Antidepressants of the latest generation. Antidepressants: which are better? Reviews of doctors, prices

SSRIs are used in the treatment of depression. The pharmacological group is represented by a wide list of active substances and an even larger list of trade names, since the same substance of the SSRI group can be produced under different trade names, depending on the pharmaceutical company. The properties of drugs, their side effects and contraindications for use are identical for all members of the group.

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    Group Description

    SSRIs are selective serotonin reuptake inhibitors, third-generation antidepressants that are used in the treatment of depression and anxiety disorders. These drugs are relatively well tolerated, unlike tricyclic antidepressants, which can cause anticholinergic side effects:

    • constipation;
    • blurred vision;
    • anorgasmia;
    • atony of the bladder;
    • increased intraocular pressure;
    • conjunctivitis;
    • tachycardia;
    • increased sweating;
    • dizziness.

    When treated with SSRIs, the risk of hypotension and toxic effects on the heart is significantly lower than with TCAs. SSRIs are classified as first-line drugs and are used in many countries around the world. Often, such medications are prescribed to patients who have contraindications to treatment with tricyclic antidepressants.

    List of representatives

    The group of selective serotonin reuptake inhibitors includes the following drugs:

    Active substance

    Tradename

    fluoxetine

    Prodep, Fluxen, Fluoxetine, Prozac, Fluval, Fluxonil, Flunisan, Deprex

    Paroxetine

    Adepress, Cloxet, Xet, Paroxin, Paxil, Reksetin, Luxotil

    Sertraline

    Asentra, Depralin, Zalox, Zoloft, Serlift, Sertraloft, Solotik, Emoton, Stimuloton, Adyuvin, Debitum-Sanovel, A-Depresin

    fluvoxamine

    Deprivox, Fevarin, Fluvoxamine Sandoz

    Citalopram

    Citol, Auropram, Citalostad, Oropram, Cipramil, Citalam, Citahexal, Pram

    Escitalopram

    Anxiozan, Depresan, Lenuxin, Elycea, Escitam, Cytoles, Cipralex, Precipra, Pandep, Medopram, Essobel, Eprakad, Tsipram

    All drugs of the SSRI group are dispensed by prescription, as they belong to the accounting list B.

    Indications for use

    The use of drugs of the SSRI group is advisable for severe depressive disorder. Medicines in this group are also effective for:

    • anxiety neurosis;
    • panic disorder;
    • social phobia;
    • obsessive-compulsive disorder;
    • chronic pain syndrome;
    • alcohol withdrawal;
    • post-traumatic stress disorder;
    • depersonalization;
    • bulimia.

    The choice of means is carried out only by a qualified specialist. Self-treatment with SSRIs is fraught with a number of side effects and deterioration in well-being.

    Efficacy in depression

    The success of treating depression with SSRIs largely depends on how severe and prolonged the patient's depression is. Several studies conducted by the US Food and Drug Administration have found that patients with severe depression experience a greater improvement in well-being than patients with moderate and mild depression.

    Researchers from Russia assess the effectiveness of SSRIs in the fight against depression in a slightly different way. IN treatment of mild and moderate depression, SSRIs can be compared to TCAs. Thus, the use of SSRIs is relevant for neurotic symptoms, anxiety and phobias.

    The drugs of this group begin to act rather slowly: the first therapeutic effects can be seen by the end of the first month of treatment. Some representatives, for example, paroxetine and citalopram, show their effect by the second week of therapy.

    The advantage of SSRIs over tricyclic antidepressants is that they can be immediately prescribed in a therapeutic dosage, without its gradual increase.

    In the treatment of childhood depression, only fluoxetine is used from the entire group. SSRIs have been shown to be effective in treating depression that has not responded to TCAs. In this case, there is an improvement in more than half of the cases.

    pharmachologic effect

    The mechanism of action of drugs in this group is based on blocking the reuptake of serotonin by neurons, since depression occurs precisely because of its lack. Therefore, SSRI antidepressants may be effective in the treatment of depressive conditions of any origin.

    The action of other drugs, for example, tricyclic or from the group of monoamine oxidase inhibitors, is also aimed at increasing the level of serotonin, but they work in a fundamentally different way. Antipsychotics of the SSRI group act specifically on serotonin receptors, so they are needed to correct phobias, anxiety, depression, and sadness.

    It is worth noting that the drugs of this group act not only on serotonin receptors in the central nervous system, but also on those located in the bronchial muscles, gastrointestinal tract and vascular walls. All representatives of this group have secondary pharmacological properties - the effect on the uptake of norepinephrine and dopamine.

    How are SSRIs different?

    The differences between the drugs of this group from each other lie in the intensity of the effect on the body's neurotransmitters. Depending on the degree of selectivity, the capture of serotonin in certain groups of receptors can be prevented.

    Each SSRI drug has its own level of selectivity for serotonin receptors and for dopamine, muscarinic and adrenoreceptors.

    Transformation of drugs in the body

    SSRIs are processed in the liver. Metabolic products are excreted by the kidneys, so dysfunction of these organs in patients is a serious contraindication to the use of SSRIs.

    The half-life of fluoxetine is the longest - three days after a single application and a week after a long one. A long half-life reduces the risk of withdrawal syndrome.

