Abnormal brain chemistry in schizophrenia. In schizophrenia, brain cells do not communicate well

There are a great many questions about schizophrenia that scientists still cannot answer. But first, let's talk about the most important thing.

Schizophrenia is a very common mental illness. Statistics show that around one in 100 people in Australia will suffer from it at some stage in their lives. Thus, almost everyone has friends or relatives with schizophrenia.

Schizophrenia is a complex condition that is difficult to diagnose, but the listed symptoms are usually identified: mental activity, perception (hallucinations), attention, will, motor skills are impaired, emotions are weakened, interpersonal relationships are observed, streams of incoherent thoughts are observed, perverted behavior, a deep feeling of apathy and sensation arises. hopelessness.

There are two main types of schizophrenia (acute and chronic), and at least six subtypes (paranoid, hebephrenic, catatonic, simple, nuclear and affective). Fortunately, schizophrenia is treated with cognitive therapy, but most often with medication.

There are many myths associated with schizophrenia. One of them is the view that this disease occurs more often in rural areas than in cities. Moreover, according to outdated information, schizophrenics from rural areas often move to cities to find privacy. However, scientists refute this myth.

A study of schizophrenia among Swedes indicates that urban residents are more susceptible to the disease and they do not move anywhere. Scientists say that the environment can push people towards illness.

But myths aside, the true source of schizophrenia is still a mystery. Previously, it was believed that the cause was the parents’ poor attitude towards the child - usually they blamed mothers who were too restrained and cold in their treatment. However, this point of view is now rejected by almost all experts. Parents are much less to blame than is commonly believed.

In 1990, researchers at Johns Hopkins University found a link between shrinkage of the superior temporal gyrus and intense schizophrenic auditory hallucinations. It has been theorized that schizophrenia results from damage to a specific area on the left side of the brain. Thus, when “voices appear” in a schizophrenic’s head, there is increased activity in the part of the brain that is responsible for thinking and speech.

In 1992, this hypothesis was bolstered by a major Harvard study that found a link between schizophrenia and shrinkage of the left temporal lobe of the brain, especially the part responsible for hearing and speech.

Scientists have found a connection between the degree of thought disorder and the size of the superior temporal gyrus. This part of the brain is formed by a fold of the cortex. The study was based on a comparison of magnetic resonance imaging of the brains of 15 patients with schizophrenia and 15 healthy people. It was found that in patients with schizophrenia this gyrus is almost 20% smaller than in normal people.

Although this work does not result in new treatments, the scientists believe that their discovery provides an opportunity to “further study this serious disease.”

Nowadays, new hope arises every now and then. A 1995 study from the University of Iowa suggests that schizophrenia may result from pathology of the thalamus and areas of the brain anatomically associated with this structure. Previous evidence indicated that the thalamus, located deep in the brain, helps focus attention, filter sensations, and process information from the senses. Indeed, “problems in the thalamus and related structures, extending from the top of the spine to the back of the frontal lobe, may create the full range of symptoms seen in schizophrenics.”

Perhaps the whole brain is involved in schizophrenia, and certain psychological ideas, for example about oneself, may have a certain connection with it. Dr. Philip McGuire says: "The predisposition [to hearing voices] may depend on abnormal activity in areas of the brain associated with the perception of internal speech and the assessment of whether it is one's own or someone else's."

Is there a specific time for such brain disorders to occur? Although symptoms of schizophrenia usually begin during adolescence, the damage that causes it can begin in infancy. "The exact nature of this neural disorder is unclear, but [it reflects] disturbances in brain development that appear before or shortly after birth."

There are experts who believe that schizophrenia can be caused by a virus, and a well-known one at that. A controversial but very intriguing version of the causes of the disease was put forward by Dr. John Eagles of the Royal Cornhill Hospital in Aberdeen. Eagles believes that the virus that causes polio can also influence the onset of schizophrenia. Moreover, he believes that schizophrenia may be part of the post-polio syndrome.

Eagles bases his belief on the fact that since the mid-1960s. in England, Wales, Scotland and New Zealand, patients with schizophrenia decreased by 50%. This coincides with the introduction of polio vaccination in these countries. In the UK, the oral vaccine was introduced in 1962. That is, when polio was stopped, the number of cases of schizophrenia decreased - no one imagined that this could happen.

According to Eagles, Connecticut scientists found that patients hospitalized with schizophrenia were “significantly more likely to be born during polio years.”

Eagles also points out that among unvaccinated Jamaicans who came to the UK, "the prevalence of schizophrenia is significantly higher compared to the local [English] population."

Eagles notes: in recent years, the existence of post-polio syndrome has been established. In this syndrome, approximately 30 years after the onset of paralysis, people begin to suffer from severe fatigue, neurological problems, joint and muscle pain, and increased sensitivity (especially to cold temperatures). Post-polio syndrome occurs in approximately 50% of polio patients. According to Eagles, “the average age of onset of schizophrenia is approaching thirty years, and this is consistent with the concept of schizophrenia as a post-polio syndrome that develops after perinatal poliovirus infection.”

Doctors David Silbersweig and Emily Stern of Cornell University believe that schizophrenics are unlikely to have serious brain problems, but nevertheless they were able to discover something very interesting. Using PET, they developed a method for detecting blood flow during schizophrenic hallucinations. They conducted a study of six either untreated or treatment-resistant schizophrenics who heard voices. One experienced visual hallucinations. During the scan, each patient was asked to press a button with their right finger if they heard sounds. It was found that during hallucinations, superficial areas of the brain involved in processing auditory information were activated. Moreover, all patients had a rush of blood to several deep areas of the brain: the hippocampus, hippocampal gyrus, cingulate gyrus, thalamus and striatum. Do schizophrenics really hear voices? Their brain data shows that this is true.

The speech of schizophrenics is often illogical, incoherent and confused. They used to think that such people were possessed by demons. Researchers have discovered a much less fantastic explanation. According to Dr. Patricia Goldman-Rakic, a neurologist, the speech problems of schizophrenics may reflect short-term memory deficits. It has been discovered that the prefrontal cortex of schizophrenics is significantly less active. This area is considered the center of short-term memory. Goldman-Rakic ​​says, “If they are unable to retain the meaning of a sentence before moving on to the verb or object, the phrase becomes devoid of content.”

In addition to all of the above, there are many questions about schizophrenia that are still unanswered.

Is schizophrenia caused by the mother's immune response or poor nutrition?

Some scientists believe that schizophrenia is caused by damage to the developing fetal brain. A study from the University of Pennsylvania, which included medical data from the entire Danish population, found that severe malnutrition in the mother early in pregnancy, as well as her body's immune response to the fetus, may influence the onset of schizophrenia.

Thanks to the memories

As the body ages, the enzyme prolyl endopeptidase increasingly destroys neuropeptides associated with learning and memory. In Alzheimer's disease, this process accelerates. It causes memory loss and a reduction in active attention time. Scientists from the city of Suresne in France have discovered medicinal compounds that prevent the destruction of neuropeptides by prolyl endopeptidase. In laboratory tests with rats that had amnesia, these compounds almost completely restored the animals' memory.

Notes:

Juan S. Einstein’s brain was doing the washing // The Sydney Morning Herald. 8 February 1990. R. 12.

McEwen B., Schmeck H. The Hostage Brain. N.Y.: Rockefeller University Press, 1994. pp. 6–7. Dr. Bruce McEwan is head of the Hutch Neuroendocrinology Laboratory at The Rockefeller University in New York. Harold Schmeck is a former national science columnist for The New York Times.

An interview with M. Merzenich is given by I. Ubell. Secrets of the brain // Parade. 9 February 1997. P. 20–22. Dr. Michael Merzenich is a neurologist at the University of California, San Francisco.

Lewis G., David A., Andreasson S., Allebeck P. Schizophrenia and urban life // The Lancet. 1992. Vol. 340. P. 137–140. Dr Glyn Lewis and colleagues are psychiatrists at the Institute of Psychiatry in London.

Barta P., Pearlson G., Powers R., Richards S., Tune L. Auditory hallucinations and smaller superior gyral volume in schizophrenia // American Journal of Psychiatry. 1990. Vol. 147. P. 1457–1462. Dr. Patrick Barta and colleagues work at Johns Hopkins University School of Medicine in Baltimore.

Ainger N. Study on schizophrenics – why they hear voices // The New York Times. 22 September 1993. P. 1.

Shenton M., Kikins R., Jolesz F., Pollak S., LeMay M., Wible C., Hokama H., Martin J., Metcalf D., Coleman M., McCarley R. Abnormalities of the left temporal lobe and thought disorder in schizophrenia // The New England Journal of Medicine. 1992. Vol. 327. P. 604–612. Dr. Martha Shenton and colleagues work at Harvard Medical School.

Flaum M., Andreasen N. The reliability of distinguishing primary versus secondary negative symptoms // Comparative Psychiatry. 1995. Vol. 36.No. 6. P. 421–427. Doctors Martin Flaum and Nancy Andresen are psychiatrists at the University of Iowa Clinics.

An interview with P. McGuire is conducted by B. Bauer. Brain scans seek roots of imagined voices // Science News. 9 September 1995. P. 166. Dr. Philip McGuire is a psychiatrist from the Institute of Psychiatry in London.

Bower B. Faulty circuit may trigger schizophrenia // Science News. 14 September 1996. P. 164.

Eagles J. Are polioviruses a cause of schizophrenia? // British Journal of Psychiatry. 1992. Vol. 160. P. 598–600. Dr John Eagles is a psychiatrist at the Royal Cornhill Hospital in Aberdeen.

A study by D. Silbersweig and E. Stern is presented by K. Leutweiler. Schizophrenia revisited // Science from American. February 1996. P. 22–23. Doctors David Silbersweig and Emily Stern work at Cornell University Medical Center.

Research by P. Goldman-Rakic ​​is presented by K. Conway. A matter of memory // Psychology Today. January – February 1995. P. 11. Dr. Patricia Goldman-Rakic ​​is a neurologist at Yale University.

Juan S. Schizophrenia – an abundance of theories // The Sydney Morning Herald. 15 October 1992. P. 14.

A study by J. Megginson Hollister et al. is cited by B. Bauer. New culprit cited for schizophrenia // Science News. 3 February, 1996. P. 68. Dr. J. Megginson Hollister and colleagues are psychologists from the University of Pennsylvania.

Sciencefi c American. Making memories // Scientific American. August 1996. P. 20.

About once a year, and sometimes a little more often, another fighter against psychiatry appears on the Internet. In general, they are very stereotypical people with a standard set of claims and a complete reluctance to read any information, much less look for it, if it does not confirm the fact that psychiatry is a pseudoscience created for the personal enrichment of psychiatrists, pharmaceutical companies and the fight against dissidents. One of the main trump cards of the fighters is the fact that people with schizophrenia turn into “vegetables” and psychiatrists with haloperidol are solely to blame for this. More than once, my colleagues, both here and in my journal, have said that the process of becoming a vegetable is inherent in the disease itself. For this same reason, it is better to treat schizophrenia than to admire the amazing and unique world of a sick person.

