How to determine schizophrenia from pictures

Posted on March 20, 2019  in Uncategorized

One of the most well-known signs of schizophrenia is the splitting of consciousness, which is subjectively experienced as a plurality of one’s own “me.” However, the feeling of a split personality can also occur in the mentally healthy, especially in a situation of making a difficult decision. Therefore, often concerned people are interested in how to recognize schizophrenia. Only a psychiatrist can figure this out with a high degree of accuracy, but there are some simple methods that can be used for initial diagnostics. These include, for example, the analysis of drawings.
How to find schizophrenia
Figures are the product of our figurative thinking and are largely related to the activity of the subconscious. Their plots, features of images, forms and lines can tell a lot about the character and mental state of a person. Scientists have proven this long ago, and now many so-called projective techniques, or drawing tests, are used in the study of the psyche.
How to determine the picture of schizophrenia
Psychologists and psychiatrists also studied the graphic activity of people with mental illness, including schizophrenia. Studies have revealed a number of features characteristic of schizophrenic figures:
randomness, lack of plot and complete images of even individual objects. The face of a person without a nose, and the nose separately aside, a house, one of the walls of which is depicted in another corner of the sheet;
a combination of images (eyes, palms, sun, monsters), signs (letters, numbers), symbols (for example, infinity signs, spirals, male and female symbols), geometric shapes, etc. in one picture;
very complex and confusing symbolism of pictures, understandable only by the patient himself;
images of the eyes and palms are often found;
strange, unusual colors and their combinations;
drawing is almost always accompanied by speech activity, which at this time is also incoherent and chaotic;
the more pronounced the disease, the harder it is for a person to draw and easier to speak.
It may seem that the drawings of people suffering from schizophrenia resemble pictures of some areas of avant-garde art: cubism, symbolism, abstract art, and psychedelic painting. This is not an accident. Many artists, creating their works, deliberately provoked a state of consciousness similar to schizophrenic nonsense. Both drugs and special meditation techniques were used for this.
Answering the question of how to define schizophrenia is not easy, as it is a complex mental disorder, and it has various symptoms. The causes of schizophrenia are not completely clear. Therefore, if there is a suspicion of the presence of this disease in you or your relatives, it is better to contact a specialist.

Night symptoms in COPD

Posted on March 16, 2019  in Uncategorized

The main symptoms of COPD are chronic and progressive dyspnea, cough and sputum production.

A number of studies have shown that most patients with COPD experience symptoms of the disease throughout the day. At the same time, violations associated with COPD cause the greatest discomfort in the morning, but also bother patients at night.

More than half of patients with COPD experience symptoms day and night. At the same time, patients with any combination of night / morning symptoms are more prone to anxiety and depression. It is also worth noting that the quality of sleep in patients with nocturnal COPD symptoms is significantly worse than in patients without nocturnal symptoms.

Patients with COPD require round-the-clock monitoring of symptoms, as most patients with COPD experience symptoms during the entire 24 hours.

Your health care provider may prescribe medications for you to reduce the frequency of COPD exacerbations. The doctor can combine the drugs of different groups with each other to enhance the therapeutic effect. If you are taking inhaled drugs, it is very important to follow the rules for using the inhaler. If you have questions about inhalation techniques, be sure to ask them to your doctor.

You can do a lot at home to feel better:

Avoid irritating the lungs – smoke, cold or dry air.

Use an air conditioner or air purifier.

Take rest breaks during the day.

Exercise regularly, especially to train your respiratory muscles, to stay in good physical shape and slow down the progression of the disease.

Eat well. It is very important to preserve your strength and well-being. If you are losing weight, ask your doctor about the need to change the diet.

Be healthy!

Depression depends on memory and pleasure

Posted on March 12, 2019  in Uncategorized

Depending on the strength of the connection between different nerve centers, the brain may tend to either be dependent on something or depression.

Our sense of pleasure depends on the reward system, or the reinforcement system, which is a complex of nerve centers. The reinforcement system does not just give us a feeling of pleasure, it connects it with this or that action or event, why it is called so — our actions are reinforced by something pleasant in the form of a reward. Therefore, it is clear that the reinforcement system plays a huge role in motivation, in training, in managing attention – all these things are somehow tied to pleasure. Roughly speaking, just as a dog is motivated to give a paw in order to get sugar, so a person is motivated to go to work to get praise and a cash reward.

Although, of course, a person is not so simple. First, our motivations can be quite complex, purely internal, depending on our personal values. Secondly, the reinforcement system does not exist by itself, other nerve centers that control the higher nervous activity constantly interact with it – they set the framework for the reinforcement system, plan its work, or simply limit it in desires. It happens, however, that the neural system of checks and balances fails, and then we are dealing with dependence — on food, on alcohol, on opiates, on purchases, etc. The other extreme is depression with anhedonia, or the inability to experience joy either from what; it is obvious that in this case, a person will completely extinct all motivation for any activity.

Since the nerve centers that make up the reinforcement system work together and must constantly exchange information with each other, it can be assumed that neuropsychiatric problems, such as addictions and depression, are at least partially related to the problems of information transfer between the centers of this system. It is known that dependencies are indeed accompanied by a too strong connection between the hippocampus (the memory center, which is included in the reward system) and the adjacent nucleus (which is often called simply the pleasure center).

Researchers at the University of Maryland decided to directly test how the gain and weakening of the connection between the hippocampus and the adjacent nucleus affect behavior. The neurons that form this connection in mice were modified by optogenetic methods so that they respond to light. With the help of optical fiber implanted in the brain, activated communication channel between the two brain centers; and this communication channel was getting stronger. As a result, as stated in an article in Nature, mice had the memory of a false reward. The animals were motivated to take certain actions, and a day later they returned to the place where they were stimulated by neurons – although they received no real reward. It is worth emphasizing that the researchers acted not on the hippocampus, not on the pleasure center, but on the information “bus” between them.

