How do antidepressants act on the nervous system? Antidepressants - what are they? Tranquilizers and antidepressants

Antidepressants are a large group of drugs for mood correction.

History

The invention of mood pills dates back to the 50s, when the first two and a half ADs were synthesized:

  • Isoniazid with Iproniazid, which were originally invented as a means to treat tuberculosis, but were found to cause unexplained euphoria in patients and attracted the interest of psychiatrists;
  • Imipramine is a tricyclic obtained by adding a pair of atoms to the nuclear neuroleptic Aminazine.

Before them, doctors tried to improve the mood of the sufferers with everything they could get their hands on: they used opiates, barbiturates, amphetamines, valerian, bromides, ginseng and rauwolfia. The effects were not bad, although far from antidepressant.

What is this

On at the moment There are three main groups of drugs, which differ greatly not only in their spectrum of action, but also in their side effects.

This is not a symptomatic treatment, they say the person became sad, they gave it and he became cheerful, no, this is pathogenetic.

TCA

Tricyclic antidepressants are the most reliable and studied group of antidepressants, which have a good list of side effects (drowsiness, dry mouth/eyes, constipation) and a low price - Amitriptyline 0.025, 17 rubles for 50 tablets. Their action is based on reducing the uptake of several mediators (serotonin, norepinephrine and dopamine), which together gives not only an antidepressant, but also a sedative effect.

The most epic of them are Imipramine, Amitriptyline and Nortriptyline. Since 2005, production of the first Soviet antidepressant Azafen began again, which is of some interest due to the absence of anticholinergic and cardiotoxic effects.

SSRIs

Selective serotonin reuptake inhibitors, as the name suggests, act primarily on serotonin, increasing its concentration and leading to the desired effect. Now this group is the most frequently used, and Flucosetine (Prozac) has been breaking all sales records for several years now, although many SSRIs have a very high price. This is facilitated by the small number of side effects when using small doses, so they are recommended for use even just in general medical practice. Also, their use helps with other conditions, such as obsessive disorders and overeating.

There are just a lot of drugs for every taste: Fluoxetine, Sertraline, Fluvoxamine, Paroxetine, Dapoxetine, Citalopram, Escitalopram, Venlafaxine, Duloxetine; For more details, see the main article.

MAOI

Inhibitors monoamine oxidases- heavy artillery, used when no other drug has worked. Their use is limited due to extensive side effects and incompatibility with a huge list of drugs and food products, increasing their toxicity. Although, due to their stimulating effect, they are highly indicated for patients with atypical and “minor” depression.

The most currently used MAOI drug is Moclobemide; in this group there is a real Russian drug - Pyrazidol, which does not have an anticholinergic effect, due to which it can be used as a replacement for tricyclic drugs in patients with glaucoma and BPH.

Other

In addition to these groups, there are drugs with a bi- and four-cyclic structure, called atypical antidepressants, some of which have a radically different mechanism of action - Mianserin does not affect either MAO or the uptake of neurotransmitters.

One of the most interesting: Bupropion.

How does this work

The basis of depression is considered to be a decrease in serotonin and norepinephrine transmission between neurons in the brain, therefore the main effects of the described group are based on an increase in the concentration of serotonin and norepinephrine. You can’t take the missing substances and put them into the brain - the administration of our body is not so stupid as to allow anything to act on them (as glutamate paranoids would like): antidepressants lead to an increase in these substances indirectly? - by blocking the enzymes that utilize them. Elimination slows down -> concentration increases, it’s simple. It is extreme idiocy to compare antidepressants with drugs; unfortunately, they do not work at all and, in principle, cannot - they do not act on a healthy person at all.

The effect of antidepressants is manifested in a positive effect on the affective sphere, which leads to an improvement in mood and a concomitant normalization of general mental state with some additional effects that differ for each specific drug: Imipramine and Fluoxetine (and some MAOIs - Nialamid, Eprobemide) have a stimulating effect, Amitriptyline (and other tricyclics) and Maprolitin act well as anti-anxiety drugs.

Doctor, what will happen to me?

An important aspect of the action of antidepressants is that their effect appears no earlier than 5-10 days of use, increasing gradually with the accumulation of target substances in the brain; and a sustained response to therapy develops within at least 2-4 months of continuous use.

They are used not only by psychiatrists, but also by neurologists for the treatment of neurovegetative conditions and chronic pain, often without real depression in the patient, so do not be surprised by such prescriptions.

More

  • Depressants are substances that depress the central nervous system. In large dosages, they remove internal inhibitions, weaken concentration and the ability to make balanced judgments. The coolest: alcohol, tranquilizers (Valium and Librium) and opiates (morphine and heroin).

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Notes

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What kind of medications are antidepressants?

Antidepressants name a group of pharmacological drugs that act on the central nervous system and eliminating the cause and symptoms of depression. In some cases, these drugs are also used to treat other diseases, but their effectiveness is significantly reduced.

The main effect of antidepressants is to change the levels of serotonin, dopamine and norepinephrine in the cells of the central nervous system. In patients with depression, they eliminate apathy, stimulate interest in physical and intellectual activity, lift the mood in general. It should be noted that people who do not suffer from depression may not experience this effect.

What is the difference between tranquilizers and antidepressants?

Tranquilizers and antidepressants are different pharmacological groups, since these drugs have different effects on the central nervous system ( CNS). Almost all tranquilizers have a pronounced sedative ( sedative) action. They can cause drowsiness, apathy, and inhibit physical activity. Their main task is to relieve psychomotor agitation if the patient is overly active or aggressive.

Antidepressants combine a fairly wide range of therapeutic effects. Only some drugs in this group produce effects more or less similar to those of tranquilizers. Basically, they relieve symptoms and eliminate the causes of depression - they activate the emotional sphere, increase internal motivation, and give strength ( in the psychological aspect).

In addition, antidepressants and tranquilizers have different chemical structure, interact with various mediators and other substances in the body. For some pathologies, doctors may prescribe parallel use of drugs from these two groups.

Is it possible to buy antidepressants in a pharmacy without a prescription or doctor's prescription?

There are a number of antidepressants that have fewer side effects. Most of these drugs also provide a weaker therapeutic effect. Taken together, their effect is considered “milder”, so in many countries they are allowed to be dispensed in pharmacies without presenting a prescription from a doctor.

It should be noted that even these drugs, which are, in principle, freely available, should not be used for active self-medication. The problem is not the direct harm from these antidepressants, but the unforeseen situations that may arise in in rare cases.