The idea that schizophrenia is associated with changes in the brain is not new. This was written about back in the 19th century. However, at that time, the main research tool was post-mortem autopsies, and for quite a long time nothing special and distinctive from all other “brain” diseases was found in the brains of patients. But with the advent of tomography in medical practice, it was nevertheless confirmed that brain changes occur in this disorder.

It has been found that people with schizophrenia lose cortical volume. The process of cortex loss sometimes begins even before the onset of clinical symptoms. It is present even when the person is not receiving treatment for schizophrenia (antipsychotics). Over five years of illness, the patient can lose up to 25% of the volume of the cortex in some areas of the brain. The process usually begins in the parietal lobe and spreads throughout the brain. The faster the volume of the cortex decreases, the faster the emotional-volitional defect occurs. A person becomes indifferent to everything and has no desire for anything - the very thing that is called a “vegetable”.

I have a little bad news. We are constantly losing nerve cells. This is actually a natural process and it goes quite slowly, but in patients with schizophrenia this process accelerates. So, for example, normally teenagers lose 1% of the cortex per year, and with schizophrenia 5%, adult men lose 0.9% of the cortex per year, patients 3%. In general, a malignant form of schizophrenia is very common in adolescence, where in just a year you can lose everything you can, and even after the first attack this process is visible to the naked eye.

For those interested, here is a picture showing how the brain loses its cortex over the course of 5 years of illness.

In addition to a decrease in the volume of the cortex, an increase in the lateral ventricles of the brain was also found. They are enlarged not because there is a lot of water there, but because the brain structures that lie in the walls are reduced in size. And this is observed from birth.

Here are pictures of twins - the first has schizophrenia (a “hole” in the middle of the brain in the image and there are dilated lateral ventricles), the second does not have the disease.

People with schizophrenia, even before developing the disease and even before using medications, had cognitive problems, including problems with information processing and language memory. All these symptoms deepened as the disease progressed. among other things, they have a reduced (also even before the disease) function of the frontal cortex, which is responsible for criticism (i.e., correct perception of oneself, one’s actions, comparing them with the norms of society), planning and forecasting activities.

Nobody really knows for sure why this happens to the brain. There are 3 theories that have fairly strong grounds.

1. Brain development disorder. It is assumed that already in utero, something goes wrong. For example, patients with schizophrenia have some problems with substances that are very important for brain development - the same Reelin, which should regulate the process of cell movement during brain development. As a result, the cells do not reach the places where they should and form incorrect and rare connections among themselves. There are many more described mechanisms of the same type, which say that a certain congenital defect causes a disease.

2. Neurodegeneration - increased cell destruction. Here we consider cases when certain reasons, including various metabolic disorders, cause their premature death.

3. Immune theory. The newest and most promising. It is believed that this disease is the result of inflammatory processes in the brain. Why they arise is now difficult to say reliably - maybe the body arranges it on its own (an autoimmune disease) or it is the result of some kind of infection (for example, there are facts that the flu suffered by the mother during pregnancy increases the risk of developing the disease). However, patients with schizophrenia have various inflammatory substances in the brain that can be quite aggressive to surrounding cells. About similar mechanisms, but for depression
No one claims that antipsychotics are a panacea for schizophrenia. To some extent, the situation with them now is obvious: we will no longer be able to squeeze out of them any greater benefit than we have now. It is possible to improve the safety profile of a drug, but neuroleptics do not radically solve the problem. We need some new ideas and discoveries in the field of schizophrenia, a new breakthrough in understanding the disease. The latest immune theory sounds very promising. However, at the moment, antipsychotics are all we have. These medications allow patients to live in society for a long time, rather than being confined to a psychiatric hospital. Let me remind you that just less than 100 years ago, mental illness was a death sentence and treatment was limited to keeping patients in hospitals. Now only a small proportion of patients are in hospitals and it is thanks to antipsychotics that this is possible. In fact, in practice, and any psychiatrist will tell you this, it is the lack of treatment that leads to a faster transformation into a vegetable. Destruction of the brain... it is destroyed by disease even without neuroleptics, and in some people this happens very quickly.

Previously, schizophrenia was listed as dementia praecox. So, in the 17th century. T. Vallisy described cases of loss of talent in adolescence and the onset of “grumpy dullness” in adolescence. Later, in 1857, B.O. Morrel identified dementia praecox as one of the forms of “hereditary degeneration.” Then hebephrenia (a mental illness that develops during puberty), chronic psychoses with hallucinations and delusions, also ending in dementia, were described. Only in 1908, the Swiss psychiatrist E. Bleuler discovered the most significant sign of dementia praecox - a violation of unity, a splitting of the psyche. He gave the disease the name “schizophrenia,” which comes from the Greek roots “split and soul, mind.” Since that time, the term “schizophrenia” has been used to designate a group of mental disorders manifested in disorders of perception, thinking, emotions, and behavior, but most often translated as split personality. The etiology of schizophrenia is still not understood; this disease still remains one of the most mysterious and often destructive mental illnesses.

Specialists (psychiatrists, neurophysiologists, neurochemists, psychotherapists, psychologists) are tirelessly trying to understand the nature of schizophrenia, this fairly common and, alas, still incurable disease. To resist schizophrenia, it is not enough to know the symptoms and try to eliminate them; it is necessary to find out the reasons that lead to the splitting of consciousness, to establish the mechanism that causes such catastrophic mental disorders.

Clinically, schizophrenia is divided into two main types - acute and chronic. Currently, this division seems to be the most correct from the point of view of the biological basis of this disease. What characteristics characterize such varieties?

In patients with acute schizophrenia, so-called positive symptoms predominate, and in chronic patients, negative symptoms predominate. In medicine, positive symptoms are usually understood as those additional signs in patients that are absent in healthy people. A tumor, for example, from this point of view is a positive sign. The most obvious symptoms of an acute, first-time attack of schizophrenia are most often two: hallucinations - the perception of non-existent visual, sound or any other images, or, as experts say, sensory stimuli, and delusion - a false, uncorrectable belief or judgment of the patient that does not correspond real reality. These symptoms are associated with disorders that make up the cognitive, cognitive, sphere: the ability to perceive incoming information, process and respond appropriately to it. Due to delusions and hallucinations, the behavior of patients with schizophrenia seems absurd and often looks like obsession. Since the disease, as a rule, begins with these symptoms, the famous German psychiatrist K. Schneider considers them primary, specifically associated with the schizophrenic process. Negative symptoms usually appear later and already include significant emotional distortions, in particular the patient’s indifference to loved ones and to himself, impaired spontaneous speech, and general suppression of the motivational sphere (wants and needs). All this is considered as a personality defect, from which, as it were, characteristic traits for a normal person have been taken away. Patients are also characterized by a reluctance to communicate with others (autism), apathy, and an inability to assess their condition. However, these signs are already secondary, and are a consequence of primary cognitive impairment.

It is natural to assume that schizophrenic psychoses, being diseases of the brain, must be accompanied by serious anatomical, physiological or some other disorders in this organ. Such anomalies are what specialists are trying to detect in various studies. But before we talk about this, let us describe very briefly and schematically the structure of the brain.

It is known that the bodies of nerve cells, neurons, form the cortex - a layer of gray matter covering the cerebral hemispheres and the cerebellum. Clusters of neurons are present in the upper region of the trunk - in the basal ganglia (assemblies lying at the base of the cerebral hemispheres), the thalamus, or thalamus optic, subthalamic nuclei and hypothalamus. Most of the rest of the brain, lying in the brain stem below the cortex, consists of white matter - bundles of axons that stretch along the spinal cord and connect one area of ​​​​gray matter to another. The hemispheres are connected to each other by the corpus callosum.

The mentioned brain structures are “responsible” for various functions of our body: the basal ganglia coordinate the movements of body parts; thalamic nuclei switch external sensory information from receptors to the cortex; the corpus callosum carries out interhemispheric information transmission; The hypothalamus regulates endocrine and autonomic processes. Note that this structure, together with the hippocampus, anterior thalamus, and entorhinal (old) cortex, are located mainly on the inner surface of the hemispheres and form the limbic system, which “guides” our emotions and is basically similar in all mammals. It also includes the cingulate gyrus, whose anterior end is in contact with the frontal, or frontal, cortex and, according to modern views, also plays a role in the regulation of emotions. The limbic system is essentially the emotional center of the brain, with the amygdala associated with aggression and the hippocampus associated with memory.

In fundamental studies of schizophrenia, along with traditional methods, different types of tomography are now used (positron emission tomography, functional magnetic resonance, single-photon magnetic emission), and electroencephalographic mapping is carried out. These new methods make it possible to obtain “images” of a living brain, as if to penetrate inside it without damaging its structures. What was it possible to discover with the help of such a powerful arsenal of instruments?

So far, only stable changes in brain tissue have been found in the anterior parts of the limbic system (especially noticeable in the tonsils and hippocampus) and the basal ganglia. Specific deviations in these brain structures are expressed in increased growth of glia (“supporting” tissue in which neurons are located), a decrease in the number of cortical neurons in the frontal cortex and cingulate gyrus, as well as in a decrease in the size of the amygdala and hippocampus and an increase in the ventricles of the brain - cavities filled with cerebrospinal fluid. Computed tomography and post-mortem examination of the patients' brains also revealed pathological changes in the corpus callosum, and with the help of functional magnetic resonance imaging - a decrease in the volume of the left temporal lobe and an intensification of metabolism in it. It turned out that in schizophrenia, as a rule, the ratio of the mass of the hemispheres is disturbed (normally, the volume of the right hemisphere is larger, but the amount of gray matter in it is less). But, such changes can sometimes be observed in people who do not suffer from schizophrenia and be features of individual development.

There is also evidence of morphological damage to brain tissue caused by infectious, degenerative and traumatic processes. Previously, it was believed that schizophrenia is the result of atrophy of brain tissue, but now some experts, for example R. Gur, are inclined to think that the disease is caused by tissue degeneration due to abnormal development, including a violation of hemispheric specialization.

In addition to the mentioned instrumental methods, other methods are used in schizophrenia research, including biochemical and neurochemical. According to biochemical data, patients have immunological disorders, which are not identical in different psychoses, combined into the group of schizophrenic ones. Neurochemists discover molecular pathology, in particular changes in the structure of certain enzymes, and as a result of this, metabolic disorders of one of the biogenic amines, namely the neurotransmitter dopamine. True, some researchers studying neurotransmitters (substances that serve as chemical messengers at the points of contact between neurons) find no changes in the concentration of dopamine or its metabolites, while others find such disturbances.

