Depression is one of the most common diseases. In terms of prevalence, it is second only to cardiovascular diseases. And of all those suffering from depression, only no more than 20% seek qualified help.
In this article we will tell you about all the drugs used to treat depression.
All medications with antidepressant effects can be divided into several groups:
- Antidepressants.
- Normotimic drugs.
- Neuroleptics.
- Tranquilizers.
- Nootropics and metabolic agents.
- Herbal remedies.
- Amino acids.
- Psychostimulants.
Normotimic drugs
Medicines in this group have an antidepressant effect only in cases where the depressive state is caused by chronic affective diseases, such as bipolar affective disorder (BD, manic-depressive psychosis), cyclothymia, dysthymia, schizoaffective disorder. Most commonly used medications:
- Carbamazepine (finlepsin)
- Depakine chrono
- Lamotrigine (Lamictal)
- Lithium carbonate
Psychotropic drugs: a guide to fears
A couple of decades ago, the use of psychotropic medications was the exclusive prerogative of the psychiatrist. Therefore, it seems to me that there remains fear and mistrust in relation to this class of drugs. However, the trends of modern medicine are such that a neurologist, working on the principles of evidence-based medicine and adhering to international clinical guidelines, must understand psychotropic medications, as they allow the doctor to improve the patient’s quality of life, avoid endless and useless consultations with doctors and additional expensive examinations. In this article I will talk about the main types of psychotropic drugs that a neurologist can prescribe at an outpatient appointment: tranquilizers/anxiolytics, antidepressants, neuroleptics, antiepileptic drugs.
Some basics. How does our brain work? The brain is made up of many neuron cells. Neurons transmit information to each other using molecules called neurotransmitters. There are a lot of neurotransmitters: acetylcholine, histamine, serotonin, dopamine, GABA, etc. The mediator is released from the process of one neuron and “sits” on a receptor that is located on the process or body of another neuron. Some transmitters activate another neuron, some inhibit it. The mechanism of action of most psychotropic drugs is associated with the effect on receptors for certain mediators - one or several at once.
What are the fundamental differences between classes of psychotropic drugs?
1. Tranquilizers (anxiolytics, anti-anxiety drugs)
Representatives: benzodiazepines (phenazepam, alprozalam, clonazepam), hydroxyzine (atarax), tofisopam (grandaxin), etifoxine (strezam) and others. They act on the receptors of “inhibitory” mediators. Due to this, they have a calming, sedative effect. The drugs differ in the “strength” of their effects and the severity of their calming effect. The effect develops quickly, but does not last long.
When prescribed: if you need to quickly relieve anxiety, a panic attack, correct insomnia, reduce anxiety before surgery or medical interventions, to reduce the side effects of antidepressants when starting to take them. Course duration: short, no more than 4 weeks, especially benzodiazepine drugs, which can become addictive with longer use. Tranquilizers are not sold without a prescription. Some drugs are only available on a special prescription with a number and series. 2. Antidepressants These include tricyclic antidepressants (amitriptyline, clomipramine), selective serotonin reuptake inhibitors (escitalopram, sertraline, fluoxetine and others), selective serotonin and norepinephrine reuptake inhibitors (venlafaxine, duloxetine) and others. Older groups of antidepressants act on the receptors of several types of mediators at once, which causes a large number of uncomfortable side effects (weight gain, drowsiness, arrhythmia, increased intraocular pressure, and others). The more modern the drug, the more “targeted” its effect. Some drugs act on a specific neurotransmitter receptor subtype. Due to this, the likelihood of developing side effects is reduced, but their effectiveness remains high. To minimize the side effects of antidepressants, which can be especially disturbing at the beginning of treatment, the doctor will select the optimal regimen for increasing the dosage (from the lowest possible dose and a gradual, smooth increase) and discontinuing the drug. The effect of this group of drugs unfolds within 2-3-4 weeks, however, after discontinuation of the drug, the “tail” of their positive effect remains for some time.
