Acute endogenous psychosis. Part 1

In the first period of development of clinical psychiatry, when psychosis was a very poorly differentiated mass, acute endogenous psychosis, naturally, did not stand out.

The clinical picture of the psychoses discussed here can be found in the descriptions of the concepts “idiocy” (Pinel), “acute dementia”, “mania”, “lipemania” (Esquirol).

As clinical psychiatry developed, mental illness began to be treated more differentially. Boismont in 1845 described in detail the clinical picture of acute delusions and differentiated it from both acute mania and meningitis. Calmeil (1851) clarified the clinical features of delirium acutum to an even greater degree, and since that time the controversy over this acute psychosis began to concern mainly its nosological evaluation. Thus, by the middle of the 19th century, one of the types of acute atypical psychosis was already identified, its clinical-psychopathological features were described quite accurately.

At about the same time, a second clinical type of acute psychosis has been noted in the literature, currently referred to as “periodic catatonia” (or oneiric catatonia). Within the framework of melancholy and acute dementia, Georget (1820) described stupidite, which he identified as a new disease. Ferrus (1838) joined Georget, emphasizing the non-febrile nature of psychosis. This author noted a favorable outcome of the attack. Ferrus described the condition of the patients as “the elimination or rather the delay of all brain processes, rapidly advancing, without temperature,“ curable ”. Soon Baillarger (1843), Griesinger (1845), and then many other psychiatrists recognized the existence of a special form of melancholy — melancholy with a stupor and described it in detail.

By this time, individual forms of mania began to be distinguished, some of which were actually described as independent types of seizures (hyperacute mania, frenzy, madness). Judging by the cited case histories, under this name, the authors described the attacks of the oneiric-catatonic, manic-delusional, paraphrenic structure. Within the framework of a single Grizipger psychosis, the psychoses considered by us were included as options in melancholia, mania and “madness”. Phase affective, affective-delusional and affective-oneiric (according to modern estimates) psychosis related to melancholia and mania. “Madness” is more consistent with modern paroxysmal progredient schizophrenia.

The process of differentiation of mania and melancholia was further intensified after the isolation of various types of circular insanity by French psychiatrists Baillarger (1854) and Falret (1851) in the middle of the 19th century. These studies confirmed the possibility of alternating mania and melancholia, which was noted long ago by doctors, and made it possible to single out a circular insanity with characteristic psychopathological picture and course.

Thus, the clinical-psychopathological contours of certain types of acute psychosis, characterized by seizures in the form of attacks, were described. In subsequent years, a group of acute psychosis began to grow in quantitative terms and be refined in its clinical and psychopathological content. A classification of acute forms of insanity began to appear. It was soon noted that circular insanity, delirium acutum, melancholy with stupor, hyperacute mania, etc., do not exhaust the whole group of acute psychoses. The concept of acute paranoia appeared (Westphal, 1876), which for a long time was the center of numerous discussions. The isolated psychosis soon turned out to be much more complicated than the simply acutely occurring delusional state.

Already in 1879, Merklin noted that acute paranoia is characterized by a darkening of consciousness or confusion, similar to those that occur in dreams or febrile delusions. Dreams, confusion of experiences of patients with acute paranoia have become more and more emphasized by psychiatrists. As a result, acute paranoia was divided into two large groups: psychosis with a predominance of delusional symptoms (without gross disturbance of consciousness) and psychosis, which were characterized not only acutely emerging delusions, but also hallucinatory, affective disorders and blackout. These two main forms of acute insanity remained at the center of controversy over the next two decades. Soon, to overcome the differences that arose, the concept of “amentia” Meinert (1893) was proposed, which included cases of acute paranoia with severe disorders of consciousness and many other acute psychoses. As it is known, the concept of amentia, which is extremely broad in the understanding of Meinert, soon began to narrow, and at present it has limited application.