Then the authors of the work acted differently: in mice, other neurons were modified, which suppress the activity of nerve cells between the hippocampus and the pleasure center. Now, when using neurons-suppressors with the help of light, they weakened this communication channel — and before that, communicative mice stopped coming to where they communicated with their comrades. For social rodents, this behavior is an anomaly that is a sign of depression; because with depression, there really is no motivation to communicate with others.

Moreover, when initially depressed mice were taken for an experiment (and animals can be simulated signs of depression, although this is not a real, “human” depression), it turned out that the connection between the hippocampus memory center and their pleasure center is weak – and what is important, direct stimulation of neurons does not enhance it. However, if the animals were given antidepressants, the information channel returned to normal, and they could create a false memory of pleasant things, as described above.

The depressed brain has other features; For example, last year we wrote that because of certain features in the structure of serotonin neurons during depression, serotonin ceases to flow into the nerve centers. On the other hand, the more we know about the mechanism of depression, the sooner we will find some effective remedy for it. Since the connection between the hippocampus and the nucleus accumbens plays a role both in the formation of dependencies and in depressions, it is possible that both dependencies and depression can be overcome by acting on the neurons connecting these two nerve centers.

“Owls” and schizophrenia

Posted on March 8, 2019  in Uncategorized

The “owls” and “larks” added DNA

People with different chronotypes, that is, “owls” and “larks”, go to bed at different times. And this is not only a matter of habit – “owl” and “larks” largely depends on genes. The other day, Nature Communications published a large-scale study in which features of chronotypes were compared with genetic data. As a result, we managed to find as many as 351 sections in our DNA, which to some extent affects the chronotype; whereas before it was believed that there are only 24 such sites in our genome. If there are certain sequences of nucleotides in these areas, a person is inclined to wake up earlier.

We are talking about DNA segments, and not specific genes, that is, there may be more than one gene, and even with regulatory sequences. Among the genes that have fallen into these areas of the genome are those that control biological clocks, those that affect glucose metabolism, those that affect the response to nicotine and caffeine, and many more. Some of them work in the brain, some kind of – in the retina, some – in other places.

Along the way, the authors of the work noticed that the “soviet” a person is, the higher his genetic predisposition to depression, anxiety and schizophrenia, and the worse he feels. This is due precisely to the chronotype, but not to insomnia and not to the quality of sleep (although it can be assumed that if a person does not just go to bed late and get up late, but also sleep poorly, then the likelihood of neuropsychiatric disorders will only increase)

At the same time, no connection was found between the “genes of the chronotype” and the likelihood of diabetes or obesity. However, it is necessary to clarify here that it is usually said about diabetes and obesity in connection with sleep, when a person randomly disrupts his daily rhythm, when his body simply cannot understand how to live – “lark” or “owl”. That is, probably, it is necessary to distinguish the chronotype, which went by genes, and the one that we impose on ourselves.

Medicines in the treatment of mental health disorders

Posted on March 4, 2019  in Uncategorized

One of the ways to treat mental health disorders is drug therapy. For some disorders, drug therapy is necessarily necessary; in the case of others, one of the possible alternatives. For example, diagnosed depression is recommended to be treated with a combination of drug and psychotherapy.

Drug therapy makes possible a meaningful life for sufferers with severe enough disorders. Every year, more than 700,000 Finns, at least from time to time, use some medicine designed to treat mental health disorders. Despite the prevalence of the use of psychotropic drugs, their use still sometimes causes shame and prejudice. In the worst cases, this leads to the fact that a person in need of medication refuses to use them, which makes them feel worse.

Psychotropic drugs should be treated in the same way as drugs for somatic diseases. With the help of drugs, it is possible to alleviate, prevent or cure the various symptoms of intolerable sensual hallucinations. Medication, quality of symptoms, and individual factors influence medication choices.

Sometimes, finding the right medicine can take a long time. Nevertheless, psychotropic drugs are well researched, so doctors can determine which group of drugs will benefit a particular patient. The effectiveness of psychotropic drugs is based on the fact that they affect the central nervous system and the substances through which electrical impulses are transmitted from nerve cells (= neurotransmitters or neurotransmitters).

Taking psychotropic drugs always ends as instructed by the doctor.

In the process of completing the medication, various symptoms may occur, such as excessive sweating, headache and dizziness. These so-called final symptoms may occur, for example, at the end of antidepressants, despite the fact that antidepressants do not cause physical dependence. The use of sedatives, in contrast, leads to addiction, but this risk can be reduced in various ways. Read more on drug addiction.

So, the final symptoms only rarely indicate the development of drug dependence, on the contrary, they arise as a natural reaction of the body that has become accustomed to using drugs to reducing the level of drugs. Because of the final symptoms, medication is usually stopped gradually, i.e. dose is reduced from time to time.

If the final symptoms do not disappear in time, for example, in cases of depression, you should consult a doctor. Sometimes it may happen that medication is stopped too early or depression has resumed. The doctor can make a prediction when the final symptoms should stop.

Do not forget to take your medication!

The drug does not have the desired effect if the instructions for use are violated.

Schizophrenia. Effective treatment with guaranteed results

What is dangerous schizophrenia?

Schizophrenia is a time bomb in your body. This severe mental illness leads to a breakdown of thinking processes and disturbances in your emotional reactions. You begin to pursue hallucinations, delusions, there are disorders of perception of reality, speech disorders. The progression of the disease is accompanied by social isolation, leading to disability and disability. Against this background severe depression develops, thoughts of suicide arise.

The main danger of the disease is the appearance of persistent mental disorders and the destruction of social ties. Losing the usual social circle and lifestyle, you exacerbate the severity of your condition, which can lead to suicide attempts and causing irreversible harm to the body.

What will happen if not treated?

In most cases, schizophrenia leads to serious complications that pose a real threat to your health and life. Among such complications:

Insomnia

Hallucinations

Disorderly thinking

Confused speech

Flattening, inadequacy and impoverishment of emotions

Identity violation

Personality changes

Attempted suicide

According to medical research, the rate of development of these pathologies and complications has been growing rapidly in recent years.

If you do not take urgent measures or use ineffective treatment, powerful pathological processes will inevitably start in your body, which will lead to aggravation of the symptoms of the disease and irreversible personality changes. This will entail not only medical complications, but also social problems.