The course of treatment is long, at least 6 months. When prescribed correctly, taking into account the individual characteristics of the patient and his concomitant pathology, taking antidepressants, even long-term, is safe. Antidepressants are not addictive or addictive. Used for: anxiety, phobias, panic attacks, as part of the treatment of post-traumatic disorder and reaction to a stressful event, for insomnia, chronic headaches, chronic back pain, for painful polyneuropathy, for psychogenic dizziness, for irritable bowel syndrome, for somatization disorders. Antidepressants are prescribed by a doctor and are not available without a prescription. 3. Neuroleptics The most frequently prescribed by a neurologist are quetiapine, olanzapine, risperidone, alimemazine (teraligen). In Russian realities, sulpiride (eglonil) is also often used, although in my opinion its purpose is not entirely justified. The main target is dopamine receptors. The indications are quite narrow and specific. Often prescribed in addition to antidepressants. Each antipsychotic has its own nuances of increasing the dosage and discontinuing the drug. Also not sold without a prescription. 4. Antiepileptic drugs (anticonvulsants, mood stabilizers). They act on receptors for certain neurotransmitters and on the ion channels of the neurons themselves. In addition to epilepsy, they are prescribed for the treatment of pain associated with irritation/inflammation/pinching of nerve structures - the root, trigeminal nerve, nerves in the arms, legs, as well as for stabilizing mood, in particular in bipolar affective disorder. The duration of treatment depends on the disease.
If your neurologist has prescribed you a psychotropic drug, be sure to discuss the following questions:
• Dosage increase and drug withdrawal regimen • The most common side effects and how to minimize them • Degree of drowsiness and ability to drive • Approximate duration of therapy • Interactions of medications and other drugs that you take on a regular basis, as well as interactions with alcohol Don’t hesitate to ask your doctor any questions that concern you in connection with the prescription of this group of drugs. Your doctor is a partner in the fight against the disease that brought you to him.
Neuroleptics
Despite the fact that most antipsychotic drugs depress the nervous system, among them there are drugs with antidepressant effects:
- Flupenthixol (fluanxol).
It has an antidepressant effect only when administered in small doses (less than 2 mg per day).
- Aripiprazole.
Effective for depression in bipolar affective disorder and schizitypal disorders.
- Levomepromazine (tizercin).
Prescribed for endogenous depression accompanied by insomnia.
Table 1 Comparison of antidepressants used in the elderly
| A drug | Starting dose | Estimated dose range | Cautions* | Perceived Benefits |
| Selective serotonin reuptake inhibitors (SSRIs)¶ | ||||
| Escitalopram | 5 mg every morning or every evening | 5 – 20 mg per day | Discontinuation of use without titration is accompanied by a mild withdrawal syndrome. | Applies to escitalopram and citalopram: Generally well tolerated. No sedative effect, low risk of developing sleep disorders, relatively few drug interactions. A good choice for initial treatment of depression in most elderly patients. |
| Citalopram | 10 mg every morning or every evening | 10 – 20 mgΔ per day | Dose-dependent increase in the duration of the QT¶Δ interval. Discontinuation of use without titration is accompanied by a mild withdrawal syndrome. | |
| Sertraline | 12.5 – 25 mg every morning | 25 – 200 mg per day | More frequent gastrointestinal adverse events, including diarrhea. Differences in bioavailability of oral dosage forms. The oral solution contains ethyl alcohol. Stopping treatment without titration is accompanied by withdrawal syndrome. | No sedation, low risk of sleep disorders, low risk of cardiotoxicity. A good choice for initial treatment of depression in most elderly patients. |
| Fluoxetine | 5 - 10 mg every morning | 5 – 60 mg per day | Activating effect. Pronounced drug interactions. Due to the long half-life of the drug and the activity of metabolites, it takes several weeks to achieve stable concentrations and evaluate the effect of dose adjustment, “washing out” or discontinuation of the drug. | The stimulant effect may be useful in treating depressed patients with decreased activity or sleepiness. Due to the long half-life, titration is not required when discontinuing the drug. |
| Paroxetine | 10 mg every evening | 10 – 40 mg every evening | Weak anticholinergic effect. May cause constipation and dry mouth. Discontinuation without titration is accompanied by more severe withdrawal symptoms. | Suitable for treating patients suffering from insomnia. Average half-life without active metabolites. |
