Etiopathogenesis of schizophrenia. Vartanyan M.E.

The statement that the etiology of schizophrenia is unknown is not entirely correct. A more precise definition would be one that clarifies the details. It is unknown within the framework that science has assigned to itself. As a result, it was necessary to create a multi-level hypothesis, which includes diathesis, stress, social factors and the level of immunity. It seems that if scientists had at least some well-developed techniques for studying the atomic structure of nerve cells of sick and healthy people, then a quantum theory of the origin of schizophrenia would also arise.

There are many different hypotheses regarding the etiology of schizophrenia.

Meanwhile, the problem itself is greatly exaggerated. And it was inflated by centuries of development of civilization. It is impossible to deny that negative and productive symptoms play their destructive role in equal measure. However, this very rarely happens abruptly. The vast majority of cases are associated with a gradual increase in negative factors. During this time, a person can have time to rebuild the psyche a hundred times, transfer it to the desired mode of operation, which will facilitate the body itself to turn on the mechanisms of self-regulation.

Schizophrenia is a change in information and energy metabolism. Looking for reasons why this happens is a thankless task. But who knows why? Let's assume that the human species is mutating, and nature is looking for ways to reorganize the psyche. Let him look for himself. We have no certainty that the human psyche has always been the way it is now. It is quite possible that in ancient times people perceived the world differently. They did not create speculative images of gods and spirits, but actually saw them. Over the centuries, this ability to expand the boundaries of perception has disappeared. However, the very fundamental possibility of activating certain layers of consciousness has been preserved. In 1% of the population, an altered state of consciousness occurs against their will and desire.

It is impossible to say whether this is good or bad. But it’s definitely bad to panic because of it. In the same way, it is precisely known that intellectual development and spiritual culture are good life preservers. What is called “schizophrenia” has only a conditional pathogenesis, since the pathology itself has become a medical problem primarily due to the fact that people have programmed themselves to get rid of everything non-standard.

People have programmed themselves to get rid of everything non-standard

The images that a person sees, the voices that he hears, the mental experiences of pseudo-hallucinations and mental automatisms in themselves are not so negative, hostile and do not carry as many problems as they are charged with.

The etiology and pathogenesis of schizophrenia are relevant as long as we are firmly convinced that it is a disease. Call a disease an altered state of consciousness and it will immediately become clear that the only pathology is that it arises on its own. The day the patient learns to change the state of consciousness according to his own choice, the justification for using medical terminology will no longer exist.

Everything is so serious that it’s time to not take it seriously...

The main mistake is that all, literally all, patients take everything seriously. The subconscious can do anything, so you don’t need to think that this is a simplified and far-fetched example. A man wakes up and sees a lizard in front of him. He walks calmly on his hind legs and wears a headdress. The lizard tells the man that he has arrived from another planet and is conducting important experiments on Earth. And this unfortunate person begins to communicate with him as if it were an external object, separate from him.

All you had to do was not pay any attention to the “lizard”. Transferring the psyche to a different operating mode is no more difficult than waking up during a nightmare. It will take one volitional effort or several, but waking up is quite possible.

The trouble is that consciousness gets involved in its own game and perceives everything as reality. This is partly correct, since psychic reality is just as real as any other. But being in this and that at the same time is impossible. The world of dreams can be scary or very beautiful, but it is completely useless in itself. The episode cannot be stopped. If someone is destined to see a talking lizard or something completely wonderful, then he will see it. But everyone has a choice limit - in which world he prefers to transfer the epicenter of his consciousness. You can go into that completely. This will be catatonic schizophrenia with a characteristic oneiric state. You can “confuse” the worlds and then the objects of the unconscious will begin to play around in this world. You can recognize that these are hallucinations and ignore them. Most often in this case they disappear.

Everyone has a choice - in which world they prefer to move the epicenter of their consciousness

Perhaps patients have some kind of genetic predisposition. But if it is fatal, then it’s time to talk about organic psychosis. Our situation is much better. Even catatonia has a way out. The author did not conduct any in-depth research. What are our years? There's more to come. However, many people who have been diagnosed or almost diagnosed with the presence of the F20 code have confirmed this fact. At a certain moment, they vaguely or clearly realized that these were hallucinations, that images came out from inside their consciousness. The word “wake up” was actually suggested by one girl. She already had one foot in the IPA corridor. And suddenly she realized that she was being pulled into some kind of dream.

Wake up!

Just don’t think that this is naive advice from an amateur. No advice. This is actually from the words of a person who almost became a patient. She walked away from the hospital, where she came on her own, so no one held her. Then she focused her consciousness on one object, then on another, then on a third. And she gave herself the command to “wake up!” So I got to the student dormitory. Then she packed her things, since everything there would remind her of this unwanted dream, and changed her habitat. Hallucinations and pseudohallucinations tried to appear for another month. But she took up Buddhism and meditated in one of the Moscow Buddhist centers. She left the institute, which she later did not regret at all. The premiere did not turn into a defect. There were no more episodes.

There are many similar stories. It seems that fate presents you with a choice. Everyone understands and can make every choice. But some people get carried away into the whirlpools of sleep, and others don’t.

There may be a genetic predisposition to schizophrenia

Here's another observation. Rehabilitation group. Rational psychotherapy is underway. The main goal is to restore the ability of patients to adapt to society. Almost everyone assumed that hallucinations, delusions, and pseudohallucinations would return. And autism was considered as a norm of life. In the same way, people prepared for post-schizophrenic depression. On the one hand, it seems like a bright and useful thing. On the other - a factory of madness. They program themselves to the fact that tomorrow the perception of the world will become different.

How to live without syndromes? What to hide behind?

• Guys, what to do if there are no hallucinations and pseudohallucinations? What to do if the psyche stops showing tricks? What to do if not a single mental automatism and even mild depersonalization appear? How to live with this?

There was an awkward pause. Then people began to wonder who I was and why I was here at all.

• Yes, I'm a fitter. I was fixing the wiring here, I heard it by accident, so I asked a question.
• Well then you won't understand...

This is one of the signs of a disorder. Please note that this is the first time this word has been used in the entire article. Now it’s time to call schizophrenia a disorder. Patients withdraw into her world and feel discomfort if they are told that they can do without hallucinations. They actually start to think of themselves as special. Not the chosen ones, although some may think of themselves that way, but special, not like that.

However, this is not hopeless. A long speech about how all people see dreams and hallucinations are no different from them convinced someone that day. Suddenly, straight to the face, without preparation, it was said that there is no disorder or “splitting” of thinking. The patient’s thinking follows strictly the same algorithms as thinking in some phases of sleep. But falling asleep does not mean going crazy.

• Well wake up! Of course, suffering exists in this world, but hiding from it in another reality is not a solution.

The world of a person with a mental disorder is a special world

This fiery cry was heard by two of the fifteen people. And these are very good results. By the way, both of them had tried to do something before: yoga, meditation... They made different choices. One decided to go to a qigong group, and the other to Buddhism. But that was a completely different story. This means that it is no longer a medical history.

SCHIZOPHRENIA (from the Greek schizo - “split, divide” and phren - “mind, mind”) - mental endogenous disease, characterized by personality changes in the form of a schizophrenic defect (such as emotional impoverishment, decreased psychological activity, impaired thinking, etc.) while maintaining acquired knowledge, memory and other formal intellectual abilities, as well as various positive disorders (delusions, hallucinations and etc.).