Main cause of schizophrenia

Absolutely all the processes in your body are controlled by the brain. The cells of your brain receive information from all organs and systems, analyze this information, produce the desired reaction and transmit the corresponding orders to various organs of your body through the nerve cells.

Schizophrenia (like any other mental disorder) arises from a combination of various factors. These factors lead to malfunction of certain parts of the brain and impaired neural connections. In other words, the brain ceases to give the “correct” orders for the precise work of your nervous system, which leads to schizophrenia, and then to more serious consequences, which were noted above.

How to conquer schizophrenia as quickly as possible?

The answer is obvious: it is necessary to restore the precise work of the brain centers responsible for the regulation of your nervous system. This problem is solved by the innovative device Neurodoctor.

The device is based on the method of pulse therapy. This is one of the most progressive and highly effective methods of treatment known to modern world medicine. Pulse therapy affects the control centers of the brain, restores the work of your nervous system, eliminating mental abnormalities and pathologies. At the same time, powerful mechanisms for restoring the nervous system are launched, and the work of damaged organs and structures is normalized. The disease quickly recedes. The risk of recurring disease is reduced to zero.

What yesterday seemed fantastic and unattainable today is becoming a reality accessible to each of us.

What is the result?

You have decreased mental arousal. Normal sleep. Streamlined thinking. Emotional responsiveness will increase. The state of anxiety and fear will disappear or decrease significantly. Increase concentration. Hallucinations and delirium will disappear or the duration and intensity of their attacks will be reduced. Reduced risk of relapse. Efficiency of the taken medicines will increase.

Powerful and effective treatment with the device Neuroditor will quickly eliminate the clinical manifestations of the disease, localize the nidus of the onset of pathologies, and reduce the dose of drugs. This will allow you to live a full life and forget about your illness forever. You will restore your lost ability to work and socialize and return to a lifestyle that led to the first signs of illness.

How can a character contribute to the development of depression?

There are general prerequisites underlying depressions, both related to a stressful situation and developing for no apparent reason. In the science of the “soul of man,” particularities of thinking and typical personality traits are known, contributing to the emergence of depressive ideas and their fixation in thinking.

Scientists have noticed that the majority of patients with depression before the illness had marked personal anxiety. Such people are sensitive in their relations with others, they subtly notice non-acceptance, rejection, are jealous of the attention of their loved ones. Since childhood, they may be timid and worry more in meaningful situations than their peers (for example, the answer at the blackboard at school, during exams). The experience of failures or grievances such individuals long stored in the memory.

With such a particular way of thinking, it is called ruminative, – thoughts about an unpleasant event spin in the head and the person longer than normal is fixed on what has been experienced.

The big fixation on the negative leads such people to the fact that they are trying to protect themselves and, as a rule, plan their day ahead. Where they go, what and how they will say or do – everything is repeatedly scrolled in the head and fixed in the “correct” order. Often they pre-write the to-do list and try to follow it clearly.

Avoiding all sorts of dangers contributes to the formation of a limited view of yourself and people (thinking “as if that didn’t work out”) hinders healthy learning, when a person is normal, getting into certain life situations, gets experience and knowledge, allows herself to develop further. Of course, this increases the risk of developing depression, when such a person finds himself in a situation to which he is not fundamentally ready.

Hence another characteristic feature – a special rigidity of thinking, which causes difficulties of unexpected switching from one business to another, because the latter is not included in the “plans”, is unfamiliar and alarming. This, incidentally, is associated with irritability over trifles, well known to the close circle of people with a similar character. Hot temper, grumbling is a direct continuation of anxiety.

With the ruminative thinking, the thoughts of an unpleasant event are steadily spinning in the head and the person lasts longer than normal, is fixed on the experience.

Another typical personality trait that increases the risk of developing depression is perfectionism. Of course, the desire to ensure that everything is done as well as possible, demanding of oneself in everyday life (cleanliness and order at home) and / or in deeds (careful fulfillment of one’s duties) is welcomed in our society and is considered a good trait of a family or exemplary worker. Scientists distinguish two forms of perfectionism: constructive and destructive. The difference between them is that in the second case people cannot accept the so-called “intermediate result”, they try so hard that they torture themselves and work hard. In addition to this, there is another feature – the crowding out (forgetting) of one’s own successes, dissatisfaction even with a perfectly accomplished deed. Such an attitude towards oneself, towards one’s work already in depressive states is transformed into a feeling of guilt, a reproach to one’s address, a feeling of hopelessness.

In the history of psychiatric science according to the classification of P. B. Gannushnkina has an idea of ​​two types of character, combining in one form or another the features listed above: psychasthenics and constitutional depressive personalities. The latter are also called obsessive-compulsive (from Lat. Obsessio – “obsession with an idea” or obsessive thoughts, and Lat. Compulsio – “coercion” or obsessive actions), as well as dependent or avoiding individuals).

Knowing about your character, its pros and cons helps people to work on themselves in a more creative way: broaden their horizons, plunge into unfamiliar situations and deal with their fears of the unexpected, solve problems on their own, give themselves an “objective” positive assessment and enjoy success. Such constructive thinking can help form a psychiatrist or psychotherapist during a psychotherapy session.

It is important to remember that even if depression has already developed or it has occurred in the past, it is never too late to pay attention to yourself, your character, and particular thinking. Psychotherapeutic work in remission (recovery period after a depressive episode), along with anti-depressive supportive treatment, is competent prevention of depression in the future.

Knowledge of your character

Knowing about your character, its pros and cons helps people to work more creatively on themselves.

Depression: causes and symptoms

Depression is a mood disorder, that is, a complex of mental disorders associated primarily with the emotional sphere. This disorder is characterized by various emotional disorders in which people experience anguish, anxiety, guilt, anhedonia, that is, the loss of the ability to experience pleasure, or apathy – a state where a person does not experience either negative or positive emotions. In addition, depression is characterized by certain disorders in the field of thinking. For example, people with depression may find it difficult to concentrate, to carry out targeted mental activity, which is associated with concentration. In a depressed state, people have difficulty making decisions. They have dark thoughts about themselves, about the world around them, about people.