Many experts note an increase in the number of specific receptors in the basal ganglia and limbic structures, especially in the hippocampus and amygdala.

Even a very cursory listing of disorders in the morphology and functioning of the brain in schizophrenia indicates the multiplicity of damage and indicates the heterogeneous nature of the disease. Unfortunately, all this so far brings specialists little closer to understanding its roots, much less its mechanisms. It is only clear that the patients have impaired interhemispheric transmission of information and its processing. In addition, the role of the genetic factor is undoubted, i.e. predisposition. Because of it, apparently, the frequency of familial schizophrenia is higher than in the general human population.

It is hoped that the unprecedented increase in knowledge about neurophysiological processes in the brains of patients with schizophrenia, observed in the last decade, will help to understand this mental illness.

The task of the brain is to perceive, process and transmit information by stimulating certain structures and establishing connections between them. In nerve cells, neurons, information is transmitted in the form of electrical signals, the meaning of which depends on the role that specific neurons play in the functioning of the nervous system. In sensory neurons, such a signal conveys information, for example, about a chemical acting on an area of ​​the body or the strength of light perceived by the eye. In motor neurons, electrical signals serve as commands for muscle contraction. The nature of the signals is a change in the electrical potential on the neuron membrane. A disturbance that occurs in one part of a nerve cell can be transmitted to other parts without changes. However, if the strength of the electrical stimulus exceeds a certain threshold value, an explosion of electrical activity occurs, which in the form of an excitation wave (action potential, or nerve impulse) propagates through the neuron at high speed - up to 100 m/s. But from one nerve cell to another, the electrical signal is transmitted indirectly, with the help of chemical signals - neurotransmitters.

The brain's electrical activity is its only natural language, which can be recorded in the form of an electroencephalogram (EEG). This recording reflects potential fluctuations in several frequency ranges, called rhythms or spectra. The main one is the alpha rhythm (frequency 8-13 Hz), which is believed to arise in the thalamo-cortical region of the brain and is most pronounced in a person at rest with his eyes closed. The alpha rhythm could only be considered a resting rhythm if the brain did not process information in its frequency range and compare it with what is already in memory and cognitive functions.

Oscillations with a frequency greater than 13 Hz belong to the beta rhythm, generated by the cerebral cortex and called activation, since it intensifies during vigorous activity. Theta rhythm (frequency 4-7 Hz) is largely determined by the limbic system and is associated with emotions. Oscillations whose frequency is less than 4 Hz belong to the delta rhythm and, as

As a rule, they are registered in the presence of organic brain damage - vascular, traumatic or tumor in nature.

Today, schizophrenia is one of those brain diseases that has not been studied the most, although it is studied the most. And, most likely, we should expect an even more significant breakthrough in research on schizophrenia in the near future, which will naturally affect specific results in treatment. Already now, in advanced clinics around the world, special neurometabolic methods for treating schizophrenia are successfully used, which give an amazing effect in treatment.

For example:

1. In 80% of cases, outpatient treatment is possible
2. The period of acute mental state (schizophrenic psychosis) has been significantly reduced.
3. A stable and long-lasting treatment effect is created.
4. There is virtually no decline in intelligence.
5. The so-called “neuroleptic defect” is significantly reduced or completely absent.
6. In most cases, brain function is largely restored.

People socialize and return to society, continue their studies, work successfully and have their own families.

Hallucinogenic psychoactive drugs drugs such as LSD can cause short-term episodes of psychosis, and frequent use or overdose of marijuana and stimulants (cocaine, amphetamines) sometimes leads to transient intoxication psychosis, the clinical picture of which resembles schizophrenia (Bowers, 1987; Tennent and Groesbeck, 1972).
Maybe Also(although this is by no means proven) that substance abuse can trigger the onset of schizophrenia.

Relatives Patients with schizophrenia sometimes see the cause of the disorder in hallucinogens, but they are mistaken: scientific facts do not support this opinion. It is known that in Great Britain and America in the 50-60s, LSD was used as an experimental drug in psychiatry, and the percentage of individuals (among voluntary trial participants and among patients) who developed long-term psychosis such as schizophrenia almost did not exceed the corresponding figure for general populations (Cohen, 1960; Malleson, 1971).

True, carried out in Sweden A study found that military recruits who used marijuana frequently and in large quantities were six times more likely to subsequently develop schizophrenia (Andreasson et al., 1987). However, this pattern may be explained by the fact that individuals predisposed to schizophrenia were more likely to resort to marijuana use as a way to cope with premorbid symptoms of the disease.

Brain in schizophrenia

In some patients schizophrenia organic changes are detected in the brain. Post-mortem analysis of brain tissue has revealed a number of structural abnormalities, and new imaging techniques have documented intravital changes in both the structure and functioning of the brain.

With the help of such techniques Magnetic resonance imaging (MRI) has revealed changes in the size of various brain structures, especially in the temporal lobes. The fluid-filled cavities (ventricles) in the depths of these lobes are often expanded, and the volume of tissue of the lobes themselves is reduced. The greater these observed changes, the more severe the patient's thought disorders and auditory hallucinations (Suddath et al., 1990).

Some techniques Imaging studies such as positron emission tomography (PET) can assess ongoing brain function and provide a similar picture of abnormalities. PET scans reveal increased activity in the temporal lobes, especially in the hippocampus, a structure located in the temporal lobe responsible for orientation and ultra-short-term memory (Tamminga et al., 1992).

Building a functional Images another kind - through recording of electrophysiological parameters of the brain using an electroencephalograph - shows that most patients with schizophrenia seem to have an excessively increased response to repeated external stimuli and a more limited (compared to other people) ability to eliminate unnecessary information (Freedman et al. , 1997).

Along with this, we received data that brain structures that are thought to screen out irrelevant stimuli (eg, the frontal lobe) show reduced activity in PET scans (Tamminga et al., 1992).

Due to this difficulty screening sensory stimuli, postmortem studies of brain tissue have revealed disturbances in a certain type of brain cells—inhibitory interneurons. These neurons inhibit the activity of the main nerve cells, preventing them from responding to too many input signals. In this way, they protect the brain from being overloaded with too much sensory information coming from the environment.

In the patient's brain schizophrenia the amount of “chemical messengers” or neurotransmitters (primarily gamma-aminobutyric acid (GABA)) released by these interneurons is reduced (Benes et al., 1991; Akbarian et al., 1993), which implies that the inhibitory function aimed at preventing brain overload is performed less effectively.

Deviation in the functioning of these interneurons appears to lead to changes in brain cells that release the neurotransmitter dopamine. Schizophrenia researchers have long been interested in the role of dopamine, since certain psychoactive drugs (such as amphetamines) that enhance the effects of dopamine can cause psychoses resembling schizophrenia, and psychoactive drugs that block or weaken its effects are effective in treating psychosis (Meltzer and Stahl, 1976). .

Dopamine enhances brain cell sensitivity to irritants. Typically, such heightened sensitivity is beneficial, increasing a person's level of awareness during periods of stress or danger, but for a person with schizophrenia, whose brain is already in a state of heightened activity, the additional exposure to dopamine can be a factor that pushes him into psychosis.

Of these research Data suggests that in schizophrenia, there is insufficient regulation of brain activity by interneurons, as a result of which the brain overreacts to numerous signals coming from the environment and has insufficient ability to filter out unwanted stimuli. This problem is exacerbated by the reduction in volume of the brain's temporal lobes, where sensory input is typically processed; as a result, it becomes even more difficult for a person to respond adequately to new stimuli.

The brain is a complex, but at the same time extremely important organ of the human body. Possible pathologies occurring in its structures manifest themselves through various neurological disorders, often due to serious brain diseases, a person becomes disabled for the rest of his life or dies, because negative processes are usually irreversible.

Many scientists are now saying that the emergence of new technologies represents a new era in medicine, because, in fact, a number of successful operations have already taken place to transplant artificial organs into humans. It is not yet possible to recreate the brain artificially, taking into account the developments of mankind - its structure is too difficult even for experienced scientific experts. Therefore, it is very important to maintain healthy brain cells and tissues; this can be the key to good health and longevity, because many processes occurring in the body are controlled and controlled by the central nervous system, which is headed by the brain.

Today, medicine has identified many dangers that can affect the brain. Among them:

Each of these dangers to the brain arises due to a specific set of causes and risk factors, but it is often impossible to predict the disease, because it may be caused by a hereditary predisposition or a malfunction of genes, in other words, gene mutations.

Considering that the brain is at the center of all endocrine processes, the processes of the sense organs carrying out their activities, the activity of the musculoskeletal system, heartbeat and blood flow, it is not difficult to predict the fact that a disease of the nervous system negatively affects the general condition of the body, and not only the physiological , but also moral and emotional.

Types of disease

Organic brain lesions are usually easily identified through certain procedures, for example, magnetic resonance or computed tomography, neuroimaging, electroencephalography. Their peculiarity lies in visible damage to certain areas of the brain; damage to the frontal lobe and temporal regions is very often observed. Organic lesions include both foreign bodies present in the structure of the brain and problems with blood vessels and the general state of blood circulation.

So, medicine identifies several types of organic lesions of the central nervous system and brain:

1. vascular lesions - most often occur in diseases such as atherosclerosis, Alzheimer's disease, cardiovascular diseases localized in other areas of the body, and spinal osteochondrosis. In many cases, brain damage is caused by squeezing or damage to blood vessels, disturbances in the speed and rhythm of blood circulation, and a state of hypoxia—oxygen starvation of the brain;
2. intoxication with chemicals, narcotic substances, alcoholic beverages. In case of poisoning, individual brain tissues and cells localized in a certain area are affected. The affected area may increase in size, very often poisoning leads to rapid dementia and other pathologies of the nervous system, as evidenced by external signs of neurological disorders of the body;
3. foreign bodies are malignant or benign tumors that can increase in size, which contributes to damage to brain tissue and compression of blood vessels.

Thus, all types of organic brain lesions are closely intertwined with each other - one type may in the future cause other signs of damage and damage. That is why doctors recommend regular observation in the clinic, since a disease detected at an early stage, of course, provides a huge chance of salvation.

Separately, medicine distinguishes residual organic damage to the brain and central nervous system, which incorporates the symptoms and causes of all three of the above types.

The main feature of residual organic brain damage is that it is residual in nature after structural damage to brain and nerve tissue. Such a lesion is mainly characteristic of newly born babies, and they are at risk until the seventh day after birth. It's all about the pathological intrauterine processes that occurred during the perinatal period. This happens as follows: at the stage of fetal development, for some reason, a certain local area of ​​the brain is affected, which after the birth of the child leads to neurological disorders and other pathologies.

