If there is not enough serotonin in a person’s body, he falls into deep depression: not only does his mood worsen, but he also experiences apathy, melancholy, anxiety, constant weakness, lethargy, irritability, worsening appetite, and decreased sex drive.

This condition is dangerous because it leads to thoughts of suicide, which a person can realize if the problem is not addressed in time. Antidepressants can relieve a patient from this state; selective serotonin reuptake inhibitors are especially effective.

Serotonin is one of the main neurotransmitters in the body. This is the name for biologically active substances that are formed as a result of certain reactions from amino acids, and whose task is to transmit nerve impulses between two cells (neurons). The transmission of such signals is carried out electrically during the transition of ions from one neuron to another.

Serotonin is produced in one of the parts of the brain, the pineal gland, and controls the functioning of the central nervous system. This makes it possible for the neurotransmitter to control many processes occurring in the human body (serotonin receptors are located not only throughout the nervous system of the body, but are also located on the walls of blood vessels in the digestive system, on the smooth muscles of the bronchi).

Thanks to serotonin, melatonin is formed in the body, which regulates the biological cycle (its deficiency often provokes insomnia). In addition, the neurotransmitter is responsible for regulating a person’s emotional state, preventing psycho-emotional disorders, creating a feeling of happiness and pleasure.

It is also responsible for the production of hormones, normalizes sexual function, takes an active part in preparing the female body for childbirth, promotes blood clotting, normal functioning of the gastrointestinal tract, and regulates brain function.

A deficiency, like an excess of serotonin, affects a person extremely negatively. The lack of a neurotransmitter makes it more sensitive to pain, the biological rhythm is disrupted, the state of the nervous system worsens, resulting in depression, obsessive disorders, and severe forms of migraine. Excess leads to hallucinations and schizophrenia.

To get a person out of this state and normalize the amount of serotonin, various antidepressants and psychotropic medications are used, the main purpose of which is to treat various forms of depression.

Such medications have no particular effect on a healthy person, whereas after a course of therapy in a person suffering from depression, they improve mood, reduce or completely eliminate anxiety, apathy, melancholy, and emotional stress. This leads to psychological stability, normalization of biological rhythm, stabilization of sleep, and improvement of appetite.

Characteristics of SSRIs

Selective serotonin reuptake inhibitors (SSRIs) include fluoxetine, paroxetine, citalopram, sertraline, fluvoxamine, dapaxetine, indalpine, efcitalopram, zimelidine. They are intended to increase the amount of serotonin in the body (it is during depression that the level of the neurotransmitter is reduced).

The active substances of the drugs act by selectively blocking (inhibiting) serotonin in the brain. The blocking occurs in the synaptic space, that is, in the places where nerve cells connect to each other, since this is where electrical impulses pass and signals are transmitted using serotonin.

This prevents the neurotransmitter from returning to the cell from which the message was sent (the medication stops the reuptake of serotonin back into the nerve cell). This leads to the fact that new serotonin is not produced and the signal is transmitted further, activating (exciting) the cells on which depression had a depressing effect, mitigating its symptoms.

It is worth noting that although all SSRI drugs block the return of the neurotransmitter, they differ in their selectivity of action on serotonin receptors and in the degree of effectiveness.

Currently, doctors prefer to work with SSRIs, which are third-generation antidepressants and, unlike earlier drugs, are characterized by milder side effects. Another advantage of drugs in this group is that they are prescribed immediately in the dosage required for successful treatment, and the dose no longer needs to be increased (this is how they differ, for example, from tricyclic antidepressants), since increasing the dosage does not have a special therapeutic effect.

For this reason, there is no particular need for constant monitoring of the amount of serotonin in the blood. An exception is made only for patients who have an accelerated or delayed process of drug withdrawal, since this results in an increased or decreased concentration of serotonin in the blood.

For this reason, selective serotonin reuptake inhibitors are widely used in medicine and can be taken at home. They are usually prescribed for the following diseases:

• major depressive disorder;
• stress, panic disorders, anxiety neurosis;
• phobias, mania;
• obsessive-compulsive disorders;
• bulimia;
• borderline personality disorder;
• chronic pain syndrome;
• alcoholism;
• depersonalization disorder (rarely prescribed because SSRIs are ineffective for this disease).