Etiology

Age is of great importance in the development of the disease. Very often the process begins in early and youthful puberty (10-25 years), less often in the involutionary period (after 40 years). Physiological changes associated with pregnancy, childbirth, and the postpartum period are also important. The occurrence of the disease is influenced by some infections and intoxications (primarily alcohol). The causes of the disease are still unclear. The hereditary factor is of great importance. Nitrogen compounds associated with DNA in patients with schizophrenia differ in their serological properties from healthy people. The patient exhibits labile immunological reactivity throughout the course of the disease. Foreign antigens are detected in the serum of patients.

Pathogenesis

Schizophrenia- This is a cerebral disease in which the main thing is a violation of higher nervous (mental) activity. There is a disruption in the relationship between the cortex and subcortex, and patients are also characterized by increased inhibition of brain activity.

Clinic

1. Perception disorders - frequent hallucinations are observed. Among them, the most typical are auditory hallucinations in the form of “voices”, which can be commanding, threatening, explanatory, accusing, defending; olfactory hallucinations are expressed in an unpleasant odor (the smell of rot, a corpse); bodily hallucinations (burning sensation, electric current, pulsation, etc.).

2. Thinking disorders. In schizophrenia, the nature of associations changes. They acquire the character of abstract ideas, fruitless philosophizing and reasoning develop. Phrases lose their logical integrity, thinking is broken (it is impossible to grasp a logical connection) and proceeds in accordance with the special, internal logic of the patient. Patients experience painful experiences and an involuntary influx of thoughts (mentism). Disorders of judgment and inferences arise (delusions, the basis of which is a violation of the course of the thinking process itself), often these are delusions of persecution, delusions of grandeur.

3. Syndrome of mental automatism (mental phenomena characterized by violence and a feeling of alienation from the individual, the so-called ideational mental automatism): patients hear their thoughts, which are repeated like an echo; sensory automatisms (combine physical delirium and poisoning): patients say that they are exposed to electric current, poison and drugs are added to food, which “take away” desires and will; motor automatisms (patients feel that they are being “turned into puppets”, they pronounce words, their tongue is moved, etc.).

Patients are convinced of the splitting of their “I” - this is delusional depersonalization.

4. Emotional disorders. Affective disorders are diverse (this is intense and excessively heightened, intense emotionality or sensory dullness - impoverishment of emotions).

5. Desire disorders. Patients experience sexual arousal, followed by a persistent decrease in libido.

6. Behavioral disorders - isolation from one’s comrades, events in the surrounding world, everyday life, and usual interests.

7. Catatonic symptoms:

1) psychomotor agitation (patients suddenly jump up, attack others, at this moment they can commit socially dangerous actions;

2) catatonic stupor (immobility of the patient);

3) catalepsy (waxy flexibility);

4) repetition of words (echolalia) or actions (echopraxia) of others;

5) catatonic excitation (one-sided, chaotic, monotype speech (talk without stopping) excitation without noticeable motor excitation). There may be motor excitation without speech, with mutism - purposeful isolated motor acts of echo reactions.

Diagnostics

Difficult. The diagnosis of “acute onset schizophrenia” is based on a thorough study of the patterns of development of psychopathological symptoms.

HEBEPHRENIAN SCHIZOPHRENIA (adolescent)- this is an early developing schizophrenia (at 14-18 years of age), also related to non-remission “nuclear” forms with a progressive course.

Etiology and pathogenesis

See "Schizophrenia simple type."

Clinic

During the first 2 years, there may be short-term episodes of rudimentary symptoms. Young, modest and reserved people suddenly change their behavior. They become rude, play pranks, behave strangely (copy the intonation and gait of their parents), curse, and strive to change their appearance. Next, motor excitement appears, the structure of which is based on foolishness, clowning, and theatricality. With increasing excitement, the patient throws off his underwear and impulsively attacks those around him. Perception disorders - auditory deceptions - are common. The delirium of greatness, giftedness, erotically colored delirium is suddenly unexpectedly replaced by the delirium of persecution, sinfulness, and hypochondriacal delirium. Violation of associations manifests itself in “verbal okroshka”, reasoning. In complex hebephrenic syndrome, elements of catatonic excitation are often present: echolalia, echopraxia, negativism, catalepsy, freezing. The course of the disease is unfavorable. Remissions are short-term and rare. Profound personality changes are rapidly increasing - emotional impoverishment with an irreversible decrease in labor and social adaptation.

Diagnosis and treatment

SCHIZOPHRENIA CATATONIC- this is a nuclear form, it can occur continuously, progressively (slow development, unfavorable prognosis) and periodically (acute onset, rapid development, proceeds favorably, often ends in deep long-term remission with labor compensation).

Etiology and pathogenesis

See Schizophrenia, simple type.

Clinic

Catatonic schizophrenia can occur with alternating states of catatonic excitation and stupor. Less commonly, these two conditions occur simultaneously. The initial period lasts from several months to a year and occurs with symptoms of lethargy: the patient suddenly freezes for a short time in an uncomfortable position while walking with a bent leg or while eating with a spoon at the mouth.

Catatonic stupor can be sluggish and rapidly developing. A flaccid stupor develops gradually: lethargy, lack of muscle tension, limited movements, and mild symptoms of waxy flexibility and negativism appear. With rapidly developing stupor, pronounced muscle tension and mutism are observed (the patient does not answer questions). Subsequently, general motor retardation, pretentious intrauterine position, air cushion symptom, and the phenomenon of waxy flexibility increase, when the patient passively remains in any position assigned to him; pronounced negativism in everything (even when trying to feed the patient, he clenches his jaw convulsively).

Symptom of catatonic stereothenia: speech stereothenia - repetition of the same words, phrases without any meaning, regardless of the situation; motor stereotenia - patients make non-purposeful movements for a long time.

Catatonic excitement manifests itself acutely. This is disorderly, chaotic, unfocused excitement, unexpected impulsive actions: a patient who has been immobilized for a long time jumps up, starts to run, and attacks those around him. Verbigeration is characteristic - patients shout out snatches of words, phrases, repeat them many times, either with monotonous or changing intonation. Echolalia and echopraxia are pronounced (patients accurately copy the words and phrases of those around them). Patients experience delusions of persecution, physical impact, and auditory hallucinations that encourage or threaten the patient. There may be confusion with disorientation in place, time and persons.

Oneiric catatonia - catatonic phenomena in combination with oneiric disorder of consciousness.

Diagnosis and treatment

See Schizophrenia, simple type.

SCHIZOPHRENIA PARANOIDAL is a form of the disease that develops over many years (10 or more), in which obvious symptoms of schizophrenia appear by the age of 30. The main psychopathological syndrome is hallucinatory-delusional.

Etiology and pathogenesis

See Schizophrenia, simple type.

In the initial stages, delirium is unstable, unsystematized, fragmentary, and ideas of relation often appear first.

Delusions can occur at different stages of schizophrenia. This may be delusions of influence, poisoning, persecution, or less often - delusions of grandeur and hallucinations.

With constant, long-term treatment with psychotropic drugs, patients adapt to work and remain in the family for a long time due to the very slow development of schizophrenia.

Hypochondriacal form is a type of paranoid schizophrenia, the main symptom of which is a pathological belief in the presence of severe incurable somatic diseases. This form can occur with senestomatia, when conviction is based on persistent, vivid, painful sensations.

Diagnosis and treatment

See Schizophrenia, simple type.