Depression has such physiological manifestations as sleep disturbances, intestinal functions, sexual needs. In patients with depression, the general energy tone is disturbed, they feel tired. With somatisation depression, the person experiences discomfort in the body. If you look at such a person, then in his behavior one can observe passivity, avoid contact with people, refusal from entertainment. Depression is often accompanied by increasing abuse of alcohol or other psychoactive substances that are used to improve mood.

Depression studies

Manifestations of melancholia have been described in Antiquity. Hippocrates introduced the terms “mania” and “depression.” At the end of the 19th century, the German psychiatrist Emil Kraepelin, the founder of the school of Crepelin, first described manic-depressive psychosis. Later they began to distinguish unipolar and bipolar forms of depressive disorder. In modern concepts, manic-depressive psychosis is called bipolar disorder. In addition, we can talk about the so-called neurotic depression, which can be exposed to people who do not suffer from mental illness, but have psychological difficulties that predispose to depression. Manic-depressive psychosis was described long ago, and now this concept is considered obsolete. In the modern world, the diagnosis of a depressive episode is more common, which can have varying degrees of severity.

Causes of Depression

Current views on depression are described in terms of biopsychosocial models. The causes of depression are never unambiguous. The biological factors of depression are confirmed by genetic studies, but the contribution of genetic factors is generally low. Neurochemical studies show that people prone to depression have impaired metabolism of neurotransmitters that contribute to the interaction between nerve cells and the passage of electrical impulses.

The psychological causes of depression can be summarized in two main directions. First of all, these are violations of self-esteem and self-esteem — introjective variants of depression, in which a person has a certain idea of ​​his own “I” as unworthy of love and respect. In connection with this, various variants of compensatory behavior are formed. For example, this may be expressed in such a personality trait as perfectionism. In this situation, a person can accept himself only when he is perfect, other people evaluate him ideally, and the products of his activity have no flaws. If the life and activity of a person is aimed at confirming a good attitude towards oneself, exhaustion depression occurs. That is, if all activity is aimed at achieving results, a person loses psychic energy, which is formed through experiencing positive emotions: joy, pleasure, interest. Such mechanisms of depression are more common in men.

Another direction in understanding the psychological causes of depression is problems in intimate relationships. When a person needs another person to feel alive and able to adapt to reality, he is inclined to merge with another person and to minimize the distance. In such cases, the person experiences himself through another person. This tendency to depend on relationships is fraught with depression. In such a relationship, the partner often feels strangled. He does not leave space, leaning too close to him. Such relationships often fall apart, and the person who needs this merger feels it as a loss of himself. People describe this experience as follows: “It’s as if I don’t exist if the other one leaves me.” Such dependence often leads to depression, because man does not have the power of the ego, which allows him to live autonomously.

In addition, depression has social mechanisms. There is a certain cultural influence that affects the severity of depression in a particular culture. In northern cultures, the incidence of depression is higher than in southern and eastern ones. Here comes to the fore the cult of success, rationality, well-being, which is implanted through the media and parenting. In the process of growing up, people introject, that is, take in, into their worldview, the idea that they need to have a certain list of achievements in order to be good. The mechanisms of social comparison are activated, and when a person compares himself with other people, and the comparison is not in his favor, it is fraught with depression. In addition, people pay a lot of attention to the achievements in relation to their own physicality: what should be the body, to be socially acceptable, and what should be done with this body to be accepted in society.

Manifestations of depression

Tosca can be felt physically, in the form of squeezing in some parts of the body. Most often, people talk about squeezing in the chest. There is the concept of vital angst when a person feels that something is bad, but does not understand what is concrete. He does not survive the loss, does not suffer from separation from a loved one, but experiences a state of life longing. Patients with this symptom often say that they are simply ill, complain of depressed mood.

Anxiety is a feeling of internal tension, an expectation of something negative. Anxiety often accompanies depression, but can manifest itself. For depression, anxiety can occur in addition to depression and depressed mood.

Guilt feelings and a general tendency to self-accusation are characteristic of people with low self-esteem. There is a connection between low self-esteem and depression. Guilt feelings, as a rule, are associated with personalization, that is, thinking error, in which a person often takes bad events on his own account, and considers good events as the result of external causes.

Anhedonia is a condition in which a person cannot experience the pleasure of something that has pleased him before. For example, a patient with depression says that he would have given half his life for a fishing trip, but now he does not even want to think about it. This is a consequence of anhedonia, a distance from everything that used to be touched.

People most often experience apathy through their own passivity. Apathy is the most severe manifestation of depression, because this condition is difficult to treat with psychological methods. When a person is apathetic, he does not touch anything emotionally, either in a bad or in a good way. In a state of apathy, a person wants to lie in bed, he has no emotions, nothing encourages him, no motive. In this case, the person has due. For example, he says to himself that he must get up, make breakfast, feed the children, but this is experienced as pressure, an obligation, and not as a goal or desire. Most often, people understand that they have apathy when they want nothing but to stay in bed.

Sleep and appetite. Emotions are psychological phenomena that have a large physiological, somatic component. They have a cognitive component at the level of experience: before we feel something, we interpret what is happening. When the emotional state is unfavorable, the functions of the autonomic nervous system are disturbed, which controls the internal organs. A person experiences a variety of physiological symptoms: appetite disturbances in one direction or another, sleep disturbances. Internal stresses make sleep superficial or impede entering sleep.

Behavior. At the level of behavior, depression manifests itself in passivity, avoidance of contacts, refusal from entertainment, gradual alcoholization or substance abuse.

In addition, emotions affect thinking. On the other hand, thinking affects emotions. In some people, depression develops due to biochemical mechanisms that do not depend on his personality. For example, a person from childhood knows that his mood is worse in the morning, and that after lunch, his mood improves. When a person feels a severe emotional state, he has an unconscious need to substantiate this state cognitively. A person has a need to think about the bad. Thinking can also affect emotions. The mechanisms of cognitive therapy of depression are based on the fact that with the help of a psychotherapist a person works on these thinking errors that are inherent in depressive thinking. He becomes aware of these errors at the cognitive level.