There is a certain risk of self-use of any antidepressants for the following reasons:

  • Possibility of an allergic reaction. Almost any drug can cause an allergic reaction. This depends on the individual characteristics of the patient’s body, and no specialist can predict such a complication in advance. If the patient has a predisposition to allergies ( to other substances), it is better to warn your doctor about this and not take any new medications yourself.
  • Possibility of diagnostic error. The patient cannot always correctly diagnose the problem. This is especially difficult to do in the case of mental and emotional disturbances. If the diagnosis was initially made incorrectly, antidepressants may not only fail to provide a therapeutic effect, but may also worsen the problem. That is why it is better to take any drug after consultation with a specialist.
  • Possibility of drug interactions. As a rule, in the instructions for a particular drug, the manufacturer indicates various undesirable interactions with other medicines. However, each drug has many brand names, and patients often do not delve into the details. Because of this, a “harmless” antidepressant sold without a prescription can be harmful to health when combined with another medication the patient is taking. In case of consultation with a qualified specialist, this risk is minimized.

Which doctor writes a prescription for antidepressants?

In principle, the main specialized doctors who often prescribe antidepressants in their practice are psychiatrists ( sign up) And neurologists ( sign up) . It is these specialists who are most closely associated with disorders of the central nervous system ( both structural and functional). In addition, other doctors usually refer patients with depression or similar disorders to them.

If necessary, antidepressants can be prescribed by other specialists. Usually these are emergency doctors, therapists ( sign up) , family doctors, etc. It should be noted that they usually prescribe more weak drugs, which do not require a prescription to purchase. However, legally, any doctor with a valid license has the right to write a patient a prescription for a more potent drug. At the same time, he takes responsibility for familiarizing the patient with the rules of admission and the possible consequences.

What are “prohibited” and “allowed” ( over-the-counter) antidepressants?

Antidepressants, like all medications, can, in principle, be divided into two large groups. These are “approved” medications, which anyone can freely purchase at a pharmacy, and conditionally “prohibited” ones, which are sold with a doctor’s prescription.
In each country, the list of permitted and prohibited drugs is slightly different. This depends on health policy, current legislation, and the prevalence of narcotic and semi-narcotic drugs.

Antidepressants sold without a prescription tend to have a weaker effect. They don't have that wide range side effects and practically cannot cause serious harm patient's health. However, the effectiveness of these drugs for serious depression is very low.

Over-the-counter antidepressants in most countries include the following:

  • Prozac;
  • zyban;
  • maprotiline;
  • deprim et al.
There are also a number of herbal products available for sale ( valerian, St. John's wort, etc.), which have an antidepressant effect.

Conditionally “prohibited” antidepressants are so called because their distribution is limited by law. This is partly done for the safety of the patients themselves. These drugs have a large number side effects, and their independent use can cause serious harm to health. Also, some drugs in this group can be equated to narcotic drugs and cause addiction. In this regard, a prescription for them is written by a specialist, who will first make sure that the patient really needs this medicine.

“Forbidden” antidepressants with a stronger effect include the following drugs:

  • imipramine;
  • maprotiline;
  • anafranil, etc.
It should be noted that as a result of changes in WHO recommendations ( world organization health) and with reforms at the national level, the list of “allowed” and “prohibited” antidepressants periodically changes.

Classification of antidepressants

The classification of antidepressants is very challenging task, since here you can take various criteria as a basis ( chemical structure, mechanism of action, etc.). Currently, it is customary to distinguish between two main groups of these drugs. The first affects the capture of neurotransmitters between membranes nerve cells. The second neutralizes the action of the enzyme, which releases the receptors. In practice, drugs from these two groups are used in almost all equally. It should also be noted that such a division is very arbitrary, since each representative of any of these groups has its own characteristics. That is why the vast majority of antidepressants are prescribed by a specialist familiar with the intricacies of the action of each drug.

Chemical and pharmacological groups of antidepressants

From a practical point of view, the most convenient classification of antidepressants is based on the chemical structure of the drug in combination with the mechanism of action. In most countries, specialists are guided by these very criteria. They allow, if necessary, to replace an intolerable or ineffective drug with another that is closest in action.

The following groups of antidepressants are distinguished according to their chemical structure:

  • Tricyclic. The chemical structure of tricyclic antidepressants contains so-called “rings” or “cycles”. These are groups of atoms united in a closed chain, which largely determine the properties of the drug.
  • Tetracyclic. There are four cycles in the structure of tetracyclic antidepressants. There are significantly fewer drugs in this group than in the tricyclic group.
  • Different structure. For convenience, this group includes substances that do not have cycles in their chemical structure ( rings), but have similar effects on the central nervous system.
According to the mechanism of action, antidepressants are usually divided depending on the enzymes and mediators with which they interact in the central nervous system.

Tricyclic antidepressants

Tricyclic antidepressants belong to the first generation of antidepressants and have been used in medical practice for several decades. What these substances have in common in their chemical structure are three interconnected “rings” or cycles. Drugs in this group are non-selective inhibitors of the reuptake of a number of substances in the central nervous system. Taking them eliminates anxiety, fear or depression, and also causes a general “lift” of mood. Currently, tricyclic antidepressants are still widely used for many mental disorders. The main disadvantage of this group is the large number of side effects. This is explained precisely by its indiscriminate effect on various processes in the brain.

The most common representatives of the group of tricyclic antidepressants are:

  • amitriptyline;
  • imipramine;
  • clomipramine;
  • trimipramine;
  • nortriptyline, etc.

Tetracyclic antidepressants ( first generation antidepressants)

This group is represented by substances that have four “rings” of atoms in their molecules. In medical practice, they are used much less frequently than tricyclic antidepressants.

The most common representatives of tetracyclic antidepressants are:

  • mianserin;
  • mirtazapine;
  • pirlindol, etc.

Selective serotonin reuptake inhibitors ( SSRIs)

SSRIs are one of the most common and popular groups of antidepressants in modern medical practice. The mechanism of action of these drugs is reduced to selective blocking of certain enzymes in the central nervous system ( CNS). This allows you to achieve the desired therapeutic effect with greater accuracy. The risk of various side effects from using the drugs is also reduced. This group includes serotonin reuptake inhibitors, but, in principle, for each neurotransmitter ( transmitter substances) their own drugs were found in the nervous system. The medicine is selected by a specialist who can accurately diagnose and identify disorders in the functioning of the central nervous system.

The following reuptake inhibitors are available for various neurotransmitters:

  • Serotonin– cipralex, fluvoxamine, etc.
  • Norepinephrine– nortriptyline, maprotiline, etc.
  • Dopamine– diclofensine.
There are also a number of drugs that block the reuptake of both norepinephrine and serotonin. These include amitriptyline, imipramine and other tricyclic antidepressants. They are called non-selective.