In the last decades of the XIX century a large number of works appeared in which it was proposed to divide the acute forms of insanity into separate types. V.P. Serbian (1892, 1906) besides mania, melancholia, and acute dementia distinguished acute amentia and acute paranoia. Contrary to the opinion of Meinert, that with amentia there are no cardinal symptoms, V.P. Serbsky singled out as characteristic signs of amentia a disorder of consciousness (according to the dream type), affect lability and disturbance of associative activity. Typical for acute paranoia, V.P. Serbsky believed: acute or subacute occurrence of unstable and unsystematized delusions, the presence of a pronounced affective state (depressive or expansive), a relatively clear consciousness. V. P. Serbsky referred to mixed forms (luck) as paroxysmal psychosis, in the clinical picture of which affective and delusional symptoms are combined with elements of confusion.

S. S. Korsakov (1901) further deepened the clinical analysis of “acute forms of insanity”. He described in detail the varieties of dysnoi (acute psychosis with a disorder of consciousness) and acute paranoia. S. Korsakov considered relative clarity of consciousness to be a characteristic sign of acute paranoia.

A similar point of view was Seglas (1895), who believed that it was necessary to distinguish between acute psychosis and confusion, that is, confusion (confusion mentale), and acute psychosis without stupefaction (acute paranoia). Within the framework of acute paranoia (simple and hallucinatory), he described depressive-paranoid oneiric attacks.

In Germany, by this time we also find a similar division of acute psychosis into psychosis without a sharp disturbance of consciousness (Wahnsinn) into psychosis with confusion (Verwirrtheit) (Kirchof, Zienn, Kraepelin).
Kraepelin himself in 1895 distinguished several forms of acute treatable psychoses: mania, melancholy, delirium, exhaustion psychosis, acute dementia, hallucinatory and depressive forms of acute delirium.

Thus, on the eve of the emergence of Kraepelin’s nosological classification with respect to acute forms of insanity, there were undoubted successes, which concerned mainly the issues of clinical differentiation of these psychoses. Most of the acute forms of psychosis were by this time grouped around affective, psychomotor, delusional disorders, and confusion syndrome.

At the end of the 19th century, principles that did not allow for a fairly complete clinical and psychopathological characterization of these complex psychoses were based on the isolation of individual forms of acute psychosis. Affective disorders (for circular insanity), febrile, catatonia, death (for delirium acutum), catatopic stupor with depressive delusions (for melancholy with stupor) were insufficient to characterize many of these psychoses. The concepts of acute paranoia, mental confusion were also unsatisfactory. As you know, for the psychoses designated by these concepts, a very different course was allowed: an exceptionally benign (one attack followed by recovery), a remitting or recurring course without gross changes (recurrent amentia, paranoia) and an unfavorable course, as a transition to a chronically current psychosis or in a state of dementia.

Particularly difficult to describe and designate were those of the acute forms of insanity, in which there was a complex clinical picture and a large variability of symptoms (affective, psychomotor, hallucinatory-delusional, impaired consciousness, etc.). These psychosis did not fit even in such broad concepts as amentia, acute paranoia, catatonia.

All this indicates that at the time of the emergence of the classifications of Krapelin’s mental diseases, many forms of acute psychosis were not yet sufficiently studied, even in their psychopathological structure. Other forms of acute mental illness were clinically quite clearly outlined, although the principles of their psychopathological description in many respects suffered from the shortcomings inherent in all static psychopathology.

Classification of mental illness Krepelin did not solve the issue of acute atypical psychosis in their essential clinical and psychopathological aspects. Moreover, against the background of a more definite situation in which other acute psychosis (typical manic-depressive psychosis, various forms of early dementia, many febrile, somatogenic and infectious psychosis) found themselves, the clinical “disorder” of acute atypical psychosis immediately appeared before psychiatrists as one of complex clinical problems.

