new synapses, lengthening and sprouting of dendrites and axons with neurogenesis. The effect of antidepressants is not limited to their regulatory influence on the content of monoaminergic neurotransmitters in the synaptic cleft and in presynaptic structures, as well as on the number and sensitivity of postsynaptic receptors, but also extends to intracellular cascades of neurochemical processes. One of the compounds formed in this case is cAMP element-binding protein (CREB), which activates the “late” gene of the brain derived neurotrophic factor (BDNF), which, in turn, enhances the expression of the gene for the main cytoprotective protein bcl-2, suppresses apoptosis, which promotes the recovery and survival of neurons.
Symptoms of depression may be obvious. Along with depression (in typical cases in the form of vital melancholy), depression includes ideational and motor inhibition with a decrease in motivation for action or anxious arousal (up to agitation). The mental hyperalgesia (mental pain) characteristic of depressed patients is associated with feelings of guilt, decreased self-esteem, suicidal thoughts, and a painful physical feeling is associated with “somatic” symptoms, such as sleep disorders with difficulty falling asleep and early awakenings; a sharp decrease in appetite and body weight; decreased libido and menstrual irregularities, including amenorrhea, etc. Low mood usually persists throughout the entire depressive attack. A typical sign of depression is also a circadian rhythm with improvement or (less often) worsening of well-being in the evening. Atypical manifestations of depression are the absence in some cases of complaints of low mood or the patient’s fixation on excitability or anxiety rather than low mood. Pain and psychosomatic disturbances may also be atypical manifestations of depression. The diagnostic criteria for masked depression are: frequent discrepancy between the patient’s complaints and the nature of the morphological changes; the possibility of the absence of objective signs of somatic disease; frequency (seasonality) of manifestation of disease symptoms; remitting course with a possible change in phases of exacerbations and relapses; connection between well-being and the biological rhythm of physiological functions (patients feel better in the evening); frequent repeated requests for medical care; insufficient effectiveness of symptomatic therapy or lack thereof; improvement of well-being while taking antidepressants.
The identification of depressive disorders is greatly facilitated by the use of psychometric scales and tests, the use of which can reduce the doctor’s time spent on examination. The most famous among the subjective psychometric scales for screening depression are the Hospital Anxiety and Depression Scale, the Zung scale, and the Beck Depression Inventory [A. Beck, 1961].
The basis for diagnosing depression is the assessment of medical history and clinical data. The results of paraclinical examination methods (including neuroimaging) are not of great importance; they only help to exclude neurological or somatic causes of the disease. The detection rate of depression by general practitioners does not exceed 50%. To a certain extent, this is due to the low specificity of the clinical manifestations of this disease. For example, weight loss and increased fatigue can occur not only with depression, but also with cancer, diabetes and thyroid diseases.
In neurological practice, diagnosing depression is difficult not only because of the frequent combination of neurological symptoms and depression when the central nervous system is damaged, but also because of the influence of neurological disease on the emotional behavior of the patient. Thus, the slowness and paucity of movements characteristic of parkinsonism, combined with a violation of the rhythm and intonation of speech, makes it difficult to correctly assess the emotional status. This task becomes even more complicated in patients with severe cognitive or speech disorders of various origins. Complaints of chronic pain, one of the most common “masks” of depression, deserve close attention. A combination of depression and chronic pain syndromes is observed in 50-60% of patients.
Antidepressant therapy is the mainstay of treatment for depressive conditions. The question of starting drug therapy becomes relevant if symptoms persist for 2-4 weeks or more. It should be noted that about 50% of cases of treatment failure are associated with its inadequate use. The most common mistakes, in addition to untimely initiation of treatment, as well as insufficient consideration of clinical indications and contraindications for the drug, are the implementation of routine (without taking into account individual characteristics) low-dose therapy or, conversely, frequent changes, “juggling” drugs without observing the required exposure duration, or premature discontinuation of therapy, or patient ignoring medical prescriptions. As is known, in many cases the clinical effect develops gradually, and suppression of current psychopathological symptoms does not yet mean achieving stable remission and the end of treatment. The effect of antidepressants usually does not appear immediately, but several weeks (usually from 3 to 6) after the start of treatment, about which the patient must be informed in a timely manner. After regression of depression symptoms, therapy is continued for 4-5 months. Treatment failure associated with true drug resistance is very rare, therefore, only if the effect of the selected drug in an adequate dose does not appear after 6-8 weeks, they switch to an antidepressant of another group. It is important to emphasize that in most cases, the lack of effect of treatment is not due to true drug resistance, but to an insufficient dose or short duration of therapy, as well as non-compliance with medical prescriptions. The possibility of psychotherapy, which, if necessary, can be supplemented with antidepressants, is currently being discussed, but the effectiveness of such a therapeutic approach requires further study.
In neurological practice, one often has to deal with restrictive tactics of using antidepressants. Of those with an epidemiological diagnosis of depression in outpatient practice (scoring more than 18 points on the depression scale of the Center for Epidemiological Studies), 72.2% of patients received treatment. However, as a rule, herbal medicines and tranquilizers were used. Only 8.7% of patients with depression took antidepressants. If drugs of this group were nevertheless prescribed, then, as a rule, in fairly low daily doses. The Russian multicenter study Compass found that neurologists are only slightly more likely than other specialists (generalists, cardiologists) to prescribe any therapy for depressive conditions in general (74% versus 67.2 and 67.8%, respectively) and thymoleptics, in in particular (14.1% versus 7.2 and 6.5%, respectively). Thus, the role of drug treatment for depression requires additional discussion.
Antidepressants are medications that help reduce ideational, motor and somato-vegetative disorders caused by depression. The clinical effect of modern antidepressants is based on the correction of the functions of the serotonergic and noradrenergic systems of the brain. The classification of antidepressants according to the mechanism of neurochemical action is very convenient (Table 1). Among the clinical classifications of antidepressants, the most widespread is the convenient and simple classification of P. Kielholtz, distinguishing drugs with predominantly sedative, stimulating or balanced effects (Table 2). The scientific development of modern antidepressants, on the one hand, is moving towards increasing the specificity of their biochemical action. In particular, selective agonists and antagonists of monoamine neuroreceptors are synthesized and tested. Substances have been found that selectively act on certain types of receptors (5HT1, 5HT2, and 5HT3 serotonin receptors). Examples include direct agonists of 5HT1a serotonin receptors (flesinoxan, ipsapirone, etc.). At the same time, there remains a tendency to develop agents with a broad effect on various monoamine systems with minimal effect on receptors, which are associated with the development of side effects (milnacipran, venlafaxine, nefazodone, mirtazapine, duloxetine, etc.). And finally, the mechanism of action of some drugs with thymoanaleptic activity is not directly related to the monoamine system or is not clear enough (for example, tianeptine, alprazolam, S-adenosylmethionine, neuropeptides, etc.).
Among the most studied on the pharmaceutical market over the past two decades, the so-called third generation antidepressants, which are representatives of a new class of pharmacological agents - selective serotonin reuptake inhibitors, have become widespread. These include, in particular, fluvoxamine.