SCHIZOPHRENIA, SIMPLE TYPE- this is a sluggishly developing schizophrenia with a progressive course, occurring without remission, belonging to the nuclear forms.

Etiology and pathogenesis

Clinic

During the first 2 years, progressive apathy, a drop in the level of intellectual activity, decreased activity, lethargy, empty philosophizing, “philosophy” abstracted from the real family and work environment, and increasing indifference to everything around and oneself are noted. Patients become sloppy, do not look after themselves, and there are no perception disorders or delusions. Then there appears disinhibition of drives, absurd behavior, swagger, rudeness against the background of emotional harshness, coldness towards parents.

Diagnosis and treatment

See Schizaffective Disorders.

Treatment

For treatment, psychotropic drugs, insulin comatose method, electroconvulsive therapy, psychotherapy, and occupational therapy are prescribed.

“The etiology and pathogenesis of schizophrenia became the subject of special study soon after the disease was identified as a separate nosological ( nosology- this is the study of diseases and their classifications, - approx. author) unit".

To date, scientists have obtained a lot of data that allows them to build one or another theory of schizophrenic etiology. Some of these theories have lost their relevance, having failed to withstand empirical testing, or being untenable due to the emergence of new scientific data. Other theories are considered the most promising today. However, as already mentioned, the etiology of schizophrenia is still considered unknown.

It is relatively unanimously recognized that the disease belongs to the group of endogenous diseases, that is, those that do not have an exogenous factor that can provoke the development of the disease (trauma, viral infections, etc.). And although there is evidence of the onset of the disease in connection with the influence of some exogenous factor, nevertheless, ““...after this” does not mean “as a result of this”.”

Genetic theory of schizophrenia. According to genetic theory, schizophrenia is a hereditary disease. The most significant evidence in favor of the genetic theory is the numerous facts of schizophrenia in individuals with a genetic burden. “Studies of identical twins indicate that the risk of schizophrenia in the sibling of an already affected twin is approximately 30 percent.”

Neurochemical theory of schizophrenia. The neurochemical theory of schizophrenia dates back to the beginning of our century. In the last two decades, much attention has been focused on dopamine, a neurotransmitter of the catecholamine class. It has been observed that large doses of amphetamines cause an increase in dopamine levels, and the resulting symptoms resemble those of schizophrenia. It has also been observed that the condition of schizophrenic patients worsens if they are given a drug containing dopamine. Scientists have also studied many other neurotransmitters, their interactions and properties (histamine, GABA, glutamic acid, and others).

Theory of developmental defects. A relatively new approach to searching for the causes of schizophrenia. More advanced methods of studying intrauterine development have made it possible to obtain many facts suggesting that the cause of schizophrenia may be intrauterine brain injury or directly at the time of birth of the child. Proponents of this theory argue that the onset of the disease may be caused by exogenous factors, namely postpartum brain injuries, immune system disorders, poisoning at an early stage of development, primary metabolic disorders and some other factors.

Other theories. There are many other theoretical developments attempting to explain the etiology and pathogenesis of schizophrenia. For example, the assertion that dominated the 19th century that masturbation can lead to insanity is considered untenable. Some theories, such as the endocrine theory of schizophrenia, the nutrition theory, or the family theory, still exist, although they are not popular.

Psychological portrait of a patient with schizophrenia.

Diagnostics.

Schizophrenia has a wide range of clinical manifestations, and in some cases its diagnosis is very difficult. The diagnostic criteria are based on the so-called negative disorders or peculiar changes in the patient’s personality. These include impoverishment of emotional manifestations, impaired thinking and interpersonal disorders. Schizophrenia is also characterized by a certain set of syndromes.

In diagnosing schizophrenia, it is important to distinguish the clinical picture of schizophrenia from exogenous psychopathologies, affective psychoses (in particular, from MDP), as well as from neuroses and psychopathy. Exogenous psychoses begin in connection with certain hazards (toxic, infectious, and other exogenous factors). With them, special personality changes are observed (of an organic type), psychopathological manifestations occur with a predominance of hallucinatory and visual disorders. For affective psychoses There are no personality changes characteristic of schizophrenia. Psychopathological manifestations are limited mainly to affective disorders. In the dynamics of the disease, there is no complication of syndromes, while in schizophrenia there is a tendency to complicate attacks. And in the case of a sluggish, inactive course of the schizophrenic process differential diagnosis of schizophrenia with neuroses and psychopathy is necessary. It should be noted that the dynamics of schizophrenia are always different from the dynamics of other nosological units, although sometimes they may be indistinguishable in cases of dishonest or incompetent attitude towards the diagnostic process. Such cases are not uncommon, which contributed to the emergence in science of a special section (or discipline) that studies errors in diagnostic and general clinical practice.

In the legal field of knowledge there is a so-called "forensic psychiatric assessment", the main task of which is to identify an accurate clinical picture of the mental state of persons who committed crimes in a state of passion or mental illness. It should be noted that “in forensic psychiatric practice, approximately half of the subjects declared insane are patients with schizophrenia.”

In schizophrenia, it is not possible to identify a single symptom that would be specific only to this disease. However, there are several symptoms that are most typical of schizophrenia, and also, as already mentioned, the pathogenesis of the disease in dynamics differs from all other mental illnesses, although not always self-evident, and sometimes difficult to distinguish even with a thorough examination.

For example, Bleuler believed that the loss of associative thinking occupies a central place in the symptomatology of the disease. K. Schneider proposed a list of symptoms he named "symptoms of the first rank". The presence of one or more of them in a patient directly indicates schizophrenia. This list included the following symptoms:

4. Tactile hallucinations, when the patient feels the touch of something foreign,

5. “Removing” thoughts from the patient’s head,

6. “Putting” thoughts into the patient’s head, carried out by strangers,

7. The belief that the patient's thoughts are transmitted to others (as on a radio), or received by him from others,

8. “Putting” into the patient’s consciousness the feelings of other people,

9. “Insertion” of irresistible impulses into the patient’s consciousness by strangers,

10. The feeling that all the patient’s actions are carried out under someone’s control, automatically,

11. Normal events are systematically given some special, hidden meaning.

American psychiatry took a significant step forward in 1980, adopting a new, significantly revised scheme for diagnosing and systematizing psychiatric diseases, enshrined in the third edition of the Diagnostic and Statistical Manual of Mental Disorders ( DSM-III). Its fourth edition was published in 1994 ( DSM-IV). According to it, a diagnosis of schizophrenia can only be made if the following conditions are met:

1. Symptoms of the disease have been present for at least six months,

2. Compared to the period preceding the disease, there are changes in the ability to perform certain activities (work, communication, personal care),

3. These symptoms are not associated with organic changes in brain tissue or mental retardation,

4. These symptoms are not associated with manic-depressive psychosis,

5. The symptoms listed in one of the points must be present - A, b, or V, namely:

A). Any two of the following symptoms must have been present for at least a month: delirium; hallucinations; disorders of thinking and speech (incoherence or frequent loss of associative connections); Severely disorganized or catatonic behavior, “negative” symptoms (blunted emotions, apathy);

b). Strange nonsense, which members of the same subculture with the patient see as groundless;

V). Obvious auditory hallucinations in the form of one or more “voices” commenting on the patient’s actions or arguing with each other.