How do different groups of antidepressants differ from each other?

Antidepressants, like most other drugs, are divided into pharmacological groups that have some characteristic differences. This is necessary for the convenience of practical use of drugs in treatment. The chemical structure of molecules is most often of secondary importance. The main criterion is the mechanism of action of the drug.

Antidepressants various groups have the following differences:

  • Mechanism of action. Each group of antidepressants has different mechanism actions. Drugs different groups interact with different substances in the central nervous system, which ultimately leads to a similar effect from taking the drug. That is, the effect of the drugs is similar, but the chain biochemical reactions that occur in the body is very different.
  • Strength of the drug. The strength of the drug is determined by how effective it is in blocking enzymes in the central nervous system. There are more strong antidepressants, which give a pronounced and stable effect. They are usually available by prescription due to the risk of severe side effects. Drugs with a weaker effect can be purchased at the pharmacy yourself.
  • Transformations of the drug in the body. The set of chemical transformations that a drug molecule undergoes in the body is called pharmacodynamics or drug metabolism. In this regard, almost every drug has its own characteristics. For example, the duration of blocking of an enzyme may vary. Accordingly, the effect of one drug will last for a long time ( up to 24 hours), and the other - just a few hours. This determines the reception mode. There is also a time for the drug to be eliminated from the body after administration. Some substances are naturally eliminated quickly, while others can accumulate during the course of treatment. This should be taken into account when choosing a medicine. The mechanism of drug elimination itself is also important. If the substance is ultimately excreted in the urine through the kidneys and the patient has renal failure ( blood filtration and urine formation are difficult), the drug will accumulate in the body, and the risk serious complications increases greatly.
  • Side effects. Depending on the characteristics of the action of a particular antidepressant on the body, it can cause various side effects. It is important for specialists to know them in order to notice their symptoms in time and take the necessary measures.
  • Interaction with other drugs. Drugs in the human body interact with various substances. Taking several medications at the same time can make their effects stronger or weaker, and sometimes produce other, unpredictable effects. In the instructions for each antidepressant, manufacturers usually indicate which drugs the substance may interact with.
  • Possibility of developing an allergic reaction. Each antidepressant has its own chemical structure. A patient can have an allergic reaction to almost any medicine ( With with different probabilities ). If you develop an allergy to one drug, you should consult a doctor and change it to another drug that differs in chemical structure, but is similar in its therapeutic effect.
  • Chemical structure of the molecule. The chemical structure of the molecule determines the properties of any drug. It is because of this that each antidepressant has its own advantages and disadvantages. In addition, features chemical structure form the basis for the classification of antidepressants.

Are there natural antidepressants ( natural herbs)?

There are not many recipes in folk medicine that could provide real help in the fight against depression. This is largely due to the complexity of the processes that occur in the central nervous system. If antidepressants act selectively, affecting certain substances ( neurotransmitters, enzymes, etc.), then their natural analogues do not have such selectivity. Their effect will be much weaker, and the likelihood of side effects increases ( Neither decoctions nor infusions make it possible to isolate only the active substance from a particular plant). That is why, in case of severe depression and other serious psychiatric diseases, it is recommended, first of all, to contact a specialist and, with his consent, begin taking folk remedies. Most often they will have to be combined with certain pharmacological drugs.

The following herbs have a weak effect similar to that of antidepressants:

  • Rhizome of lure. The crushed rhizome is poured with medical alcohol ( 70% ethyl alcohol solution) in a ratio of 1 to 10 and leave for several hours. The infusion is taken 1 teaspoon 2 times a day.
  • Chamomile aster flowers. For 1 tablespoon of dried flowers you need 200 ml of boiling water. Infusion lasts at least 4 hours. The resulting product is taken 1 tablespoon 3 times a day.
  • Bird's knotweed. 3 - 5 grams of dried knotweed are poured into 2 cups of boiled water and left until the water cools to room temperature on its own. Drink half a glass of infusion before meals ( 3 times a day).
  • Aralia Manchurian. Crushed Aralia roots are poured with medical alcohol in a ratio of 1 to 5 and left for 24 hours. The resulting tincture is taken 10 drops 2-3 times a day, diluted in boiled water.
  • Ginseng root. Dried ginseng root is crushed and poured alcohol solution (50 – 60% ) in a ratio of 1 to 10. The mixture is infused for 2 - 3 days in a closed container. The resulting tincture is drunk 10-15 drops 2 times a day.

Properties and action of antidepressants

Antidepressants, as a separate pharmacological group, have certain general properties. First of all, this concerns the predominant effect on the central nervous system. Any antidepressant affects the transmission of nerve impulses in the brain, and its effect on other organs and systems will be secondary. Otherwise, most drugs in this group have their own characteristics. For example, antidepressants include drugs that give a hypnotic or, conversely, an invigorating effect. Side effects can affect almost any organ or system. This is explained by the fact that the brain, one way or another, regulates the vital functions of the entire organism, and any changes in its work will inevitably affect the body as a whole.

Mechanism of action of antidepressants

To better understand the mechanism of action of antidepressants, you need to imagine in general terms the principle of operation of the human central nervous system. The brain consists of many nerve cells, neurons, which perform the most important functions. Neurons have a large number of different processes that connect to other nerve cells. As a result, a kind of network of cellular contacts is formed. The impulses entering the brain are distributed in this network in a certain way, and the brain reacts to the information received. Each part of the brain is responsible for regulating certain processes in the body. Depression, as well as various nervous and mental disorders, are primarily a consequence of excitation of certain parts of the brain. Antidepressants affect the junctions of nerve cells, speeding up or slowing down the transmission of nerve impulses in various ways (depends on the specific drug).

The transmission of nerve impulses in the brain occurs as follows:

  • An impulse is formed in a nerve cell as a result of chemical interactions and travels along one of the processes to the junction with another nerve cell.
  • The junction of two nerve cells is called a synapse. Here, two cell membranes are located at a very close distance. The gap between them is called the synaptic cleft.
  • The nerve impulse reaches the presynaptic membrane ( cells that transmit impulses). Here are bubbles with a special substance - a neurotransmitter.
  • As a result of excitation, enzymes are activated, which lead to the release of the transmitter from the vesicles and its entry into the synaptic cleft.
  • In the synaptic cleft, neurotransmitter molecules interact with receptors on the postsynaptic membrane ( cell membrane that “receives” the impulse). As a result, a chemical reaction occurs, and a nerve impulse arises, which is transmitted throughout the cell.
  • The transmitter molecules that transmit the impulse between cells are captured back by special receptors and concentrated in vesicles or destroyed in the synaptic cleft.
Thus, a number of different substances take part in the process of propagation of nerve impulses in the central nervous system. There are also enzymes that prevent the propagation of the impulse. That is, both excitation and inhibition can occur between cells.