Unlike tricyclic antidepressants, selective serotonin reuptake inhibitors are more targeted to a wide range of neurotic-level depressive conditions. They have a greater spectrum of psychotropic effects with fewer side effects. Nuclear variants of the melancholic syndrome of endogenous depression with typical circadian symptoms, severe (psychotic) depression and depressive-delusional states respond worse to therapy with serotonin reuptake inhibitors. On the contrary, depressive states with obsessive-phobic, hypochondriacal and anxious symptoms of a neurotic level are treated quite successfully. In addition to depression with atypical symptoms, serotonergic antidepressants have been shown to be highly effective in anxiety and obsessive-compulsive disorders in their pure form or comorbid with depression, as well as panic disorder, post-traumatic stress disorder, social phobia, somatoform disorders and other anxiety disorders.
An analysis of a number of randomized trials comparing the clinical effect of a group of selective neuronal reuptake inhibitors with tricyclic antidepressants, such as imipramine, found similar beneficial effects of non-selective and selective drugs. When summing up the results of all clinical trials, it became clear that selective drugs do not have any clear advantages over the standard tricyclic antidepressants. The negative effects of drugs in these groups differ significantly. For example, sedation, anticholinergic effects, and cardiac arrhythmias are less likely to occur with selective serotonin reuptake inhibitors than with conventional antidepressants. On the other hand, the negative effects of selective neuronal reuptake inhibitors affect the gastrointestinal tract, causing nausea and diarrhea, and may also lead to insomnia, agitation, extrapyramidal disorders (drug-induced parkinsonism) and withdrawal symptoms. When comparing the negative effects of selective neuronal reuptake inhibitors and conventional antidepressants, one cannot help but come to the conclusion that one group of negative effects is replaced by another and there is no difference in the number of people who can take these two groups of antidepressants. Fifty-eight clinical trials looked at patients who stopped taking antidepressants and found no significant difference between selective neuronal reuptake inhibitors and conventional antidepressants.
Thus, numerous scientific studies of this group of drugs, including those conducted in comparison with standard tricyclic antidepressants traditionally used in psychiatry and neurology in the treatment of depression (amitriptyline, imipramine, clomipramine, etc.), have shown their high therapeutic effectiveness, comparable to tricyclics compounds, with fewer side effects. However, despite belonging to the same group of chemical compounds, the spectrum of antidepressant activity of various selective neuronal reuptake inhibitors has its own characteristics, which determine the preferential indications for their individual use and deserve discussion.
Fluvoxamine is the founder of the antidepressants of the group of selective serotonin reuptake inhibitors, the first and most widely studied drug of this group. Fluvoxamine is registered in more than 80 countries and has the largest database of clinical studies (among antidepressants), including a description of the treatment results of 38 thousand patients. To date, more than 5,000 scientific papers devoted to the study of the drug have been published. The drug has been successfully used since 1983 in the treatment of depressive disorders of varying severity, as well as so-called borderline mental disorders (anxiety, panic, obsessive-compulsive, behavioral, etc., including in children over 8 years old). The mechanism of action of fluvoxamine is associated with selective inhibition of serotonin reuptake by brain neurons and is characterized by minimal effects on noradrenergic transmission. Fluvoxamine has an unexpressed ability to bind to a-adrenergic, b-adrenergic, histaminergic, muscarinic cholinergic, dopaminergic or serotonergic receptors. Fluvoxamine has pronounced anxiolytic and sedative properties and is the drug of choice for the treatment of depression in combination with anxiety, panic and psychomotor agitation. The drug is also distinguished by moderate psychostimulating activity, which results in the absence of suicidogenicity, hyperstimulation, increased irritability, and sleep disturbances. The powerful vegetative stabilizing effect of fluvoxamine is especially important in the treatment of neurotic, somatized depression and dysthymia. Lack of behavioral toxicity does not impair attention, memory and cognitive function. Fluvoxamine is an effective antidepressant in the treatment of depression of various types and varying degrees of severity. This is confirmed, in particular, by meta-analysis data, according to which fluvoxamine is the drug of choice in the treatment of patients with severe depression in a hospital setting. In addition, fluvoxamine has been shown to be effective in preventing relapses of depression. After a course of treatment with the drug, relapses developed three times less often, and the period of remission before the first relapse was twice as long as when using placebo. The pronounced antiqueering effect of fluvoxamine eliminates or reduces pathological craving for alcohol. In psychiatric practice, the drug has demonstrated good effectiveness in correcting negative (deficient) symptoms in patients with schizophrenia.
In the clinical department of endogenous mental disorders and affective states of the Scientific Center for Mental Health of the Russian Academy of Medical Sciences, fluoxetine, fluvoxamine, sertraline and paroxetine were clinically studied at different periods. A total of 129 patients with endogenous depression underwent a course of treatment with these drugs. Fluvoxamine reduced the severity of depression in this group to a mild degree already by the 5th day of treatment, but its “significant” therapeutic effect was recorded after the 14th day (second week) of treatment, and by the end of the course of treatment, the total score of depressive symptoms on the Hamilton scale decreased by 64.6%. Fluvoxamine has shown a good therapeutic effect equally in mild and moderate depressive states, which, provided it has been well studied, makes it the drug of choice for this group of conditions. The thymoleptic effect of fluvoxamine appeared at the level of 76.1%, while the sedative-anxiolytic and stimulating components of the action of fluvoxamine were almost the same and less profound, they appeared at the level of 67.8 and 64.5%, respectively. Izmailova I.G. et al. evaluated the effect of fluvoxamine in a group of children with tension-type headache. The initial dose of fluvoxamine was 12.5 mg at night, with a further gradual increase in the dose of 12.5 mg every two days to the optimal daily dose of 50-75 mg. The course of treatment was 1.5-2 months. This pharmacotherapy was combined with massage, psychotherapy, and physiotherapy. Patients began to notice a clinical effect in the form of a reduction in headaches and an improvement in mood by the end of the first week of treatment; no side effects were observed. After 1.5 months of therapy, the existing disorders were completely relieved in 25 children; 5 children showed a decrease in the intensity and frequency of cephalalgia attacks. A dynamic study of psycho-vegetative status showed a significant decrease in astheno-vegetative and anxiety-depressive disorders to values ​​close to normal, which confirms the anxiolytic, antidepressant, vegetotropic and mild antiasthenic effect of the drug in the pediatric population. Follow-up (6 months) confirmed the preservation of the achieved results in 20 children.
Therapy with antidepressants of various structures has traditionally been used for a long time in chronic alcoholism. A number of domestic and European researchers convincingly speak out in favor of central serotonin deficiency as the main neurochemical mechanism for the development of depression in alcoholism. With the help of antidepressants, you can not only influence depressive disorders, but also stop the pathological craving for alcohol. And in this regard, selective serotonin reuptake inhibitors, which reduce pathological craving for alcohol, are most preferable. According to numerous domestic data, it is fluvoxamine - an antidepressant “predominantly sedative with pronounced not only thymoanaleptic, but also vegetostabilizing and anxiolytic effects” - that is most preferable for chronic alcoholism and drug addiction due to the high comorbidity of alcoholic depression, anxiety, phobia, somnology, somatovegetative disorders, and also aggressiveness and suicidal behavior.
The good tolerability of fluvoxamine, in particular the absence of sedative side effects, allows it to be used in outpatient practice, without reducing the patient’s quality of life. It is important to emphasize that fluvoxamine is not only the most studied, but also the most economically accessible drug from the group of selective serotonin uptake inhibitors. The most important condition for the success of treatment is a rational combination of pharmacotherapy with social rehabilitation and psychotherapeutic measures, including psychoeducational work with the active involvement of the patient and his relatives in the treatment process.