| Fluvoxamine | 25 mg every evening | 25 – 200 mg every evening | Significant drug interactions. Due to the short half-life, discontinuation without titration is accompanied by a more severe withdrawal syndrome. | Can be used in patients with insomnia. |
| Serotonin and norepinephrine reuptake inhibitors (SSRIs)◊ | ||||
| Venlafaxine (slow release) | 37.5 mg once daily | 75 – 225 mg once daily | Refers to venlafaxine or desvenlafaxine: Activating effect. May cause a dose-dependent increase in blood pressure (mainly diastolic) and heart rate. Regular monitoring of blood pressure is required. Gastrointestinal disturbances (for example, nausea) may be more severe than when taking the immediate-release dosage form of venlafaxine. Discontinuation without titration is accompanied by withdrawal syndrome. Titrate desvenlafaxine with increasing interval between doses. | Refers to venlafaxine or desvenlafaxine: The activating effect may be useful in the treatment of depressed patients with melancholic features, low energy or increased sleepiness. Suitable for the treatment of patients suffering from pain due to comorbidities such as diabetic neuropathy. |
| Venlafaxine (immediate-release tablets) | 18.75 - 37.5 mg every morning or twice a day | 75 – 150 mg twice daily | ||
| Duloxetine | 10 – 20 mg per day | 20 – 60 mg once daily | Significant drug interactions. | Mild sedative effect. Low risk of insomnia. Suitable for the treatment of patients suffering from pain due to underlying diseases such as diabetic neuropathy or chronic pain. |
| Atypical antidepressants◊ | ||||
| Mirtazapine | 7.5 mg every evening | 15 – 60 mg every evening | Increased half-life of the drug and active metabolites. Risk of accumulation in patients with renal and/or liver failure. Dose reduction required. Lethargy, weight gain. Rare reports of the development of agranulocytosis. | Sedative effect. Low risk of sexual dysfunction. During the first few days of use, stimulation of appetite and reduction of nausea may be noted. Suitable for treating patients suffering from insomnia or those who need to gain weight. |
| Bupropion sustained release | at the beginning - 75 mg in the morning, then - twice a day | 150 mg morning and afternoon (twice daily) | Avoid use in patients with seizures and agitation. Dose-dependent increase in diastolic blood pressure May increase the severity of sleep disorders. | The stimulant effect may be useful in the treatment of patients suffering from depression with low activity levels and apathy. Low risk of “cognitive toxicity” (negative effects on cognitive function). Dopaminergic effects may be beneficial for Parkinson's patients suffering from depression. |
| Vilazodone | 10 mg once daily with food for 7 days or more | 20 - 40 mg once a day with food | Take food to ensure bioavailability. Diarrhea, nausea, vomiting, dizziness, insomnia. Significant drug interactions mediated by effects on CYP 3A4 require dose adjustment. | Low incidence of weight gain or sexual dysfunction. Role in treatment of elderly, depressed, or adults with underlying medical conditions has not been established. |
| Trazodone | 12.5 - 25 mg 30 - 60 minutes before bedtime may have a hypnotic effect | 25 - 100 mg 30 - 60 minutes before bedtime can have a hypnotic effect; a higher dose is required to develop an antidepressant effect. | Sedation, orthostatic hypotension, nausea. Increases cognitive impairment, the sedative effect persists during the day. Reports of hyponatremia. | Used in low dose as an adjunct to SSRIs to treat insomnia. |
| Tricyclic antidepressants (TCAs)§ | ||||
| Amitriptyline | 6.25-12.5 mg at night | 75-200 mg per day (literature data) more often, patients do not tolerate doses > 50 mg | Similar to nortriptyline and desipramine: May be poorly tolerated by patients with comorbidities and older patients due to anticholinergic effects causing dry mouth, constipation, urinary retention or visual disturbances (the drug should be avoided in patients with prostate diseases, angle-closure glaucoma). Overdose can be fatal. Potential for cardiotoxicity: May cause arrhythmia or orthostatic hypotension. Multiple significant drug interactions. | Mild sedative effect. Patients suffering from insomnia take the drug before bedtime. Can be used for patients suffering from depression with melancholic and anxious features in whom first-line antidepressants fail to achieve effect. Pronounced analgesic effect for neuropathic pain. |
Tranquilizers
- Bromodihydrochlorophenylbenzodiazepine (phenazepam).