You need to know that even the smallest area of ​​damage can provoke various bodily anomalies in all internal systems. That is why the term residual organic brain damage is not used by doctors as the name of the disease. This concept is extremely general, which includes a lot of possible pathologies, dangerous symptoms and their development.

Despite the fact that more often newborn children suffer from residual organic damage to the central nervous system and brain, nevertheless, there is a possibility of such damage in adults, arising due to local lesions - for example, damage to the frontal lobes of the brain or damage to the white matter of the brain or due to poisoning, viral diseases, inflammatory processes.

The symptoms of residual organic damage in both adults and children depend on the degree of damage to areas of the brain, because each element in this organ is responsible for a certain set of body functions; accordingly, the more areas affected in the process of damage, the more clearly various dangerous signs will manifest themselves .

Reasons for origin

Medicine identifies four types of perinatal pathologies that increase the risk for the child due to the possible appearance of residual organic damage to the brain and central nervous system, which can manifest itself immediately after birth. These include:

So, the traumatic nature of perinatal pathology is caused by falls of a pregnant woman, blows to the abdominal area. Thus, the child may experience congenital brain injuries associated with mechanical impact. Therefore, expectant mothers are advised to be careful when moving, to stay at home in bad weather, especially when it’s icy, and to eliminate as much as possible all the risks of external influences on the child.

Hypoxic damage can be caused by certain pathologies of the mother or her bad habits, in particular, smoking and drinking alcohol. At the same time, the child in the womb experiences oxygen deficiency, and even a short-term state of hypoxia can cause irreversible damage to the structures of the brain, since both the nervous system and the brain of the fetus are still only at the stage of their formation.

The dismetabolic nature of residual organic brain damage is a consequence of a malfunction in the endocrine system in the body of the expectant mother. Metabolic disorders are directly related to hypoxia - the fetus, even at the development stage, begins to receive less nutrients, which negatively affects the state of the brain.

Finally, the viral or infectious nature of the lesion is nothing more than existing or severely suffered in the past infections and viruses of the expectant mother. This also includes intrauterine infections that enter through the woman’s vagina and directly affect the child’s body in the perinatal period.

Medical experts include the following parameters as risk factors that can cause residual organic damage to the central nervous system and brain:

4. malfunction of genes, gene mutations;
5. hereditary predisposition;
6. influence of environmental quality. This includes possible air pollution with chemicals and toxins, radiation exposure above the norm, harmful emissions from cars, reduced levels of oxygen in the air, in general terms, poor and ruined ecology;
7. toxic and chemical intoxication with vapors, gases, alcohol, drugs, other compounds, including certain medications;
8. pregnancy pathologies, for example, too early birth, umbilical cord abnormalities, bleeding;
9. infections and viruses that occurred during pregnancy or in the past;
10. weakened immunity of women;
11. unbalanced poor nutrition, lack of proteins, vitamins of all groups, minerals (calcium, potassium, magnesium), fiber. At the stage of pregnancy, any diets are prohibited; nutrition must be standardized, not necessarily regimented, the main thing is that the expectant mother gets all the substances she needs into her body. After all, you need to remember that by eating, the mother is already feeding not only herself, but also her baby;
12. pathologies of the birth process itself - either rapid or too prolonged labor;
13. chronic maternal diseases, mostly associated with damage to the nervous system, endocrine processes, cardiovascular diseases;
14. frequent stress during pregnancy, mental and emotional instability of the expectant mother.

As already mentioned, in children the symptoms of residual organic damage are observed immediately after birth, in some less pronounced, in others more, but this does not change the essence. Based on the baby’s behavior, the doctor may immediately suspect certain neurological problems, for example, tremors of the limbs, constant crying and restlessness, delay in certain movements, unhealthy facial expressions, tone disorders.

In adult patients, symptoms appear in the same order, only at a different level, that is, more vividly.

If the doctor suspects possible neurological problems in the baby, he can immediately send the mother and newborn for a neuroimaging procedure, neurosonography, or, in extreme cases, an MRI of the brain.

So, the clinical picture of residual organic damage to the brain and central nervous system consists of the following symptoms:

15. external mental disorders - fatigue, moodiness, constant crying, anxiety, restlessness;
16. rather rapid exhaustion of the body, this is visible not only through the baby’s food intake, but also by his weight - instead of gaining weight, some newborns stop in their development;
17. mental instability, unhealthy behavior towards oneself and others - applies not only to children, but also to adults. A person may begin to hurt himself, and he also behaves inappropriately towards those close to him, turning against them in a very aggressive way;
18. absent-mindedness, significant impairment of attention, lack of perseverance, sometimes increased activity of the limbs;
19. apathy, indifference to everything that happens;
20. encephalopathy;
21. headaches and dizziness - especially if the frontal lobe of the brain is affected;
22. disorders in the mental and emotional sphere - stress, irritability;
23. insomnia, increased excitability even at night;
24. disruption of the visual and auditory organs - in particular, with damage to the brain stem;
25. impaired coordination of movements - with disorders in the cerebellum.

Organic lesions are easy to detect using technological procedures such as magnetic resonance imaging, electroencephalography, and neurosonography. The affected areas are usually visible on the images; as a result, the doctor, having noticed the affected area, will base his prognosis on what this local area is responsible for. For example, when the brain stem is damaged, some functions suffer, while when the cerebral cortex is damaged, others suffer.

It is important to understand that the effectiveness of a person’s treatment depends on the quality of diagnosis.

Treatment of organic brain damage involves a long process, so the relatives of a sick adult or child need to devote more time to him, caring for him, and, if possible, tolerate his antics and negative mental states.

With timely detection of the lesion and proper therapy, the prognosis gradually improves.

If we talk about drug treatment, then you need to take sedatives, nootropics and vitamins.

Also, physiotherapy, therapeutic baths, and massages should not be neglected.

Clinical and diagnostic symptoms and signs of schizophrenia

What is schizophrenia, what are the symptoms and treatment of this pathology, can it be inherited?

Definition of schizophrenia. This is a chronic mental disorder, which is accompanied by a violation of the cognitive and personal spheres of a person. This pathology is equally common in both men and women. However, signs and symptoms of schizophrenia appear earlier in men (18–25 years) than in women (25–30 years). To find out whether schizophrenia is treatable, you need to become familiar with the signs of pathology and study the causes of schizophrenia.

Etiology of the disease

What are the causes of the development of schizophrenia today is not known exactly. However, experts in the field of psychiatry argue that the etiology of this disease is heterogeneous. There are both endogenous and exogenous causes of schizophrenia.

Many people wonder whether schizophrenia is inherited or not. Long-term research in this area has revealed a direct connection between schizophrenia and heredity. So, if there are close relatives with schizophrenia, then the likelihood of developing this pathology increases significantly. However, there are many patients whose family history is not burdened. This indicates that the causes of schizophrenia are varied. But whether schizophrenia is inherited, this question can be answered in the affirmative, but there must be other etiological factors that provoke an impetus in the development of the disease.

Etiological factors contributing to the onset of schizophrenia:

26. Viral infections that affect brain tissue (meningitis, encephalitis).
27. Infectious diseases suffered by the mother during pregnancy. They can lead to organic changes in the brain, which over time manifest themselves with characteristic symptoms.
28. Seasonality. People born in the spring months get sick more often.
29. Location. The incidence is higher in urban residents than in people living in rural areas.
30. Low level of material wealth, that is, poverty.
31. Antisocial family lifestyle. In this case, the child’s psyche is subjected to a severe test, and if there is a hereditary predisposition, then the possibility of developing the disease schizophrenia increases sharply.
32. Mental trauma inflicted in childhood. Signs of the disease are found in people who were subjected to physical, sexual and mental abuse in childhood.
33. Lack of upbringing, neglect of the child, lack of proper support and mutual understanding on the part of parents.
34. The presence of various types of addictions: alcohol, drugs, toxic (substance abuse).
35. Structural abnormalities and underdevelopment of the brain. They can be the cause of the pathology or its consequence.

Stages of development of the pathological process

What is schizophrenia and how is it treated? The disorder progresses over a long period of time and goes through a number of stages. Depending on the stage of development at which the disease is located, appropriate treatment for schizophrenia is carried out.

Having studied the course of the disease, specialists in the field of psychiatry identified four main stages of the pathological process:

36. the primordial stage is characterized by initial pathological changes in the personal sphere of the human psyche; previously unusual traits such as suspicion, inappropriate behavior, and wariness are observed;
37. prodromal stage, during this period the first obvious syndromes of schizophrenia are determined: alienation and isolation from all kinds of contacts with loved ones and surrounding people, absent-mindedness, inability to perform usual work and household chores;
38. the stage of the first mental episodes is characterized by the presence of delusions, hallucinations of various types and obsessions;
39. remission, at this stage the patient has no pathological symptoms. The duration of remission varies, from several weeks to several years.

Classification of the disease

There are several classifications of this mental disorder. They differ in the characteristic taken as a basis. Types of schizophrenia based on clinical symptoms:

40. Paranoid form of the disease. Hallucinations and delusions are observed, but disturbances in thinking and behavior in schizophrenia are not detected.
41. Catatonic schizophrenia is characterized by psychomotor disorders.
42. Disorganized (heberphrenic) type of schizophrenia. Emotional and mental disorders are noted.
43. Residual schizophrenia is characterized by the presence of positive symptoms that are not brightly colored.
44. Undifferentiated – the clinical picture does not fit into the above listed types of disease.

Types of schizophrenia identified by psychiatrists based on the course of the pathological process:

45. paroxysmal-progressive;
46. periodic (recurrent);
47. continuously flowing;
48. sluggish.

In the international classification of diseases, there are two types of schizophrenia:

49. Simple schizophrenia. A gradual increase in pathological symptoms, acute psychoses are not observed in this case.
50. Post-schizophrenic depression. This condition occurs after an exacerbation of the disease. There are residual pathological symptoms and a persistent decrease in the emotional sphere.

All these classifications help prescribe correct and effective treatment for schizophrenia.

To answer the question of how to recognize schizophrenia, you need to know its manifestations. There is a severe disturbance of thinking in schizophrenia, which is manifested by various symptoms. In this case, it is necessary to distinguish between concepts such as “signs” and “symptoms”. There are four signs that are scientifically called “Bleuler’s tetralogy.” They characterize disorders of areas of brain activity.

1. Autism is manifested by alienation and immersion of a person in his inner world. How to recognize a schizophrenic in this case? His actions are constrained, somewhat awkward, and his thinking is stereotypical. Communication with other people does not work out; the sick person lacks a sense of humor. All jokes addressed to him are perceived as truth, which is why he withdraws even more into himself and avoids people.