Antidepressant molecules interact with certain receptors, mediators or enzymes, and affect the impulse transmission mechanism as a whole. Thus, excitation or inhibition of processes in various departments brain

What side effects do antidepressants have?

The vast majority of antidepressants have a fairly wide range of side effects, which greatly limit the use of these drugs. More often similar phenomena arise due to the parallel effect of the drug on receptors in the peripheral nervous system. This affects the functioning of many internal organs. However, there are other mechanisms for the development of side effects.

Side effects from taking antidepressants can be divided into the following groups:

  • Dose dependent. This group of side effects includes problems that arise when the therapeutic level is exceeded ( medicinal) doses. All medications without exception have them. Many of these side effects can be interpreted as signs of overdose. In the case of tricyclic antidepressants, for example, this may be a hypotensive effect ( lowering blood pressure). As a rule, all such effects disappear when the dose is reduced.
  • Dose independent. This group of side effects usually appears against the background long-term treatment. A drug with a similar structure and effect affects the functioning of certain cells or tissues, which can sooner or later cause various problems. For example, when using tricyclic antidepressants, leukopenia is possible ( reduced level leukocytes and weakened immunity), and when treated with serotonergic antidepressants – inflammation and pain in the joints ( arthropathy). In such cases, lowering the dose will not solve the problem. It is recommended to stop treatment and prescribe drugs from a different pharmacological group to the patient. This gives the body time to recover a little.
  • Pseudo-allergic. This group of side effects resembles common ones allergic reactions (urticaria, etc.). Similar problems are quite rare, mainly when taking serotonergic antidepressants.
In general, the range of side effects that can occur while taking antidepressants is very wide. Disturbances in the functioning of a variety of organs and systems are possible. Patients often not only develop any symptoms and complaints, but also experience deviations from the norm when various studies (for example, in a blood test).

Possible side effects when taking antidepressants

Affected organs or systems

Complaints and violations

Possible ways problem solving

Cardiovascular system

Reducing the dose of antidepressant. If not possible, use medications to eliminate symptoms ( at the discretion of the cardiologist).

Heart rhythm disturbances ( on the electrocardiogram)

Increased blood pressure ( sometimes harsh)

Strong changes in blood pressure with changes in body position ( orthostatic hypotension)

Digestive system

Reducing the dose of the drug. Changing the reception mode ( more often, but in smaller doses), gradually increasing the dose at the beginning of treatment. If jaundice appears, it is recommended to stop treatment or change the drug.

Bitter taste in mouth

Blood and hematopoietic system

Increase or decrease in white blood cell count ( leukocytosis or leukopenia, respectively), decreased platelet count ( thrombocytopenia), increased level eosinophils ( eosinophilia). These disorders are detected during a general blood test

Stopping treatment, changing the drug.

Central nervous system

Lethargy and drowsiness ( in severe cases and confusion)

At the discretion of the attending physician ( psychiatrist or neurologist) you can reduce the dose, stop taking the drug or prescribe symptomatic treatment in parallel ( lithium salts, antipsychotics, phenobarbital, beta blockers - depending on the symptoms).

Nervous excitement, increased activity

Irritability

Hives

Swelling and pain in the joints

A sharp increase in blood pressure (hypertensive crisis)

Nausea and vomiting

General disorders and symptoms

Decreased sex drive

Hormonal imbalances

Hearing impairment


In principle, if, against the background of a one-time or long-term use of antidepressants, the patient begins to experience any unusual symptoms, you should consult your doctor. Many of the above side effects indicate poor tolerability of the drug. If treatment is not stopped, the patient may develop severe serious damage organs or systems that will require additional treatment.

Also, the side effects of many antidepressants include addiction, and, as a result, withdrawal syndrome that occurs after stopping treatment. In these cases, treatment tactics may be different. Treatment is prescribed by the specialist who is caring for the patient.

Are there antidepressants without side effects?

In principle, any pharmacological drug can potentially cause certain side effects. Among the antidepressants that have a very wide spectrum of action, there are no drugs that would be ideal for all patients. This is explained by the characteristics of the underlying disease ( Antidepressants are prescribed not only for depression) and individual characteristics of the body.

To reduce the likelihood of side effects when choosing a drug, you should pay attention to following points. First, newer drugs ( "new generation") have a highly targeted effect on the body and usually have fewer side effects. Secondly, over-the-counter antidepressants have more weak impact on the body as a whole. That is why they are available for free sale. As a rule, serious side effects occur much less frequently when taken.

Ideally, the selection of the drug is carried out by the attending physician. To avoid serious side effects, he conducts a series of tests and better understands the characteristics of the individual patient’s body ( concomitant diseases, accurate diagnosis etc.). Of course, in this case there is no 100% guarantee. However, under the supervision of a doctor, you can always replace the drug or select an effective symptomatic treatment that will eliminate complaints and allow you to continue the course of treatment.

Compatibility of antidepressants with other drugs ( neuroleptics, hypnotics, sedatives, psychotropics, etc.)

The simultaneous use of several drugs in medicine is very actual problem. In the case of antidepressants, it should be noted that they are often used as part of complex therapy. This is necessary to achieve a more complete and quick effect for a number of mental disorders.

The following combinations of antidepressants are very relevant in psychiatry:

  • Tranquilizers– for neuroses, psychopathy, reactive psychoses.
  • Lithium salts or carbamazepine– with affective psychoses.
  • Neuroleptics- for schizophrenia.
According to statistics, almost 80% of patients in psychiatric departments receive such combinations. However, in this case, therapy is prescribed by a specialist, and the patient is always under the supervision of doctors - in a hospital.

In general, the combination of antidepressants with many other pharmacological drugs often gives negative consequences. You may experience unexpected side effects or reduce the effectiveness of any drug ( no expected therapeutic effect). This is explained by several mechanisms.