Forms of depression

One form of depression is bipolar disorder. It manifests itself as a mood disorder that proceeds with a phase flow. Phases are periods of time that last for weeks or months. Moreover, in bipolar disorder, the phase of depression replaces the phase of mania. Mania is characterized by a positive mood. In this state, a person is full of plans, sleeps little, does not analyze obstacles, commits rash acts.

In bipolar disorder, significant coefficients of the genetic contribution are observed. In neurotic depression, the genetic contribution is lower, and psychosocial factors play a more significant role. With such a disorder, there is no phase of mania, disturbed thinking and reality testing, delusions or hallucinations. Treatment of neurotic depression is more dependent on psychotherapeutic procedures.

Another form of depression is unipolar depression, that is, a depressive episode. It can have three degrees of severity: mild, moderate, and severe. This condition lasts at least two weeks. If the depressive episode is repeated, then the diagnosis changes from a depressive episode to a recurrent depressive disorder, that is, to a periodically pop-up depression. A person can suffer depression once in a lifetime, and can suffer from it twice a year.

In addition, there are such forms of mood disorders as cyclothymia and dysthymia. These are personality characteristics rather than illness. Dysthymia is a property of a person to remain in a gloomy mood, to have a pessimistic picture of the world, but at the same time to function all his life, never addressing psychiatrists. The intensity of depressive symptoms in dysthymic low, but lasts for years.

Cyclothymia is dysthymia with the presence of phases in which the dysthymic phase gives way to a good mood phase and so on. The difference from bipolar disorder is that it is a characteristic associated with a person’s worldview and personality. You can talk about cyclothymic or dysthymic personality. Such depression takes a lifetime if the person does not specifically work on it. And this does not radically restrict his ability to live. But when there is a real clinical depression, a person is limited in life activity. Often he cannot work due to the fact that he cannot concentrate, get out of bed, he has no mental tone, but there is a strong longing.

Treatment of depression

There are several psychotherapeutic areas for the treatment of depression. In particular, psychoanalysts work with depression. They are more focused on the analysis of early losses and injuries. One of the most effective is cognitive-behavioral therapy for depression, the author of which is Aaron Beck. Beck’s concept is called depression cognitive therapy. The basic theoretical premise is that a person has negative basic beliefs, ideas about himself, the world, and his future, which keep him inside the depressive pit.

A person follows a compensatory strategy of behavior in that he should like everyone and should not be mistaken. These behavioral strategies lead to exhaustion or frustration. In cognitive therapy, there are a number of techniques that are designed to correct these basic beliefs. First, more superficial beliefs are corrected. A person learns to recognize these thinking errors. When he tests this in his life, basic beliefs also begin to be corrected, too. He begins to accept himself as he is, ceases to depend on the opinions and assessments of others, allows himself to make mistakes and to treat them adequately. Beliefs are corrected, and the life situation begins to be interpreted through the prism of other beliefs and a worldview that is more adaptive.

In addition, depression is treated with medication. It is known that half of the inhabitants of the United States take antidepressants. In Russia, this practice is also common, but far fewer people turn to psychiatrists. The history of Soviet psychiatry in the Soviet period is rather repressive. There are prejudices in people’s minds.

Depression should be treated comprehensively. If a person treats depression with antidepressants, the mechanisms of psychological coping with emotions do not mature. As a result, sooner or later he attacks the same rake.

Frequency of depression

According to statistics, depression occurs more often in women than in men. This is due to the fact that women as a whole have a more delicate nervous organization and there are cyclical hormonal changes. The most vulnerable age range is after 45 years. In old age, depression is associated with anxiety. There are predictions that in the 21st century depression will take the second place after cardiovascular diseases for reasons of disability. In general, in Western countries, this is indeed a social disaster.

The effect of depression on physical health

There are two mechanisms of the effect of depression on physical health. First, there is somatization, in which it is not about physical health, but about the symptoms that a person experiences as a violation of physical health. Often, when a person is depressed, there are so-called psychalgia, that is, pain in different parts of the body. In this case, medical research does not lead to any results. But a person suffers systematically from the body: he may have a bad headache or, for example, a knee; besides, there are stomach or heart pains.

Another mechanism is the effect of depression on health, on changes in body tissues that are associated with depression. By itself, depression does not cause damage to internal organs. But a person who is depressed often leads an unhealthy lifestyle. Having a dark look at the state of things in life, he may not go to the doctors or, conversely, turn too often. The physiological, biochemical components of depression are not fully understood. As for psychology, there are also many white spots, in particular in the description of family and cultural mechanisms of depression. Scientists are trying to understand why, for example, in the southern countries patients with depression are less than in the north, but at the same time in India more than all over the world.

Efficacy of Quetiapine as an Antidepressant. Part 1

Quetiapine was first approved by the United States Food and Drug Administration (FDA) in 1997? for the treatment of acute episodes of schizophrenia in adults. Over time, the wide possibilities of the pharmacological properties of the drug, due to which in 2003? It was approved for the treatment of manic episodes in bipolar affective disorder (BAR), in 2006? for the treatment of depressive episodes with BAR, and in 2008? has been recommended as maintenance therapy for BAR (Hawkins et al., 2013; Sanford, 2011). Since 2009?

Quetiapine has been used as an adjunct in the treatment of major depressive disorder (MDD) in combination with antidepressants without FDA approval (Mauri et al., 2007). Currently, this drug is not registered indications (off-label) is used for mental disorders such as generalized anxiety disorders, as monotherapy for monopolar depression, with delirium, psychotic symptoms associated with dementia and obsessive-compulsive disorder. Thus, the range of Quetiapine use has gone far beyond that approved by the FDA.

The use of quetiapine in affective disorders has been reviewed in a large number of double-blind, randomized clinical trials (RCTs). Currently, quetiapine is one of the most commonly used drugs for bipolar and monopolar disorders (Lopez-Munoz et al., 2013).