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Numerous studies have shown that selective serotonin reuptake inhibitors (SSRIs) are as effective as TCAs but are better tolerated by patients. The most common side effects of SSRIs are nausea, headache,

nervousness, sleep disturbances and diarrhea are quickly transient.

The better tolerability of drugs in this group makes it possible to use them to treat elderly and somatically weakened patients. In addition, compared to TCAs, SSRIs have a wider safety margin in the event of overdose. Selective serotonin reuptake inhibitors include drugs such as paroxetine, sertraline, fluvoxamine, fluoxetine and citalopram.

Fluoxetine. Syn. Prozac, Fluxonil. The drug is completely devoid of antihistamine, anticholinergic and adrenolytic effects. The drug has a distinct thymoanaleptic effect with a predominantly stimulating component and is especially effective for obsessive-phobic symptoms. Mainly used

for depression of a neurotic level, including somatization and dysthymic disorders, and shallow endogenous depression with lethargy. According to Mosolov (1995), when using fluoxetine, the reduction of symptoms develops quite harmoniously, apathetic depressive affect, somato-vegetative manifestations, ideas of low value and other symptoms are gradually reduced. In general medical practice, for mildly expressed anxiety depression, the use of the drug in a standard dosage gives a clear tranquilizing effect. Fluoxetine is also indicated for obsessive-phobic disorders, premenstrual tension syndrome, and personality pathology accompanied by excessive irritability and increased aggressiveness. Side effects when using fluoxetine are as follows: dyspeptic disorders, allergic reactions, sexual dysfunction. Since fluoxetine is a fairly powerful inhibitor of the activity of cytochrome P 450 IID6 and P 450 IIIA4 enzymes, it can increase the clearance, half-life and blood levels of all drugs metabolized through them. Due to the long half-life from the body, the drug is used with caution in patients with liver disease, kidney disease, pregnancy and lactation.

Doses and application. The drug is used once a day or once every 2-3 days in average doses of 20 to 40 mg in the morning with food. In elderly patients, the drug can be taken at a dose of 5-10 mg/day. The clinical effect develops from the end of 1 week to 4 weeks of therapy, and in some patients after 8-12 weeks of therapy.

Available in capsules containing 20 mg of fluoxetine hydrochloride (Prozac), or 10 and 20 mg of fluoxetine.