Negative combinations of antidepressants with a number of medications can be dangerous for the following reasons:

  • Pharmacodynamic interactions. In this case we're talking about about difficulty in learning medicinal substances. After taking an antidepressant ( in tablet form) the active substance must be normally absorbed in the intestines, enter the liver, and combine with blood proteins. Taking other pharmacological drugs can disrupt this chain at any stage. For example, many drugs are converted in one way or another by the liver. Taking several drugs that interact with the same enzymes may weaken the effect of each of them individually or cause some complications in the liver itself. To avoid such complications, the doctor prescribes drugs taking into account the time of their absorption, specifying the dosage regimen.
  • Pharmacokinetic interactions. In this case, we are talking about the effect of several drugs on the same body system ( same target cells or enzymes). Antidepressants work at the nerve connections in the central nervous system. Taking other drugs that affect the nervous system can enhance their effect or, conversely, neutralize it. In both cases, there will be no expected therapeutic effect, and the risk of side effects will greatly increase.
That is why during the course of treatment with antidepressants you should be very careful and not take even the usual and familiar drugs that are sold in pharmacies without a prescription without a doctor’s prescription. In some cases, incorrect drug combinations can seriously harm the patient's health or even endanger his life. If you need to take any medication, it is advisable to consult your doctor or pharmacist. On most drugs ( in the instructions) often indicate the most dangerous drug combinations for a particular drug.

Do antidepressants have a stimulant effect?

In principle, most antidepressants have a stimulating effect on the central nervous system to some extent. Depression itself is accompanied by a state of depression. The patient is passive because he has no desire to do anything. A properly selected antidepressant restores the desire to do something and, thus, gives strength.

However, the stimulating effect of antidepressants should not be confused with the effect of energy drinks or certain drugs. The stimulating effect manifests itself more in the emotional and mental sphere. Physical fatigue decreases due to the removal of some “psychological block.” The drugs promote motivation and interest in various activities.

MAO inhibitors have the greatest stimulating effect in this regard ( monoamine oxidases). However, even in them this effect develops gradually, as the corresponding enzymes and mediators accumulate in the body. You can feel the changes 1 – 2 weeks after starting to take the drug ( provided that it is correctly selected and taken in the required dose).

There are also antidepressants that have a hypnotic and sedative effect. They stimulate mental and emotional activity, but physical condition a person changes little. These include, for example, amitriptyline, azaphene, pyrazidol. Thus, the patient may not get the expected result. To avoid mistakes, it is better to consult in advance with a specialist who can explain in detail what effect he expects from treatment with a particular drug.

Do antidepressants have an analgesic effect?

The main effect of antidepressants is to relieve the patient of symptoms and signs of depression, including drowsiness, passivity, lack of motivation, mental and emotional depression. None of the drugs in this group has a pronounced analgesic effect in the generally accepted sense. In other words, when there is an obvious source of acute pain ( inflammation, injury, etc.) taking antidepressants will not alleviate the patient's condition.

However, some drugs from the antidepressant group are successfully used to combat chronic pain. The fact is that chronic pain often accompanies long-term depressive states. Mental disorders are not the only source of pain, but may well intensify it and, thereby, greatly worsen the patient’s condition. Experts have noticed that a number of antidepressants can relieve such chronic pain. In this case, we are talking more about reducing the perception of pain than about the analgesic effect.

The following antidepressants can be used in the treatment of chronic pain syndromes:

  • venlafaxine;
  • amitriptyline;
  • clomipramine;
  • desipramine.
Of course, you should not start taking antidepressants on your own if you have chronic pain. Firstly, this group The drugs have a wide range of side effects, and the patient may experience other problems. Secondly, by eliminating pain syndrome, the patient runs the risk of “masking” the problem. After all, back pain, muscle pain or headaches do not always accompany depression. Most often they have a very specific reason that needs to be eliminated. That is why patients need to contact a specialist for staging correct diagnosis. Only if depression in combination with chronic pain is confirmed, the use of the above antidepressants will be justified and rational. Before use, you should consult a specialist.

    Monoamine oxidase inhibitors:

    1. I generation (non-selective irreversible MAO inhibitors): nialamide, tranylcypromine.

      II generation (selective irreversible MAO-A inhibitors): chlorgyline.

      III generation (selective reversible MAO-A inhibitors): pirlindole, moclobemide.

    Neuronal monoamine reuptake inhibitors:

    1. Non-selective neuronal reuptake inhibitors:

      1. tricyclic structure: imipramine, amitriptyline, amoxapine;

        tetracyclic structure: maprotiline.

    2. Selective noradernaline and serotonin uptake inhibitors: venlafaxine.

      Selective serotonin uptake inhibitors: trazodone, sertraline, fluoxetine.

      Selective norepinephrine uptake inhibitors: reboxetine.

      Selective dopamine uptake inhibitors: amphebutamon.

    Atypical antidepressants: mianserin, mirtazapine, tianeptine..

Monoamine oxidase inhibitors

MD: The action of all antidepressants in this group is associated with an effect on the activity of monoamine oxidase (MAO), an enzyme from the group of flavin oxidases. MAO is a mitochondrial enzyme that takes part in the deamination of biogenic amines (norepinephrine, adrenaline, dopamine, serotonin). There are 2 isoforms of this enzyme, the characteristics of which are presented in Table 18.

Table 18. Monoamine oxidase isoforms and consequences of their blockade.

Sign

MAO-A

MAO-V

Localization

Intestine, liver, placenta, adrenergic and serotonergic neurons

Liver, brain nuclei and platelets

Oxidizable substrate

Serotonin, norepinephrine, dopamine

Phenylethylamine, tyramine, dopamine

Inhibitor

Chlorgyline

Selegilin

Positive effect of the blockade

    Psychostimulant

    Antidepressant

    Hypotensive

    Antiparkinsonian

Negative effect of the blockade

    Increased anxiety

    Insomnia

    Headache

    "Cheese" syndrome

    Neurotoxic solutions

    Hemodynamic parameters

    Hepatotoxic disorders

Blockade of MAO activity leads to the cessation of oxidation and inactivation of monoamines in the synapses of the nervous system after their reverse neuronal uptake and, as a consequence, an increase in the reserves of monoamine stores in the neuron. With each subsequent nerve impulse, the release of monoamines into the synaptic cleft increases sharply and the transmission of the impulse is facilitated.

Scheme 14. Effect of MAO inhibitors on a neuron. IN normal conditions(left), after the release of the transmitter into the synapse, part of it undergoes reverse neuronal uptake, where monoamine oxidase oxidizes its excess in the mitochondria. That. MAO acts as a “safety valve”, preventing the vesicles from becoming overloaded with transmitter. MAO inhibitors (right) disrupt this process and the transmitter continues to accumulate in the vesicles after each pulse. An excess of transmitter occurs in the vesicles, and its release into the synapse increases.