The drug of choice for neurotic conditions with depression and post-stress conditions. That is, in cases where short-term treatment is required.
- Clonazepam.
Strong anti-anxiety and sedative effect. When taken for a long time it causes dependence.
- Alprazolam.
Prescribed for anxiety and depression. Recommended for short courses (no more than 10 days) due to the risk of developing addiction and dependence.
Antidepressants: how do they work?
Depression. Its vice squeezes the heart and tears the soul apart. Rest and sedative medications do not help. The only effective means of combating it are medications from the antidepressant group.
The root of sad troubles
Lethargy, decreased vitality, gloomy mood and self-accusation of all mortal sins most often have nothing to do with bad character or unfavorable life circumstances. These symptoms are evidence of depression, which mercilessly breaks up families, deprives one of a career, and sometimes gives rise to terrible thoughts of putting an end to all this trouble once and for all.
According to the World Health Organization, about 350 million people in the world suffer from depression. Most patients, unfortunately, do not seek medical help, blaming their sad condition on anything but biochemical changes in the body. Meanwhile, they are the ones responsible for the development of depressive symptoms.
Nootropics and Metabolic Aids
The remedies in this group help to get out of a depressive state that has developed against the background of stress, overwork, encephalopathy, the consequences of injuries and poisoning. By improving the blood supply to neurons and energy metabolism within cells, they contribute to the activation of cognitive functions and memory. The most effective drugs in this group:
- Phenibut
- Mexidol
- Aminalon (GABA)
- Piracetam (nootropil)
- Picamilon
- Pyriditol (encephabol)
- B vitamins.
Antidepressants
Antidepressants are psychotropic medications used primarily to treat depression. In a depressed patient, they improve mood, reduce or relieve melancholy, lethargy, apathy, anxiety and emotional stress, increase mental activity, normalize the phase structure and duration of sleep, and appetite. Action diagram
What is common to all known modern antidepressants is that all of them in one way or another - either by blocking the reuptake of monoamines or by blocking their destruction by monoamine oxidase - increase the content of one or more neurotransmitter monoamines (norepinephrine, serotonin, dopamine, phenylethylamine and others) in the synaptic cleft and enhance monoaminergic (monoamine-mediated) transmission of nerve impulses (neurotransmission).
All modern antidepressants are characterized by the phenomenon of an “antidepressive threshold” that is individual for each patient and depends on the severity of depression and the degree of resistance to antidepressants (experience of previous treatment).
Below this threshold, there is no antidepressant effect and only nonspecific effects appear - in particular side effects, sedative or stimulant properties. It turned out that for the antidepressant effect of drugs acting through their influence on the reuptake of monoamines to occur, it is necessary to block the reuptake of at least one of the monoamines by at least 80-90% (that is, a decrease in monoamine reuptake by at least 5-10 times), and for the antidepressant effect of MAO inhibitors to manifest, it is necessary to reduce MAO activity by at least 40-50%, that is, at least 2 times. Classes of antidepressants Monoamine oxidase inhibitors (MAOIs)
Non-selective and irreversible Monoamine oxidase inhibitors (MAOIs) are first-generation antidepressants.