    Side effects

    Mostly undesirable reactions are observed from the gastrointestinal tract and the central nervous system. Adverse reactions according to the frequency of occurrence:

    Organ System/Frequency

    Often

    Infrequently

    Very rarely

    The cardiovascular system

    Hot flashes

    hypotension

    Vasculitis

    Diarrhea, nausea, dry mouth, vomiting

    Taste perversion

    Pain in the esophagus

    The immune system

    Anaphylactic reactions

    Musculoskeletal system

    muscle twitches

    Headache, decreased activity, dizziness, drowsiness

    Coordination disorders, bruxism, hyperactivity

    Seizures, serotonin syndrome

    Insomnia, nightmares, nervousness, decreased libido, euphoria

    Depersonalization, anorgasmia

    manic disorders

    Skin covering

    Increased sweating, itching, hives, rash

    Alopecia, cold sweat

    Increased skin sensitivity to sunlight

    genitourinary system

    Ejaculation disorder, frequent urination, erectile dysfunction, gynecological bleeding

    Sexual dysfunction, priapism

    sense organs

    Blurred vision

    If adverse reactions are detected, the drug should be discontinued until consultation with a specialist, who will consider the possibility of correcting the treatment regimen or canceling the drug by choosing another one.

    Contraindications

    SSRI drugs are contraindicated in the following cases:

    • manic states;
    • treatment with MAO inhibitors;
    • lactation and pregnancy;
    • epilepsy;
    • mania in the history of the disease;
    • renal and liver failure;
    • angle-closure glaucoma;
    • intoxication with alcohol, medicines, drugs.

    In old age, dosages should be carefully monitored, since the functions of the kidneys and liver are reduced, and adverse reactions may increase.

    Application features

    Caution is required when prescribing drugs to patients with epilepsy, cardiovascular diseases. The use of SSRIs is associated with a high risk of bleeding in elderly patients, as well as in those who suffer from ulcerative and erosive diseases of the gastrointestinal tract.

    Suicide risk

    The use of SSRIs is associated with an increased risk of suicidal thoughts and behavior in children, adolescents, and young adults under 25 years of age. Drugs in this group, like tricyclic antidepressants, can lead to an increase in suicidal thoughts inherent in most depressive conditions.

    This effect is associated with the excitation of the central nervous system at the beginning of treatment, so it is observed most often in the first weeks of admission. Patients prone to suicidal thoughts and behavior should be closely monitored.

    The risk of suicide with SSRIs is lower than with tricyclic antidepressants. The latter are also more dangerous in overdoses.

    withdrawal syndrome

    The risk of drug dependence is inherent in all antidepressants. SSRI withdrawal syndrome may occur in the first days after discontinuation of treatment and disappear on its own in a few weeks.

    The severity of this syndrome directly depends on the half-life of the drug from the body. Paroxetine, which has a short half-life, causes more difficult withdrawal than fluoxetine.

    This condition is accompanied by the following symptoms:

    • dizziness;
    • goosebumps on the skin;
    • nausea, vomiting, diarrhea;
    • insomnia;
    • tremor of the limbs;
    • unsteady gait;
    • anxiety, apathy;
    • panic attacks, arrhythmia.

    With the development of severe withdrawal symptoms, patients are forced to re-take the drug and stop treatment more smoothly. The use of SSRI drugs during pregnancy leads to withdrawal syndrome in the newborn.

    Serotonin syndrome

    This is a rare but life-threatening side effect of antidepressants. It occurs when SSRIs are combined with other drugs that affect the concentration of serotonin in the central nervous system.

    To prevent serotonin syndrome, it is strictly forbidden to combine SSRIs with MAO inhibitors and other antidepressants that affect serotonin levels.

    This syndrome manifests itself in the following symptoms:

    • anxiety;
    • manic behavior;
    • insomnia;
    • abdominal pain, diarrhea;
    • increase in body temperature;
    • lacrimation, dilated pupils;
    • tachycardia, rapid breathing;
    • chills, incoordination;
    • tremor, increased reflexes.

    Serotonin syndrome can manifest itself in severe conditions that threaten life. These include insufficiency of the liver, kidneys, blood circulation, pneumonia, coma.

    Treatment of serotonin syndrome begins immediately and is carried out in a hospital in an intensive care unit or intensive care unit.

    Prohibited drug combinations

    To prevent the development of serotonin syndrome, the combination of SSRIs with the following drugs should be avoided:

    • tricyclic antidepressants;
    • adenosylmethionine;
    • St. John's wort preparations;
    • normotimics;
    • levodopa;
    • opioid painkillers;
    • dextromethorphan preparations;
    • migraine medicines;
    • drugs that affect the activity of liver enzymes.

    Before starting treatment, tell your doctor about any medications you have taken in the last two weeks.

    Conclusion

    The pharmacological group of SSRIs is the group of first choice for depression and anxiety. Its representatives show high efficiency in the fight against mental disorders, if selected by a specialist with an individual treatment regimen. Self-administration of such drugs can not only worsen well-being, but also threaten health and life.

There are many groups medicines which are aimed at psychotropic correction in the treatment of anxiety and depressive conditions.

All of them have a common mechanism of action, the essence of which is to control the effect of certain neurotransmitters on the state of the central nervous system, depending on the genesis of the disease. According to studies, a central deficiency of serotonin in synoptic transmission has a special effect on the pathogenesis of depression, by controlling which it is possible to regulate mental activity.

Selective serotonin reuptake inhibitors (SSRIs) are the third generation that are relatively well tolerated by patients. They are used for the treatment of depressive and disorders in mono and poly-therapy.

This group of medicines works by maintaining the prolonged activity of central serotonergic processes by preventing the capture of serotonin by brain tissues, as a result of which the mediator, accumulating in the receptor area, exerts its effect on them for a longer time.

The main advantage of SSRIs over other groups is the selective inhibition of only one type of biogenic amines, which helps prevent unwanted side effects on the body. This has a positive effect on the tolerance of this group of drugs by the body, due to which their popularity among patients and specialists is growing every year.

Mechanism of action and pharmacological properties

When serotonin is released from nerve fibers in the area of ​​the reticular formation responsible for wakefulness, as well as the limbic system responsible for controlling the emotional state, it enters a space called the synoptic cleft, where it attaches to special serotonin receptors.

During this interaction, the neurotransmitter excites the cell membranes of these structures, thereby increasing their activity. As a result, this substance breaks down under the action of special enzymes, after which its elements are recaptured by those structures through which its initial release was made.