N
ialamide (
Nialamid, Nuredal) It is a derivative of isonicotinic acid hydrazide. MD: Acts as a “suicidal substrate” for MAO. MAO metabolizes nialamide to a highly reactive intermediate product, hydrazide, which oxidizes the prosthetic flavin group of the enzyme and MAO loses its activity.

Nialamide irreversibly and non-selectively blocks both types of enzyme - MAO-A and MAO-B. Restoration of oxidative deamination of amines occurs only during the resynthesis of new MAO molecules, which requires about 10-14 days.

    Thymoanaleptic effect - has an antidepressant effect (reduces melancholy, depression, pessimism) in combination with a psychostimulating component (causes excitement, euphoria, insomnia). The antidepressant effect develops after 7-10 days of course administration and reaches a maximum by 3-4 weeks. Due to the psychostimulating component, depression can transition into a hypomanic and manic state in people with manic-depressive psychosis.

    Analgesic effect - suppresses chronic pain caused by injuries, tumors, neuritis and rheumatic diseases. A decrease in the sensation of pain occurs due to a decrease in its emotional coloring, but nialamide has virtually no effect on the intensity of pain. Nialamid potentiates the effect of analgesics. The exact mechanism of the analgesic effect of nialamide is not clear; it is believed that it suppresses the transmission of nociceptive impulses in the spinal cord pathways due to the activation of monoaminergic descending transmission in the antinociceptive system.

    Hypotensive effect. With the use of nialamide and other MAO inhibitors, blood pressure decreases despite an increase in the release of monoamines from the endings of the sympathetic nerves. The reasons for this are unclear, but several mechanisms may be at play:

    reduction in the activity of the central parts of the baroreflex arc and higher sympathetic centers due to the facilitation of catecholaminergic transmission in inhibitory neurons;

    disruption of the transmission of sympathetic impulses at the ganglion level.

    Anti-aggregation effect. By inhibiting the activity of MAO-B in platelets, nialamide promotes the accumulation of dopamine in them, which inhibits platelet aggregation (sticking together) and improves the rheological properties of blood. In addition, nialamide causes vasodilation of cerebral vessels.

Indications for use and dosage regimen. Currently, the use of nialamide and other irreversible inhibitors MAO in the Russian Federation and a number of other CIS countries has been discontinued. This is due to the large number of serious and potentially fatal adverse effects that occur due to the interaction of MAO inhibitors with other drugs. Previously, nialamide was used to treat:

    Astheno-adynamic and melancholic forms of major depression and the depressive phase of manic-depressive psychosis.

    Atypical depression, as well as depression resistant to traditional pharmacotherapy.

The initial dose was 25-75 mg/day (⅔ doses taken in the morning and ⅓ in the afternoon) with a daily increase of 25-50 mg/day to an average effective dose of 200-800 mg/day.

    Nialamide, like all other irreversible MAO inhibitors, is characterized by a number of undesirable interactions with other drugs:

    Nialamide potentiates the inhibitory effect on the central nervous system of barbiturates, ethanol, opioid analgesics, antihistamines and antiparkinsonian drugs from the group of M-anticholinergic drugs. In severe cases, respiratory depression may occur.

    When interacting with sympathomimetics (including drugs for the treatment of cold symptoms that contain pseudoephedrine or phenylethylamine), their hypertensive effect may be potentiated, because sympathomimetics cause the release of excess transmitter accumulated in nerve endings during MAO blockade 25 .

    When interacting with sympatholytics (reserpine, guanethidine), their hypotensive effect may be distorted with agitation and hyperthermia. This is due to the fact that at the beginning of their action, in order to empty the neurotransmitter depot, sympatholytics cause the release of all accumulated neurotransmitter into the synapse. Since, against the background of MAO inhibitors, the reserves of the mediator in the vesicles are increased, the release of such an amount of norepinephrine causes the development of the above-described hypercatecholamine syndrome.

    When interacting with tricyclic antidepressants, nialamide and other MAO inhibitors also cause hypercatecholamine syndrome: arterial hypertension, hyperthermia, psychomotor agitation, tremor. This is due to the fact that MAO inhibitors increase the stores of norepinephrine, serotonin and dopamine in the neuron and they are released into the synapse in large quantities. Tricyclic antidepressants block the reuptake of these monoamines and promote an even greater increase in their level in the synaptic cleft during the passage of subsequent nerve impulses.

These interactions should be remembered because, due to the irreversibility of MAO blockade, the effect of inhibitors of this enzyme (and nialamide among them) persists not only during the entire course of treatment, but also for another 10-14 days after stopping their use. Therefore, when transferring a patient who has been taking MAO inhibitors to tricyclic antidepressants, it is necessary to take a break of 2-3 weeks.

    "Cheese crisis" or tyramine syndrome. Characterized by sharp increase Blood pressure, tachycardia and arrhythmia, increased body temperature, in severe cases – attacks of angina pectoris and myocardial infarction. The cause of the syndrome is the consumption of foods containing tyramine. Tyramine is a product of protein tyrosine decarboxylation, which is formed during the fermentation of foods. By acting on nerve terminals, tyramine displaces monoamines from the depot, which (due to MAO blockade) accumulate in them in large quantities. In the average person, tyramine from foods is neutralized by the MAO system of the intestines and liver. However, in individuals who use MAO inhibitors, these enzymes do not work and they are unprotected 26 .

The doctor is obliged to inform the patient about the list of food products, the use of which is undesirable due to the content of tyramine:

    cheeses, especially “ripened” varieties (the highest concentration of tyramine is observed under the rind and around the enzymatic cavities);

    smoked sausages, herring, ham;

    overripe bananas, avocados, figs;

    wines and beer (including non-alcoholic);

    fermented legumes, beans, soy sauce;

    chicken liver;

    tea, coffee.

If tyramine syndrome occurs, help consists of the immediate administration of α-adrenergic blocking agents - phentolamine, prazosin or chlorpromazine.

    An overdose of nialamide is accompanied by agitation, confusion, a manic or hallucinatory state, and sudden sweating.

    Specific to nialamide, as a representative of the group of hydrazine derivatives, is peripheral neuropathy (possibly associated with impaired absorption of vitamin B6) and hepatocellular damage.

    A big disadvantage of MAO inhibitors with psychoactivating effects (which include nialamide) is the ability to increase suicidal tendencies in a patient when he recovers from depression 27 .

    MAO inhibitors help increase intraocular pressure, cause acute delay urine (especially in older people with benign prostatic hyperplasia).

FV: tablets and even 25 mg.