Trazodone. Selective serotonin reuptake inhibitor; characterized by moderate antidepressant and tranquilizing properties. Contraindications: hypersensitivity; pregnancy and breastfeeding. Side effects: increased fatigue, drowsiness, headache, dizziness, insomnia, decreased blood pressure, nausea, vomiting, priapism. Precautionary measures. For epilepsy, liver and kidney diseases, myocardial infarction, the drug is prescribed with caution and according to strict indications. The use of trazodone, as well as other SSRIs with MAOIs and some other drugs (furazolidone, procarbazine, selegiline) is unacceptable. Doses and application. Single dose 25-50 mg, average daily dose 100-300 mg. Syn. Azona. Table 25, 50 and 100 mg. Trittico. Retard tablets 75 and 150 mg.

Fluvoxamine. Selective serotonin reuptake inhibitor (SSRI). It has antidepressant anxiolytic and vegetostabilizing effects. It does not have anticholinergic, antihistamine or adrenolytic effects. Does not have cardiotoxic or hypotensive side effects. Indications: a wide range of depressive conditions, obsessive-compulsive disorders. Doses and application. The average dose is 100-200 mg once a day, the maximum dose is 400 mg. Syn. Fevarin. Table 50 and 100 mg.

Sertraline Syn. Zoloft®, Stimuloton®. It is a powerful selective inhibitor of serotonin reuptake and does not cause blockade of muscarinic, serotonin, adrenergic and GABAergic receptors. The basis of the profile of psychotropic activity is a clear thymoanaleptic effect with a weak stimulating component. In terms of the rate of reduction of depressive symptoms, sertraline is somewhat inferior to fluoxetine. Sertraline has a positive effect on patients with anxious depression and sleep disorders. The drug is effective for somatized and atypical depression with symptoms of bulimia and weight gain, for obsessive-phobic disorders, in elderly patients or with concomitant somatic pathology without reducing the effective dose - 50-200 mg/day.

Side effects include dry mouth, delayed ejaculation in men, tremors and sweating. Precautionary measures. The use of sertraline with MAO inhibitors is unacceptable, since the development of serotonin syndrome (confusion, hypomanic state, psychomotor agitation, chills, tremor, diarrhea) is possible. At least 2 weeks should elapse from the moment of discontinuation of MAOI therapy before starting sertraline therapy; after stopping sertraline before starting MAOI therapy - at least 5 weeks.

The drug is prescribed with caution for epilepsy. Doses and application. The initial dose for depression and obsessive-compulsive disorder is 50 mg/day, regardless of food intake and time of day. For panic and post-traumatic stress disorder, the initial dose may be 25 mg/day. If necessary, the dose can be increased gradually over several weeks to a maximum of 200 mg/day. Available in the form of tablets 50 and 100 mg No. 28.

Paroxetine (syn. Paxil, Paroxin) is one of the most powerful specific serotonin reuptake blockers among the SSRIs. The drug has a thymoanaleptic, anxiolytic and stimulating effect. Unlike other SSRIs, paroxetine can be successfully used not only for mild, but also for severe classic endogenous depression. Reduction of symptoms occurs from 1 week of treatment. Unlike fluoxetine, paroxetine does not cause hyperstimulation, increased agitation, or sleep disturbance. It is indicated for pain in patients with diabetic neuropathy and is safe for elderly patients. Doses and application. The doses used are 10-50 mg/day. The optimal dose is 20 mg of the drug taken with food once a day. The drug should not be prescribed for impaired liver and kidney function, during pregnancy and lactation. Available in tablets of 20 mg No. 30.

Citalopram - in vitro is the “standard of selectivity” among SSRIs. It has no or very weak ability to bind to a number of receptors, including histamine, muscarinic and adrenergic receptors. This circumstance largely explains the absence of such side effects as cardiotoxicity, orthostatic hypotension, sedation and dry mouth. Cipramil inhibits cytochrome P 450 IID6 only to a very small extent and, therefore, does not interact with drugs metabolized by this enzyme. It does not affect the conduction system of the heart and blood pressure, hematological parameters, liver and kidney function. Tsipramil does not reduce intellectual abilities and psychomotor reactions. Therefore, cipramil is the drug of choice for the treatment of depression in general medical practice. It exceeds the speed of onset of effect of typical SSRIs, is non-toxic and does not lead to death even with a significant overdose. Easy to use and can be used to prevent depression. Doses and application. Tsipramil is taken 1 time per day, regardless of meals, at any time of the day. The initial dose is 20 mg. Depending on the patient's individual response and the severity of depression, the dose may be increased to 60 mg. In general medical practice, elderly patients are prescribed 20-40 mg orally per day at a time. Available in tablets of 20. No. 14, 28, 56 and 40 mg No. 28.

Escitalopram Syn. Cipralex® - S is an enantiomer of the racemic drug citalopram. The drug is a highly selective SSRI that acts by specifically competitively inhibiting the membrane serotonin transporter. Studies have demonstrated the effectiveness of escitalopram at a dose of 10-20 mg/day in the treatment of depression, with higher efficacy and earlier correction of symptoms compared to citalopram. The effectiveness of escitalopram is comparable to that of venlafaxine. It has been proven that escitalopram at a dose of 10-20 mg/day reliably corrects symptoms of anxiety and depression in patients with major depressive disorder, and also causes faster elimination of anxiety symptoms compared to citalopram. The drug is also effective for panic attacks and generalized anxiety disorder. Adverse events that may occur in the first weeks of treatment decrease during therapy. Contraindications: pregnancy and breastfeeding. Issued in table. 10 and 20 mg No. 28.

Serotonin is an important substance related to the mediators of the nervous system of the human body. People call it the hormone of happiness.

Serotonin received its name due to the activation of positive emotions and a beneficial effect on the psychoneurological state of a person.