Application

The effectiveness of SSRIs in the treatment of depression largely depends on at what stage the disease was started to be treated. For mild or moderate depression, the difference between reuptake inhibitors and ordinary antidepressants is small, sometimes even completely absent.

But when it comes to severe depression, the difference is large and even incomparable: it has been clinically proven that after tricyclic antidepressants were replaced by SSRIs, the condition of patients improved in more than thirty percent of cases.

You should not expect instant results from SSRIs: the first signs of the drug’s effectiveness can be seen by the end of the second to fifth, sometimes even the eighth week after the first dose of the medication. How often you need to take the drug depends not only on the severity of the disease, but also on the speed of elimination from the body.

Almost all inhibitors, with the exception of fluvoxamine, have a long half-life (more than a day), which makes it possible to take them only once a day. Fluvoxamine is eliminated after fifteen hours, so you need to take it twice a day.

Side effects

Side effects appear precisely due to an increase in the concentration of serotonin. First of all, this substance is produced in the structures of the brain, so its increase cannot but affect mental activity.

Some studies have shown that after the use of SSRIs in children and adolescents, suicidal thoughts and various types of mania increase. Therefore, they must be carefully monitored during treatment. As for adults, whether suicidal behavior is associated with taking the drug is controversial and has not been proven.

This reaction is due to the fact that while the therapeutic effect of antidepressants is noticeable only after a few weeks, the stimulating or sedative (calming) effect appears within a week after the first dose of the medicine. Eliminate the stimulating effect by prescribing the use of a tranquilizer simultaneously with taking the medication. Despite the risk of suicidal thoughts, various manias during the use of SSRIs are lower when compared with TCAs and MAO inhibitors.

If the patient has thoughts of suicide, it is undesirable to use drugs that can activate the psychomotor sphere, and stick to antidepressants with a sedative (calming) effect. One such SSRI drug is fluoxetine (this drug can trigger the development of mania). There are different opinions about citalopram: some believe that it has a balanced effect, others claim that it has a stimulating effect. There is also no consensus on the effect of paroxetine.

Side effects are also often associated with the fact that serotonin receptors are located not only in the central and peripheral nervous system, but also in the gastrointestinal tract, as well as in the smooth muscles of the bronchi and on the walls of blood vessels. For this reason, people who have serious liver or kidney problems should not use SSRIs. Stimulation of receptors affects their activity and provokes various disorders, including:

• problems with the digestive system (nausea, diarrhea, constipation, vomiting, possible development of anorexia);
• increased arousal, restlessness, anxiety;
• headache;
• fast fatiguability;
• insomnia (in 20-25% of cases) or increased drowsiness;
• diarrhea;
• motor dysfunction (hand tremors).

This reaction of the body is typical in the first stages of taking SSRIs and usually goes away after a month. Sometimes patients complain of decreased sexual desire, delayed orgasm, or inability to feel it. If you take medications for too long, there is a risk of bleeding.

Patients with very serious psychological disorders who take too many medications may experience serotonic syndrome, characterized by seizures, high fever, and cardiac arrhythmias. In this case, the drug must be discontinued and replaced with a more effective one.

SSRI drugs are interchangeable and if one drug fails, you can use a drug from the same group (if it so happens that one of your relatives was also treated with a similar drug and the result was positive, preference should be given to this drug).

If it is necessary to take serotonin reuptake inhibitors with other drugs, especially tricyclic antidepressants, you must strictly follow the doctor's instructions and follow the prescribed dose. An overdose can be fatal.