2. Alogia (associative defect). In this case, the person experiences impoverished speech and an inability to think logically. The patient is unable to have a constructive conversation. His answers are monosyllabic and require constant clarification. There is a “slipping”, that is, a sudden transition from one topic to another.

3. Ambivalence is characterized by a schizophrenic’s dual attitude towards any object, person, and so on. For example, he may like daisies, and at the same time he begins to hate them. It is customary to distinguish three types of ambivalence:

51. strong-willed – indecision when making any decision;
52. emotional – inconsistency of feelings towards events, things, people, and so on;
53. intellectual – ideas and solutions that are opposite in nature.

4. Affective inadequacy - an abnormal response to everything that happens. If any tragedy occurs in the family, the sick person reacts to it joyfully. But in fact, his internal feelings and external manifestations do not coincide. He also worries, but expresses it with opposite emotions.

Having become familiar with these signs, a person knows how to recognize a schizophrenic. But you also need to remember about the symptoms, which will also help answer the question of how to recognize the presence of schizophrenia.

Symptoms of the disease

What is schizophrenia and what manifestations does it have? In the development of this pathology, it is customary to distinguish several types of symptoms. They help to understand who schizophrenics are.

1. Positive symptoms. In this case, symptoms that were previously not characteristic of this person are considered. This is something new, but far from positive:

54. Rave. This condition is common to all people suffering from this pathology. There are several types of this positive symptom: delusions of persecution, influence, persuasion, unreasonable jealousy, delusional ideas. In this case, a person is divorced from reality. He comes up with something and sincerely believes in it. It seems to him that he is under constant surveillance or that he suspects his spouse of infidelity, although there is no reason for this.
55. Hallucinations. The following types of hallucinations are distinguished: visual, auditory, tactile, sound and olfactory. The most common auditory form of this pathological symptom. A person hears voices that can be intrusive or even aggressive.
56. Inappropriate behavior. The patient may laugh loudly or talk when it is inappropriate (this is called hebephrenia - a type of inappropriate behavior), show aggression or, conversely, tender feelings in inappropriate situations.
57. Illusion. Surrounding objects are perceived incorrectly. Instead of one, another object appears.
58. Catatonia is another manifestation of inappropriate behavior. In this case, the schizophrenic may take various uncomfortable and unnatural poses or, conversely, continuously and randomly swing various parts of the body.
59. Obsession. A person constantly thinks about her, these thoughts do not give him peace day or night.
60. Impaired thinking and speech function. Confused or incoherent speech, illogical and inappropriate statements.

2. Negative symptoms. This term refers to qualities lost due to illness. Manifestations characteristic of negative symptoms:

61. autism;
62. poverty of emotions and their manifestations;
63. inability to find the right solution in the current situation;
64. mood swings that occur with enviable frequency;
65. passivity in behavior and actions;
66. disorders of speech, thinking and attention;
67. apathy;
68. decrease in volitional manifestations;
69. cruelty or indifference towards others;
70. selfish behavior;
71. motor activity decreases sharply;
72. lack of initiative;
73. no satisfaction with what is happening, loss of interest in one’s own life due to its dissatisfaction;
74. the patient cannot control his actions, thoughts and behavior in general;
75. the person is unable to carry on a conversation;
76. the sequence of habitual actions is disrupted.

First manifestations of the disease

The first signs of schizophrenia may be mild, which is why family and friends are not immediately able to recognize the onset of the disease:

77. It is difficult for a person to concentrate on an object or perform any action.
78. Habitual manipulations are not performed, since they make no sense for the patient. Refusal of hygiene procedures: a person does not change clothes, does not take off shoes when coming home, and so on.
79. Loss of interest in activities and hobbies.
80. Emotional poverty.
81. Speech dysfunction.
82. Excessive suspicion.

Early or initial signs are few in number, they can be confused with nervous disorders due to severe stress, depression and nervous exhaustion. However, over time, these symptoms become more noticeable and other pathological signs appear.

Features of delusions and hallucinations

How to determine schizophrenia in a loved one? Relatives may suspect the presence of the disease if the main symptoms of schizophrenia (delusions and hallucinations) are present. But you need to know how they manifest themselves and what you should pay attention to.

Patients most often experience auditory and visual hallucinations. What are their manifestations?

83. Reasonless laughter. The patient suddenly begins to laugh.
84. The patient has a detached look, as if his mind is somewhere far away. He gets distracted while talking.
85. Suddenly begins to listen to something or abruptly interrupts the conversation and withdraws into himself.
86. Talks to himself, it looks like answers or dialogue, a story.
87. By a person's appearance it is noticeable that he sees or hears something.

Delirium is also one of the early signs. It is characterized by the following features:

88. Excessive suspicion. A person begins to complain about relatives, neighbors and acquaintances. He accuses them of stalking, cruel treatment and attempt on life and limb.
89. Strange actions are observed: locking the room, curtaining the windows during the day, turning off the lights at night, and so on.
90. The patient does not eat food prepared by another person and checks the food.
91. He talks about fear for his health and the health of those around him.
92. Fear and panic.
93. Spying on a spouse, speaking out about his infidelity.

All of the above symptoms are characteristic of the schizophrenic personality type of a sick person.

Diagnostic measures

How to diagnose schizophrenia? If you suspect that a loved one has this pathology, you should seek help from a psychiatrist. Diagnosis of schizophrenia is carried out on the basis of identifying pathological signs and symptoms of the disease. This requires long-term monitoring of the patient by both relatives and medical workers. It is important to determine the type of schizophrenia in order to select the correct treatment for schizophrenia.

The diagnosis of paranoid schizophrenia is made if general and characteristic symptoms are observed:

The diagnosis of catatonic schizophrenia is made when the following symptoms are present:

94. Increased physical activity.
95. Stupor.
96. Resistance to words and actions (negativism).
97. Automation of actions. The patient follows instructions coming from outside.
98. Waxy flexibility. If you give a person a certain pose, he will remain in it.
99. If a person is frozen in a certain position, then it is impossible to change it (rigidity).
100. Changes in a person’s socialization: refusal to communicate, neglect of hygiene and care procedures.
101. Work, school and other activities become less productive.
102. Increasing apathy, loss of interest in what is happening.
103. Speech becomes poor.
104. Activity decreases, obvious passivity appears.

Schizophrenia is said to occur when symptoms have been observed in a patient for a long time. Heredity is taken into account, since pathology can be transmitted from parents to a child. Also, schizophrenia is diagnosed using psychological tests, which are carried out and interpreted by the attending psychiatrist. After the diagnosis is made, the question of how to cure schizophrenia is decided.

Can schizophrenia be cured? This question is often asked by relatives. The answer to the question of whether schizophrenia is curable is negative. It is possible to achieve stable remission when there are no pathological manifestations. However, it is impossible to say that schizophrenia is completely curable. Even remission of several years can, in the presence of favorable factors, move into the active phase of the disease.

How to treat schizophrenia? Treatment of schizophrenia is aimed at getting rid of symptoms and achieving long-term and stable remission. The following types of treatment for schizophrenia are distinguished:

Social therapy is based on psychotherapy and social rehabilitation of the patient. This is a long-term work that can continue during the period of remission.

Biological treatments for schizophrenia:

105. Drug treatment.
106. Insulin comatose therapy.
107. Electroconvulsive therapy.
108. Phototherapy.
109. Sleep deprivation.
110. Detoxification of the body.
111. Diet-fasting therapy.
112. Psychosurgery.

Drug therapy is of particular importance. It helps to get rid of hallucinations, delusional and catatonic manifestations, and psychomotor agitation. This is how the pathology was treated before.

Medicines used in the treatment of schizophrenia:

In what cases is schizophrenia treated in a hospital?

113. Aggression towards oneself and others.
114. If the patient does not eat, with weight loss of more than 20%.
115. Nervous and motor excitement.
116. The presence of hallucinations that are threatening, commanding in nature.
117. Suicidal tendencies and behavior.
118. The patient refuses treatment, he does not recognize himself as sick.

Cases when a patient is hospitalized without his consent:

119. if the patient poses a danger to others and himself;
120. if a person is unable to provide personal care and meet the needs of life;
121. a severe disorder that can lead to deterioration of health.

During the period of remission, maintenance treatment for schizophrenia is necessary. This is important to prevent the condition from getting worse. Medicines prescribed by a doctor must be taken constantly. Otherwise, the symptoms of the disease will return.

How to remove the diagnosis of schizophrenia? This disease is chronic and incurable, so such a procedure is practically impossible. But if the patient or his legal representative insists, then a serious psychological examination should be undertaken.

Hematoma and brain contusion: why is it dangerous?

An intracranial hematoma can be caused by a brain contusion. This is a serious disease that threatens human health and even life! A brain hematoma can form even due to a minor blow to the head. Medium and large areas of hemorrhage are treated with surgical intervention during surgery. Why is a bruise of the soft tissues of the head dangerous?

How does a brain bruise and hematoma occur? ^

The brain is protected by a liquid consistency that surrounds it and prevents it from being injured by the inner walls of the skull. With a strong push, the liquid does not cope with this task and then the tissue is sharply shaken and, with pressure, comes into contact with the inner shell of the skull. The result is a brain contusion or traumatic brain injury.

Brain contusion occurs in parallel with vascular damage and, as a result, a hematoma is formed. It is dangerous because its placement causes compression of the brain.

To remove hemorrhage, a surgical treatment method such as craniotomy is most often used. A small hematoma is treated with medication.

A brain contusion is almost impossible to visually recognize. A person begins to feel the first signs immediately after the injury or after some time. The stronger the brain contusion, the higher the area of ​​damage and the force of pressure on the meninges.

Traumatic brain injury. What symptoms characterize a brain injury?

122. pain in the head, namely where the blow was;
123. nausea, vomiting;
124. hematoma on the head
125. lump at the site of impact;
126. dizziness, memory loss;
127. sluggish, confused speech;
128. short-term loss of consciousness;
129. drowsiness, apathy;
130. darkening before the eyes, the presence of “spots” or dark circles;
131. the circumference of the diameter of the pupils of both eyes of different sizes;
132. impaired pain sensitivity of the limbs on the affected side.

If a large hematoma occurs due to compression of the brain, then there is a risk of observing dangerous signs:

A brain hematoma occurs due to severe head trauma. Traumatic brain injury very often occurs in a car accident, a fall, in athletes during training, in children under 3 years old, when they walk unsteadily and like to experiment. In older people, due to age, there is a lack of intracranial fluid, so even a minor head injury can cause a fracture of the base of the skull. Traumatic brain injury is characterized by the fact that it can preserve the integrity of the outer integument, that is, there is no bump or bruise.

It can also be noted about the risk group of newborn children. In a small child at birth, the skull bones do not have a full structure that can protect the brain from damage. Thus, during a prolonged labor period, there is a huge risk of rupture of blood vessels in the head and, as a result, traumatic brain injury.