The main task of serotonin is to regulate neuronal function. In the central nervous system, this substance has the following effects:

• improves mood;
• improves memory;
• regulates the speed of cognitive reactions;
• normalizes appetite;
• organizes food cravings;
• regulates sexual desire;
• responsible for social behavior.

It is accompanied by muscular, autonomic and mental disorders, which have a high risk of death.

To prevent the syndrome, it is unacceptable to take SSRIs together with MAO inhibitors.

Combinations with the following types of drugs can lead to the same condition:

• tetracyclic antidepressants;
• herbal remedies with the addition of St. John's wort;
• Levodopa;
• antimigraine drugs;
• mood stabilizers;
• atypical antipsychotics.

If you have previously used any medications, you must wait at least two weeks before starting to take an SSRI.

Depending on the type of drug, this period may be changed. Replacing Fluoxetine with Paroxetine requires a break of 2-3 weeks. For older patients, this period increases to 8 weeks.

Comparison of reuptake inhibitors: which is better?

If you seek medical help, a specialist will definitely select the appropriate medicine and tell you how to use it as productively as possible for your health.

Many years of experience in use and consumer reviews allow us to schematically outline the advantages and disadvantages of the drugs.

It is impossible to say for sure which is the best selective serotonin reuptake inhibitor.

All medications have features of use, restrictions and individual dosage regimens.

Depression is a very common phenomenon that is difficult to ignore. The chronic form of this condition can become a threat not only to health, but also to human life. People perceive the world around them differently and find themselves in different life situations. If a person’s potential is not realized, he faces an insoluble problem - they develop depression.

They can be caused by hormonal age-related changes, frequent stressful situations, chronic (or incurable) illness, or disability. These factors lead to a general biochemical failure. The level of pleasure hormones (endorphins, in particular) in the body sharply decreases serotonin). This is expressed in dissatisfaction with oneself, a depressed state, lack of will and desire to change anything.

SSRI - C Selective Serotonin Reuptake Inhibitors

It is very difficult to get out of this state. Support from loved ones, specialist help, and medication are often necessary. Medicines, developed to treat depression, are called antidepressants. They have a different mechanism of action, but the dynamics of the patient’s condition when using them is definitely positive.

Such facilities have virtually no effect on a healthy person. In people who suffer from depression after treatment antidepressants, mood improves, anxiety, melancholy, and apathy go away. Their psychological stability returns, sleep and biological rhythms normalize, and their appetite improves.

Third-generation drugs for effectively combating depression are selective serotonin reuptake inhibitors.

Classification of antidepressants

Depression has been known to mankind since time immemorial, as have ways to overcome it. In ancient Rome, the famous physician Soranus of Ephesus used lithium salts to treat them, for example. Cannabis, opium, barbiturates, amphetamines are all numerous attempts to chemically manipulate the body to help people cope with emotional exhaustion.

The first drug to combat depression was Imipramine, which was synthesized in 1948. To date, many have been developed antidepressants, which are currently classified. Depending on the general picture of the manifestation of the mental processes of patients:

• Thymiretics are used for depressed and depressed states;
• thymoleptics have a calming effect, so they are used when there is increased mental arousal.

According to biochemical effects on the body antidepressants there are :

• non-selective action (for example, Melipramine, Amizol),
• selective action: blocking serotonin uptake (for example, Sertraline), blocking norepinephrine uptake (for example, Reboxetine),
• inhibition monoamine oxidases: non-selective action (for example, Transamine), selective action (for example, Autorix).

There are other pharmacological groups of drugs against depression.

How do antidepressants work?

Antidepressants are able to control some processes that occur in brain cells. This organ consists of a huge number of nerve cells. The body and processes are the components of neurons. They transmit impulses between themselves using processes and through the synapse (the space that is located between two neurons).

Antidepressants were discovered by accident while testing drugs against tuberculosis

This space is filled with a special substance (mediator), through which information is transmitted from one neuron to another. About 30 mediators are currently known in biochemistry. But depressive states are associated, as a rule, with only three hormones that function as neurotransmitters: dopamine, norepinephrine.
The mechanism of action of antidepressants is aimed at regulating the concentration of these hormones in the brain and correcting its functioning, impaired as a result of depression.

What are SSRIs

In modern medical practice, the most popular are third generation drugs - selective serotonin reuptake inhibitors. These drugs differ from traditional tricyclic drugs for depression by having fewer side effects and being more effective.

With an overdose of these drugs, virtually no cardiotoxic effect is observed. SSRIs are recommended for patients who have contraindications to the use of conventional antidepressants (for example, closed glaucoma, cardiac arrhythmias).

How the drugs work

One of the causes of depression is decreased concentration of serotonin in the brain. This important neurotransmitter, hormone is called the hormone of happiness, joy, pleasure. Moreover, its normal concentration provides a long-lasting, stable feeling of quiet happiness and harmony.

Serotonin reuptake inhibitor works to increase the concentration of the hormone serotonin in the brain. The active ingredients of this antidepressant selectively block (inhibit) serotonin in the brain. This process occurs directly at the synapse. That is, the reuptake of the hormone by the adhesive does not occur; this process is prevented by the drug.

Serotonin remains in place, so the circulation of nerve impulses continues. They activate cells who are depressed, softening its manifestation. The advantage of drugs in this group is that the dosage is immediately determined by the attending physician; there is no need to increase it, since the additional therapeutic effect does not depend on it.

When using a group of inhibitors, there is no point in monitoring the concentration of serotonin in the blood. An exception may be some diseases of patients, due to which the elimination of drugs from the body slows down.

When are SSRIs prescribed?