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 help; 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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Interactions with other drugs when taking SSRIs are associated with their ability to affect cytochrome P450 isoenzymes. Combination use with other drugs is one of the main risk factors for undesirable effects of antidepressants in this group. A high risk of drug interactions exists when taking fluoxetine, which interacts with four types of cytochrome P450 isoenzymes - 2 D62, C9/10, 2 C19 and 3 A3/4 - and fluvoxamine, which interacts with isoenzymes 1 A2, 2 C19 and 3 A3/4. Paroxetine is also a powerful inhibitor of liver enzymes. Sertraline is less problematic in this regard, although its effect on enzyme inhibition is dose dependent; Citalopram and escitalopram are relatively safe.
SSRIs should not be combined with MAO inhibitors as this may cause severe serotonin syndrome.
When TCAs are coadministered with an SSRI, tricyclic antidepressants should be used in lower doses and plasma levels monitored as the combination may result in elevated TCA blood levels and an increased risk of toxicity.
The combined use of SSRIs and lithium salts enhances the serotonergic effects of antidepressants, and also increases the side effects of lithium salts and changes their concentrations in the blood.
SSRIs may increase the extrapyramidal side effects of typical antipsychotics. Fluoxetine and paroxetine are more likely than other SSRIs to increase blood levels of typical antipsychotics and therefore increase their side effects or toxicity. Blood concentrations of many atypical antipsychotics also increase when taking SSRIs.
Cimetidine can lead to inhibition of the metabolism of SSRIs, increasing their concentration in the blood with an increase in their main effect and side effects.
SSRIs increase plasma concentrations of benzodiazepines.
Warfarin in combination with SSRIs leads to an increase in prothrombin time and increased bleeding.
When taken simultaneously with SSRIs, aspirin or other non-steroidal anti-inflammatory drugs, as well as anticoagulants and antiplatelet agents, increases the risk of gastrointestinal bleeding. Painkillers of non-steroidal anti-inflammatory drugs (aspirin, ibuprofen, naproxen) may reduce the effectiveness of SSRIs:
In combination with alcohol or sedative-hypnotics, SSRIs lead to an increase in the inhibitory effect of sedative-hypnotics and alcohol on the central nervous system with the development of undesirable effects.
Some drugs may increase the toxicity of SSRIs, such as zolpidem.
SSRIs may potentiate the development of extrapyramidal disorders caused by the use of bupropion and psychostimulants.
Some antibiotics (in particular, erythromycin) can increase the concentration of sertraline and citalopram in the blood and even cause psychosis when combined with fluoxetine (clarithromycin).
In patients taking SSRIs, the analgesic effect of tramadol or codeine may be reduced.
Some SSRIs interact unfavorably with statins - for example, fluoxetine in combination with some statins can cause manifestations of myositis.
SSRIs greatly attenuate the effects of tryptamines (e.g., psilocybin), LSD, 2C-family psychedelics, and almost completely abolish the serotonergic effects of MDxx (e.g., MDMA, methylone, butylone).
Drug interactions of individual SSRIs.
Paroxetine. Sodium valproate slows down the metabolism of paroxetine and increases its concentration in the blood. Paroxetine slows down the metabolism of some antipsychotics (pimozide, etaprazine and) and tricyclic antidepressants and increases their concentration in the blood with a possible increase in their side effects.
Fluvoxamine. Slows down the metabolism of haloperidol (as well as other neuroleptics of the group of butyrophenone derivatives) and increases its concentration in the blood by 2 times (at the same time the concentration of fluvoxamine increases by 2-10 times), as a result of which it can reach a toxic level. When fluvoxamine is combined with atypical antipsychotics olanzapine or clozapine, the metabolism of the antipsychotic also slows down and its concentration in the blood increases (when combined with clozapine - several times). In addition, fluvoxamine slows down the metabolism of some tricyclic antidepressants with a possible increase in their concentration and the development of intoxication; The combined use of fluvoxamine with beta-blockers, theophylline, caffeine, alprazolam, carbamazepine leads to similar effects.
Fluoxetine. Macrolide antibiotics (erythromycin, clarithromycin, etc.) increase the concentration of fluoxetine in the blood with the possible development of toxic effects. Fluoxetine has a similar effect on the metabolism of drugs such as TCAs, trazodone, alprazolam, beta-blockers, carbamazepine, sodium valproate, phenytoin, and barbiturates. Fluoxetine enhances the sedative effect and motor retardation when taking barbiturates and triazolobenzodiazepines (alprazolam, triazolam). Reduces the anti-anxiety effect of buspirone. Lithium enhances both the antidepressant and toxic effects of fluoxetine. Fluoxetine causes an increase in the level of the main metabolite of bupropion - hydrox-bupropion, which can lead to clinical manifestations of the toxic effects of this metabolite: catatonia, confusion and agitation. When fluoxetine was used together with calcium channel blockers (verapamil, nifedipine), headaches, swelling, and nausea were observed.
Sertraline. Slows down the metabolism of desipramine (as well as imipramine) and increases the concentration of this antidepressant in the blood by 50%. Reduces the plasma clearance of diazepam and tolbutamide, slightly increasing their concentrations in the blood. It enhances the side effects of lithium salts, but the effect of sertraline on the concentration of lithium salts in the blood has not been detected.