Depending on the location and severity of the pathology, head contusion and hematoma are divided into three groups:

Let's look at each of them.

Subdural hematoma^

It is considered the most dangerous and requires immediate diagnosis and treatment! It occurs due to rupture of the veins that pass at the border of the brain and the dura mater. The resulting bleeding forms a subdural hematoma, which is dangerous because it can compress important areas of the brain. If treatment is not started promptly with medications or surgery, a decline in the conscious state may occur, which often leads to biological death.

There are three types of subdural hemorrhage:

133. Progressive. The most dangerous, as it develops rapidly immediately after a brain contusion occurs. Its signs appear immediately, so they are difficult to hide. If at least one symptom is present, immediate treatment is required.
134. Subacute. Symptoms develop 2-3 hours after injury.
135. Prolonged flow. Occurs after a blow in which hemorrhage slightly compresses the brain. There may be no symptoms of a hematoma at first, and the victim may not even be aware that there is a problem. The first “bells” appear after a couple of days, weeks and, less often, months.

The protracted chronic course of the pathology carries a hidden danger. After an injury, a person usually feels well and leads a standard life, despite the compression of the brain. But one day, a headache, muscle weakness in the limbs (especially on the injured side), slurred speech, clouding of consciousness and convulsions begin to develop. Clinically, this resembles signs of a lesion in the brain. Very often, a subdural hematoma is mistaken for an ordinary stroke, since the symptoms are very similar to each other. At the same time, patients may not even associate the deterioration in well-being with a condition such as a traumatic brain injury or brain contusion that occurred several days or weeks ago. The final diagnosis is made by deciphering the results of computed tomography or magnetic resonance imaging. Subdural hematoma of the brain (chronic) develops mainly in people of retirement age.

Traumatic brain injury, whatever it may be, requires immediate treatment, otherwise compression of the brain and irreversible processes in the organ of the central nervous system may develop. A head injury often has serious consequences.

The degree of formation and extent of lesions can be influenced by blood clotting and fragility of blood vessels. Thus, with the systematic use of aspirin, anticoagulants or alcohol, there is a risk of getting a serious problem that can cause compression of the brain.

Epidural hemorrhage^

An epidural hematoma develops due to a rupture of the artery that passes between the skull and the dura mater of the brain. The blood mass, which automatically enters the resulting space, causes compression of the soft tissues.

An epidural hematoma often leads to serious consequences and threatens the life of the victim. Hematoma formation most often occurs in the temporal and parietal lobes.

Epidural hematoma has an acute development. Subacute and protracted stages occur less frequently and most often in older people.

An epidural hematoma has the following symptoms:

136. Availability of “transparent” time. After a head injury occurs, the victim may temporarily lose consciousness, and then, as if nothing had happened, get back to his feet and feel fine. However, after some time (from 10 minutes to several hours and even days), a sharp pain in the head, nausea, and muscle weakness appears. This may signal that the “transparent” gap is coming to an end;
137. On the side where there is a traumatic brain injury, there is a significant enlargement of the pupil and drooping of the lower eyelid;
138. Part of the healthy hemisphere also exhibits certain malfunctions, which signal a pathological condition. Thus, pyramidal insufficiency syndrome is noted - increased tendon reflexes, pathological Babinski syndrome, general muscle weakness.

As already mentioned, these symptoms develop due to compression of the soft tissues of the brain by the hematoma. The compression occurs in the area where the traumatic brain injury occurred, while the rest of the brain is subject to displacement. Next, there is an increase in intracranial pressure, which causes psychomotor agitation, then inhibition and the development of a coma. Before the onset of serious consequences, the patient experiences severe and constant headache, nausea, vomiting, and deterioration of coordination. With increasing compression of the cerebral column, areas of the brain important for human life can be damaged. This means that an epidural hematoma in some cases causes difficulty breathing, arrhythmia with short-term cardiac arrest, which can be fatal.

An internal hematoma is a hemorrhage inside the head, which often affects the temporal and frontal parts, sometimes the parietal part. The accumulation of blood is observed in the brain tissue and has a spherical appearance.

External symptoms of internal hemorrhage:

• deterioration in speech production and understanding;
• paresis of arms and legs;
• asymmetry of the front part;
• loss of sensitivity in a certain area of ​​the body, a lump in the head area;
• psychical deviations;
• impairment of motor ability.

From the side of the eyes, twitching or floating of the eyeballs and squint may occur. In some cases, there are disruptions in respiratory and cardiac function, increased body temperature, and a fracture of the base of the skull.

Correct and effective treatment depends on diagnosis, which begins with collecting an anamnesis: complaints are taken into account, it is found out what period of time has passed since the injury, when there was a brain injury and whether there was a “bright” period. However, in order to make an accurate diagnosis, they resort to more informative research methods:

The data obtained is carefully studied to determine the type of hemorrhage. Thanks to this, the doctor has information about the location of the hematoma, its size, and also finds out whether there was a fracture of the base of the skull. At this stage, the question of the need for surgery is decided.

Treatment depends entirely on the type of hematoma and its complexity and can be medicinal or by removing the area through surgery (craniotomy).

Let's look at each of them.

Drug therapy^

A conservative treatment method is indicated in the presence of a small lesion that does not grow. Patients require careful medical monitoring, since the disease may progress at any time and there will be an urgent need for surgery.

First, intracerebral bleeding is stopped, and then resorption therapy is performed. Diuretics are also recommended to help reduce intracranial pressure.

If drug treatment does not help to cope with the symptoms and there is a deterioration in the patient’s condition, then a decision is made on surgical intervention (craniotomy and removal of the hematoma).

Surgical intervention ^

Craniotomy is indicated for those victims who need to remove a medium or large hematoma. A fracture of the base of the skull is also a direct indication for surgery. Very often, surgical intervention occurs as an emergency, when the health and life of the patient depends on every split second.

Craniotomy is far from the only surgical solution. Sometimes the hematoma is removed using the endoscopic method.

The prognosis of surgical therapy depends entirely on the speed of delivery of the victim to a medical facility. Thus, prolonged compression of the brain can cause an irreversible reaction, in which even craniotomy will not give a good result.

What happens when cerebral vessels narrow, symptoms and treatment of pathology

From this article you will learn: what is called cerebral vasoconstriction, treatment, symptoms, causes of the disease. The mechanism of development of pathology and diagnostic methods. Prognosis for recovery.

Pathological stenosis (narrowing) of the capillaries, veins and arteries supplying blood to the brain is called cerebral vasoconstriction.

What happens during pathology? Under the influence of atherosclerosis (formation of cholesterol plaque, 60%), arterial hypertension (up to 30%) and other pathologies (developmental defects, osteochondrosis), the lumen of the blood vessels providing blood supply to the brain narrows. The amount of blood required for the organ to function properly is reduced; disturbances lead to tissue ischemia (oxygen starvation), changes in the structure of cells, and subsequently to their mass death (the appearance of foci of necrosis).

Changed or dead nerve cells of the brain are not able to perform their functions (conducting bioelectric impulses), so vasoconstriction is manifested by numerous neurological symptoms (headaches, dizziness, insomnia).

The pathology develops slowly and is almost asymptomatic in the initial stages. If the cause of stenosis is eliminated at this moment, the disease can be cured, completely restoring brain function (92%).

The pathology becomes dangerous at stages when the narrowing of the vessel increases by more than 50%. The patient develops serious disorders of brain activity (decreased ability to perceive and analyze information, behavioral disorders, dementia, impaired coordination of movements). They are joined by hypertensive crises and strokes (acute cerebrovascular accidents), which quickly lead to a complete loss of physical and mental disability.

The causes of narrowing of cerebral vessels in the early stages are treated by a general practitioner; in case of severe neurological symptoms, a neurologist or psychiatrist is involved; surgical correction is carried out by angiosurgeons.

The mechanism of pathology development

The most common causes of cerebral vasoconstriction are atherosclerosis and hypertension:

1. With atherosclerosis, the amount of “bad” cholesterol in the patient’s blood increases; in the wall of the vessel, a cholesterol plaque is formed from it and specific plasma proteins (fibrin), which gradually grows, increases in size and over time is able to completely block the lumen of the vessel and blood flow.
2. In hypertension, small vessels and capillaries are the first to suffer. Under the influence of blood flow pressure on the walls, a mechanism of protection against ruptures and damage is triggered - first there is an increase in tone and narrowing of the capillaries and arterioles, over time their walls thicken, building up layers inward, into the lumen of the vessel, and reduce the volume of blood flow.

As a result of stenosis, chronic ischemic (oxygen) starvation develops, which leads to changes in the structure of brain tissue in the subcortex (centers of speech, thinking, hearing, memory, movement) and white matter (“bridge” connecting the departments):

• foci of non-functioning cells are small (“silent”, asymptomatic infarction);
• very tiny, but numerous, form small “gaps”, almost imperceptible defects (sparse tissue).

The connections between these parts of the brain are interrupted (“disconnection”) and provoke a group of multiple disorders – impairments of memory, speech, motor activity, mental abnormalities in behavior, dementia, the ability to analyze and draw conclusions.

Causes and risk factors

The main, but not the only, cause of stenosis is the formation of cholesterol plaques during atherosclerosis (60%).

Schizophrenia - description, causes, symptoms (signs), diagnosis, treatment.

Schizophrenia is a mental illness of a continuous or paroxysmal course, begins mainly at a young age, is accompanied by characteristic personality changes (autization, emotional and volitional disorders, inappropriate behavior), thought disorders and various psychotic manifestations. Frequency- 0.5% of the population. 50% of beds in psychiatric hospitals are occupied by patients with schizophrenia.

Code according to the international classification of diseases ICD-10:

• F20 Schizophrenia

Genetic aspects. A priori, polygenic inheritance seems most likely. Non-scientific application of a broader definition of schizophrenia leads to an increase in population frequency estimates to 3%. The existence of several loci that contribute to the development of schizophrenia has been proven or suggested (SCZD1, 181510, 5q11.2-q13.3; amyloid b A4 precursor protein, AAA, CVAP, AD1, 104760, 21q21.3-q22.05; DRD3 , 126451, 3q13.3; SCZD3, 600511, 6p23; SCZD4, 600850, 22q11‑q13; EMX2, 600035, 10q26.1.

Clinical manifestations of schizophrenia are polymorphic. Various combinations of symptoms and syndromes are observed.

Negative symptoms. In psychiatry, the term “negative” means the absence of certain manifestations inherent in a healthy person, i.e. loss or distortion of mental functions (for example, impoverishment of emotional reactions). Negative symptoms are decisive in diagnosis.