Drugs in this group are prescribed for:

• deep depressive disorders;
• stress, panic attacks, neurotic anxiety;
• manias, phobias;
• obsessive-compulsive neuroses;
• bulimia;
• alcoholism;
• chronic pain syndrome;
• emotionally unstable personality disorder.

The effectiveness of treatment largely determines the timeliness of therapeutic measures. For minor manifestations of depressive conditions, there is no significant difference between the effectiveness of treatment with tricyclic antidepressants and SSRIs. But the effectiveness of the latter in the treatment of advanced nervous disorders has been proven by medical practice.

SSRI drugs do not have a therapeutic effect immediately. Depending on the severity of the disease and the individual characteristics of the body, positive dynamics are observed in the second, fifth, and sometimes only the eighth week from the start of taking the medicine.

The daily dosage depends on the rate of elimination of drugs from the body. Most often, the drug is prescribed to be taken once a day, since the half-life of most SSRIs is more than a day.

Side effects

Side effects include some disorders of the digestive system - nausea, vomiting. When using selective serotonin reuptake inhibitors, the following may occur:

• anxiety;
• anxiety;
• dizziness;
• fast fatiguability;
• sleep disturbance;
• sexual disorders.

Reactions to reception blockers depend on the individual characteristics of the organism.

If the patient has problems with the liver, kidneys selective serotonin reuptake inhibitors should be used with caution. Serotonin receptors are located in the human body not only in the brain, but also in the spinal cord. There are many of them in the gastrointestinal tract, respiratory system, and on the walls of blood vessels. When using inhibitors, the above conditions develop, which usually disappear after a month. That is side effects are observed only in the first stages of taking inhibitors.

Side effects of drugs are associated with an increase in the amount of neurotransmitter serotonin in the brain, this affects mental activity. Medical practice describes cases appearance of suicidal thoughts, mania during treatment with inhibitors in adolescents. This manifestation has not been proven in adult patients.

This reaction is individual in nature; among SSRIs, you can choose drugs that do not affect the activation of the psychomotor sphere and have a sedative effect.

If SSRI regimen involves a large dosage, it can develop, which causes convulsions, fever, and heart rhythm disturbances. In this case, the drug is discontinued. Third generation antidepressants easily replace each other, so if treatment is not effective, you can choose another drug. If any of the family members used inhibitors and achieved positive results, it makes sense to opt for this drug.

For treatment complex mental disorders, conditions of chronic depression, SSRIs are prescribed together with other drugs, for example, tranquilizers, tricyclic antidepressants. Complex therapy requires strict adherence to the doctor’s recommendations regarding the regimen and dosage of medications. There are known cases of death due to overdose.

SSRI drugs

List of drugs SSRIs are extensive. Today they are in great demand for treating depression, improving mood, and normalizing sleep. These medicines are available and sold in the pharmacy network without prescriptions. The most common are:

• Paroxetine;
• Fluvoxamine;
• Sertraline;
• Cipramil;
• Fluoxetine.

When choosing a drug, it is worth analyzing the effect of the drug:

Paroxetine

Of all the serotonin reuptake inhibitors Paroxetine is the most effective drug. It is prescribed in an initial concentration of 10 mg or 20 mg. In some cases, the dosage is gradually increased to 50 mg per day. Take the medicine once a day. The half-life of Paroxetine occurs in almost a day. Within a week of taking the drug, a stable concentration is achieved. The drug may cause slight weight gain.

Fluvoxamine

For manifestations of depression in combination with increased anxiety, Fluvoxamine is prescribed. The effectiveness of this drug appears almost immediately after starting treatment and subsequently has a smooth effect on the patient. The drug has proven itself positively in the manifestation of obsessive-compulsive disorder neuroses, social phobias (including in children), and in combination with other drugs has proven itself well in the treatment of schizophrenia.

The initial concentration of the drug is 50 mg once a day; it is recommended to take the drug in the evening. The initial dosage can be increased to 100 mg, the maximum amount is 500 mg (in this case, the regimen includes several doses of the drug). Within 5-7 days, the effective concentration of the active substance is achieved. Fluvoxamine has the largest number of side effects.

Sertraline

Indications for the use of Sertraline are mild depressive states. It does not affect psychomotor functions and has a weak antiphobic effect. The drug is prescribed for the treatment of obsessive-compulsive disorder. It gives a good therapeutic effect and can prevent relapse and the development of depression in the future.

The initial dose of Sertraline is 50 mg per day. The dosage can be gradually increased to 200 mg (50 mg per week). Half-life of active substances affected by the patient's age. With prolonged use of the drug, addiction develops.

Cipramil

Tsipramil is most often prescribed for the treatment of depressive conditions that arise as a result of chronic somatic diseases. In addition, it is indicated for elderly patients who have suffered a cerebral stroke.

The initial dose of Tsipramil is 20 mg per day. The drug is taken once a day in the morning. In most cases, this dose of the drug has a good therapeutic effect. The daily concentration can be increased to 60 mg, depending depending on the severity of the patient's condition.

In the practice of using Tsipramil, its interaction with other drugs is not described. The half-life of the inhibitor is 30 hours. Among the most common side effects are nausea and headache, but they are observed only in the initial stages of taking the drug.

Fluoxetine

Fluoxetine is known as one of the first serotonin reuptake inhibitors. It has been used in medical practice since the early 80s. Prescribed for the treatment of depressive symptoms of varying degrees. Known as an effective drug in the treatment of bulimia.

The medicine is taken in the morning, once a day at a dosage of 20 mg. It can be increased to 40-80 mg. The maximum concentration is observed after 6 hours. This drug has longest half-life- about 3 days, and the half-life of its active metabolite is up to 9 days. This circumstance provides benefits to patients who may miss doses of the drug.