“Symptom lists like the one above can give the impression that schizophrenia is easy to diagnose. This is true when dealing with an advanced form of the disease, but in the early stages, diagnosing schizophrenia is difficult. Symptoms can appear with varying degrees of frequency, they can be mild, and the patient can skillfully hide some manifestations of his disease. Therefore, it is a widespread practice among specialists when, at the first meetings with a patient, they write down in the medical history: "suspicion of schizophrenia". This means their diagnosis is in doubt until the clinical picture becomes clearer.”

Currently, the possibility is being considered that there is not “one” schizophrenia, the etiology of which we are trying to determine, but several (possibly hundreds) of different diseases, the clinical manifestations of which are similar; or schizophrenia is a fusion of different dimensions ( dimension - cluster of symptoms) with different etiologies), but we must explain why they coexist. Figure 1 presents these models alongside the traditional understanding of schizophrenia.

Picture 1.

Influence of genetic and environmental factors.

Table 1 describes the most studied risk factors for the development of schizophrenia.

Table 1 Estimation of the relative risk of developing schizophrenia depending on environmental and genetic factors.

Currently, schizophrenia is considered a heterogeneous and polygenic disease with multiple gene polymorphisms, each of which has a small contribution to susceptibility to the disease. Most often in schizophrenia, abnormalities are found in three chromosomal regions (22q11, 1q42/11q14, X chromosome), which are considered a possible location for the localization of genes involved in the development of schizophrenia. But the total number of genes in these regions is about 4000 and specific genes have not been identified.

This is interesting:
A study was conducted to distinguish between the influence of the family environment and hereditary burden on the development of schizophrenia. The risk of developing schizophrenia was compared in adopted children whose parents had schizophrenia, but were raised in a healthy family, and in adopted children born from healthy parents, but raised by sick parents. It was found that the risk of schizophrenia depended on the presence of schizophrenia in biological parents, but not in adoptive parents.

Environmental factors.

As for environmental factors, there is not a single environmental factor that is necessary and sufficient for the occurrence of schizophrenia. Assumptions are made about the role of environmental factors. For example, the risk of developing schizophrenia in the presence of ante- and perinatal complications is well known. Influenza suffered by the mother most often attracts attention as a risk factor, while other infections (rubella, toxoplasmosis, etc.) during this period are also associated with an increased risk of developing schizophrenia. Although the exact neurobiological mechanism is unknown, most researchers point to the role of cytokines and an aberrant immune response that interfere with normal fetal brain development. Hypoxia of the fetal brain plays a leading role in various perinatal disorders.

Advanced paternal age approximately doubles the risk of developing schizophrenia. The leading role is played by impaired spermatogenesis, leading to an increased likelihood of mutations and disruption of epigenetic regulation. Birth in late winter or early spring is considered a risk factor in terms of the possible presence of three factors: prenatal infection, prenatal malnutrition and risk of mutations.

This is interesting:
For many years, there was no consensus among researchers about whether living in urban areas is a risk factor for developing schizophrenia or whether people with schizophrenia move to cities. Over the past half century, the latter assumption has gained more weight, attributed to the "social drift" of people with schizophrenia to cities with cheaper public services and relative anonymity. Of course, the causal role of factors associated with living in urban conditions (stress, unfavorable environmental conditions, relative availability of surfactants, etc.) for the occurrence of schizophrenia is not denied.

Only in the last 20 years have researchers begun to specifically study how genetic and environmental factors interact in the onset of schizophrenia, and through what neurobiological mechanism this occurs. At the moment there are no reliable facts.

Models of schizophrenia.

Pathophysiological models(which focus on "what's wrong" in the neurobiology of the disease) have been around since the 1906s, when the effectiveness of dopamine blockers led to neurochemical theories that emphasized disruption of the dopamine system. Later theories included disorders of the glutamatergic, GABAergic, cholinergic, and serotonergic systems.

Neuroanatomical models, which arose as a result of neuroimaging and neuropathological observations of structural and functional disorders. These theories include: disruption of the heteromodal association cortex (Ross and Pearlson, 1996), disruption of interhemispheric communication as evidenced by loss or reversal of hemispheric asymmetry (Crow et al., 1989) or damage to the striatum (Nasrallah, 1985), dysfunction of the corticothalamo- cerebellar pathway (Andreasen, 1999) and disturbances in the basal ganglia-thalamocortical pathway system (Williamson, 2007).

Pathogenesis models focused on the question of “when” does pathology occur. These include models of neurodevelopment that include early disturbances in neuronal migration or proliferation (Murray and Lewis, 1987; Weinberger, 1987), disruption of synaptic pruning during adolescence (Feinberg, 1982; Keshavan et al., 1994; Murray and Lewis , 1987; Weinberger, 1987) and neurodegenerative theories, which include neuronal excitotoxicity or neurochemical sensitization that leads to progressive deterioration after disease onset (DeLisi, 1997; Lieberman et al., 1997).

Etiological models(which attempt to answer the “why” question) point to varying degrees of the role of genetic factors (Gottesman and Shields, 1967), disrupted gene expression or epigenetic factors (Petronis, 2004) and a variety of environmental factors (van Os et al., 2005 ).

Which of the presented models is the main one is a difficult, and perhaps futile question, since each model can be addressed to different aspects of schizophrenia, and the integration of these theories is an extremely pressing issue. In an attempt to propose a unifying hypothesis, Olney and Farber (1995) proposed that NMDA receptor (NRH) hypofunction may account for multiple features of schizophrenia, including premorbid worsening, adolescent onset, the role of dopamine, and progressive worsening after illness onset. Dysfunction of the glutamatergic system can explain many things - its disturbances are consistent with structural, functional and electrophysiological abnormalities, as well as with early and late neurological aspects of schizophrenia (Keshavan, 1999); hypofunction of NMDA receptors also corresponds to dysfunction of the dopaminergic (Grace, 1991; Weinberger, 1987) and GABAergic systems (Zhang et al., 2008). Several genes implicated in the development of schizophrenia are thought to act on the glutamatergic system (Arnold et al., 2005; Coyle, 2006). However, to date there is insufficient evidence to support a primary disorder in the glutamatergic system.

On the other hand, Crow (1995), arguing that no existing theory explains all key aspects of the disease, suggests that many manifestations of schizophrenia can be explained by asynchrony in the development of the cerebral hemispheres, which is caused by the gene(s) involved in the development of speech , and thus specific to Homo sapiens.

But perhaps no single theory can explain all aspects of schizophrenia, just as no single model can help us understand all the causes of heart failure.

Literature

1. Tandon, R., Keshavan M., Nasrallah H., 2008. Schizophrenia, “Just the Facts”What we know in 2008. 2. Epidemiology and etiology. Schizophr. Res.102, 1-18 4.
2. Keshavan M., Tandon R., Boutros N., Nasrallah H., 2008. Schizophrenia, “Just the Facts”What we know in 2008. Part 3: Neurobiology. Schizophr. Res. 106, 89-107 5.

We do not know the cause of schizophrenia, and given the state of modern science, it is unlikely that this could be the only cause. With the help of psychiatric research, a number of conditions for the occurrence of the disease have been established. These data on etiology and pathogenesis will be reviewed in the following sections and then synthesized in the form of a preliminary theory.

Genetic factors

Family studies have shown that people with schizophrenia have significantly more relatives who also have schizophrenia than the average population. While the overall morbidity rate is about 1%, in the patient’s parents it reaches 2-10, in brothers and sisters - 6-12, in children 9-13, and in grandchildren - 3%. If both parents have schizophrenia, the percentage of the disease in children reaches about 40%. Other psychoses, including melancholic mania, are much less common in the family environment of patients with schizophrenia.