The authors of the article conducted a thorough search in the PUBMED database of all RCTs published before December 2015? In which quetiapine IR or XR was used in patients with depressive episodes in bipolar and monopolar disorders. Among all the studies, RCTs were selected that meet the criteria for the analysis.

Pharmacokinetic Profile of Quetiapine

Quetiapine belongs to the group of preparations of dibenzothiazepine derivatives. Available in two forms: with immediate (IR) and prolonged (XR) release. With a single dose in therapeutic doses, the drug demonstrates linear kinetics with a half-life of about 7 hours. Both forms have the same bioavailability. At the same time, the peak plasma concentration in Quetiapine IR is 2 hours, and Quetiapine XR – 5 hours. Quetiapine XR is also characterized by a longer maintenance of high plasma concentrations. Therefore, to maintain therapeutic concentrations, it is possible to take the drug once a day, while Quetiapine IR should be taken 2 times a day (Mauri et al., 2007; Bui, 2013).

Quetiapine is metabolized in the liver to form various derivatives, and only 1?% Is excreted unchanged in the urine. N-dezalkilkvetiapin (norkvetiapin) is the most important metabolite of the drug. Norkvetiapin is formed by CYP3A4 isoenzymes of the cytochrome P450 system (Lopez-Munoz et al., 2013). Due to the lack of genetic polymorphism of CYP3A4, any differences in quetiapine metabolism associated with racial or genetic traits are unlikely. Nevertheless, some inducers (carbamazepine, phenytoin), which increase the amount of norkvetiapine, or inhibitors (ketoconazole, itraconazole, erythromycin, and fluvoxamine), which decrease its production, affect the activity of this isoenzyme (Winter et al., 2008; Prieto et al., 2010). In elderly patients and patients taking concomitant medications, pharmacokinetic variability was more pronounced in quetiapine than in norkvetiapin, hence the concentrations of norkvetiapin were more stable (Bakken et al., 2011).

The less significant metabolic pathway of quetiapine occurs through CYP2D6 to form 7-hydroxy-quetiapine, which is not supposed to have pharmacological activity (Fisher et al., 2012), and 7-hydroxy-dealkyl-quetiapine, which has pharmacological activity (Bakken et al., 2012). According to Mauri et al. (2007), the plasma concentrations of quetiapine are not high enough to determine its effect on the receptors or its clinical effects. According to scientists, the active metabolites of the drug are also responsible for its pharmacodynamic characteristics.

Pharmacodynamic profile of quetiapine

The main mechanism underlying the antipsychotic activity of quetiapine is the blockade of the dopamine D2 receptors of the mesolimbic nerve pathways. Both quetiapine and norkvetiapin have a moderate affinity for D1 and D2 receptors, and the former quickly dissociates with D2 receptors. This explains the need to receive sufficiently high doses of quetiapine for the development of antipsychotic effect (Altamura et al., 2012). However, quetiapine does not affect the regulation of the activity of these receptors, which explains the low level of development of tardive dyskinesia during prolonged therapy with this drug. In the nigrostrial and tuberoinfundibular dopaminergic nerve pathways, serotonin acts as an inhibitor due to its effect on 5HT2A receptors.

Quetiapine and norkvetiapin have a strong antagonistic effect on these receptors, which contributes to the release of dopamine and provides a low level of extrapyramidal side effects and hyperprolactinemia (Kapur et al., 2000). A large number of depressive symptoms, such as agedonia, psychomotor retardation, social exclusion and loss of motivation are the result of reduced dopamine neurotransmission in the prefrontal cortex. According to some scientists, norkvetiapin due to antagonism with 5HT2A – and 5HT2C-receptors promotes the release of dopamine in the prefrontal cortex and reduces the symptoms of depression in patients with affective disorders (Mundo et al., 2006).

Dopamine reuptake is carried out by a norepinephrine carrier protein. Quetiapine and norkvetiapin potentiate serotonergic transmission of nerve impulses, acting as partial 5HT1A receptor agonists, which are associated with antidepressant and anxiolytic effects. In particular, norkvetiapin has a high affinity for 5HT1A receptors, similar to buspirone and gepironom. Thus, it increases serotonergic neurotransmission in neurons of the brain stem seam, and also modulates the 5HT activity of the cortex and limbic system (Bjorkholm et al., 2013). Activating these receptors in the hippocampus, norkvetiapin affects the increase in trophic factors and activates the regeneration of nerve cells (Silverstone et al., 2012).

In addition, it has a high affinity for 5HT7 receptors, the association of which with symptoms of depression and circadian rhythm disorders has been proven experimentally. Antagonism of norkvetiapine in relation to these receptors contributes to the manifestation of the antidepressant effects of quetiapine (Sumegi et al., 2008). When comparing quetiapine and norkvetiapine with antidepressants in vitro, norkvetiapin showed the same activity against the norepinephrine transporter, as well as some antidepressants, while quetiapine was inactive.

In view of the foregoing, it can be concluded that quetiapine’s effectiveness for reducing depression symptoms is due, in part, to the pharmacological properties of its active metabolite, norkvetiapin, which selectively inhibits the reuptake of noradrenaline, acts as a partial agonist of 5-HT1A receptors, as well as antagonist of presinaptic? 2, 5-HT2C and 5-HT7 receptors (Bortnick et al., 2011).

Monopolar and bipolar depression

The clinical activity of quetiapine has a number of differences from other atypical antipsychotics, which is why this drug is quite effective in treating bipolar depression, MDD, and generalized anxiety disorder (GAD) (Suppes et al., 2008). For a long time, atypical antipsychotics have been banned for use in the treatment of BAR, as they were thought to provoke the symptoms of depression. However, recent studies have found that drugs such as quetiapine, aripiprazole, and lurazidone can be used in the treatment of both phases of BAR (Riedel et al., 2011). The affinity of these drugs for various 5HT receptors has a significant effect on their normo-chemical properties. By binding to these receptors, they, as well as lithium, alter the signal transduction along the intracellular pathways and the activity of nerve growth factor (Rush, 2010; Connolly et al., 2011).