The inhibitor has an effect on the body disinhibitory effect, in the first weeks of use, states of anxiety and restlessness may be observed. This drug slowly relieves signs of depression. The effect is observed only after 2-3 weeks of treatment. At the initial stages and with further use, side effects are noted in the form nausea, headaches, decreased vision, skin allergic manifestations, sexual dysfunction.

Selective serotonin reuptake inhibitors are third generation antidepressants. They allow you to stabilize a person’s emotional state at the biochemical level. SSRIs are effective in treating depression, neuroses, phobias, and obsessive disorders. At maximum efficiency they have minimal side effects.

Antidepressants are medications that are active against depressive conditions. Depression is a mental disorder characterized by decreased mood, weakened motor activity, intellectual poverty, erroneous assessment of one’s “I” in the surrounding reality, and somatovegetative disorders.

The most likely cause of depression is the biochemical theory, according to which there is a decrease in the level of neurotransmitters - nutrients in the brain, as well as a decreased sensitivity of receptors to these substances.

All drugs in this group are divided into several classes, but now let’s talk about history.

History of the discovery of antidepressants

Since ancient times, humanity has approached the issue of treating depression with different theories and hypotheses. Ancient Rome was famous for its ancient Greek physician named Soranus of Ephesus, who proposed lithium salts for the treatment of mental disorders, including depression.

As scientific and medical progress progressed, some scientists resorted to a variety of substances that were used against the war against depression - from cannabis, opium and barbiturates to amphetamine. The last of them, however, was used in the treatment of apathetic and lethargic depression, which was accompanied by stupor and refusal to eat.

The first antidepressant was synthesized in the laboratories of the Geigy company in 1948. This drug became. After this, clinical studies were carried out, but they did not release it until 1954, when it was obtained. Since then, many antidepressants have been discovered, the classification of which we will talk about later.

Magic pills - their groups

All antidepressants are divided into 2 large groups:

1. Thymiretics– drugs with a stimulating effect, which are used to treat depressive conditions with signs of depression and depression.
2. Thymoleptics– drugs with sedative properties. Treatment of depression with predominantly excitatory processes.

Indiscriminate action:

Selective action:

• block serotonin uptake– Flunisan, Sertraline, ;
• block norepinephrine uptake— Maproteline, Reboxetine.

Monoamine oxidase inhibitors:

• indiscriminate(inhibit monoamine oxidase A and B) – Transamine;
• electoral(inhibit monoamine oxidase A) – Autorix.

Antidepressants of other pharmacological groups - Coaxil, Mirtazapine.

Mechanism of action of antidepressants

In short, antidepressants can correct some processes occurring in the brain. The human brain is made up of a colossal number of nerve cells called neurons. A neuron consists of a body (soma) and processes - axons and dendrites. The neurons communicate with each other through these processes.

It should be clarified that they communicate with each other by a synapse (synaptic cleft), which is located between them. Information from one neuron to another is transmitted using a biochemical substance - a transmitter. At the moment, about 30 different mediators are known, but the following triad is associated with depression: serotonin, norepinephrine, dopamine. By regulating their concentration, antidepressants correct impaired brain function due to depression.

The mechanism of action differs depending on the group of antidepressants:

1. Neuronal uptake inhibitors(non-selective action) block the reuptake of mediators - serotonin and norepinephrine.
2. Neuronal serotonin uptake inhibitors: Inhibit the process of serotonin uptake, increasing its concentration in the synaptic cleft. A distinctive feature of this group is the absence of m-anticholinergic activity. There is only a slight effect on α-adrenergic receptors. For this reason, such antidepressants have virtually no side effects.
3. Neuronal norepinephrine uptake inhibitors: prevent the reuptake of norepinephrine.
4. Monoamine oxidase inhibitors: monoamine oxidase is an enzyme that destroys the structure of neurotransmitters, resulting in their inactivation. Monoamine oxidase exists in two forms: MAO-A and MAO-B. MAO-A acts on serotonin and norepinephrine, MAO-B acts on dopamine. MAO inhibitors block the action of this enzyme, thereby increasing the concentration of mediators. The drugs of choice for treating depression are often MAO-A inhibitors.

Modern classification of antidepressants

Tricyclic antidepressants

There is evidence of the effective use of antidepressants as auxiliary pharmacotherapy for early ejaculation and smoking.

Side effects

Since these antidepressants have a diverse chemical structure and mechanism of action, side effects may vary. But all antidepressants have the following common symptoms when taking them: hallucinations, agitation, insomnia, and the development of manic syndrome.

Thymoleptics cause psychomotor retardation, drowsiness and lethargy, and decreased concentration. Thymiretics can lead to psychoproductive symptoms (psychosis) and increased.

The most common side effects include:

• constipation;
• mydriasis;
• urinary retention;
• intestinal atony;
• violation of the act of swallowing;
• tachycardia;
• impairment of cognitive functions (impaired memory and learning processes).

Elderly patients may experience - disorientation, anxiety, visual hallucinations. In addition, the risk of weight gain, the development of orthostatic hypotension, and neurological disorders increases (,).

With long-term use - cardiotoxic effects (cardiac conduction disturbances, arrhythmias, ischemic disorders), decreased libido.

When taking selective inhibitors of neuronal serotonin uptake, the following reactions are possible: gastroenterological - dyspeptic syndrome: abdominal pain, dyspepsia, constipation, vomiting and nausea. Increased anxiety levels, insomnia, increased fatigue, tremors, impaired libido, loss of motivation and emotional dulling.

Selective norepinephrine reuptake inhibitors cause side effects such as insomnia, dry mouth, dizziness, constipation, bladder atony, irritability and aggressiveness.

Tranquilizers and antidepressants: what's the difference?

From this we can conclude that tranquilizers and antidepressants have different mechanisms of action and differ significantly from each other. Tranquilizers are unable to treat depressive disorders, so their prescription and use is irrational.