Reuptake inhibitors exert their influence at the stage of the enzymatic breakdown of serotonin, preventing its destruction, contributing to the subsequent accumulation and prolongation of its excitatory effects.

As a result of an increase in the activity of the neurotransmitter, the pathological processes of depressive and phobic disorders are leveled, the deficit of emotional behavior and the regulation of mental states are compensated.

Scope of application

The main purpose of using this group of antidepressants is to suppress various types of depression by providing a stimulating effect on brain structures.

SSRIs are also used in the following cases:

Also, this group of drugs is effective in the treatment of alcoholism and withdrawal symptoms.

Restrictions and contraindications

Taking SSRI antidepressants is prohibited in the presence of psychostimulant drugs in the blood, in a state of alcoholic or drug intoxication.

The combination of several drugs with a serotonergic effect is contraindicated. Also incompatible is the use of serotonin reuptake inhibitors in the presence of a history.

Hepatic and renal insufficiency, as well as cardiovascular diseases in the stage of decompensation, are a contraindication to the use of selective inhibitors.

  1. Nausea, vomiting, congestion in the intestines and, as a result, constipation.
  2. Restless states may be noted, develop up to insomnia or reversion to increased drowsiness.
  3. Increased nervous agitation, appearance, loss of visual acuity, the appearance of a skin rash are possible, a change in the phase of the disease is possible with the transition from depressive to manic.
  4. There may be an appearance, a decrease in libido, development in the form of, or acute. There is an increase in the production of prolactin.
  5. With prolonged use, a phenomenon such as loss of motivation with emotional dulling, which is also known as SSRI-induced apathetic syndrome, is possible.
  6. Bradycardia may develop, a decrease in the sodium content in the blood can be observed, leading to edema.
  7. When taking drugs during pregnancy, spontaneous abortions are possible as a result of a teratogenic effect on the fetus, as well as developmental anomalies on later dates pregnancy.
  8. In rare cases, it is possible with the corresponding mental, autonomic and neuromuscular disorders.

Information for thought

According to recent studies, the treatment of endogenous depression in adolescence is effective and safe when used as therapy with SSRI antidepressants, due to the absence of such side effects as when taking tricyclic drugs.

The predictability of the therapeutic effect makes it possible to provide the correct treatment to this group of patients, despite the atypical symptoms of depression of this age associated with neurobiological changes in adolescence.

SSRIs make it possible already at the initial stages of treatment to prevent an exacerbation of the condition and reduce the relevance of suicidal behavior, which is inherent in people suffering from juvenile depression.

Also, serotonin reuptake inhibitors have proven effective in the treatment of postpartum depression, have positive influence in menopausal syndrome in the form of depression and depression, which allows the use of antidepressants as a replacement for hormone therapy.

TOP-10 popular drugs of the SSRI group

Ten selective serotonin reuptake inhibitors that are deservedly popular among patients and doctors:

Full list of drugs available for 2017

An exhaustive list of SSRIs, which consists of all the active substances of the group, as well as drugs based on them (trade names).

Structural formulas of popular SSRIs (clickable)

Preparations based on;

  • Prozac;
  • Deprex;
  • Flunisan;
  • Fluval;
  • Profluzak;
  • APO-fluoxetine;
  • Prodep;
  • Flunat;
  • Fluxonil;
  • Fludak.

This group of drugs has a stimulating and thymoanaleptic effect. Medicines are used for different types depression.

  • Avoxin.

The drugs specifically inhibit the reuptake of serotonin and have an anxiolytic effect. They are used to prevent and treat obsessive-compulsive disorders. They also have an effect on adrenergic, histamine and dopamine receptors.

  • paroxetine;
  • Rexitin;
  • Serestill;
  • Pleased;
  • Actaparoxetine;
  • Apo-paroxetine.

The group has anxiolytic and sedative properties. The active substance has a bicyclic structure, which distinguishes it from other drugs.

With a long course, the pharmacokinetic properties do not change. The main indications apply to endogenous, neurotic and reactive depressions.

Preparations based on Sertraline:

  • Oprah;
  • Pram;
  • Sedopram;
  • Siozam;
  • died;
  • Citalift;
  • Citalorin;
  • Cytol;
  • Citalopram.

The group minimally has third-party effects on dopamine and adrenergic receptors. The main therapeutic effect is aimed at correcting emotional behavior, leveling feelings of fear and. The therapeutic effect of other groups of antidepressants may be enhanced by simultaneous interaction with citalopram derivatives.

Medicines based on Escitalopram:

Medicines are used for. Maximum therapeutic effect develops 3 months after the start of taking this group of SSRI drugs. Medicines practically do not interact with other types of receptors. Most of the metabolites are excreted by the kidneys, which is hallmark these derivatives.

General treatment regimen

Preparations from the group of selective serotonin reuptake inhibitors are used once a day. It can be a different time period, but most often it is taken in the morning before meals.

The medicinal effect occurs after 3-6 weeks of continuous treatment. The result of the body's response to therapy is a regression of the symptoms of depressive conditions, after the complete suppression of which the therapeutic course is continued for 4 to 5 months.

It is also worth considering that in the presence of individual intolerance or resistance of the body, manifested in the absence of a positive result within 6-8 months, the group of antidepressants is replaced with another one. The dosage of the drug at one time depends on the derivative of the substance, as a rule, it ranges from 20 to 100 mg per day.

Once again about the warnings!

Antidepressants are contraindicated in renal and hepatic insufficiency, due to a violation of the elimination of drug metabolites from the body, resulting in its toxic poisoning.

Serotonin reuptake inhibitors should be used with caution in people whose work requires high concentration and attention.

In diseases that cause tremors, such as antidepressants, they can increase the negative clinic, which can negatively respond to the patient's condition.