As is known, in the initial nosological classification of Kraepelin, as well as in the classifications of his supporters, at first there was a desire to abstract from many psychopathological, clinical aspects of these psychoses, to a significant simplification of their structure, thanks to which it was possible to attribute them to one of the two main endogenous diseases . Thus, acute delusional psychosis (acute paranoia) was treated by many psychiatrists to manic-depressive psychosis; acute catatonic psychosis without an outcome in dementia was more readily regarded as a catatonic form of early dementia. Such a hasty nosological formulation of insufficiently studied forms of acute psychosis immediately led to difficulties in attempting to classify psychoses that do not fit into the concepts of manic-depressive psychosis and early dementia. This soon led psychiatrists to amend and supplement the original scheme. Such a need was due to the fact that the clinical picture of many endogenous psychosis was closer to early dementia, while their paroxysmal course and the appearance of affective attacks more resembled manic-depressive psychosis. Rehm (1919) described a catatonic form of remitting insanity with a clearly circular course, despite the fact that many attacks were in the nature of a catatonic stupor. Tamburini described catatonic manic-depressive psychosis, etc. Urstein (1912) came to the conclusion that early dementia can occur circularly and that it is legitimate to include manic-depressive psychosis in catatonia. Other psychiatrists described cases of early dementia with a depressive onset (Pascal, 1911).

Thus, almost simultaneously with the spread of the nosological concept of Kraepelin, the disadvantages of the dichotomous division of endogenous psychoses began to be revealed. It is important to note that among the psychoses that do not fit into the scheme, acute psychosis with severe affective disorders and catatonia with remitting course, ie, psychoses, considered up to the present time as acute atypical psychosis, occupied a large place.

Hippocampal neuroanatomy in schizophrenia.

Reducing the size of the hippocampus in schizophrenia was found in a study of autopsy brain by a number of authors in the 80s, although other researchers could not confirm these data. This may be due to the fact that the decrease in the volume of the hippocampus in absolute terms is very small and is subject to the influence of clinical and demographic factors.

The data concerning the number of glutamatergic pyramidal neurons and cytoarchitecture of the hippocampus in schizophrenia are also rather contradictory, as reflected in the review by D. Weinberger. On the one hand, both the decrease in the numerical density of pyramidal neurons in the hippocampus during schizophrenia and its local increase were revealed, on the other hand, no such significant changes were found. Some publications have described the disorientation of pyramidal neurons in some areas of the hippocampus in schizophrenia, which has not been confirmed by other researchers. Data on the reduction of the size of the bodies of pyramidal neurons in the hippocampus, obtained by a number of researchers, also did not find confirmation in subsequent studies. The reason for such contradictions, in addition to the above, may also be errors in the methodological approach. We are talking about the absence in quantitative studies of the stereological approach, which allows to avoid distortion of the results associated with the effect on the studied parameters of the thickness of the slices, the size and distribution of the studied cells, etc. Recent studies performed using stereological methods on large groups of schizophrenic patients and mentally healthy people showed not only the absence of changes in the size and number of pyramidal neurons of the hippocampus, but also in the volume of the hippocampus or its regions.

Nevertheless, due to the use of the Golgi method, it was possible to reveal a decrease in the numerical density of the spines and a violation of the arborization of the dendritic tree of the pyramidal neurons of the subicle and the granular neurons of the dentate fascia. Immunocytochemical studies using antibodies to a specific dendritic marker – microtubule-associated protein 2 (MAP2) and the subunits of the kainate receptor GluR5,6,7 confirmed these findings. Although data on immunoreactivity and mRNA expression for the MAP2 dendrites marker are rather contradictory, these findings, together with the results of classical neuromorphological studies, indicate a significant reduction in the dendritic tree of the pyramidal neurons of the hippocampus in schizophrenia. The significance of this fact is determined by the fact that, as is known, the size of the processes is closely related to the size of the neuron body. Therefore, the question of reducing the size of the pyramidal neurons of the hippocampus in schizophrenia cannot be considered finally resolved.

As for the inhibitory GABAergic interneurons, which, along with pyramidal neurons, are the most numerous in the hippocampus, a decrease in their number in schizophrenia was first detected in the CA2 region of the hippocampus using neurohistological techniques of F. Benes et al. In the future, these data were confirmed by methods of immunocytochemistry and in situ hybridization. According to S. Heckers et al., the density of neurons containing the mRNA of the two isoforms of the main enzyme for the synthesis of GABA-glutamate decarboxylase (isoform 65 kilodalton – GD65 and isoform 67 kilodalton – GD67) was reduced in the hippocampus with schizophrenia by an average of 10%, with mRNA expression for both isoforms of the enzyme did not change. However, other authors have found a significant decrease in both the expression and the protein content of GD67- (but not GD65-) enzyme isoform in the hippocampus in schizophrenia. When interpreting these data, one should take into account that the authors of the relevant works did not reveal the effect of neuroleptic therapy on the expression of HD.