Twin studies provide clearer evidence. According to the latest data, concordance for identical twins is 31-78%, for fraternal twins - 6-28% (as for brothers and sisters in general). The differences are impressive. In identical twins, concordance is 3-5 times higher than in fraternal twins (with neuroses it is 1.5-2 times higher). These data are assessed as a hereditary factor, but they also indicate that there are other conditions of occurrence, since if the condition were exclusively hereditary, the concordance of identical twins would be one hundred percent.

If identical twins live separately, then concordance for schizophrenia is lower than that. those who live together, although observations of twins who would live apart from an early age are not enough. These differences in the influence of the external environment are explained by the opposition between the internal environment (genetic environment) and the external environment (environment). If one of identical twins develops schizophrenia, and the other remains healthy, then the children of the healthy one develop schizophrenia no less often than those of the sick one.

To differentiate genetic and social inheritance, adopted children whose biological and social spheres are not identical are studied. Children of mothers with schizophrenia adopted into a new family develop schizophrenia more often than those adopted from a healthy mother. Studies of adopted ill children show that the rate of schizophrenia among their biological parents is significantly higher than among the adoptive parents; Children often get sick only when their biological parents also get sick.

There is no consensus on the nature of inheritance. On the one hand, a dominant type of inheritance with low penetrance is considered, and on the other, a monohybrid-recessive type. Multifactorial polygenetic inheritance could best explain the large variability of schizophrenic patterns and types of course (the severity of schizophrenic symptoms again depends on living conditions). Modern psychiatric genetics, using molecular biological methods, searches for phenotypic markers, for example, neuronal metabolism in schizophrenia. An individual forecast is not yet possible.

Summarizing the above, we can state that the study of families, twins and adopted children speaks in favor of genetic determination of schizophrenia (not just about heredity) and, in addition, about other pathogenetic factors. What is inherited is, in any case, unknown; the presence of a biochemical defect or predisposing structure is assumed, up to a tendency for pathological personality development and partial lack of activity.

Constitution

Kretschmer's data on the bodily constitution indicate biological relationships: in patients with schizophrenia, the leptosomal-asthenic, only sometimes pyknic, body type predominates, and in affective psychoses the relationships are the opposite. However, these data, as well as their interpretation (the biological affinity between psychosis and bodily constitution), are questioned. In addition, Kretschmer described the relationship between personality and psychosis, namely the schizoid structure (or less clearly the schizoid temperament) and schizophrenia. However, here we are not talking about close correlations. Many schizoids do not become psychotic, and many patients with schizophrenia have other features in their personality structure or an unremarkable structure in the premorbid period.

Psychophysiological studies in patients with schizophrenia (heart rate, EEG, skin resistance) have just begun.

Morphological data

For a long time, the organic brain substrate of schizophrenia was intensively searched. The results are disappointing. If changes were found, they turned out to be secondary (for example, cerebral circulation disturbances due to severe catatonic agitation), nonspecific findings not related to psychosis, or artifacts of the technique.

Clinical studies using computed tomography show differences between healthy people and some patients with schizophrenia in the dilation of the ventricles, especially the third ventricle (possibly also the frontal and temporal subarachnoid spaces). Findings indicating predominantly diencephalic morphological brain lesions, and corresponding autopsy findings indicating inferiority of the brain substance in some patients with schizophrenia, especially in the limbic and paralimbic areas, are in direct connection with the unfavorable outcome of schizophrenia.

The etiology is difficult to interpret, but it is possible that we are talking about impaired brain maturation (due to early brain damage). Some observations indicate this. In patients with schizophrenia, there are definitely frequent anamnestic neurological and psychopathological indications of brain damage. In the anamnesis, patients with schizophrenia are more likely than their healthy brothers and sisters to indicate complications during pregnancy, during and after childbirth.

These findings are not found in all patients with schizophrenia and cannot, even if present, be considered a cause of psychosis. Here we are obviously talking about one of the factors in the conditions of the disease. Perinatal brain disorders can cause general mental retardation in the sense of increased vulnerability. The associated partial weakness of the ability to function can make it difficult to build normal relationships with reality and thus contribute to the predisposition factors for the occurrence of schizophrenic psychoses.

“Building relationships as an activity that children perform from preschool to primary school depends on many factors, which include the neurophysiological ability to act, excitability and the ability to differentiate excitation, the ability to process and accumulate information in the child’s brain...” (Lemp).

The underlying cognitive impairments that Syllvold studies have something in common with partial weaknesses in judgment.

Neurobiochemical data

When searching for somatic causes of schizophrenia, numerous findings are discovered and hypotheses are put forward, which for the most part are not supported (rheumatic, allergic or viral genesis; oxygen consumption disorders, various endocrine hypotheses). The hypothesis of modeling psychoses was inspired by observations of pharmacogenic psychoses (LSD 25, mescaline, cocaine), but they do not add anything either psychopathologically or neurobiologically.

Only psychopharmacological studies have revealed significant data. It is noteworthy that psychopharmacological agents were discovered not at the level of basic research, but through clinical observations and largely by accident. This is how widespread neurobiochemical studies of the mechanisms of action of psychopharmacological drugs and, based on this, the pathogenesis of psychoses arose. The first biochemical hypotheses for the occurrence of schizophrenia (serotonin, transmethylation, etc.) were later abandoned. The following hypotheses are much more important.

Dopamine hypothesis: antipsychotics (along with other biochemical effects) cause blockade of dopamine receptors, due to which the transmitter function of dopamine is reduced. Certain antipsychotics act differently on D|- and Eg receptors. It is possible that targeting specific portions of dopamine receptors predicts neuroleptic effects. Nowadays, the antipsychotic effect is explained by the antagonism of antipsychotics with dopamine.

Based on this, schizophrenic symptoms are associated with the relative predominance of dopamine in relation to other neurotransmitters, including hyperactivity or hypersensitivity of dopamine neurons. In amphetamine psychoses (with schizophrenia-like symptoms), dopamine is released from presynaptic membranes; neuroleptics also have an effect on them.

In particular, the antipsychotic effect of antipsychotics is explained by the blockade of dopamine receptors in the limbic (as well as in the cortical) region, while side extrapyramidal-motor effects depend on the corresponding effect on the nigrostriatal system, on neuroendocrine side effects in the tubero-infundibular system.

Along with the dopamine hypothesis, the reduction of glutamatergic transmission and the participation of serotonergic, cholinergic and other neurochemical systems were also the subject of discussion. In general, knowledge about neurochemical processes is riddled with gaps. There is still no sufficiently reasoned theory. We hardly know which of these conditions lead to pathogenetic changes, and which are only epiphenomena.

It is clearly established that, from a psychoneuroimmunological point of view, activation of the immune system occurs in patients with schizophrenia, so the hypotheses of viral genesis or autoimmune pathology are still being discussed.

Somatic participation

The opinion that somatic factors are involved in the genesis of schizophrenia is based on clinical observations. Although in most cases there is no connection between a somatic illness and the development of schizophrenia, in a few cases the onset and/or course of psychosis has such a close connection with a somatic illness that it is difficult to detect only a coincidence in this.

So-called symptomatic schizophrenia. If schizophrenic symptoms occur in close temporal connection with a somatic illness and, moreover, disappear after treatment and elimination of the underlying disease, then this is not schizophrenia, but organic (symptomatic) psychosis with a schizophrenia-like picture. Such symptomatic schizophrenia is observed in various somatic diseases, for example, encephalitis, progressive paralysis, brain injuries, and metabolic diseases. More often they occur during intoxication with psychoanaleptics and psychodisaleptics. These psychoses are today explained as an organic-paranoid syndrome and are classified as organic psychoses of the second stage.