Given the fact that inhibitors are teratogenic, they are not recommended for use during pregnancy and lactation.

It should be remembered that with severe physical exhaustion of the body, drugs of this group cannot be used because of the risk of even greater suppression of appetite.

It is also always worth remembering about the withdrawal syndrome, which is a complex of negative symptoms that develop when the course of treatment is abruptly stopped:

However, these drugs have their own drawbacks, manifested in the incomplete study of all their properties and the presence of individual, characteristic only for SSRIs, side effects.

Interactions with other drugs when taking SSRIs are associated with their ability to influence cytochrome P450 isoenzymes. Combined use with other drugs is one of the main risk factors for the 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 potent 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 prescribing tricyclic antidepressants with SSRIs, tricyclic antidepressants should be used at lower doses and their plasma levels should be monitored, since this combination can lead to an increase in blood levels of tricyclic antidepressants and an increased risk of toxicity.
The combined use of SSRIs and lithium salts enhances the serotonergic effects of antidepressants, and also enhances the side effects of lithium salts and changes their blood concentrations.
SSRIs may increase the extrapyramidal side effects of typical antipsychotics. Fluoxetine and paroxetine are more likely than other SSRIs to cause an increase in blood levels of typical antipsychotics and thus increase their side effects or toxicity. The blood concentration of many atypical antipsychotics also increases with SSRIs.
Cimetidine can lead to inhibition of the metabolism of SSRIs, an increase in their concentration in the blood with an increase in their main action and side effects.
SSRIs increase the concentration of benzodiazepines in the blood plasma.
Warfarin in combination with SSRIs leads to an increase in prothrombin time and increased bleeding.
When taking aspirin or other non-steroidal anti-inflammatory drugs, as well as anticoagulants and antiplatelet agents with SSRIs, the risk of gastrointestinal bleeding increases. Non-steroidal anti-inflammatory drug painkillers (aspirin, ibuprofen, naproxen) may reduce the effectiveness of SSRIs:
In combination with alcohol or sedative, hypnotic drugs, 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 can 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 (particularly erythromycin) can increase blood levels of sertraline and citalopram and even cause psychosis when combined with fluoxetine (clarithromycin).
In patients taking SSRIs, the analgesic effect of tramadol or codeine may be weakened.
Some SSRIs interact adversely with statins - for example, fluoxetine in combination with some statins can cause myositis.
SSRIs greatly attenuate the effects of tryptamines (eg, psilocybin), LSD, psychedelics of the 2C family, and almost completely abolish the serotonergic effects of MDxx (eg, 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 certain neuroleptics (pimozide, etaperazine and) and tricyclic antidepressants and increases their concentration in the blood with a possible increase in their side effects.
fluvoxamine. It slows down the metabolism of haloperidol (as well as other antipsychotics 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, it also slows down the metabolism of the antipsychotic and increases its concentration in the blood (several times when combined with clozapine). 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 and) 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, 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 - hydroxbupropion, which can lead to clinical manifestations of the toxic effect of this metabolite: catatonia, confusion and agitation. When using fluoxetine in conjunction with calcium channel blockers (verapamil, nifedipine), headaches, swelling, and nausea were noted.
Sertraline. Slows down the metabolism of desipramine (as well as imipramine) and increases the concentration of this antidepressant in the blood by 50%. Reduces plasma clearance of diazepam and tolbutamide, slightly increases their concentration in the blood. It enhances the side effects of lithium salts, however, the effect of sertraline on the concentration of lithium salts in the blood was not found.

Antidepressants

Serotonin and norepinephrine reuptake inhibitors (tricyclic antidepressants and selective inhibitors):

Mechanism of action: increase noradrenergic and serotonergic activity as a result of suppression of the reuptake of both neurotransmitters; also have anticholinergic, antihistamine action and antagonism to alpha-adrenergic receptors.

Amitriptyline

Imipramine

Clomipramine

Opipramol

Doxepin

Dibenzepine

Nortriptyline

melitracene

Trimipramine

Amoxapine

Butriptyline

Lofepramine

Dosulepin

Maprotiline

Fluorocyzine

Desipramine

Viloxazine

Venlafaxine

Irreversible non-selective monoamine oxidase inhibitors:

Mechanism of action: increase noradrenergic and serotonergic activity, suppressing the destruction of serotonin and norepinephrine by inhibiting the enzyme - monoamine oxidase. Due to the non-specific action of drugs (inhibition of monoamine oxidase type A and type B), it is necessary to follow a tyramine-free diet, due to the possibility of developing "cheese reactions". It is also impossible to combine MAOIs with SSRIs due to the possibility of developing serotonin syndrome. SSRIs can be prescribed after a 2-week period has elapsed since the last intake of MAOIs.

Hydrosine derivatives:

Nialamide

Non-hydrozine:

Phenelzine

Tranylcypromine

Isocarboxazid

Reversible selective monoamine oxidase type A inhibitors:

Mechanism of action: they increase noradrenergic and serotonergic activity, suppressing the destruction of serotonin and norepinephrine by inhibiting monoamine oxidase type A, and the inhibition of the enzyme is reversible. In this regard, the need for a tyramine-free diet disappears. However, it is not recommended to prescribe type A MAOIs in combination with SSRIs.

Moclobemide

pyrazidol

Tetrindol

Selective serotonin reuptake inhibitors:

Mechanism of action: it is based on the suppression of rebtake systems of serotonin, as a result of which it accumulates in the synaptic cleft.

Trazodone

fluoxetine

fluvoxamine

Sertraline

Paroxetine

Citalopram

Minaprin

Selective dopamine reuptake inhibitors:

Mechanism of action: it is based on the suppression of rebtake systems of dopamine, as a result of which it accumulates in the synaptic cleft.

Nomifenzine

Amineptine

Bupropion

Selective norepinephrine reuptake inhibitors:

Mechanism of action: it is based on the suppression of norepinephrine rebtake systems, as a result of which it accumulates in the synaptic cleft.