Today, there are many different types of medications that act on the central nervous system. For depressive or other personality disorders, medications are widely used to relieve the patient of melancholy, lethargy, apathy, anxiety and irritability, while improving his mood.

The mechanism of action of most antidepressants is associated with correction of the level of certain neurotransmitters, in particular serotonin, dopamine and norepinephrine. According to studies conducted in the first half of the 20th century, it is a change in the ratio of neurotransmitters that leads to the appearance of symptoms of clinical depression and other mental illnesses. A special role in the occurrence and development of mental diseases is assigned to a deficiency of serotonin in synapses. By influencing this link, it becomes possible to control the course of depressive disorders.

Brief description of the pharmacological group and classification

Selective serotonin reuptake inhibitors (SSRIs) work by maintaining long-term activity of serotonergic transmission by preventing the uptake of the neurotransmitter serotonin into nervous tissue.

Accumulating in the synaptic cleft, serotonin acts longer on specific receptors, preventing the depletion of synaptic transmission.

A synapse is a special structure that forms between two neurons or between a neuron and an effector cell. Its function is to transmit nerve impulses between two cells

The main advantage of antidepressants of this group is the selective and targeted inhibition of exclusively serotonin, which helps prevent the development of a large number of side effects on the patient’s body. That is why drugs from the SSRI group are among the most modern and clinically effective and are relatively easily tolerated by patients.

Today, in addition to drugs from the SSRI group, the following antidepressants are distinguished:

Group	Mechanism of action	Representatives
Tricyclic antidepressants (TCAs)	Block the reuptake of some neurotransmitters by the presynaptic membrane	Amitriptyline, Imipramine, Clomipramine, Maprotiline, Mianserin, Trazodone
Monoamine oxidase inhibitors (MAOIs)	They inhibit monoamine oxidase, an enzyme found in nerve endings. Thus, biologically active substances prevent the destruction of serotonin, dopamine, norepinephrine, phenylethylamine and other monoamines by this enzyme	Moclobemide, Pirlindol
Selective norepinephrine reuptake inhibitors	Selectively prevent the occurrence of norepinephrine “deficiency” in synapses	Reboxetine (the drug is not available in Russia)
Serotonin norepinephrine reuptake inhibitors (SNRIs)	Inhibits the uptake of both serotonin and norepinephrine without participating in changes in the concentrations of other neurotransmitters	Milnacipran, Mirtazapine, Venlafaxine
Antidepressants of other groups	Have different mechanisms of action, depending on the specific drug	Ademethionine, Tianeptine, etc.

Mechanism of action and pharmacological properties

Serotonin is released from nerve endings in the area of ​​the reticular formation, which is responsible for wakefulness, and in the area of ​​the limbic system, which regulates the emotional and behavioral sphere.

After serotonin leaves these areas, it is transferred to the synaptic cleft - a special space between the pre- and postsynaptic membranes. There, the neurotransmitter seeks to bind to specific serotonin receptors.

As a result of a chain of complex physicochemical transformations, serotonin excites the cell membranes of the reticular formation and limbic system, selectively increasing their activity. Under the influence of special enzymes, serotonin breaks down, after which its components are passively captured by the same elements that were responsible for its release at the very beginning of the chain described above.

Selective serotonin reuptake inhibitors act on its structure, preventing its destruction with the subsequent accumulation and prolongation of its effector actions that excite the nervous system.

As a result of an increase in the activity of this neurotransmitter, pathological links in the development of depressive, anxious, anxious-depressive and other mental disorders are stopped by regulating the emotional and mental function of the brain.

Indications and contraindications for use

The main indication for the prescription and use of antidepressants, regardless of their affiliation, is the treatment and prevention of depression, including bipolar personality disorder.