Observing patients with ARD, clinicians determined that they most often had symptoms of depression rather than mania (Bakken et al., 2011). In this case, depression may be in the form of a major depressive episode requiring hospitalization, or chronic with subthreshold symptoms, as well as other symptoms, such as anxiety, somatic complaints, substance abuse, etc. Therefore, it is very important to choose the optimal treatment for the depressive phase of BAR. Data from several studies have shown that quetiapine monotherapy can be effective in this case. The recommended dosage regimen for quetiapine for depressive episodes: 1st day — 50 mg, 2nd — 100 mg, 3rd day — 200 mg, 4th and the next 300 mg. With BDR, quetiapine is recommended as an additional therapy according to the following scheme: 1st day – 50? Mg, 2nd – 100? Mg, 3rd and 4th – 150? Mg, the recommended daily dose is 150-300? Mg.

Quetiapine Safety Profile in older age

The problem of mental disorders in the elderly and senile age is one of the most important sections of modern gerontology and psychiatry, which formed a separate research direction – gerontopsychiatry. However, in this area, the focus is on senile dementia and other forms of involutional psychosis, affective disorders, and much less on the clinical and therapy features of schizophrenia.

Epidemiology and clinical features

Today in US, schizophrenia is 1.7% of the incidence of elderly and old people . About 10 ­ 15% of patients with schizophrenia pathology manifest uet after the age of 60 years. It is important to emphasize that in old age both a certain syndromological dynamics in patients with the onset of the disease at a younger age are revealed , as well as features of the clinical picture of schizophrenia in later age, namely: complication of productive symptoms due to the expansion and deepening of hallucinatory ­ delusions, paranoia Destroy PTS straight and absence of growth deficitsymptoms and even shenii Decrease the manifestations of autism. Attention is drawn to the frequency of the relationship of schizophrenia with senile dementia. It is the development of concomitant senile dementia that contributes to the further development of the mentioned clinical manifestations in the elderly.

Dementia modifies the course of the schizophrenic process in two opposite directions – smoothing out specific personality changes, simultaneously aggravating and weighing down productive psychopathology disorders . In cases of schizophrenia combination with senile dementia age recesses Destroy productive endogenous PTS etc. Practical coincides with the manifestation of dementia. In addition, schizophrenia in old age is characterized by increased and prolonged exacerbations, a decrease in the quality of remissions, a transition to a chronic course, greater acuity and worse compensation for paranoid and paranoid manifestations .

From the point of view of pharmacotherapy, schizophrenia in old age is also characterized by a number of features. The most important of these is the increase in resistance to preparations of conventional neuroleptics and the incidence of their side effects. Especially often in gerontopsychiatry, extrapyramidal disorders and cardiotoxic reactions are observed with the use of phenothiazine and butyrophenone derivatives, which is associated with the age-related weakening of dopaminergic processes, primarily in the nigrostriatal system, impaired conduction and metabolism in the myocardium, as well as slowing down the biotranslation patterns and aspirant patterns. in an aging body.

As a result, the development of neuroleptics, which are not inferior in effectiveness to conventional means, but surpass them in breadth of therapeutic action and safety criteria, has become one of the most important tasks of the development of psychopharmacology. The emerging drugs of the new generation have received the general name of atypical antipsychotics, which currently include clozapine, olanzapine, risperidone, quetiapine, ziprasidone, amisulpride, aripiprazole, and some others.

The specific antipsychotic activity of atypical antipsychotics is generally comparable to that of traditional antipsychotics and is associated with the general mechanism of action of drugs in this group – the blockade of dopamine D2 receptors. ­ type At the same time, the selective tropicity of theaction of atypical antipsychotics on the mesolimbic and mesocortical dopaminergic systems of the brain, as well as a much less pronounced effect on the nigrostriatal system, which is directly related to a significantly more favorable safety profile.

As a result, atypical antipsychotics optimally meet the following criteria for the effectiveness of antipsychotic therapy in geriatric practice, which implies:

  • antipsychotic action, comparable in its severity with the classical representatives;
  • effects on negative symptoms;
  • effects on cognitive symptoms;
  • effects on affective symptoms;
  • effectiveness in many cases of resistance to conventional neuroleptics.

Finally, it is the assessment of the safety of pharmacotherapy with these drugs, based on the knowledge of the characteristics of the development of certain side effects, that becomes the decisive factor in choosing an instrument of treatment with neuroleptics in a particular patient in old age. As a result, the question arises about the criteria for choosing one or another atypical in gerontopsychiatry.

Each of the atypical antipsychotics is characterized by a peculiarity of the mechanisms of action, clinical effects, and finally, significant differences in the safety profile and, accordingly, differences in the therapeutic spectrum, which determines the feasibility of administering a particular drug in certain clinical forms and syndromes.

One of the most peculiar atypical antipsychotics is quetiapine . It is quetiapine that is considered today by many authors as one of the optimal antipsychotics for treating older patients of their age groups , which is largely due to its original, very own ­ figurative mechanism of action.

Mechanisms of action of quetiapine

Quetiapine blocks D2 receptors ­ type only in mesolimbic and mesocortical dopaminergic systems in the central nervous system, having a very low resistance to D2 ­ nigrostriatal and hypothalamic receptors ­ pituitary ary systems. According to modern ideas, D2 blockade ­ mesolimbic andmesocortical receptors are directly associated with manifestations of the antipsychotic effect, and interaction with D2 ­ receptors in the substantia nigra and striatum are associated with the development of extrapyramidal complications – syndrome of drug parkinsonism and late dyskinesias .Thus, it becomes clear one of the most important clinical benefits of quetiapine – the presence of a pronounced antipsychotic effect in combination with a minimal risk of neurological motor disorders.