Tomoxetine

Pizoxetine

Alpha-2 receptor blockers:

Mechanism of action: Refers to alpha-2 receptor antagonists. Blocking these presynaptic receptors increases the release of norepinephrine and serotonin.

Mirtazapine

Mianserin

Other antidepressants:

Nefazodon. Mechanism of action: has a strong antagonism to serotonin receptors. It is assumed that antagonism to receptors enhances serotonergic transmission through postsynaptic serotonin receptors, which provides an antidepressant effect.

Tianeptine. Mechanism of action: stimulates the reuptake of serotonin at the presynaptic level. Tianeptine corrects the stress-induced increase in adrenaline release and increases extracellular dopamine content in the prefrontal cortex. In addition, stress-induced excitation of the HPA system is stopped.

Classification of antidepressants by pharmacological action:

Stimulant antidepressants:

Imipramine (melipramine, tofranil, priloygan)

Nortriptyline (Aventil, Psychostyle, Nortrilene)

Viloxazine

Desipramine (pertofran, petilil, norpramine)

Nialamide (Nuderal, Novazid)

Tranylcypromine (transamine, parnot)

Phenelzine (nardil)

Inkazan (Metralindol)

Moclobemide (Aurorix)

Fluoxetine (Prozac, Prodel)

Sertraline

Minaprin (cantor)

Amineptine (survector)

Bupropion

Tomoxetine

Sedative antidepressants:

Fluorocyzine

Amitriptyline (Laroxil, Elavil, Damilene, Triptizol)

Azaphen (pipofezin)

Amoxapine (moxadil, azendin, demolox)

Doxepin (sinequan, novoxapin, aponal)

Opipramol (Insidon, Pramalon)

Trimipramine (surmontil, gerfonal, sapilent)

Butriptyline (evaden)

Mianserin

Mirtazapine (remeron, mepirzapine)

fluvoxamine

Trazodone (deseryl, trittiko, pragmarel)

Nefazodon (serzon)

Balanced antidepressants:

Clomipramine (Anafranil, Hydifen)

Dosulepin (dothiepin, protiaden, idom)

Melitracen (Trausabun, Adaptol, Metraxil)

Lofepramine (Gamonyl, Thymelite)

Maprotiline (Ludiomil)

Venlafaxine

Sertraline

Paroxetine

Tianeptine (stablon, coaxil)

Pyrazidol (Pirlindol)

Antipsychotics

Mechanism of action: the antipsychotic effect of neuroleptics is due to the blocking of central dopamine receptors. Some neuroleptics also block adrenergic and serotonin receptors. In more detail, the mechanism of action will be analyzed using the example of chlorpromazine.

Phenothiazine derivatives (typical antipsychotics):

Aminazine

Propazine

Levomepromazine (tisercin)

Alimemazine

Meterazine

Etaperazine

Metophenazate

Triftazin

Fluorphenazine

Fluorphenazine Decanoate

Thioproperazine

Pipothiazine

Periciazine

Thioridazine

Thioxanthene derivatives (typical antipsychotics):

Chlorprothixene

Zuclopenthixol:

Clopixol Acufaz

Clopixol Depot

Clopixol

Flupentixol:

Fluanxol

Fluanxol Depot

Fluanxol Drops

Buterophenone derivatives (typical antipsychotics):

Haloperidol

Trifluperidol

Droperidol

Benperidol

Diphenylbutylpiperidine derivatives (typical antipsychotics):

Fluspirilen (Orap)

Penfluridol

Indole derivatives (typical antipsychotics):

Carbidine

Dibenzodiazepine derivatives (atypical antipsychotics):

Azaleptin (Clozapine)

Cholanzapine

Seroquel

Substituted benzamides (atypical antipsychotics):

Sulpiride

Sultopride

Prosulpin

Benzisoxazole derivatives (atypical antipsychotics):

Rispolept

Anxiolytics

Excite benzodiazepine receptors, which are GABA-benzodiazepine-chlorionoform, located on the postsynaptic membrane of the neurons of the limbic system, hippocampus, hypothalamus. As a result, a channel for chloride ions is formed in the CPM, its concentration increases, which leads to allosteric activation of GABA receptors, and as a result, the duration of action of the inhibitory mediator GABA is prolonged. These receptors are found in both the spinal cord and skeletal muscles. As a result of their activation, the effect of muscle relaxation is observed.

Benzodiazepine derivatives:

Chlosepides

Phenazepam

Lorazepam

Bromazepam

Gidazepam

Clobazam

Alprazolam

Tetrezepam

Carbamic esters of substituted propanediol:

Meprotan

Diphenylmethane derivatives:

Oxylidine

Trioxazine

Tofisopam

Sedatives

Rhizomes with valerian roots

Valocormid

Valosedan

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motherwort herb

stressplant

Sodium bromide

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Nootropic drugs

Piracetam

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Arylalkylamines:

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Benzimidazole derivatives:

Fundamentals of adequate use of drugs in psychiatry

V. Kozlovsky

The adequacy of the ongoing drug therapy is important, given the rich choice of drugs. There is no doubt that now in any medical specialty this issue is quite acute. Violation of the rational use of drugs is not always noticeable when it comes to the treatment of chronic diseases or when it is difficult to objectify the dynamics of the treatment process. These branches of medicine include psychiatry, in which the question of the correct prescription of individual drugs and even entire classes is most acute. This is due to the fact that the number of new drugs is constantly growing, the effect of their use develops rather slowly, and the spectrum of their psychotropic activity often does not fit into the usual patterns of action of classical drugs. As an illustration of alternative indications, we can recall the recommendations for prescribing antidepressants from the group of serotonin reuptake inhibitors in addition to depression in various anxiety disorders, the use of atypical antipsychotics in depressive states or anticonvulsants and calcium channel blockers in bipolar disorders, etc., there are many examples of this.