In these psychoses, schizophrenic symptoms arise only in a transient manner (the so-called transitional syndrome) and in connection with transient symptoms of organic psychosis. Sometimes organic psychoses occur exclusively with the picture of schizophrenia. These observations suggest that somatic factors may be involved in the genesis of schizophrenia.

More often than organic psychoses with schizophrenic symptoms, there are schizophrenias, which, although they arise in a temporary and perhaps even causal connection with a somatic disease, should not be associated with it, since psychoses proceed further as schizophrenia. With such somatic participation, it is believed that when one is prepared for a disease, a somatic disease leads to its manifestation. This participation is nonspecific, since it is observed in many somatic diseases. It is difficult to judge the frequency of somatic provocation of schizophrenia, since there is no criterion that would determine the pathogenetic significance of a previous somatic disease. In general, somatic involvement is less common than psychoreactive involvement.

Psychoreactive participation

According to old psychiatric concepts, schizophrenia is defined as independent of somatic or mental influences, that is, it arises “endogenously.” However, the results of epidemiological and anamnestic, psychodynamic and follow-up studies show that psychosocial factors are also involved in the emergence and course of schizophrenic psychoses. Stressful life situations (life incidents) before the onset of the disease often do not occur by chance, as comparison with healthy people shows. Of course, it is not always possible to obtain enough information about the life of a withdrawn and autistic patient to reliably judge the frequency and pathogenetic significance of such stress. In addition, the digital data is different. Approximately half of schizophrenic diseases (attacks) are attributed to psychoreactive provocation. This is one condition among others, but not the cause.

At the same time, external pressures (somatic overstrain, a situation of need, etc.) apparently have less importance than conflicts in interpersonal relationships: on the one hand, lack of attention and loss of human connections, and on the other, too much closeness and intimacy lead to to schizophrenia. Fear of the danger of becoming too close while simultaneously needing intimacy and love is a characteristic conflict of ambivalence in a patient with schizophrenia. For the patient, the problem of experiencing interpersonal relationships without fear, without danger to one’s own self is insoluble. A decrease in distance is more often a cause of illness than an increase in this distance.

This is also supported by the experience that in schizophrenia, relapses are especially frequent in those patients who live with overly caring relatives than in those who are in hostile relationships with them, or when they are indifferent. If the patient is in contact with relatives for many hours a day, the risk of relapse increases, especially if he does not take antipsychotics. It does not follow from this that the patient should live outside the home; Rather, the solution is that it is necessary to eliminate the possibility of an emerging conflict psychotherapeutically, and relatives need to be involved in treatment, ensuring that they themselves restore an atmosphere of balance in the family. Many cases of the course show that individual schizophrenic manifestations are caused by the same difficult situations, so that there is an individual specific provocation.

However, it is often difficult to determine whether this is the same situation, the same experiences are observed before the next exacerbation of psychosis, or whether the signs of the disease developed on their own. Upon careful analysis of the situation, it becomes clear that there is no clear boundary in time between not yet painful and already schizophrenic experiences, and therefore the onset of psychosis in most cases cannot be unambiguously determined.

Prepsychotic conflict experiences and psychotically altered experiences are closely intertwined (“situational unity of cause and reaction”).

Nowadays, schizophrenia is often detected in individuals taking part in group dynamic, meditative and other classes and activities. As a result of uncontrolled influences of this kind, the function of the ego is so disrupted that psychotic decompensation occurs.

So-called schizophrenic reactions. Despite the fact that in most cases a psychoreactive predisposition is determined, psychosis proceeds basically in the same way as other schizophrenias, and in addition, there are other, quite often observed forms of the course: severe, insurmountable conflicts are followed by acute and pronounced schizophrenic symptoms, which soon disappears (after a few weeks, in extreme cases, months, and sometimes after a few days), without showing any tendency towards an undulating course with relapses or to a chronic course and residual conditions. These forms of the disease - schizophrenic reactions - are considered as an independent disease.

However, even with this disease, conflict cannot be the only cause, because only a few people develop schizophrenic symptoms after such conflicts. They talk about genetically determined readiness for the disease, since in these families there are more cases of schizophrenia than in the general population, although not as many as in families where the disease of schizophrenia is severe and long-lasting. Careful observations of the course of the disease show that in most cases, patients with a disease regarded as a schizophrenic reaction and with complete recovery later experience schizophrenic episodes and even residual states. Consequently, we can assume that with the so-called schizophrenic reactions, we are presumably not talking about an independent disease, but about schizophrenia with a favorable course.

Psychodynamic aspects

If you are not satisfied with the statement of the possible psychoreactive provocation of the disease, and based on this ask from a psychodynamic position what happens to a patient with schizophrenia, you should start with analytical psychology of the Self, with which the new theory of vulnerability converges to a large extent. According to Federn, in neuroses the ego can be restored thanks to defense mechanisms, but in schizophrenic psychoses the ego disintegrates.

“Where there is a lack of control of the ego, it is impossible to keep the highly developed and organized ego in sufficient control throughout all its boundaries, and therefore invasion by the impersonal unconscious is possible. After returning to an earlier state of the Self, the boundaries of the distribution of this state are significantly reduced, but remain inactive as such. In such a case, the regression of the Self can serve an earlier state, which makes fewer demands on the possession of the Self and protection from false reality.”

Based on this, Federn identifies the main signs of schizophrenia:

1. invasion of “false” reality, which manifests itself in the identification of previously repressed contents of the unconscious or delusional experiences associated with the unconscious;
2. this invasion can move the ego by regression to an earlier stage of development. This regression in schizophrenia manifests itself in a more radical form than in neuroses. First of all, juvenile schizophrenia can cause regression to the level of a small child and even to the level of an infant: at a deep point of regression, many children stop speaking and it is difficult to feed them. Such conditions are in no way prognostically unfavorable. This indicates that it is less about the expression of the disease process and more about psychodynamic processes;
3. insufficient control of the boundaries of the Self becomes the basis for mixing the untrue and the true in reality and thus disrupting conceptual, abstracting and integrating thinking.

This so-called deficit theory cannot explain the etiology of schizophrenia, but it is a useful psychodynamic model for diagnosis and therapy, and it prompts the following observations, which lead to the so-called conflict theory. Just one example of this is given.

Winkler, in the “dynamic-phenomenological method of analysis,” described two forms of defense mechanisms of the Self, which serve to resolve intolerable (not related to the Self) feelings of guilt. One form is anachoresis-I, the withdrawal of the I from feelings of guilt. In contrast to repression, the content of experiences remains in consciousness, but the qualities of the Self are lost, so that the Self becomes irresponsible for content alien to the Self. As a result of anachoresis-I, physical sensations of a sexual nature can turn into a feeling of foreign influence or one’s thoughts are perceived as alien in the form of suggestion and auditory hallucinations. Anachoresis-I is the last resort when unacceptable content bursts with particular intensity and penetrance into the I, which cannot defend itself. This is the case when there is weakness of the ego and insufficient control of the ego according to Federn, therefore active opposition or repression is impossible.