In addition, in the practice of psychiatrists, antidepressants are prescribed to correct other disorders of the central nervous system:

Instructions for use	Detailed description
Indications	1. Panic states. 2. Neuroses of various origins. 3. Obsessive-compulsive disorders. 4. Enuresis. 5. Chronic pain syndromes. 6. Correction of sleep disorders. There are known cases of effective use of drugs from the group of antidepressants for the complex treatment of tobacco addiction, bulimia nervosa, and early ejaculation. For mild depression, the use of SSRIs is not recommended, since the undesirable effects associated with taking antidepressants can outweigh the benefits of their use. As an exception, clinical cases are considered in which other therapy is ineffective, as well as depression of moderate and severe severity. Taking drugs in this group does not cause addiction
Contraindications	1. Individual intolerance to drugs. 2. Alcohol and drug intoxication. 3. Pregnancy and breastfeeding. 4. Thyrotoxicosis. 5. Persistent arterial hypotension. 6. Prescription together with other drugs of serotonergic type of action (neuroleptics and tranquilizers). 7. The patient has a history of epileptic seizures. 8. Kidney and liver failure. 9. Cardiovascular diseases in the stage of decompensation (acute and recovery period of myocardial infarction, decompensated heart defects)
Side effects	The risk of side effects and their severity when taking SSRI antidepressants is significantly lower than when using TCAs. Side effects include: 1. Dyspeptic disorders (nausea, vomiting, constipation). 2. Sleep disorders (insomnia or drowsiness). 3. The occurrence of anxiety states (mania, anxiety), increased nervous excitability. 4. Migraine-like headache. 5. Loss of visual acuity. 6. The appearance of skin rashes. 7. In the case of prescribing medications for depressive-manic personality disorder, a change from one phase to another is possible. 8. Parkinsonism symptoms, tremor, decreased libido, erectile dysfunction. 9. SSRI-induced apathy syndrome – loss of motivation with dulling of emotions. 10. If antidepressants are used during pregnancy, there is a risk of miscarriage and fetal abnormalities

According to foreign studies, the prescription of SSRIs as the main drug is effective in the treatment of childhood and adolescent depression due to the absence of a wide range of contraindications, “side effects” (side effects) and undesirable effects, as when prescribing tricyclic antidepressants (TCAs).

The ability to “predict” the therapeutic effect of drugs allows us to prescribe treatment to this group of patients most correctly and with less risk of side effects. SSRIs provide the opportunity to relieve the symptoms of the disease, prevent a period of exacerbation and correct the behavior of patients prone to suicide, which is especially important in patients with juvenile depression.

In addition, selective serotonin reuptake inhibitors are extremely effective in the treatment of postpartum depression and have a positive effect on women with menopausal syndrome, as they reduce anxiety and stop painful thoughts.

List of drugs

There are many different SSRI antidepressants. This table provides a list of the most popular names:

Active substance	Description	Side effects	Image
Fluoxetine	Increases the serotonergic effect according to the principle of negative feedback. Has virtually no effect on the concentration of dopamine and norepinephrine. Rapidly absorbed through the gastrointestinal tract. The maximum concentration in the blood is observed after 6-8 hours	Nausea and vomiting; drowsiness; loss of appetite; decreased libido
Fluvoxamine	It is a drug with an anxiolytic (anxiety-relieving) effect. Bioavailability is about 53%. 3-4 hours after administration, the maximum concentration of the drug in the blood is observed. Metabolized in the liver to nurfluoxetine, a specific active substance	Manic states; tachycardia; arthralgia (joint pain); xerostomia (dry mouth)
Sertraline	It is one of the most balanced drugs in this group. Used for the most severe depressive conditions. The therapeutic effect is observed after 2-4 weeks of starting the course	Hyperkinesis; swelling; bronchospasm
	Prescribed for the prevention of depression and other unexpressed mental disorders	Nausea, vomiting, constipation; tachycardia, feeling of heartbeat, chest pain; tinnitus; headache
Paroxetine	The pharmacological properties of Paroxetine show pronounced anxiolytic and sedative effects. It has a high degree of absorption, reaching maximum concentration in the blood 5 hours after administration. Prescribed for panic attacks and obsessive-compulsive disorders	Nausea, vomiting; incompatibility with monoamine oxidase inhibitors (MAOIs)
	It is used for moderate depressive conditions, since it does not have a pronounced sedative and anxiolytic effect	Loss of appetite; swelling; worsening existing depressive conditions
Citalopram	Together with serotonin receptors, it participates in blocking adrenergic receptors, H1-histamine receptors and M-cholinergic receptors. The maximum concentration in the blood is reached 2 hours after administration	Tremor of fingers; migraine; orthostatic hypotension; urinary disorders
Trazodone	In addition to anxiolytic and sedative effects, it has a pronounced thymoanaleptic effect (improves mood). The maximum concentration of the drug in the patient’s blood is observed one hour after administration. Used to reduce anxiety, hypothymia and other similar conditions	Fatigue; weakness; headache and dizziness; increased appetite; dryness and unpleasant taste in the mouth; retention and increased frequency of urination; premature menstruation
Escitalopram	Prescribed for mild to moderate mental illness. The peculiarities of the drug include the absence of an effect on hepatocytes - liver cells, which allows it to be used with other drugs without fear of hepatotoxicity	Sleep disorders; weakness, impaired concentration and performance; loss of appetite