The purpose of this work was to consider the basic principles of rational therapy of mentally ill patients. First of all, a few words about the meaning of this question. As is known, the adequacy of prescribing drugs is associated with the doctor's actions in accordance with two areas that determine the effectiveness of therapy: pharmacokinetics and pharmacodynamics. Compliance with the general rules of pharmacokinetics is aimed at achieving therapeutic concentrations of drugs at the target point, and pharmacodynamics - at the choice of the drug in accordance with the mechanism of its action and the specifics of the pathology.

Issues of psychopharmacology related to the observance of the general principles of pharmacokinetics are rarely considered in the scientific press. This is probably due to the fact that the chemical structure, which determines the chemical and physical properties of all psychotropic drugs, must always satisfy the main criterion of "psychotropy" - solubility in lipoids. The latter is directly related to the distribution of drugs in the body and their penetration into the CNS through the blood-brain barrier (BBB). It should be noted that the concept of the BBB implies the presence of not a static formation, but a functionally active system, the adequate operation of which depends on the state of the organism as a whole and at the same time is itself capable of controlling the normal course of physiological processes. For example, it is well known that the permeability of the BBB increases dramatically with convulsions, arterial hypertension, allergic and infectious injuries. In addition, it is well known that intravenous administration of hyperosmolar solutions (40% glucose solution, 30% sodium thiosulfate solution, 25% magnesium sulfate solution, etc.) can provoke a greater penetration of substances through the BBB. It is also known that in the brain there are areas of high BBB permeability for physiologically active substances and the presence of such points (pituitary and epiphyseal regions, postrema region, preoptic cavity) is necessary for normal functioning, for example, neurohumoral and protective reactions (adequate functioning of biological feedback ). Therefore, to say that the substance is not capable of penetrating the BBB at all can only be very conditional, since small amounts of it are still able to enter the brain tissue and have a corresponding effect.

One of the important parameters characterizing the pharmacokinetics of drugs is the apparent volume of distribution. It shows the hypothetical volume of fluid in which the intravenously administered dose of the drug is distributed so that the resulting concentration at the end of its administration becomes equal to that determined in the blood plasma. Since most psychotropic drugs, in contrast to drugs of peripheral action, have a larger volume of distribution, they can to a certain extent almost evenly saturate all tissues of the body. For comparison: the volume of distribution of amitriptyline, nortriptyline, haloperidol is 20, 21, 23 l/kg, and for digitoxin, anaprilin, oxprenolol - 0.5, 4, 6 l/kg, respectively. However, it should be emphasized that the volume of distribution is not only determined by the solubility of drugs in lipoids, but also in water, and also depends on other properties of the drug molecule. In general, it is believed that the larger the volume of distribution, the better the penetration of the drug into various tissues of the body and the more difficult it is for the latter to get rid of it, even in the case of methods such as forced diuresis or renal dialysis. Nevertheless, it should be noted that endogenous substances and preparations similar to them, necessary for the normal functioning of the brain, are able to actively penetrate the BBB through specific transport systems that deliver them to the brain tissue (vitamins, hormones).

It is clear that the active therapeutic concentration of drugs in the blood plasma and brain, provided that there is good solubility in lipoids, primarily depends on the administered dose, and the constancy of the concentration will be determined by the rate of elimination of drugs from the body.

Mostly in psychiatry, the oral route of drug administration is used, in emergency cases intramuscular, and extremely rarely in urgent situations - intravenous. The peculiarities of drug entry into the blood plasma by these routes of administration are well known and, therefore, there is no need to dwell on them in detail. The elimination of the drug is associated with the work of the kidneys, liver and the activity of metabolic processes, all these characteristics depend on the chemical structure of the drugs and individual differences in the intensity of the work of the corresponding body systems.

It is believed that the determination of the concentration of the drug in the blood plasma is of great importance, since it can reflect the content of the active substance, including in the brain tissue, and the quality of the action depends on it - therapeutic or toxic. However, in relation to psychopharmacology, this provision in more may reflect the risk of "peripheral" side effects from the psychotropic drugs used, than to characterize their psychotropic activity. This is confirmed by the fact that for such classes of psychotropic drugs as antidepressants and antipsychotics, no direct and absolute dependence was found: dose-severity of the psychotropic effect. This fact is associated with the peculiarities of the action of psychotropic drugs on the endogenous neurochemical systems through which their action is realized. The features of pharmacodynamics or the mechanism of action of psychotropic drugs are determined, on the one hand, by the functional state of the corresponding neurochemical systems (their ability to react / change under the influence of a psychotropic drug), and on the other hand, by the selectivity / specificity of their action on the target system. Due to the limited volume of this work, it is not possible to speak in more detail about the pharmacodynamics and pathophysiology of mental disorders.

With the dynamics of changes in the concentration of the drug in the body, the most well-known indicator that characterizes this process is associated - the half-life of the drug from the blood plasma. It is generally believed that during the normal functioning of the organs responsible for the excretion of xenobiotics, the substance is completely removed from the body during its half-life, multiplied by 5. As a rule, for the vast majority of psychotropic drugs, this indicator is higher than for drugs of other groups used in related fields of medicine, in which drugs with less stringent requirements are used regarding their penetration through histohematological barriers. If we assume that for psychotropic drugs, the half-life almost always exceeds 12 hours, then the frequency of administration of these drugs should not be more than 2-3 times a day, and in most cases even a single prescription of drugs is sufficient. It is appropriate to say that in many guidelines on pharmacotherapy, the frequency of administration of drugs is often silent, and this reduces the value of the corresponding manuals for practicing physicians.