These include derivatives of isonicotinic acid hydrazide (GINK), or the so-called “hydrazine” MAOIs - iproniazid (iprazide), isocarboxazid, nialamide, as well as amphetamine derivatives - tranylcypromine, pargyline. Most of the drugs in this group cannot be combined with a number of other drugs and require a special diet to prevent the development of tyramine (“cheese”) syndrome. Newer drugs of this class - selective MAO-A inhibitors (moclobemide, pirlindole, metralindole, befol) or MAO-B (selegiline) are used more widely, as they give significantly fewer side effects, are better tolerated and do not require a special diet, and are also compatible with many drugs with which non-selective MAOIs are incompatible. However, selective MAO-A and selective MAO-B have significantly weaker antidepressant activity compared to non-selective MAOIs, and are also weaker than tricyclic antidepressants. Strictly speaking, it is not entirely correct to classify tranylcypromine, pargyline and other amphetamine derivatives into the group of non-selective and irreversible MAO inhibitors along with hydrazine MAOIs such as nialamide and isocarboxazid. Tranylcypromine and pargyline, unlike GINK derivatives, partially reversibly block MAO and exhibit greater selectivity towards MAO-A, and the likelihood of developing cheese syndrome when treated with tranylcypromine or pargyline is lower, and the cheese syndrome itself, if it develops, is milder. However, it is also impossible to classify tranylcypromine and pargyline into the group of modern, fairly safe selective and reversible MAO-A, since cheese syndrome is still possible when treated with them. Tranylcypromine and pargyline seem to occupy an intermediate position between the irreversibly blocking MAO derivatives of GINK and the reversibly blocking MAO-A such as moclobemide and pirlindole. On the other hand, the selectivity of modern MAO-A such as pirlindole, moclobemide and the reversibility of the MAO blockade they cause is not absolute, and at high doses (submaximal or maximum, or exceeding those usually used in clinical practice), some of them can still cause cheese syndrome, although milder than tranylcypromine, pargyline and hydrazine MAOIs. Tricyclic antidepressants (TCA, English TCA)
Tricyclic antidepressants (TCA), or tricyclics, are a group of highly effective antidepressants with much fewer side effects compared to MAOIs, which do not require a special diet and do not impose large restrictions on the medications used simultaneously.
They are called tricyclics because they all have a common chemical structure - three rings connected together (condensed) in a molecule. Although the structure of these rings and the radicals attached to them can be very different. Within the class of tricyclics, there are two subclasses that differ in the characteristics of their chemical structure - tricyclics, which are tertiary amine tricyclics, and tricyclics, which are secondary amines (secondary amine tricyclics). Many of the tricyclics of the secondary amine subgroup are active metabolites of tricyclics - tertiary amines, formed from them in the body. For example, desipramine is one of the active metabolites of imipramine, nortriptyline is one of the active metabolites of amitriptyline. Tricyclics - tertiary amines, as a rule, are distinguished by stronger sedative and anti-anxiety activity, more pronounced side effects (M-anticholinergic, antihistamine, alpha-blocking), stronger antidepressant activity and a more balanced effect on the reuptake of both norepinephrine and serotonin. Typical representatives of tertiary amines are amitriptyline, clomipramine (anafranil), imipramine (melipramine, tofranil), trimipramine (gerfonal), doxepin, dothiepin (dosulepin). Tricyclics - secondary amines (desipramine, nortriptyline, protriptyline), as a rule, are distinguished by more pronounced stimulating activity, less sedative and anti-anxiety effects, are better tolerated and give fewer M-anticholinergic, antihistamine and alpha-blocking side effects, but also have less antidepressant activity and imbalance (they inhibit the reuptake of norepinephrine to a greater extent, with almost no effect on the reuptake of serotonin). There is also a special subgroup of so-called atypical tricyclics. Atypical tricyclics are drugs that have a tricyclic structure (having three connected rings in the molecule), but for which the antidepressant effect is either not the main one or the main one in the spectrum of their pharmacological activity, or has a different mechanism than the effect on the reuptake of monoamines, characteristic of classical tricyclics . Atypical tricyclics include: * the tranquilizer alprazolam (Xanax), which is a triazolo-benzodiazepine in structure and combines the properties of a strong benzodiazepine tranquilizer and a tricyclic antidepressant; * antiparkinsonian drug amantadine (midantan), which is a tricyclic aminoadamantan in structure and combines the properties of an antiparkinsonian drug and a tricyclic; * anticonvulsant drug carbamazepine (finlepsin), which is a tricyclic iminostilbene in structure and combines the properties of an anticonvulsant drug, a tricyclic antidepressant and a mood stabilizer (mood stabilizer); * a number of so-called antidepressant neuroleptics of a tricyclic structure, in particular phenothiazine derivatives - thioridazine (sonapax), levomepromazine (tizercin), alimemazine (teralen), frenolone; thioxanthene derivatives - chlorprothixene, flupenthixol (fluanxol); dibenzodiazepine derivatives - clozapine (azaleptin, leponex); * the drug tianeptine (Coaxil), which is a tricyclic in structure, but has a fundamentally different mechanism of action than that of typical, classical tricyclics, namely facilitating the reuptake of serotonin with a simultaneous blockade of its destruction (that is, an increase in serotonin reserves in neuronal depots); On the territory of the Russian Federation, it will currently be included in the PKU list (subject-quantitative registration) due to abuse as a narcotic drug. Many drug users tried to replace heroin with it, which led to serious consequences: blindness, amputations, and death. * the drug amineptine (survector), which is a tricyclic in structure (close to tianeptine), but has a special mechanism of action (selective blockade of dopamine reuptake with an almost complete absence of blockade of the reuptake of other monoamines) and is distinguished by the fact that it is almost the only antidepressant for which known drug addiction and which is included in the international Schedule II (Controlled Substances). Heterocyclic antidepressants (HCAs, English HCA)
Heterocyclic antidepressants (HCAs) - this group includes antidepressants that have a tetracyclic structure and similarity in the mechanism of action (the effect on the reuptake of monoamines) with tricyclic antidepressants.