Another process of defense is identification with a mythical figure. With this mythization of the Self, which is also a pronounced form of suppression of the feeling of guilt, it is eliminated from personal existence. These observations show: it is not the imposition of difficulties on oneself, but certain conflicts that become risk factors in the genesis of schizophrenia, or more precisely, the failed processing of the conflict of a weakened self when protective mechanisms of a different nature enter into force than in neuroses.

It remains to ask: why exactly these and not other defense mechanisms come into play and why does the weakness of the ego arise in general?

Explanation from the perspective of developmental psychology. If you try to answer this question, you must immediately point out that the described weakness of the ego has been present in at least some patients since childhood: already in infancy, weak facial, motor and social activity is detected. Later, although mental development is not delayed (how the anamnesis of these children differs from early childhood exogenous psychosyndrome), parents do not note difficulties in upbringing; rather, these are good children, but upon painstaking questioning they reveal a lack of spontaneity and ability to respond. Their complaisance can be the result of parental dominance, which leads to the child’s dependence (especially on the mother), lack of independence, and lack of resistance, which constitutes the weakness of the ego.

These children do not exhibit a phase of stubbornness, make few contacts, and are rather passive and unnoticeable at school. The puberty period proceeds surprisingly calmly. In subsequent years, and even in adolescence, the weakness of the ego increasingly contrasts with the demands of life, and personality changes may gradually occur, especially depersonalization and autism. The development of psychosis stems more from the internal consequences of previous life than appears at first glance.

To generalize, they speak of a basic weakness of the constitution of the ego or egopathy (Kisker). But again the question arises: how does this disorder appear? In general, it is possible to determine persistently persistent structures of human temperament from the first weeks or months of life, as evidenced by rigorous studies of the activity and behavior of children of Thomas and Chess. The originality and immutability of the individual have been known for a long time, therefore mental structures bear the imprint of not only external influences. On the other hand, it does not follow from this that the structure of temperament is simply determined by heredity. Observations suggest that conditions of a hereditary nature and the influence of the surrounding world are inseparable in their impact on mental development. Increased vulnerability, which predisposes to schizophrenia, usually occurs in childhood. Here there are connections between schizophrenia and early childhood autism, which can be considered congenital or early-onset schizophrenia.

Here the contribution of psychology to the development of the doctrine of schizophrenia (Lempp) is assessed. Schizophrenia is seen as a condition that is recognized as a loss of "coping ability". The ability to overcome corresponds to the sovereign ability to rotate between the common reality that a person shares with his environment and the individual world of ideas (parallelism). The general attitude towards reality is experiences in the process of mental development in the first years of life. “While young children place general reality and the individual world of ideas on the same level, general reality later, at the beginning of school, acquires absolute dominance.” The stability of the construction of this general reality depends on cognitive structures, as well as on the information that the child receives from his environment in the first years of life. Violations in the construction of this attitude to reality can occur both due to cognitive disorders caused by congenital or acquired weak ability to judge, and due to the inconsistency of information coming from the outside world. Instability during maturation, along with other factors, can lead to exercise intolerance and the development of schizophrenia.

Family Studies

The individual development of the patient, as well as his family and its dynamic structures, deserve attention. It has long been known that a difficult situation and conflicts are established not only at the time of the onset of the disease (psychoreactive impulse), but in most cases it haunts the patient from childhood: birth out of wedlock, neglect of a child, psychotic or neurotic parents, alcoholic father, divorce of parents , family breakdown. However, more important than the signs of a broken home are other (often difficult to identify by anamnestic) difficulties in the family: an unsuccessful marriage of parents, reluctance to have a child, inconsistent upbringing, pronounced rivalry among children. Of course, such disorders can be found in the anamnesis of neurotics, personality disorders, and healthy people. But with schizophrenia, this obvious or hidden breakdown in the family occurs almost constantly and, moreover, to a severe degree, as careful family studies show.

Psychoanalytic attitudes in family research proceed mainly from abnormal early mother-child relationships and lead to the hypothesis of the “schizophrenogenic mother”, which they still could not prove. Accordingly, an attempt to define the role of the father in a child with future schizophrenia is regarded as weakness and powerlessness. New family research follows a transactional approach.

Brief results of the studies of Lidz, Fleck and Cornelson: psychotic parents are more likely than others to come into the field of attention when studying heredity, since even mild schizophrenic diseases as such are taken into account, while other diseases fall out of observation. Two thirds of patients have at least one sick parent, if the concept of schizophrenia is taken broadly. Of the families surveyed, not a single one was even more or less integrated: the relationship between parents was seriously disturbed; often families are divided into two camps. In other families, open confrontation is avoided only through subordination, even with pathological or psychotic behavior of family members. The relationship between the mother and the future child with schizophrenia is especially disturbed due to the mother’s lack of understanding and at the same time due to her excessive care and guardianship. The mother's uncertainty and anxiety lead to inconsistent changes between strictness and pampering of the child. In this case, more often there is not an isolated violation of the mother’s behavior, but a violation of the entire situation in the family.

Wynn and Singer found in the families of people with schizophrenia a style of broken speech and broken thinking. Parents talk to each other in a vague and meaningful style. Concepts are used in unusual and variable meanings. Conversations lack precision and purpose. The behavior of parents may also be incomprehensible, and in the eyes of the child it contrasts with generally accepted principles of life. Thus, children grow up in an atmosphere of uncertainty and inconsistency, which explains the subsequent disorders of communication and thinking. Alanen's family studies yielded similar results.

And in a later period of life, as well as after the onset of the disease process, the emotional relationships between the patient and his parents were studied and their significance for the results of treatment and the course of the disease was determined. The periods of living together, the nature of emotional relationships (expressed emotions, EE) were determined and correlations were established with relapses of the disease, special and clearly manifested emotional relationships to the manifestation of schizophrenic disorders (Brown, Leff).

These briefly described data, which were only partially confirmed by subsequent monitoring, do not indicate a single form of disturbance in family relationships, but reveal severe and unusual deviations. There is no definite judgment yet whether these data are specific for families of patients with schizophrenia, as well as for families of other patients, especially with anorexia, depressive and other severe neuroses with a borderline structure. Perhaps a patient with schizophrenia, due to his special disposition (predisposition), reacts with such certain disturbances to influences that do not affect others.

The dynamics of the described family processes contribute to the development of schizophrenic disease and, moreover, determine its course (hypothesis of cause). The described parental behavior causes early onset disturbances in the child who respects them (response hypothesis). Because of this, causes and effects can be difficult to distinguish. In system theory they do not talk about causality, but only about changing relationships and patterns of family life.

A hypothesis is proposed about the joint responsibility of close relatives. It is not the family that is “pathogenic”, but the unfavorable conditions of existence. For patients with schizophrenia, a family and social environment is considered favorable, which is protective (protective), but not pampering (aggressively indulgent), stimulating, stress-free, emotionally warm and at the same time maintaining the necessary distance.

Although family studies cannot explain the etiology of schizophrenia, their data still convincingly indicate the creation of conditions for the development of a prudent attitude of a patient with schizophrenia towards his life and treatment.

Among other numerous studies and theories, the theory of double blindness should be mentioned (Bateson et al.), which seems very clear, although unprovable: in families of patients with schizophrenia, mutual understanding is disturbed and the understanding of the unambiguity of certain messages is lost, they talk about them jokingly or seriously, with friendliness or hostility. In a situation of double blindness to the meaning of this information, these relationships (like the game “double mill”), the child cannot help but make mistakes. Perhaps such situations occur frequently, but only those children who are susceptible to the disease for other reasons experience a psychotic processing of their attitude to the world and reality.