T
ranylcypromine (
Tranylcypromine, Transamine, Parnate) MD: Unlike nialamide, it has a different mechanism of irreversible MAO inhibition. It is metabolized under the influence of MAO to form an active imine product, which interacts with the SH group of the active center of the enzyme. Tranylcypromine has no effect on the flavin prosthetic group.

IN
Unlike nialamide, the effect manifests itself more quickly (on days 2-5), is tolerated somewhat better, and in doses up to 40 mg/day it is much less likely to cause undesirable effects characteristic of nialamide. Otherwise similar to other irreversible MAO inhibitors. Tranylcypromine is used occasionally in the United States as an alternative to nialamide.

FV: 10 mg tablets.

Chlorgyline (Clorgyline) MAO-A is oxidized to an active acetylene intermediate, which, according to the “suicidal metabolite” principle, irreversibly inactivates the flavin prosthetic group of MAO-A.

It has virtually no effect on the activity of MAO-B. Chlorgyline did not find widespread clinical use because it did not have any advantages over nialamide in terms of safety and tolerability. It also often caused the development of tyramine syndrome and orthostatic hypotension like nialamide.

P
irlindol (
Pearlindole, Pyrazidolum) MD: It is a reversible selective inhibitor of MAO-A, which only temporarily blocks the active site of the enzyme, with virtually no effect on MAO-B. The blockade of the enzyme lasts 6-24 hours. Pirlindole is characterized by a certain substrate specificity - it inhibits MAO-A to a greater extent in the brain than in the liver. Preservation of the hepatic pool of MAO-B and MAO-A during treatment with pirlindole allows the liver to oxidize food tyramine, while “cheese syndrome” rarely develops when taking pirlindole.

    Thymoregulatory effect. Pirlindol increases mood and activity in patients with astheno-apathetic forms of depression and has a psychosedative effect in the agitated form of depression. Like other MAO inhibitors, the effect of pirlindole is enhanced in older patients age groups.

    Pirlindol has a nootropic effect in patients of older age groups (improves memory, associative thinking, cognitive functions of the brain).

    Unlike nialamide, it does not cause increased intraocular pressure or acute urinary retention in elderly people.

Indications for use and dosage regimen. Pirlindol is used primarily in geriatric practice for the treatment of involutive depression, atypical depression in the elderly, and for anxiety and depression in patients suffering from alcohol dependence.

The initial dose of pirlindole is 50-75 mg/day in 2 doses orally. Gradually increasing the dose by 25-50 mg/day, it is brought to the average therapeutic dose of 150-400 mg/day. A clear and sustainable effect can usually be achieved by the end of the first week.

NE: Pirlindol is well tolerated and rarely causes the undesirable effects characteristic of nialamide. However, it is not recommended to use other MAO inhibitors, tricyclic antidepressants, psychotropic drugs and central nervous system depressants simultaneously during treatment with pirlindole.

The most common undesirable effects during treatment with pirlindole are dry mouth, sweating, tremor, tachycardia, nausea and dizziness, which are associated with an excess of catecholamines in the central parts of the nervous system and a relative deficiency of M-cholinergic effects against this background.

FV: tablets of 25 and 50 mg.

M
oclobemide (
Moclobemide, Aurorix) MD: Selectively and reversibly blocks the MAO-A isoform of the enzyme. It is believed that both moclobemide itself and the metabolite formed from it during oxidation act as an enzyme inhibitor.

    Timostimulating effect – moclobemide improves the mood of patients and increases their psychomotor activity.

    Anxiolytic effect. It manifests itself in moclobemide in obsessive-phobic forms of neuroses and is most pronounced in relation to the so-called. social phobias – agoraphobia (fear of open spaces, fear of finding yourself in places or situations from which leaving may be difficult or shameful, or fear of being in places where in case of panic it is impossible to get help – crowd, queue, train, etc.) , claustrophobia (fear of closed spaces).

Indications for use and dosage regimen. Mclobemide is used for astheno-adynamic forms of depression and social phobia. The initial dose is 300 mg/day in 2-3 doses; if well tolerated, it can be increased after 5-6 days to 600 mg/day.

NE: Moclobemide is well tolerated, cases of “cheese syndrome” with its use have not been described, however, the patient should be warned about the need to limit the consumption of tyramine-containing products during treatment with moclobemide.

Long-term use of moclobemide is accompanied by an increase in prolactin concentrations. This is associated with its ability to activate 5-HT 2 -type serotonin receptors of the pituitary gland and cause the release of prolactin into the blood.

A feature of moclobemide is its extremely short half-life (1-4 hours), therefore, when replacing moclobemide with another drug from the antidepressant group, there is no need to take a break in treatment.

FV: film-coated tablets of 150 and 300 mg.

Table 19. Comparative characteristics of the action of MAO inhibitors

Preparation

Blockable Action Targets

-AR

5-HT-R

M 1 - R

H 1 -R

nialamide

pirlindole

moclobemide

Note: SCR - serotonin reuptake, SNR - norepinephrine reuptake, OCR - dopamine reuptake,- AR-adrenoreceptors, 5-HT-R– serotonin receptors,M 1 - R– muscarinic cholinergic receptors, N 1 - R– histamine receptors

Chemicals found in the human brain that affect mood are called neurotransmitters or neurotransmitters. People suffering from depression and other mood disorders have altered levels of these chemicals. Antidepressants work by helping to normalize the levels of these compounds, which in turn normalizes the functioning of neurotransmitters in the brain. Depression and mental health disorders are serious problems that need to be treated. In our country, antidepressants are prescribed by doctors of all specialties, but in fact only a psychiatrist should prescribe them, since only a psychiatrist can make a conclusion about the severity of mood imbalance and prescribe adequate therapy to help balance chemical composition neurotransmitters.

Types of Antidepressants

Antidepressants These are psychotropic drugs used to treat depression, affecting the level of neurotransmitters such as serotonin, norepinephrine and dopamine. In patients with depression, they improve mood, reduce or completely relieve melancholy, lethargy, a feeling of indifference, neutralize anxiety, restlessness, irritability and emotional stress, increase mental activity, normalize the structure of sleep phases, affect the duration of sleep, appetite.

There are the following classes of antidepressants working in different directions.

They act similarly to SSRIs, but allow more norepinephrine to be produced in the synaptic cleft. TCAs include Protriptyline (Vivactil), trimipramine (Surmontil) and (Tofranil)

    Monoamine oxidase inhibitors (MAOIs).
    MAO inhibitors slow the breakdown of serotonin, dopamine and norepinephrine in the brain. Isocarboxazid (Marplan), Phenelzine (Nardil), and Razageline (Azilect) are examples of monoamine oxidase inhibitors.