That is, they are “like tricyclics” in terms of their mechanism of action, but not tricyclics in terms of their chemical structure. This group includes maprotiline (ludiomil). Conventionally, if desired, it can also include pirlindole, metralindole, mirtazapine (Remeron) and mianserin (Lerivon), since these drugs also have a 4-cyclic structure, and as one of the mechanisms of action (but not the main one) they have an effect on reuptake monoamines, but do not have all the side effects characteristic of both tricyclics and maprotiline. Selective serotonin reuptake inhibitors (SSRIs)
Selective serotonin reuptake inhibitors (SSRIs) are a modern group of antidepressants with minimal side effects.
Today they are prescribed most often. For mild and moderate depression, SSRIs are comparable in effectiveness to TCAs, but for severe depression they are significantly less effective than TCAs. Well-known representatives - fluoxetine (Prozac, Portal, Prodep, Fontex, Seromex, Seronil, Sarafem), paroxetine (Paxil, Rexetine, Paxet, Seroxat, Aropax), citalopram (Celexa, Cipramil, Emocal, Sepram), escitalopram (Lexapro, Cipralex) , sertraline (Zoloft, Lustral, Stimuloton), fluvoxamine (Fevarin, Luvox, Favoxil, Faverine). The most common side effects of SSRIs include: insomnia, akathisia (restless restlessness), extrapyramidal effects (increased parkinsonism or its appearance, muscle hypertonicity, jaw trismus, acute dyskinesia), headache, dizziness, nausea and vomiting, lack or decreased appetite, asthenia (physical weakness), increased fatigue, drowsiness, tremor (shaking), sweating, weakened libido or potency, inhibition (slowdown) of ejaculation or anorgasmia, frigidity, worsening anxiety. Irritability, aggressiveness, increased excitability and nervousness, dysphoria, inversion of the phase sign from depression to mania or hypomania, or increased frequency and acceleration of the cycle with the formation of a “fast cycle” are also possible. Clinical trials involving more than 3,000 people have shown that many of these side effects are due entirely or mainly to the placebo effect (a patient who thinks a drug must have side effects “finds” them). Selective norepinephrine reuptake inhibitors (SNRIs)
Selective norepinephrine reuptake inhibitors (NARIs) are a modern group of antidepressants with minimal side effects and good tolerability.
A characteristic property of this group is a pronounced stimulating effect in the absence or low severity of a sedative effect. Well-known representatives of this group are reboxetine (edronax), atomoxetine (straterra). Some RCTs suggest that SSRIs are superior to SSRIs, at least in the subgroup of severe depression. However, it remains unclear whether SSRIs can be considered equivalent in strength to tricyclic antidepressants and “dual-acting” antidepressants (SSRIs), or whether SSRIs are still weaker than TCAs and SSRIs. Selective serotonin and norepinephrine reuptake inhibitors (SNRIs)
Selective serotonin and norepinephrine reuptake inhibitors (SNRIs), or double-action antidepressants, are a modern group of antidepressants with low or minimal side effects and good tolerability.
Drugs in this group are powerful antidepressants, superior in antidepressant activity to SSRIs, and approaching the strength of tricyclic antidepressants (TCAs). Their superiority over SSRIs is especially pronounced in the treatment of severe depression. Well-known representatives of this group are venlafaxine (Velaxin), duloxetine (Cymbalta), milnacipran (Ixel). Selective norepinephrine and dopamine reuptake inhibitors (SNRIs)
Selective norepinephrine and dopamine reuptake inhibitors (SNRIs) are a modern group of antidepressants with minimal side effects and good tolerability.