Thinking disorders. Patients with schizophrenia rarely have only one type of impaired thinking; Usually a combination of different types of thinking disorder is noted. Diversity. Minor features of everyday things seem more significant than the object as a whole or the general situation. Manifested by ambiguity, vagueness, and thoroughness of speech.. Discontinuity. There is no semantic connection between concepts while the grammatical structure of speech is preserved. Speech loses its communication properties, ceases to be a means of communication between people, retaining only its external form. Characterized by a gradual or sudden deviation in the thought process towards random associations, a tendency towards symbolic thinking, characterized by the coexistence of the direct and figurative meaning of concepts. There are sudden and incomprehensible transitions from one topic to another, a comparison of the incomparable. In extreme cases, speech is devoid of semantic meaning and is inaccessible to understanding if it is constructed outwardly correctly. In severe cases of disrupted thinking, the patient spews out a sequence of completely unrelated words, and pronounces them as one sentence (verbal okroshka).. Sperrung (blockage of thinking) - an unexpected break in the train of thought or a long delay in the thought process, loss of the thread of conversation. The disorder occurs with clear consciousness, which is different from absence seizure. The patient begins a thought or response and suddenly stops, often in the middle of a sentence. .. Reasoning is thinking with a predominance of florid, unsubstantial, empty and fruitless reasoning, devoid of cognitive meaning.. Neologisms are new words invented by the patient, often by combining syllables taken from different words; the meaning of neologisms is understandable only to the patient himself (for example, the neologism “tabushka” is created from the words “stool” and “cabinet”). To the listener they sound like absolute nonsense, but to the speaker these neologisms are a kind of reaction to the inability to find the right words.

Emotional disorders.. Emotional disorders in schizophrenia are manifested primarily by the extinction of emotional reactions, emotional coldness. Due to decreased emotionality, patients lose their sense of affection and compassion for loved ones. Patients become unable to express any emotions. This makes it difficult to communicate with patients, causing them to withdraw even more into themselves. Patients in the later stages of schizophrenia do not have strong emotions; if they appear, one should doubt whether the diagnosis of schizophrenia was correctly made. Emotional coldness manifests itself first and to the greatest extent in feelings towards parents (usually the patient responds to the care of parents with irritation; the warmer the attitude of the parents, the more obvious the patient’s hostility towards them). As the disease progresses, such dulling or atrophy of emotions becomes more and more noticeable: patients become indifferent and indifferent to their surroundings. However, it should be argued that a patient with schizophrenia, who looks like he does not experience any emotions, actually does not experience them, should be with great caution. People with schizophrenia exhibit both positive and negative emotions, although not as strongly as healthy people. Some people with schizophrenia, who seem to experience no emotions, actually live a rich emotional inner life and have a hard time experiencing their inability to show emotions. Ambivalence. The coexistence of two opposing tendencies (thoughts, emotions, actions) towards the same object in the same person at the same time. It manifests itself as the inability to complete certain actions or make a decision.

Volitional disorders. Emotional disorders are often associated with decreased activity, apathy, lethargy and lack of energy. A similar picture is often observed in patients who have suffered from schizophrenia for many years. Severe volitional disorders lead to an unconscious withdrawal from the outside world, a preference for the world of one’s own thoughts and fantasies, divorced from reality (autism). Patients with severe volitional disorders look inactive, passive, and lacking initiative. As a rule, emotional and volitional disorders are combined with each other; they are designated by the same term “emotional-volitional disorders.” Each patient has an individual relationship between emotional and volitional disorders in the clinical picture. The severity of emotional and volitional disorders correlates with the progression of the disease.

Personality changes result from the progression of negative symptoms. They manifest themselves in pretentiousness, mannerism, absurdity of behavior and actions, emotional coldness, paradox, and unsociability.

Positive (psychotic) manifestations. The term “positive” (“productive”) in psychiatry means the appearance of states that are not characteristic of a healthy psyche (for example, hallucinations, delusions). Positive symptoms are not specific to schizophrenia, because also occur in other psychotic conditions (for example, organic psychoses, temporal lobe epilepsy). The predominance of positive symptoms in the clinical picture indicates an exacerbation of the disease.

Hallucinatory-paranoid syndrome is manifested by a combination of poorly systematized, inconsistent delusional ideas, often persecution, with a syndrome of mental automatism and/or verbal hallucinations. For the patient, apparent images are as real as objectively existing ones. Patients actually see, hear, smell, and do not imagine. For patients, their subjective sensory sensations are as valid as those emanating from the objective world.. The behavior of a patient experiencing hallucinations seems crazy only from the point of view of an outside observer; to the patient himself it seems quite logical and clear.. Delusions and hallucinations are considered one of the the most important and common symptoms of schizophrenia, but one symptom is not enough to diagnose this disease. Many patients with schizophrenia with a whole range of other symptoms, such as thought disorders, emotional and volitional disorders, have never experienced delusions or hallucinations. It must also be remembered that delusions and hallucinations are inherent not only in schizophrenia, but also in other mental illnesses, so their presence does not necessarily indicate that the patient has schizophrenia.

Mental automatism syndrome (Kandinsky-Clerambault syndrome) is the most typical type of hallucinatory-paranoid syndrome for schizophrenia. The essence of the syndrome is the feeling of the violent origin of the disorders, their “madeness” .. Alienation or loss of belonging to one’s “I” of one’s own mental processes (thoughts, emotions, physiological functions of the body, movements and actions performed), the experience of their involuntary, madeness, imposition from the outside. Symptoms of openness, withdrawal of thoughts and mentism (an involuntary influx of thoughts) are characteristic.. Pseudo-hallucinations (sensations and images that arise involuntarily without a real stimulus, differing from hallucinations in the patient’s lack of a sense of the objective reality of these images).. The syndrome of mental automatism usually accompanies systematized delusions of persecution and impact. Patients no longer belong to themselves - they are at the mercy of their persecutors, they are puppets, toys in their hands (sense of mastery), they are under the constant influence of organizations, agents, research institutes, etc.

Paraphrenic syndrome is a combination of expansive delusions with delusions of persecution, auditory hallucinations and (or) mental automatisms. In this state, along with complaints about persecution and influence, the patient expresses ideas about his world power, cosmic power, calls himself the god of all gods, the ruler of the Earth; promises the creation of heaven on earth, the transformation of the laws of nature, radical climate change. Delusional statements are characterized by absurdity, grotesqueness, statements are given without evidence. The patient is always at the center of unusual and sometimes grandiose events. Various manifestations of mental automatism and verbal hallucinosis are observed. Affective disorders manifest themselves in the form of elevated mood, which can reach the level of mania. Paraphrenic syndrome, as a rule, indicates the age of onset of schizophrenia.

Capgras syndrome (a delusional belief that people around them are capable of changing their appearance for a specific purpose).

Affective - paranoid syndrome.. Depressive - paranoid syndrome is manifested by a combination of depressive syndrome, delusional ideas of persecution, self-accusation, verbal hallucinations of an accusing nature.. Manic - paranoid syndrome is manifested by a combination of manic syndrome, delusional ideas of grandeur, noble origin, verbal hallucinations of an approving, praising nature.

Catatonic syndrome.. Catatonic stupor. Characterized by increased muscle tone, catalepsy (freezing for a long time in a certain position), negativism (unreasonable refusal, resistance, opposition to any outside influence), mutism (lack of speech with a intact speech apparatus). Cold, uncomfortable posture, wet bed, thirst, hunger, danger (for example, a fire in a hospital) are not reflected in any way on their frozen, amicable face. Patients remain in the same position for a long time; all their muscles are tense. A transition from catatonic stupor to excitement and vice versa is possible. Catatonic excitement. Characterized by an acute onset, suddenness, chaoticity, lack of focus, impulsiveness of movements and actions, senseless pretentiousness and mannerisms of movements, absurd unmotivated exaltation, aggression.

Hebephrenic syndrome. Characterized by silly, ridiculous behavior, mannerisms, grimacing, lisping speech, paradoxical emotions, impulsive actions. May be accompanied by hallucinatory-paranoid and catatonic syndromes.

Depersonalization-derealization syndrome is characterized by a painful experience of changes in one’s own personality and the surrounding world that cannot be described.

Depression in schizophrenia

Depressive symptoms in schizophrenia (both during exacerbation and in remission) are often observed. Depression is one of the most common causes of suicidal behavior in patients with schizophrenia. It should be remembered that 50% of patients with schizophrenia make suicide attempts (15% are fatal). In most cases, depression is due to three reasons.

Depressive symptoms may be an integral part of the schizophrenic process (for example, when depressive-paranoid syndrome predominates in the clinical picture).

Depression can be caused by awareness of the severity of their illness and the social problems that patients face (narrowing of their social circle, misunderstanding on the part of loved ones, being labeled as “crazy,” work maladjustment, etc.). In this case, depression is a normal personality reaction to a serious illness.

Depression often occurs as a side effect of antipsychotic medications.

The division of schizophrenia according to its clinical forms is carried out according to the predominance of a particular syndrome in the clinical picture. This division is conditional, because only a small number of patients can be confidently classified as one type or another. Patients with schizophrenia are characterized by significant changes in the clinical picture during the course of the disease, for example, at the beginning of the disease the patient is noted to have a catatonic form, and after a few years he also experiences symptoms of the hebephrenic form.

. Simple form characterized by a predominance of negative symptoms without psychotic episodes. A simple form of schizophrenia begins with the loss of previous motivations for life and interests, idle and meaningless behavior, and isolation from real events. It progresses slowly, and the negative manifestations of the disease gradually deepen: decreased activity, emotional flatness, poor speech and other means of communication (facial expressions, eye contact, gestures). Efficiency in study and work decreases until they stop completely. Hallucinations and delusions are absent or occupy a small place in the picture of the disease.

. Paranoid form- the most common form; The clinical picture is dominated by hallucinatory-paranoid syndrome and mental automatism syndrome. The paranoid form is characterized by the predominance in the picture of the disease of delusional and hallucinatory disorders, forming paranoid, paranoid syndromes, Kandinsky-Clerambault syndrome of mental automatism and paraphrenic syndrome. At first, they note a tendency towards systematization of nonsense, but later it becomes more and more fragmentary, absurd and fantastic. As the disease progresses, negative symptoms appear and intensify, creating a picture of an emotional and volitional defect.

. Hebephrenic form characterized by the predominance of hebephrenic syndrome. This form differs from the simple one in the patients’ greater mobility, fussiness with a touch of foolishness and mannerisms, and instability of mood is characteristic. Patients are verbose, prone to reasoning, stereotypical statements, their thinking is poor and monotonous. Hallucinatory and delusional experiences are fragmentary and striking in their absurdity. According to E. Kraepelin, only 8% of patients experience favorable remissions, but in general the course of the disease is characterized by malignancy.