It has also been established that the number of interneurons containing parvalbumin (but not calretinin) decreases in the hippocampus in schizophrenia. As mentioned above, parvalbumin-containing neurons are a special subclass of inhibitory interneurons that innervate the bodies of pyramidal neurons and the initial segments of their axons. It should be emphasized that the lack of interneurons, including parvalbumin, in schizophrenia is not a phenomenon inherent only in the hippocampus, it was also detected in the prefrontal cortex. On the other hand, the results of immunocytochemical determination of the number of parvalbumin-immunoreactive neurons can be significantly influenced by the level of expression of the antigen. In schizophrenia in the hippocampus, a decrease in parvalbumin expression has been shown. Although the use of histological methods revealed a decrease in the number of inhibitory interneurons in schizophrenia only in the CA2 region of the hippocampus, this contradiction may be explained by the fact that parvalbumin neurons constitute only a part of the population of hippocampal interneurons. In this regard, it should be noted that there is a decrease in the expression of not only parvalbumin, but also Kalbindin, mainly in the CA2 region of the hippocampus. Although it was not possible to detect in schizophrenia a decrease in the numerical density of Kalbindin-immunoreactive neurons in the hippocampus, these data are consistent with the previously described selective deficit of interneurons in the CA2 region of the hippocampus.

Unfortunately, data on the effect of antipsychotic drugs on morphology and the number of pyramidal neurons in the hippocampus are not available. It was found that the expression of the dendritic marker MAP2 in the hippocampus of experimental animals increases with the introduction of neuroleptics. Experimental studies of the possible effect of antipsychotic therapy on the number and size of GABAergic neurons in the hippocampus or its individual sectors did not reveal changes in these parameters in response to a 3-week introduction of haloperidol or olanzapine.
Thus, data from neuroanatomical (histological) studies of the hippocampus in schizophrenia indicate more likely quantitative changes in cytoarchitectonic parameters that are not reflected in the overall histological pattern of the structure. There were no significant changes in the total number of hippocampal neurons in schizophrenia, with the exception of one of the subpopulations of GABAergic interneurons. However, the data presented on the reduction of the dendritic tree of the pyramidal neurons of the hippocampus suggest disorders in schizophrenia of the interneuronal connections, which is, according to some authors, the main component of the pathology of the hippocampus in this disease.

Lifetime studies of the hippocampus in schizophrenia

There are numerous studies of the hippocampus in schizophrenia, which were performed using modern methods of computer x-ray and magnetic resonance (MPT) tomography. The findings suggest a decrease in the volume of this structure in patients with schizophrenia compared with healthy people. Sensitive modern methods of multidimensional brain mapping revealed that in some cases, in the absence of volume changes, there is a deformation of the hippocampus, manifested in a decrease in the curvature of its posterior section.

It is important to emphasize that both the reduction in the volume of the hippocampus and the changes in its shape were observed in patients who first became ill and did not receive antipsychotic therapy, as well as in their mentally healthy relatives. This suggests that these changes are not brought about by disease or therapy, and, most likely, are an important feature of the brain in schizophrenia. This interpretation is supported by the presence of general morphological features of the hippocampus (volume reduction) in schizophrenia and schizoaffective disorders. Some authors suggest that a decrease in the volume of the hippocampus in schizophrenia may be the basis of a predisposition to the development of this disease.