General treatment regimen

Drugs from this group of antidepressants are used 1–2 times a day in the morning before meals. The expected therapeutic effect does not occur immediately, but after 3–6 weeks of continuous use of SSRIs.

The result of therapy is the relief of depressive symptoms, after which drug treatment should be continued to prevent relapses. If there are contraindications, as well as individual intolerance, resistance or other circumstances that do not allow prescribing medications from the SSRI group, the attending physician selects similar drugs of a different type.

Patients undergoing drug treatment should take into account the likelihood of developing withdrawal syndrome - a set of negative symptoms that develop against the background of abrupt cessation of medication:

• decreased mood;
• weakness, decreased performance, attention and concentration;
• nausea, vomiting and diarrhea;
• Strong headache;
• drowsiness;
• impaired coordination of movements;
• influenza-like syndrome, etc.

To avoid withdrawal syndrome, under the supervision of your attending physician, you should gradually reduce the doses of medications taken until you stop taking them completely. This usually takes 2-4 weeks.

Due to the current legislation of the Russian Federation, antidepressants are prescription drugs and are not sold in pharmacy chains without a prescription.

Drugs from the SSRI group are widely used in psychiatry due to the absence of severe side effects, as well as their “softness” and direction of action.

Antidepressants are used in the treatment of depression, a list of which can be seen below. Antidepressants are drugs that selectively affect a person’s depressive state. These drugs and antipsychotics for depression can be used to relieve affective-delusional syndromes in children and adults.

• Moclobemide;
• Bethol;
• Toloxatone;
• Pyrazidol;
• Imipramine;
• Amitriptyline;
• Anafranil;
• Pertofran;
• Trimipramine;
• Azafen;
• Maprotiline;
• Mianserin;
• Fluoxetine;
• Fevarin;
• Citalopram;
• Sertraline;
• Paroxetine;
• Cymbalta.

This is only some of the antidepressants used to combat nervous disorders and depression. All of them are divided into several classifications.

Calming

Anti-depressants are a classification of the most common drugs used to combat depression.

Amitriptyline belongs to the classic type of mild antidepressants with a tricyclic structure. It is distinguished from Imipramine by its rather strong sedative effect. It is used to get rid of depression of anxious and agitated types, which can manifest themselves with “vitality”. This drug is available in the form of tablets and injections.

Another domestic antidepressant is Azafen, or Hypophysin. It is used to combat the symptoms of “minor” depressive disorders of the cyclothymic register. The drug has moderate sedative and thymoanaleptic effects.

Mianserin, or Lerivon, is a drug that has a strong sedative effect when used in small doses. Due to this effect, it can be used to treat cyclothymia in combination with insomnia. It is able to cure depression with major episodes.

Stimulating

Moclobemide, or Aurorix, is a selective MAO inhibitor. The drug has a powerful stimulating effect on people suffering from inhibited types of depression. It is prescribed for somatized types of depression. But the drug is strictly prohibited for use in anxiety depression.

Imipramine, or Melipramine, is the first fully studied tricyclic antidepressant. It is used in the treatment of severe depression with a high prevalence of sadness and lethargy, and with suicidal thoughts. The drug is available both in the form of tablets and as intramuscular injections.

Fluoxetine is a drug that has a thymoanaleptic effect. Its second name is Prozac. The drug is effective during the treatment of depression with obsessive-phobic symptoms.

This type of medication is called a selective serotonin reuptake inhibitor (SSRI). The drug is devoid of some effects of clinical tricyclic antidepressants:

• antihistamine;
• adrenolytic;
• cholinolytic.

Pertofran is a more powerful version of Imipramine (desmethylated). It has a brighter activating effect. The drug is used to combat depression combined with depersonalization.