. Catatonic form characterized by the predominance of catatonic syndrome in the clinical picture of the disease. This form manifests itself as a catatonic stupor or agitation. These two states can alternate with each other. Catatonic disorders are usually combined with hallucinatory-delusional syndrome, and in the case of an acute paroxysmal course of the disease - with oneiric syndrome.

There are continuous and paroxysmal-progressive types of schizophrenia. Before the advent of ICD-10, there were two more types of progression in Russian psychiatry: recurrent and sluggish. In ICD-10 (as well as in DSM-IV), there are no diagnoses of recurrent schizophrenia and low-grade schizophrenia. Currently, these disorders are identified as separate nosological units - schizoaffective disorder and schizotypal disorder, respectively (see Schizoaffective disorder, Schizotypal disorder).

The continuous type of course is characterized by the absence of clear remissions during treatment and the steady progression of negative symptoms. Spontaneous (without treatment) remissions are not observed with this type of course. Subsequently, the severity of productive symptoms decreases, while negative symptoms become more and more pronounced, and in the absence of treatment effect, it comes to the complete disappearance of positive symptoms and pronounced negative symptoms. A continuous type of course is observed in all forms of schizophrenia, but it is exceptional for simple and hebephrenic forms.

The paroxysmal - progressive type of course is characterized by complete remissions between attacks of the disease against the background of progression of negative symptoms. This type of schizophrenia in adulthood is the most common (according to various authors, it is observed in 54-72% of patients). Attacks vary in severity, clinical manifestations and duration. The appearance of delusions and hallucinations is preceded by a period of severe affective disorders - depressive or manic, often replacing each other. Mood fluctuations are reflected in the content of hallucinations and delusions. With each subsequent attack, the intervals between attacks become shorter and the negative symptoms worsen. During the period of incomplete remission, patients retain anxiety, suspicion, a tendency to interpret any actions of others in a delusional manner, and hallucinations occasionally occur. Particularly characteristic are persistent subdepressive states with decreased activity and a hypochondriacal orientation of experiences.

Research methods. There is no effective test to diagnose schizophrenia. All studies are aimed mainly at excluding an organic factor that could cause the disorder. Laboratory research methods: .. KBC and OAM .. biochemical blood test .. study of thyroid function .. blood test for vitamin B 12 and folic acid .. blood test for the content of heavy metals, medications, psychoactive drugs, alcohol. Special methods.. CT and MRI: exclude intracranial hypertension, brain tumors.. EEG: exclude temporal lobe epilepsy. Psychological methods (personality questionnaires, tests [eg, Rorschach tests, MMPI]).

Psychotic disorders caused by somatic and neurological diseases. Symptoms similar to those of schizophrenia are observed in many neurological and somatic diseases. Mental disorders in these diseases usually appear at the onset of the disease and precede the development of other symptoms. Patients with neurological disorders tend to be more critical of their illness and more concerned about the onset of symptoms of mental illness than those with schizophrenia. When evaluating a patient with psychotic symptoms, an organic etiological factor is always excluded, especially if the patient exhibits unusual or rare symptoms. The possibility of superimposed organic disease should always be kept in mind, especially when a patient with schizophrenia has been in remission for a long time or when the quality of symptoms changes.

Simulation. Schizophrenic symptoms can be invented by the patient or for the purpose of obtaining “secondary benefit” (simulation). Schizophrenia can be simulated, because The diagnosis is largely based on the patient's statements. Patients who actually suffer from schizophrenia sometimes make false complaints about their supposed symptoms in order to receive some benefits (for example, a transfer from disability group 3 to disability group 2).

Mood disorder. Psychotic symptoms are observed in both manic and depressive states. If a mood disorder is accompanied by hallucinations and delusions, their development occurs after pathological changes in mood occur, and they are not stable.

Schizoaffective disorder. In some patients, symptoms of mood disorders and symptoms of schizophrenia develop simultaneously and are expressed equally; Therefore, it is extremely difficult to determine which disorder is primary - schizophrenia or a mood disorder. In these cases, a diagnosis of schizoaffective disorder is made.

Chronic delusional disorder. The diagnosis of delusional disorder is valid for systematized delusions of non-bizarre content, lasting at least 6 months, with the preservation of normal, relatively high personality functioning without pronounced hallucinations, mood disorders and the absence of negative symptoms. The disorder occurs in adulthood and old age.

Personality disorders. Personality disorders can be combined with manifestations characteristic of schizophrenia. Personality disorders are stable characteristics that determine behavior; the time of their appearance is more difficult to determine than the moment of onset of schizophrenia. As a rule, there are no psychotic symptoms, and if they are present, they are transient and unexpressed.

Reactive psychosis (brief psychotic disorder). Symptoms last less than 1 month and occur after a clearly defined stressful situation.

Social and psychological support in combination with drug therapy can reduce the frequency of exacerbations by 25-30% compared to the results of treatment with antipsychotics alone. Psychotherapy for schizophrenia is ineffective, so this treatment method is rarely used.

The nature of the disease is explained to the patient, they are reassured, and their problems are discussed with him. They try to form an adequate attitude towards the disease and treatment in the patient, and the skills to timely recognize signs of an impending relapse. An excessive emotional reaction of the patient’s relatives to his illness leads to frequent stressful situations in the family and provokes exacerbations of the disease. Therefore, the patient’s relatives must be explained the nature of the disease, treatment methods and side effects (the side effects of antipsychotics often frighten relatives).

Basic principles of drug therapy

Drugs, doses, and duration of treatment are selected individually, strictly according to indications, depending on the symptoms, severity of the disorder and stage of the disease.

Preference should be given to a drug that has previously been effective in a given patient.

Treatment usually begins with small doses of drugs, gradually increasing them until the optimal effect is obtained. In case of acute development of an attack with severe psychomotor agitation, the drug is administered parenterally; if necessary, injections are repeated until the excitement is completely relieved, and subsequently the treatment method is determined by the dynamics of the psychopathological syndrome.

The most common mistake is prescribing more antipsychotics to patients than necessary. Studies have shown that smaller amounts of antipsychotics usually produce the same effect. When a clinic increases a patient’s dose of antipsychotic medications every day, creating the impression that this is intensifying treatment and reducing psychotic symptoms, in fact, this effect depends only on the duration of exposure to the drug. Long-term administration of antipsychotics in large doses often leads to the development of side effects.

Subjective severe sensations after the first dose of the drug (usually associated with side effects) increase the risk of a negative treatment outcome and patient evasion from treatment. In such cases, you need to think about changing the drug.

The duration of treatment is 4-6 weeks, then, if there is no effect, the treatment regimen is changed.

When incomplete and unstable remission occurs, the dose of drugs is reduced to a level that ensures the maintenance of remission, but does not cause depression of mental activity and pronounced side effects. This maintenance therapy is prescribed for a long time on an outpatient basis.

Neuroleptics - chlorpromazine, levomepromazine, clozapine, haloperidol, trifluoperazine, flupentixol, pipothiazine, zuclopenthixol, sulpiride, quetiapine, risperidone, olanzapine.

Antidepressants and tranquilizers are prescribed for depression and anxiety, respectively. When the depressive effect is combined with anxiety and motor restlessness, antidepressants with a sedative effect, such as amitriptyline, are used. For depression with lethargy and decreased behavioral energy, antidepressants with a stimulating effect, such as imipramine, or without a sedative effect, such as fluoxetine, paroxetine, citalopram, are used. Tranquilizers (eg, diazepam,zepine) are used short-term to treat anxiety.

Complications during treatment with neuroleptics

Long-term therapy with antipsychotics can lead to the development of persistent complications. Therefore, it is important to avoid unnecessary treatment by varying doses depending on the patient's condition. Anticholinergic drugs prescribed to relieve adverse extrapyramidal symptoms, with long-term continuous use, increase the risk of tardive dyskinesia. That's why anticholinergic drugs are not used continuously and for prophylactic purposes, and are prescribed only in case of adverse extrapyramidal symptoms.

Akineto - hypertensive syndrome.. Clinical picture: mask-like face, rare blinking, stiffness of movements.. Treatment: trihexyphenidyl, biperiden.

Hyperkinetic - hypertensive syndrome.. Clinical picture: akathisia (restlessness, feeling of restlessness in the legs), tasykinesia (restlessness, the desire to constantly move, change position), hyperkinesis (choreiform, athetoid, oral).. Treatment: trihexyphenidyl, biperiden.

Dyskinetic syndrome.. Clinical picture: oral dyskinesia (tension of the masticatory, swallowing, tongue muscles, an irresistible desire to stick out the tongue), oculogyric crises (painful rolling of the eyes).. Treatment: trihexyphenidyl (6-12 mg/day), 20% p - caffeine 2 ml s.c., chlorpromazine 25-50 mg i.m.

Chronic dyskinetic syndrome.. Clinical picture: hypokinesia, increased muscle tone, hypomimia in combination with local hyperkinesis (complex oral automatisms, tics), decreased motivation and activity, acairia (intrusiveness), emotional instability.. Treatment: nootropics (piracetam 1200-2400 mg/day for 2-3 months), multivitamins, tranquilizers.

Malignant neuroleptic syndrome.. Clinical picture: dry skin, acrocyanosis, sebaceous hyperemic face, forced posture - on the back, oliguria, increased blood clotting time, increased residual nitrogen in the blood, renal failure, decreased blood pressure, increased body temperature.. Treatment : infusion therapy (reopoliglucin, hemodez, crystalloids), parenteral nutrition (proteins, carbohydrates).

Intoxication delirium develops more often in men over 40 years of age (with a combination of chlorpromazine, haloperidol, amitriptyline. Treatment is detoxification.

Forecast for 20 years: recovery - 25%, improvement in condition - 30%, care and/or hospitalization required - 20%. 50% of patients with schizophrenia make suicide attempts (15% are fatal). The older the age of onset of the disease, the more favorable the prognosis. The more pronounced the affective component of the disorder, the more acute and shorter the attack, the better it responds to treatment, and the greater the chance of achieving complete and sustainable remission.

Synonyms. Bleuler's disease, Dementia praecox, Discordant psychosis, Dementia praecox

Pfropfschizophrenia (from German Pfropfung - grafting) - schizophrenia developing in an oligophrenic "oligoschizophrenia" pfropfhebephrenia "vaccinated schizophrenia

Huber's senesthetic schizophrenia is schizophrenia with a predominance of senestopathy in the form of burning sensations, constriction, tearing, turning over, etc.

Schizophrenia-like psychosis (pseudoschizophrenia) is a psychosis similar or identical in clinical picture to schizophrenia.

Schizophrenia-like syndrome is the general name for psychopathological syndromes similar in manifestations to schizophrenia, but occurring in other psychoses.

Nuclear schizophrenia (galloping) is the rapid development of emotional devastation with the disintegration of pre-existing positive symptoms (end state).