Sociocultural aspects

In addition to the “microsocial” environment of the family, the “macrosocial” society of a person with schizophrenia should also be studied. Psychiatric epidemiology primarily examines whether the patient has connections with different sectors of society.

There is evidence that there are more patients with schizophrenia in the lower strata of the population and in the industrial centers of large cities, and there are also more patients with severe forms of the disease. Whether poorer psychohygienic conditions lead to the development of schizophrenia (social conditioning) or whether in these cases low social status is rather a consequence of psychosis or a prepsychotic state (social selection), there is no clear answer to these questions. The fact that a patient with schizophrenia, due to repeated attacks of the disease, declines socially (social mobility) has not yet been clearly decided.

If a patient with schizophrenia lives alone for a long time, it is difficult to judge whether this isolation is a condition for the onset or a consequence of the disease. There are more people with schizophrenia among vagabonds than among the settled population, and more often among newcomers than among those living at home. The question remains open here: do the difficulties of resettlement and adaptation to a new place have a pathogenic effect, or are there more people with schizophrenia among the resettlers?

The theory that schizophrenia is a disease of civilization is not supported by transcultural research. Schizophrenics are also found in primitive cultures. Whether people with schizophrenia occur at different frequencies in different countries and cultures is still unclear, since epidemiological surveys are more difficult to conduct in less developed countries and therefore are likely to have fewer patients under observation. The symptoms of schizophrenia depend little on sociocultural influences; they are the same in different cultural circles and even in different time periods. It is only unknown where the prognosis of the disease is better - in developing countries or in industrialized ones.

Data from epidemiological studies of schizophrenia are sometimes contradictory, their assessment is controversial, and the significance for etiology is unclear. Since clinical observations and systematic studies throughout the life of patients show that the course of the disease depends on psychosocial factors, data on specific strata of society should also be studied in a prognostic aspect.

Conclusion on the causes and mechanisms of development.

1. The only and fully provable cause of schizophrenia has not been established, but only individual factors have been identified.
2. None of these factors alone explains the cause of schizophrenia.
3. The combined action of a number of factors is knowable.

Consequently, we do not have any full-fledged theory of the emergence of schizophrenia and a common causative factor, but we can identify a number of conditions for the emergence of etiopathogenetic components. In this case, they talk about multifactorial genesis.

And yet there are schizophrenias in which their own patterns are visible and the disease proceeds largely independently of environmental influences. This applies, for example, to a simple form of schizophrenia with a pronounced family history. There are, although less frequently, symptomatic schizophrenia as somatically caused psychoses and, further, schizophrenic diseases, in the origin and course of which psychoreactive factors are clearly involved. Accordingly, the results of pharmacotherapy and psychotherapy are impressive. But if we absolutize in an inadmissible way and ignore everything else, we can define schizophrenia as hereditary diseases or as organic psychoses, as a result of stress or social disorder. Clinically, it should be noted that even today there are almost as many theories of schizophrenia as there are individual etiopathogenetic observations. Most of both biological and psychological research into schizophrenia is not free from speculative elements.

The totality of data does not allow us to build a unified theory, but brings us closer to a multidimensional approach. How do these separate conditions of origin work together? The components of the occurrence of schizophrenic psychoses today can be presented as follows: there is a readiness for the disease, which is determined by a chromosomal or enzyme defect or a predisposition to pathological personality development. Along with genetic factors, the resulting organic brain disorders and psychosocial influences in childhood contribute to the preparedness for the disease.

These factors interfere in some yet unknown way. They cause vulnerability in the sense of an unstable balance, which is easily disturbed or intensified by external influences of both a somatic and mental nature. As a result, the patient develops defense mechanisms that act on withdrawal and isolation and are expressed in symptoms such as autism, disturbances of the self and self-limitation. If the threshold of vulnerability is overcome by various kinds of harmful factors, then a schizophrenic disease occurs.

Vulnerability (damageability, susceptibility to influence) is a clear model that has long been used to explain the multi-cause genesis of schizophrenia (and other mental illnesses): if the endurance threshold is exceeded by overloads (of various kinds), the disease develops or its relapse. With a high readiness for the disease (low threshold of vulnerability), it may be only a small part in the further pathogenetic influence (and vice versa).

The vulnerability model is needed theoretically, diagnostically and therapeutically. Theoretically, it allows us to avoid the pitfalls of monocausal thinking. Diagnostically, it allows for careful examination of early symptoms (threshold symptoms). Therapeutically, it allows one to approach indications and treatment not symptomatically, but based on the situation and characteristics of the patient’s reaction, which are indicators of therapy. Any vulnerability model cannot capture all observations and explain all data on schizophrenia, including the primary chronic course or low-expected late improvements.

Model of diathesis stress- this is the modern designation of these relationships. In this definition, diathesis means readiness for illness. Stress must be understood in its broadest sense, encompassing biochemical, pathophysiological and psychoreactive influences.

If psychosis already occurs or recurs, it depends not only and not so much on predisposition, but on premorbid or situational factors, as well as on somatic influences (for example, on metabolism). What kind of psychosis this is, whether stress or conflict will cause schizophrenia or other psychosis, cannot be explained psychologically or psychodynamically, since it is mainly due to heredity. Individual schizophrenic symptoms are not the meaningless product of a disease process, but the result of combined processes of impairment and deficit, on the one hand, and processes of defense and coping, on the other. The course of the disease ultimately depends largely on environmental conditions.

“A flow is like a street that has crossroads and blocks, intersections and forks, slopes and rises, ditches and gullies, but there are no way signs to which attention would be drawn. Both the disease and the person suffering from this disease, whether the person stumbles or falls, stays down or gets up again, whether he crosses the intersection in the right or wrong direction, decides to cross or stops at the fork - all this cannot be explained by endogeneity. And as for the possible process of recovery, the current does not show us a transition - from red to green, since the street has long been free” (Mauts).

Schizophrenia is not only a disease process and not only a mental reaction or human failure, it is a multidimensional combination of both. The multifactorial etiology of schizophrenia, although not disputed today, affects mainly issues of diagnosis and therapy, and is not entirely transferred to practice. Of course, the multifactorial concept can become an expression of difficulties in diagnosis and refusal of therapy. If the conditions for the onset of schizophrenic psychosis in a patient are unclear (maybe due to a short period of observation), indications of a multifactorial etiology become very convenient. If the prescribed psychotherapy fails or pharmacotherapy remains ineffective, the doctor may be content to indicate a particularly unfavorable prognosis due to living conditions or too strong influence of hereditary burden.

Long-term course and especially chronicity largely depend on psychosocial influences, therefore, for chronic schizophrenia, its own model of etiology (Chompi) was created. A number of observations make it incredible that the course of the disease is determined only by the disease processes themselves: there is also decompensation due to conflicts, social harm (including due to society’s attitude towards the mentally ill), and the extreme diversity of individual varieties of the course. In addition, family studies show that chronification generally does not coincide with hereditary burden (relatives with schizophrenia), as is the case with acute diseases. Further, the symptoms of chronically residual schizophrenia are in many respects similar to the residual states of other mentally ill patients (with neuroses and personality pathologies), as well as with mental impoverishment in healthy people in certain situations (in sanatoriums, prisons). These observations suggest the thesis that chronic schizophrenia is more of an “artifact” than a disease, but this is only one perspective of etiopathogenesis, at least an aspect of serious therapeutic significance.