The only representative of this class of antidepressants known today is bupropion (Wellbutrin, Zyban). Distinctive features of bupropion are the low probability of phase sign inversion into mania or hypomania and the low probability of provoking a “rapid cycle” - less than that of SSRIs, and much less than that of TCAs or MAOIs and other powerful antidepressants. In this regard, bupropion is especially recommended for patients with bipolar depression who are prone to phase inversion or the development of a “rapid cycle” when treated with various antidepressants. Bupropion also has the ability to reduce the need for nicotine and cravings for it, as well as the physical and mental manifestations of nicotine withdrawal, and therefore, under the name “Zyban”, it is specially proposed to facilitate tobacco withdrawal. Important features of bupropion are also a pronounced general stimulating and psycho-energizing effect (so pronounced that a number of experts previously classified it not as an antidepressant, but as a psychostimulant, despite the lack of narcotic properties), as well as a disinhibiting effect on libido, sexual activity and the quality of orgasm. Due to its libido-disinhibiting effect, bupropion is often used to correct the sexual side effects of TCAs, SSRIs, or SSRIs. Noradrenergic and specific serotonergic antidepressants (NaSSA, English NaSSA)
Noradrenergic and specific serotonergic antidepressants (NaSSA), English.
NaSSA is a modern group of antidepressants with minimal side effects and good tolerability. They are called specific serotonergic because, by blocking “inhibitory” presynaptic alpha-2 adrenergic receptors and increasing the content of norepinephrine and serotonin in synapses, drugs of this group simultaneously strongly block postsynaptic serotonin 5-HT2 and 5-HT3 receptors, responsible for the manifestation of a number of “serotonergic » side effects of SSRI drugs. In particular, excessive stimulation of 5-HT2 receptors has been associated with decreased libido, anorgasmia, frigidity in women and inhibition of ejaculation in men, as well as insomnia, anxiety and nervousness. Excessive stimulation of 5-HT3 receptors has been associated with nausea and vomiting, decreased appetite, and anorexia. Since drugs of the HaSCA group block serotonin receptors of the 5-HT2 and 5-HT3 subtypes, which are “bad” in the context of blood pressure treatment, and specifically increase serotonergic neurotransmission only through the 5-HT1 type receptors necessary for the antidepressant effect, they do not produce the side effects characteristic of SSRIs, such as a decrease in libido, increased anxiety, insomnia, decreased appetite or nausea. Moreover, drugs of the NaSCA group are often used as correctors of these side effects during SSRI therapy (in addition to summing up and potentiating the antidepressant effect, a number of side effects of SSRIs are weakened). Due to the blocking of 5-HT3 serotonin receptors, the stimulation of which is associated with the appearance of nausea and vomiting during chemotherapy of malignant tumors, drugs of the HaCCA group are very well suited for the treatment of depression in cancer patients receiving chemotherapy - in addition to the antidepressant effect itself, it is possible to reduce nausea and vomiting during chemotherapy and improvement of the antiemetic effect of drugs from the setron group. Due to the blocking of 5-HT2 and 5-HT3 serotonin receptors, drugs from the NaSCA group tend to increase libido, improve the quality of orgasm, and have a disinhibiting effect on the sexual activity of patients. Unfortunately, drugs from the NaSCA group are also not without side effects associated with strong antihistamine activity - they have pronounced (sometimes excessive) sedative activity, greatly increase appetite, and tend to cause significant weight gain. Sometimes there are bright colored dreams and even nightmares, a violation of the phase structure of sleep. Due to the blockade of alpha-2 adrenergic receptors of the pancreas, there is a significant increase in insulin secretion, which can lead not only to increased appetite and weight gain, but also to the development of hypoglycemic conditions, especially in patients with type II diabetes. Well-known representatives of the NaSCA group are the structurally similar drugs mianserin (lerivon, bonserin) and mirtazapine (Remeron). Specific serotonergic antidepressants (SSA, English SSA)
Specific serotonergic antidepressants (SSA), English.