Returning to the indicator of the half-life or half-life of the drug, it should be noted that it must be distinguished from another indicator - the half-life of biological activity, which reflects the physiological or therapeutic effect of the substance. This indicator becomes important when the drug, metabolizing, forms active metabolites of the same spectrum of action as the main “mother” product. With the appearance of active and passive (inactive) metabolites, one of the stages of elimination (liberation of the body from the xenobiotic) is associated - biotransformation. Most often, drugs are metabolized in the liver, then in the blood, lungs, and muscles. This phase of metabolic transformations is also present when the drug is administered intramuscularly or subcutaneously, but is less significant when administered intravenously. As a rule, at this stage there is a biological oxidation of substances with the participation of a system of cytochrome P-450 isoenzymes. In addition, some drugs that enter the liver and are excreted unchanged with bile are able to be reabsorbed, entering the systemic circulation, the portal vein system, and again into the bile, repeating this cycle many times, they can be determined in the body for a long time at low concentrations. (chlorpromazine, chloral hydrate, methaqualone, diphenin, tricyclic antidepressants).

The concept of bioavailability is associated with biotransformation, which reflects the percentage of the active substance that enters the systemic circulation, remaining after the first passage through the liver. Already at this stage, substances may appear that are formed during the metabolism of the drug and have very active biological properties. They can cause not only therapeutic, but also toxic, oncogenic, teratogenic and other effects. The total amount of metabolites formed in the process of primary biotransformation reduces the amount of the active substance precisely by the part that they account for. Some drugs, having a relatively short half-life, can form long-lived active metabolites, the appearance of which in the blood plasma may suggest the development of cumulative effects. As an example, we can recall that the well-known drug from the group of selective serotonin reuptake inhibitors fluoxetine (T1 / 2 \u003d 50–70 h) - Prozac, Prodep, Portal, etc. - forms an active long-lived metabolite (T1 / 2 = 160–360 h), similar in spectrum of psychotropic activity to the drug itself. This, depending on the clinical situation, can be considered both as a positive moment and as a negative one. For example, with the successful use of a drug by a patient suffering from depression, the regimen of its use may be more free, skipping 1–2 or even 3–4 days in admission will not significantly affect the therapeutic effect of this drug. On the other hand, if the patient is resistant to this agent, the transition to another drug (MAO inhibitors, tricyclic antidepressants) or a combination of several should be done with extreme caution because of the risk of developing severe consequences in the form of a malignant serotonin syndrome.

At the stage of biotransformation, it is possible to change the pharmacokinetics of the main drug if it is administered in combination with other concomitant drugs. Particularly noteworthy are drug combinations containing inducers (ethanol, phenobarbital, diphenin, carbamazepine, hexamidine, diphenhydramine) and liver enzyme inhibitors (pyriditol, cimetidine).

Attempts to use the metabolic stage of drug transformations for the benefit of the patient were implemented when creating the so-called inactive prodrug, a drug from which a physiologically active substance is formed as a result of metabolism. Bupropion, a dopamine-positive antidepressant, is a prodrug among psychotropic drugs.

Unfortunately, reference books on psychopharmacology will never have a hypothetical indicator that can reflect the equipotentiality of the action of analogues. Any doctor is well aware of the differences in the biological effect of drugs from different manufacturers that have one active substance, such as diazepam (Valium, Relanium, Seduxen, Sibazon, Apaurin, Saromet, etc.). Despite the fact that all these drugs contain diazepam, the spectrum of their activity varies from a pronounced hypnotic to a mild sedative, and at the same time, both the severity and the speed of onset of the anxiolytic action characteristic of this drug change. Such differences in clinical performance are likely due to the fact that manufacturing companies use different excipients (“neutral” substances) necessary for the preparation of the dosage form. Most likely, the differences in the magnitude of some pharmacokinetic parameters that determine the level of concentration of the active substance in the blood plasma and target tissue are also due to the same reason.

In conclusion of this part of the work, it is also necessary to mention one more pharmacokinetic characteristic, which reflects the duration of the presence of the active substance in the body - binding to blood plasma proteins. As well as in the case of penetration through the histohematological barriers, psychotropic drugs, as a rule, to a much greater extent than other drugs, are able to bind to blood plasma proteins (albumins, acidic 1-glycoprotein). For example, protein binding for thioridazine is 99.5%, chlorprothixene is 97%, aminazine is 90%, haloperidol is 90%, amitriptyline is 95%, desipramine and doxepin are 80%, and for amidopyrine is 27%, digoxin is 30%, atropine - 50%, pindolol - 60%. Since the bound fraction of the drug is considered as a kind of depot from which the active substance gradually enters the blood plasma, then, as in the situations described above, the release of the body from the psychotropic drug is slower than elimination from another drug less associated with the protein fraction.

So, when considering the appearance of psychotropic effects, pharmacokinetic parameters were identified that can be used to control the therapeutic concentration of drugs in blood plasma. However, in contrast to therapeutic practice, in which the effect of the prescribed drug, as a rule, correlates with the content of the drug in the blood plasma, only a part of psychotropic drugs has a dependent psychotropic effect in accordance with changes in the dose and concentration of the drug. Such drugs include thymostabilizers (valproic acid derivatives, lithium preparations, carbamazepine), antiepileptic and anticonvulsant drugs, hypnotics, but, unfortunately, the main psychotropic classes - antidepressants and antipsychotics, do not have such an effect, both typical and atypical drugs of the new generations. If the absence of such a dependence was noted in special studies, then indirect, additional evidence of the correctness of this conclusion is that the therapeutic effect in the appointment of these drugs is formed from 2 to 6 weeks. When it comes to such a long period of therapeutic “inactivity” of drugs (this is a difficult period in the professional life of a psychiatrist), it can be assumed that some kind of restructuring of the neurochemical systems of the brain is required for the development of a psychotropic effect. They can be associated with both a change in the content of mediators and/or a change in the number of receptors in certain brain structures. In psychiatric practice, not only the period of "therapeutic inactivity" acquires importance, but also the absence in this period of undesirable effects from the prescribed drug. If within 2–3 weeks from the start of drug therapy the patient does not feel any effects from taking it, then it is possible that even an objective improvement in the condition may be underestimated in a subjective assessment (it seems to the patient that the medicine does not work on him, because he does not feel it). If the drug at the very beginning of therapy, without having a therapeutic effect, still causes the appearance of undesirable effects, then with the development of even minimal positive changes, the condition can be assessed not only by the patient, but also by the doctor with a clear overestimation of effectiveness. The role of psychological factors in drug therapy is described in detail in the monographs of I.P. Lapin.