Every patient is different, but many for depressed patients one of the SSRIs is prescribed for the first time. If drugs in this group do not work, then next drug a tricyclic antidepressant is prescribed. Last but not least, monoamine oxidase inhibitors (MAOIs) are prescribed. This is due to the fact that all antidepressants have many side effects and restrictions on use.

May take time

Antidepressants work best for treating depression when given in conjunction with psychotherapy, but they do not work right away. Many antidepressants have a cumulative effect and it will take 1 to 3 weeks for it to start working, and about 2 more weeks for the effect to reach its maximum. Most symptoms associated with depression—a lack of interest in things that were once enjoyable, as well as feelings of hopelessness and sadness—eventually improve with antidepressants. In rare cases, some people may be resistant to certain antidepressants, and finding what works may require trial and error with other medications. The effect of the drug may not be noticeable for weeks or months. Each different type and class may be associated with different potential risks.

Make adjustments if necessary

In general, it takes about 4-6 weeks for antidepressants to take effect. If you are still experiencing symptoms after this amount of time, talk to your doctor. You may need to increase the dose of your current antidepressant medication or switch to another one. Some people experience treatment failure with the first antidepressant they try. In these cases, switching to a drug in a different class may be a better option. Antidepressant treatment may take up to three months to achieve maximum effect. Very rarely, some people who take antidepressants notice that the drug stops working. Such cases, as well as any other difficulties associated with treatment, must be reported to your doctor. Remember that depression left unattended is a risk to your mental health.

Regular visits to your doctor are necessary in order to adjust treatment in the changing picture of the disease. Depression and anxiety are serious illnesses and can be associated with suicidal ideation and other symptoms. It is extremely important to address complaints that concern you in a timely manner. Treatment with selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs) and other antidepressants requires monitoring and exact dosages. The goal is to relieve depression and anxiety without side effects or symptoms. You may also need treatment adjustments if you have undergone a major life change, such as being diagnosed with a serious illness or losing your job. Women who are pregnant may also need to adjust the type or dose of medications they take. Some medications may have negative impact on developing fetus.

How long does treatment last?

Treatment with antidepressants for depression can last from several months to a year. It is very important not to stop treatment or reduce the dose of your prescribed medication just because you start to feel better. If you do this, the depression will return. It is important to stay on your prescribed dose for as long as your doctor tells you to do so. Take the medication at the same time each day for maximum benefit. You can take your tablets with breakfast each morning as an easy way to remember to take your medications.

Tell your doctor about side effects

Some people may experience side effects from antidepressants. Be sure to discuss them with your doctor. Some common side effects may include increased or decreased appetite; difficulty falling asleep or excessive sleepiness; weight gain or loss, problems with libido. Some people may experience nausea. Your doctor can help you come up with solutions to potential side effects. Often, side effects from antidepressants are temporary and may go away after a few weeks of taking them. If the side effects are severe, your doctor may prescribe a different medicine for you. Never stop taking your antidepressants. This may lead to severe symptoms withdrawal and depression.

Interaction with other drugs

Antidepressants prescribed today are often of much higher quality and have fewer side effects and drug interactions than older drugs across different classes. However, reactions with other medications, herbs, and supplements you take are always possible. Interactions may interfere with how the drug works or may reduce the effectiveness of the drug. Always make sure your healthcare provider knows about all the prescriptions and medications, supplements, and herbs you are taking.

Myths about antidepressants as drugs

Many people are afraid to take antidepressants to treat depression and anxiety because they believe that antidepressants are drugs and are addictive. Some fear that antidepressants will make them robotic and emotionless. Yes, they can help relieve feelings of sadness and hopelessness, but they will not make you detach from your emotions. Some people also mistakenly believe that they will need to be treated with antidepressants for life. Most people are treated for 6 to 12 months. Follow your doctor's instructions about starting, increasing, decreasing, or stopping medications and you will receive good treatment. Abruptly stopping antidepressants is dangerous and can lead to withdrawal symptoms.

It is best to combine treatment

Several studies show that combining antidepressants with psychotherapy is the most effective method treatment of depression. Mental illness is serious. It is important to take your depression medications as directed and see your GP regularly. Mental illness is first and foremost a disease and is nothing to be ashamed of. Millions of people suffer from depression, anxiety and other mental health disorders. People should feel comfortable seeking help for mental health conditions as they would for others organic diseases such as heart disease or diabetes. Cognitive behavioral therapy(CBT) helps control and change unwanted thoughts and behaviors. Interpersonal therapy helps patients interact better and more effectively with others.

Stopping antidepressants

Antidepressant withdrawal should be carried out very carefully by a specialist to avoid withdrawal symptoms. Follow your doctor's instructions to reduce your dose and eventually stop the medication. If you stop taking antidepressants too early, depression will return. In general, dose reduction is very gradual best plan. Tell your doctor if you experience side effects or symptoms when you reduce the dose of your medication or stop it altogether.

Getting help for depression is the right thing to do. The risks of untreated depression outweigh the potential side effects of medications. Current clinical trials continue to explore new potential treatments for depression and other mood disorders. The FDA has issued a warning that some SSRIs, MAOIs, and TCAs may increase the risk of suicidal thoughts and behavior in adolescents and young adults aged 18 to 24 years during the first two months of treatment.

Antidepressants – medicines, which are active in relation to depressive states. Depression is a mental disorder characterized by decreased mood, weakened motor activity, intellectual poverty, erroneous assessment of one’s “I” in the surrounding reality, and somatovegetative disorders.

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

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

History of the discovery of antidepressants

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

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

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

Magic pills - their groups

All antidepressants are divided into 2 large groups:

  1. Thymiretics- drugs with a stimulating effect that are used to treat depressive states with signs of depression and oppression.
  2. Thymoleptics– drugs with sedative properties. Treatment of depression with predominantly excitatory processes.

Indiscriminate action:

Selective action:

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

Monoamine oxidase inhibitors:

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

Antidepressants of others pharmacological groups– Coaxil, Mirtazapine.

Mechanism of action of antidepressants

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

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

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

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

Modern classification of antidepressants

Tricyclic antidepressants

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

Side effects

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

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

The most common side effects include:

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

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

At long-term use– cardiotoxic effect (cardiac conduction disturbances, arrhythmias, ischemic disorders), decreased libido.

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

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

Tranquilizers and antidepressants: what's the difference?

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

The power of "magic pills"

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

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

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

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

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

Herbal natural antidepressants:

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

Our TOP 30: the best antidepressants

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

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

There's something for everyone

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

The truth is always beyond theory

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

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

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

Karina, 27

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

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