Balanced drugs

The second name of Pyrazidol is Pirlindol. The drug is produced in Russia. It is a reversible inhibitor of MAO type A, like Moclobemide. This drug is used to prevent and treat depression of the inhibited type, as well as depressive disorders with pronounced anxiety manifestations. The advantages of the drug are that it can be taken for glaucoma, prostatitis and heart pathologies.

Another powerful drug created as a result of the synthesis and introduction of a chlorine atom into the imipramine molecule is Anafranil. It is used to treat resistant depression and to relieve the affective phases of severe depression.

Maprotiline, or Ludiomil, is an antidepressant with a tetracyclic structure. It has a fairly powerful thymoanaleptic effect when interacting with anxiolytic and sedative components. It can be used for circular depression in combination with ideas of self-blame. The drug is used for involutional melancholia. Maprotiline is produced in the form of oral medications and injections.

Reversible monoamine oxidase inhibitors and selective reuptake inhibitors

Befol is one of the domestic drugs that are prescribed for depressive disorders of asthenic and anergic types. It is used to treat the depressive phase of cyclothymia.

Fevarin and Fluoxetine belong to the classification of drugs with thymoanaleptic action. The drugs have a vegetative stabilizing effect.

Citalopram and Tsipramil are other names for thymoanaleptic antidepressants that can be used to treat depression. They belong to the group of sedating serotonin reuptake inhibitors (SSRIs).

Afobazole is an over-the-counter antidepressant. It is used to combat somatic diseases with adaptation disorders, anxiety, neurasthenia and oncological and dermatological diseases.

The drug has a good effect in treating sleep disorders and relieving PMS symptoms. But it is worth considering that it is contraindicated for children and women during pregnancy and lactation.

Tricyclic

Trimipramine, or Gerfonal, is used in the treatment of depression with increased anxiety. This is one of the most powerful drugs of this kind. Its psychotropic activity is similar to Amitriptyline. When carrying out treatment, it is worth considering the list of contraindications of this antidepressant:

• dry mouth;
• orthostatic hypotension;
• problems with urination.

New generation antidepressants

Sertraline and Zoloft are names of antidepressants with a strong thymoanaleptic effect with a weak stimulating effect. Moreover, the drugs do not have anticholinergic or cardiotoxic properties.

They achieve maximum effect when fighting somatized atypical depression with some manifestations of bulimia.

Paroxetine is a derivative of piperidine. It has a rather complex bicyclic structure. The main properties of Paroxetine are thymoanaleptic and anxiolytic. They appear when there is stimulation.

The drug shows itself well in the fight against endogenous and neurotic depression, their melancholy or inhibited variants.

Venlafaxine is an antidepressant used for depression associated with severe mental disorders such as schizophrenia, etc.

Opipramol is used to treat somatized and alcoholic depression. It is able to prevent vomiting, convulsions and generally stabilize the autonomic nervous system.

Toloxatone, or Humoril, is similar in its effect on the human body to Moclobemide. The drug does not have anticholinergic or cardiotoxic properties. But it copes well with treating depression with pronounced inhibition.

Cymbalta or Duloxetine are used to combat depression with panic attacks.

Side effects

Most antidepressants have a fair number of side effects. Their list is quite long:

• hypotension;
• arrhythmia;
• sinus tachycardia;
• violation of intracardiac conduction;
• suppression of bone marrow functions;
• agranulocytosis;
• thrombocytopenia;
• hemolytic anemia;
• dry mucous membranes;
• violation of accommodation;
• intestinal hypotension;
• problems with urination;
• increased appetite;
• increase in body weight.

Such side effects occur quite often due to the use of tricyclic antidepressants. In contrast, antidepressants that are serotonin reuptake inhibitors have less pronounced side effects. But it could be:

• frequent headaches;
• insomnia;
• anxiety states;
• depotentiating effects.

If combination therapy is used for treatment, that is, drugs of both types are used simultaneously, then serotonin syndrome may occur, characterized by an increase in temperature, signs of intoxication of the body, and disturbances in the functioning of the heart and blood vessels.

Any antidepressants for depression should be taken only after a complete medical examination and an accurate and complete diagnosis.

And for children they are prescribed with extreme caution. Be sure to do this under the supervision of a doctor so as not to harm the body.