The power of "magic pills"

Depending on the severity of the disease and the effect of use, several groups of drugs can be distinguished.

Strong antidepressants - effectively used in the treatment of severe depression:

1. – has pronounced antidepressant and sedative properties. The onset of the therapeutic effect is observed after 2-3 weeks. Side effects: tachycardia, constipation, difficulty urinating and dry mouth.
2. Maprotiline,– similar to Imipramine.
3. Paroxetine– high antidepressant activity and anxiolytic effect. Taken once a day. The therapeutic effect develops within 1-4 weeks after the start of administration.

Mild antidepressants - prescribed in cases of moderate and mild depression:

1. Doxepin– improves mood, eliminates apathy and depression. A positive effect of therapy is observed after 2-3 weeks of taking the drug.
2. - has antidepressant, sedative and hypnotic properties.
3. Tianeptine– relieves motor retardation, improves mood, increases the overall tone of the body. Leads to the disappearance of somatic complaints caused by anxiety. Due to the presence of a balanced action, it is indicated for anxious and inhibited depression.

Herbal natural antidepressants:

1. St. John's wort– contains hepericin, which has antidepressant properties.
2. Novo-Passit– it contains valerian, hops, St. John's wort, hawthorn, lemon balm. Contributes to the disappearance, and.
3. Persen– also contains a collection of herbs: peppermint, lemon balm, and valerian. Has a sedative effect.
   Hawthorn, rose hips - have sedative properties.

Our TOP 30: the best antidepressants

We analyzed almost all antidepressants that were available for sale at the end of 2016, studied reviews and compiled a list of the 30 best drugs that have virtually no side effects, but at the same time are very effective and perform their tasks well (each to their own):

1. Agomelatine– used for episodes of major depression of various origins. The effect occurs after 2 weeks.
2. – provokes inhibition of serotonin uptake, used for depressive episodes, the effect occurs after 7-14 days.
3. Azafen– used for depressive episodes. The treatment course is at least 1.5 months.
4. Azona– increases the content of serotonin, is part of the group of strong antidepressants.
5. Aleval– prevention and treatment of depressive conditions of various etiologies.
6. Amizol– prescribed for agitation, behavioral disorders, and depressive episodes.
7. – stimulation of catecholaminergic transmission. It has adrenergic blocking and anticholinergic effects. Scope of application: depressive episodes.
8. Asentra– a specific serotonin uptake inhibitor. Indicated for the treatment of depression.
9. Aurorix– MAO-A inhibitor. Used for depression and phobias.
10. Brintellix– antagonist of serotonin receptors 3, 7, 1d, agonist of serotonin receptors 1a, correction of depressive states.
11. Valdoxan– a stimulator of melatonin receptors, to a small extent a blocker of a subgroup of serotonin receptors. Therapy.
12. Velaxin– an antidepressant of another chemical group, enhances neurotransmitter activity.
13. – used for mild depression.
14. Venlaxor– a powerful serotonin reuptake inhibitor. Weak β-blocker. Treatment of depression and anxiety disorders.
15. Heptor– in addition to antidepressant activity, it has antioxidant and hepatoprotective effects. Well tolerated.
16. Herbion Hypericum– a herbal-based drug, part of the group of natural antidepressants. Prescribed for mild depression and.
17. Deprex– an antidepressant has an antihistamine effect, used in the treatment.
18. Deprefault– a serotonin uptake inhibitor, has a weak effect on dopamine and norepinephrine. There is no stimulating or sedative effect. The effect develops 2 weeks after administration.
19. – antidepressant and sedative effects occur due to the presence of St. John's wort herb extract. Approved for use in the treatment of children.
20. Doxepin– blocker of H1 serotonin receptors. The action develops 10-14 days after the start of administration. Indications -
21. Miansan– stimulator of adrenergic transmission in the brain. Prescribed for depression of various origins.
22. Miracitol– enhances the effect of serotonin, increases its content in the synapse. In combination with monoamine oxidase inhibitors, it causes severe side effects.
23. Negrustin– an antidepressant of plant origin. Effective for mild depressive disorders.
24. Newwelong– serotonin and norepinephrine reuptake inhibitor.
25. Prodep– selectively blocks the uptake of serotonin, increasing its concentration. Does not cause a decrease in the activity of β-adrenergic receptors. Effective for depression.
26. Citalon– a high-precision serotonin uptake blocker with minimal effect on the concentration of dopamine and norepinephrine.

There's something for everyone

Antidepressants are most often not cheap, we have compiled a list of the most inexpensive of them in ascending order of price, with the cheapest drugs at the beginning and the more expensive ones at the end:

The truth is always beyond theory

To understand the whole point about modern, even the best, antidepressants, to understand what their benefits and harms are, it is also necessary to study the reviews of people who had to take them. As you can see, there is nothing good in taking them.

I tried to fight depression with antidepressants. I quit because the result was depressing. I looked for a lot of information about them, read many sites. There is contradictory information everywhere, but everywhere I read it, they write that there is nothing good about them. I myself experienced shaking, pain, and dilated pupils. I got scared and decided that I didn’t need them.

Three years ago, depression began, while I was running to clinics to see doctors, it was getting worse. There was no appetite, she lost interest in life, there was no sleep, her memory deteriorated. I visited a psychiatrist, he prescribed Stimulaton for me. I felt the effect after 3 months of taking it, I stopped thinking about the disease. I drank for about 10 months. Helped me.

Karina, 27

It is important to remember that antidepressants are not harmless drugs and you should consult your doctor before using them. He will be able to choose the right drug and its dosage.

You should monitor your mental health very carefully and contact specialized institutions in a timely manner so as not to aggravate the situation, but to get rid of the disease in time.