Quetiapine is also quite intensively bound to serotonin 5 ­ NT2A ­by receptors. It is known that serotonin receptors of this type are widely represented in the frontal cortex and various parts of the brain, and that the serotonergic system after 5 ­NT2A ­receptors have a modulating effect ondopaminergic structures. According to modern concepts, the serotonergic system plays a key role in the pathogenesis of schizophrenia, in particular, its disorders are directly related to the development of negative symptoms, affective disorders, and secondary cognitive deficits.

Finally, the weakening of serotonergic processes and the imbalance between individual subtypes 5 ­ NT2 ­ receptors – one of the leading mechanisms of brain aging and development in zrastzavisimoy CNS pathology. Therefore, the serotonergic mechanisms of quetiapine action are of particular interest from the point of view of its use in gerontopsychiatry.

It is also important to emphasize the absence of any ­either quetiapine interactions with postsynaptic M ­cholinoreceptors, which is one of the most important clinical benefits of this drug – the almost complete lack of risk of extrapyramidal adverse reactions (acute dystonia, akathisia, catalepsy, tardive dyskinesia, drug parkinsonism) – the leading side effect of conventional antipsychotics.

In general, it seems today that the basis of the pharmacological effects of this drug is not so much blockade of certain receptors per se (in its neurochemical sense), but rather a modulating action aimed at normalizing the imbalance of activity of both individual neurotransmitter systems and within the same system (dopamine ­ and serotonergic ), mediated by different receptor subtypes. At the same time, it is this imbalance that serves as the foundation for aging of the brain and disorders of the integrative function of the central nervous system. Quetiapine, like no other atypic, has a normalizing effect on the imbalance mentioned, that is, to a certain extent one can speak of the presence of geroprotective (in their psychiatric understanding) properties of this drug.

In clinical practice, equal efficacy of quetiapine and conventional neuroleptics ( haloperidol , chlorpromazine , fluphenazine , etc.) was demonstrated in reducing positive clinical symptoms based on analysis of various clinical scales (short psychiatric rating scale, scale of overall clinical impression, assessment scale of negative symptoms, etc. ) both during the acute as well as stabilizing and n rotivoretsidivnoy therapy. At the same time, the most important aspect of quetiapine action , in contrast to classic drugs, is the beneficial effect on negative symptoms.

In gerontopsychiatry, an effective effect on hallucinatory ­ delusional symptomatology expressed Decrease the shenie paranoid symptoms.

The beneficial effects of quetiapine on cognitive functions, such as attention, performing functions, and verbal memory, deserve special attention . The severity of cognitive deficit in schizophrenia in old age is considered as the most important indicator in assessing the social and therapeuticprognosis of the disease.

Finally, quetiapine demonstrated the possibility of correcting affective symptoms (depression) in schizophrenic patients by positively affecting the entire cluster of affective disorders, according to a short psychiatric rating scale. Given the importance of the problem of depression in geriatrics, as well as the poor efficacy in stopping these symptoms of traditional antipsychotics and antidepressants, this property of quetiapine deserves special attention.

Quetiapine Safety Profile

Quetiapine optimally meets the criteria for selecting an atypical neuroleptic for geriatric practice in terms of effectiveness, breadth and variety of clinical ­ pharmacological action. However, the main advantage of Quetiapine, which ensured its wide popularity in the world psychiatric practice and, in particular, in gerontopsychiatry, is safety. It is by this criterion that it significantly exceeds not only conventional, but also the majority of atypical neuroleptics .

As already mentioned, due to the lack of affinity for M ­ brain cholinergic receptors, as well as a slight affinity for D ­ to the receptors in the nigrostriatal system, quetiapine is practically devoid of extrapyramidal side effects – the most important negative effect of the use of antipsychotics.

In this respect, the safety of quetiapine significantly higher than traditional drugs, and that kzhe risperidone and olanzapine, is important to emphasize that this characteristic of quetiapine is celebrated all over the therapeutic dose range (100 – 800 mg/day), that is, with increasing doses, as well as with long courses of use, the risk of developing extrapyramidal complications (including tardive dyskinesia) remains minimal.

As you know, serious problems associated with the use of both classical and atypical neuroleptics are the development of hyperprolactinemia (due to the effect on D ­receptors in the hypothalamo ­ pituitary system) and related sexual dysfunction (including gynecomastia, galactorrhea), as well as the formation of osteoporosis, disorders of water ­ salt metabolism, etc. Many atypical neuroleptics (risperidone, olanzapine, amisulpride) to some extent cause hyperprolactinemia, which in some cases can become a serious clinical problem and lead to the replacement of the drug.Quetiapine is almost completely devoid of the ability to cause these disorders, which significantly increases the safety of its use.

Finally, quetiapine has minimal risk (unlike traditional drugs and olanzapine) for developing metabolic disorders, such as weight gain and diabetes.

The most common side effects of quetiapine are sedation, somnolence, orthostatic hypotension, dizziness, dyspepsia, that is quite soft manifestations are typically dealt with decreasing dose. The likelihood of complications such as malignant neuroleptic syndrome and leukopenia is very low and does not differ in this respect from that of other atypical antipsychotics. Quetiapine, unlike clozapine, does not cause agranulocytosis.

In general, quetiapine can be characterized as one of the atypical antipsychotics most favorable in terms of safety. In combination with the characteristics of the clinical spectrum of action and pharmacokinetics, this allows recommending it as the drug of choice in elderly and senile patients, with a combination of psychotic disorders with dementia and Parkinson’s disease .

Quetiapine preparations Seroquel deserves special attention in the pharmaceutical market in the form of tablets of 25, 100 and 200 mg, which allows you to fully meet the needs for individualization of the dose regimen in different categories of patients depending on the clinical form of the pathology, severity of the condition, age, presence of concomitant diseases, features of combined pharmacotherapy, etc.

Seroquel It is produced in full compliance with all GMP requirements and European quality criteria and, at the same time, it is the most economically available drug Quetiapine , which significantly expands its prospects in domestic clinical practice and is a significant advantage over foreign counterparts.

In general, quetiapine is a promising atypical neuroleptic that deserves widespread introduction into domestic clinical practice. Further accumulation of experience in its use will allow optimizing the pharmacotherapy of schizophrenia in old age in accordance with modern international standards.