It is probably legitimate to assume that the effect of psychotropic drugs on the mental state of healthy and mentally ill people differs. Moreover, it is likely that the differences between healthy and sick people are associated with the peculiarities of neurochemistry, against which the effect of the drug develops. Since antipsychotics and antidepressants have the corresponding (antipsychotic and antidepressant) effect only in patients and the reduction of pathological symptoms is clearly associated with their action, it is likely that their activity is aimed at changing the stable brain metabolism formed by the pathological system.

Researchers N.P. Bekhtereva et al. spoke about the development of a stable pathological condition in brain diseases. and G.N. Kryzhanovsky, noting stable changes both in the functioning of neurochemical systems and in the work of neurophysiological mechanisms that determine the corresponding changes in mental functions. Since most mental illnesses are chronic, often progressive either in the severity and severity of mental symptoms, or in the nature of changes in the relapse-remission cycle, neurochemical changes do not stand still, but undergo some changes associated with the involvement of more and more new neurochemical systems. In connection with such dynamics, the activity of some drugs can also change in comparison with others, and previously inactive drugs at some stage of the disease may turn out to be effective.

If there is not enough serotonin in the human body, he falls into a deep depression: not only does his mood worsen, but apathy, melancholy, anxiety are also observed, there is constant weakness, lethargy, irritability, appetite worsens, sexual desire decreases.

This state is dangerous, because it leads to thoughts of suicide, which a person, if he does not deal with the problem in time, can realize. Antidepressants are able to get the patient out of this state, selective serotonin reuptake inhibitors are especially effective.

Serotonin is one of the main neurotransmitters in the body. This is the name of 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 direct many processes occurring in 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 the emotional state of a person, prevents 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 goes astray, the state of the nervous system worsens, resulting in depression, obsessive-compulsive disorders, and severe migraines. Excess leads to hallucinations and schizophrenia.

To bring a person out of this state and normalize the amount of serotonin, various antidepressants, psychotropic medications, the main purpose of which is the treatment of various forms of depression.

Such drugs do not particularly affect a healthy person, while after a course of therapy in a person suffering from depression, they improve mood, reduce or completely relieve anxiety, apathy, melancholy, and emotional stress. This leads to psychological stability, normalization of the biological rhythm, stabilization of sleep, 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 lowered).

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

Due to this, the neurotransmitter does not return to the cell from which the message was sent (the drug 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 that were oppressed by depression, alleviating its symptoms.

It should be noted that although all SSRI drugs block the return of the neurotransmitter, they differ in their selectivity of action (selectivity) 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 this group of drugs is that they are prescribed immediately in the dosage necessary 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 has no special therapeutic effect.

For this reason, there is no special 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 drug withdrawal process, 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 in home treatment. 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;
  • pain chronic syndrome;
  • alcoholism;
  • depersonalization disorder (rarely prescribed, since SSRIs are ineffective in this disease).

Application

The effectiveness of SSRIs in the treatment of depression largely depends on the stage at which the disease was started to be treated. In mild to moderate depression, there is little, if any, difference between reuptake inhibitors and conventional antidepressants.

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 with SSRIs, the condition of patients improved in more than thirty percent of cases.

There is no need to expect immediate results from SSRIs: the first signs of the effectiveness of the drug can be seen by the end of the second to fifth, sometimes even the eighth week after the first dose of the drug. How often you need to take the drug depends not only on the severity of the disease, but also on the rate of excretion 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 only once a day. Fluvoxamine is excreted after fifteen hours, so you need to drink it twice a day.

Side effects

Side effects are manifested precisely because of the 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, various types of mania, increase. Therefore, during treatment, they must be carefully monitored. In adults, whether drug-related suicidal behavior 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 already a week after the first dose of the drug. Eliminate the stimulating effect by prescribing the use of a tranquilizer at the same time as taking the medication. Despite the risk of suicidal thoughts, various manias during the use of SSRIs are lower when compared with TCAs, MAO inhibitors.

If the patient has thoughts of suicide, it is undesirable to use drugs that can activate the psychomotor sphere, but to stop at antidepressants with a sedative (sedative) effect. Such a drug from the SSRI group is fluoxetine (this drug can provoke the development of mania). There are different opinions about citalopram: some believe that it has a balanced effect, others argue that it is stimulating. There is also no consensus on the effect of paroxetine.

Side effects are often also associated with the fact that serotonin receptors are located not only in the central and peripheral nervous system, but also gastrointestinal tract, as well as the smooth muscles of the bronchi, on the walls of blood vessels. For this reason, people who have severe 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, anorexia may develop);
  • increased arousal, anxiety, anxiety;
  • headache;
  • fast fatiguability;
  • insomnia (in 20-25% of cases) or increased drowsiness;
  • diarrhea;
  • motor function disorders (hand trembling).

This reaction of the body is typical in the first stages of taking SSRIs and usually disappears after a month. Sometimes patients complain of a decrease in sexual desire, a delay in orgasm, or an inability to feel it. If the drugs are taken for too long, there is a risk of bleeding.

In patients with very serious psychological disorders who take too much a large number of drugs, serotonic syndrome may occur, characterized by convulsions, high temperature, 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, a drug from the same group can be used (if it so happened that one of the 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.

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