SSA is a group of antidepressants with relatively few side effects and good tolerability. Along with blocking the reverse capture of serotonin and an increase in serotonergic neurotransmission, the drugs of this group strongly block “bad” treatment of the treatment of 5-HT2 serotonin receptors, which explains the low probability of sexual side effects (reduction of libido, anorgazmia, frigidness or ejaculation inhibition), as well as The low probability of exacerbation of anxiety, insomnia and nervousness in comparison with the SIOS. Often, on the contrary, an increase in libido and sexual disinsection, improvement of the quality and brightness of orgasm, and therefore the SSA is sometimes used as proofreaders of sexual side effects of the SIOS. The drugs of this group include trazodon (Tritico) and its more new nefazodone derivative (Serzon). The antidepressant activity of the SSA is evaluated as moderate. With severe depression, the SSA is ineffective or not effective enough. A specific feature of the SSA, especially trapodon, is a strong normalizing effect on the phase structure of sleep and the ability to suppress nightmares by reducing the share of the REM-SNN, increased with depression and anxious conditions. This influence is realized even in small doses that do not have a noticeable antidepressant effect. Therefore, trazodon was widespread and the special love of psychiatrists in Western countries as a sleeping pill and sedative drug in insomnia (not only depressive origin), as well as as a corrector of insomnia and nightmares in therapy of Sioxes or TCA. A specific feature of trapodon is also the ability to improve the erectile function in men, up to causing priapism (painful spontaneous erections), not related to antidepressant activity and is realized with any type of functional (not organic) impaired erection. Due to this property, trazodon is widely used to treat impotence, erectile dysfunction, including not related to depression or anxiety. Unfortunately, in Nephasodon, shortly after the start of its clinical use, a rather significant (1 %) hepatotoxicity (toxicity for the liver) was revealed, in some cases leading to deaths, which forced the American FDA to first demand the mention of this in large letters in the black frame at the beginning of the tab -nnations to the drug and informed consent of the patient for treatment with Nefazodon, and then generally prohibit the production and spread of non -phaseDone in the United States. After that, the manufacturer of Nefazodon Organon announced the recall of the drug from the pharmacy network in all countries and the termination of its production. Meanwhile, if it were not for the toxicity for the liver, it would be a very good expansion of the arsenal of antidepressants - it, unlike trapodon, does not cause jokesism (involuntary painful erections), has a significantly less sedative effect and better tolerance, almost does not reduce blood pressure ( It does not have alpha-adrenoing and hypotensive activity) and at the same time has a clearly stronger antidepressant activity. Features of the action
of antidepressants are serious drugs that always require an individual selection of a particular drug and dose and therefore their independent intake without a doctor’s prescription is strictly not recommended. Antidepressants are practically not able to improve the mood in a healthy person, so their recreational use is unlikely or almost impossible. An exception is a coaxil, which was often used for recreational purposes, which led to it in the lists of PCU (subject-quality accounting). Antidepressants do not work right away - usually they should go from two to four weeks before they start working. Nevertheless, there is often an immediate effect that can be explained by sedative or, conversely, with a stimulating effect. Studies have shown that many antidepressants, in particular fluoxetine, can increase the likelihood of suicide at the beginning of therapy, especially in children and adolescents. This is due to the rapidly advancing stimulating, energy -izing action, which occurs before the onset of the true antidepressant effect. Consequently, still suicidal patient in this way can receive enough energy and effort to realize suicidal thoughts against the background of a still preserved poor mood and longing. In addition, many antidepressants can cause or aggravate anxiety, insomnia or irritability, impulsivity at the beginning of therapy, which can also lead to an increase in suicide.
Are there non-drug treatments for depression?
In addition to medications, there are many non-drug treatments for depression. These are psychotherapy, biofeedback therapy, diet therapy, physical therapy, exercise therapy, reflexology, light and color therapy, sleep deprivation, etc. Most often, a combination of several methods is used to treat depression. For example: psychotherapy + drug treatment, biofeedback therapy + psychotherapy, medication + diet therapy, etc.
You cannot prescribe or use medications on your own. If you or your loved one is faced with the problem of depression, you need to see a psychiatrist or psychotherapist! Only according to his recommendations can you use drugs. Self-medication is life-threatening!