Some authors, however, failed to detect a decrease in the volume of the hippocampus in schizophrenia. Naturally, these contradictions have led to attempts to identify their possible causes. This was done, in particular, M. Nelson et al. based on the analysis of a large number of papers published before 1998. They concluded that the constant, although small (on average, 5%) deficit of the hippocampus is a characteristic feature of schizophrenia, the main reason for the contradictions is the use of inadequate statistical methods, especially in cases where a small amplitude of change is combined with significant individual variability. Other researchers believe that the cause of the contradictions may be the clinical heterogeneity of schizophrenia itself and, accordingly, differences in patient samples. Moreover, some authors have noted the link between the decrease in the volume of the hippocampus and some psychopathological phenomena — thought disorders and auditory hallucinations. In addition, the available data do not allow us to conclude unambiguously whether the reduction of the hippocampus progresses with an increase in the duration of the disease. Attention is drawn to the fact that atypical antipsychotics (olanzapine) can cause an increase in the temporal lobe of the brain, thereby masking the decrease in the size of the hippocampus.

Of particular interest are lifetime changes in the function of the hippocampus in schizophrenia. The corresponding data were obtained using magnetic resonance spectroscopy (MRS) with mapping and positron emission tomography (PET) with the registration of regional cerebral blood flow.

In MDR, it was possible to detect dysfunction of the glutamatergic neurons of the hippocampus during schizophrenia in vivo, as indicated by a decrease in the content of N-acetyaspartate (NAA) in it, including in patients who did not receive neuroleptic therapy. NAA is known to be a neuronal marker that serves as an indicator of both the deficiency of glutamatergic neurons and their dysfunction. However, a decrease in the NAA signal in the hippocampus in schizophrenia is more a result of dysfunction of glutamatergic neurons than their deficit, since these changes were detected in the absence of changes in the volume of the hippocampus and were not accompanied by changes in the choline signal, an indicator of the state of cell membranes. Experimental studies confirm that the suppression of the intensity of the NAA signal may correlate directly with a decrease in the functional activity of glutamatergic neurons even in the absence of their deficiency. The severity of NAA-signal suppression in the hippocampus in schizophrenia, according to a number of authors, correlates positively with both the severity of positive symptoms (delusions, hallucinations, etc.) and the severity of memory and attention disorders.

In PET studies, it was shown that a decrease in blood flow in the hippocampus in patients who did not receive neuroleptic therapy for 2–3 weeks also correlates with the severity of positive symptoms. The suppression of the involvement of the hippocampus in the implementation of tasks associated with verbal memory has also been shown previously. The authors attribute this specific cognitive deficit to manifestations of psychosis, such as auditory hallucinations and disorganized speech. However, a comparison of groups of patients separated by the presence or absence of a pronounced mental defect in them revealed a similar suppression of the activation of the hippocampus when solving problems associated with the reproduction of new words. These data may indicate that the dysfunction of the hippocampus in schizophrenia, associated with the implementation of cognitive processes, can be universal and underlie a wide range of symptoms of the disease in question.

It remains unclear whether changes in the structure of the hippocampus, which were detected during post-mortem studies, can be a cause of disorders in the size and shape of the hippocampus observed at the MRI level. Obviously, this relationship may not be direct. In the already classic works of R. Sapolsky et al. showed that the impact of chronic stress on primates causes pronounced changes in the cytoarchitecture of the hippocampus, associated with the loss of neurons and gliosis, but is not accompanied by significant in vivo changes in the volume of the hippocampus. On the other hand, it was shown that a decrease in the volume of the hippocampus is characteristic of Alzheimer’s disease, accompanied by marked neurodegenerative changes in it  However, with other mental illnesses that are accompanied, like schizophrenia, by minimal cytoarchitectonic disorders in the hippocampus, intravital MRI studies show different directions for changes in the volume of this structure. Thus, in manic-depressive psychosis, the volume of the hippocampus increased or did not change, whereas in depression, a decrease in the volume of the hippocampus, often depending on the age of onset of the disease, was shown. In schizophrenia, neuroendocrine disorders of some patients, associated with polydipsia and hyponatremia, may have a certain effect on the lifetime reduction of the hippocampus.

Thus, data from in vivo studies indicate that a decrease in volume and / or a change in the shape of the hippocampus, as well as a disruption of its functional activity, may be an important feature of the brain in schizophrenia. Although the severity of structural and functional disorders of the hippocampus is associated mainly with the predominant, mostly positive symptoms, the basis for this relationship may be a violation of the cognitive functions determined by the hippocampus. Therefore, we dwell on them in more detail.

Personality Psychopathology

In modern psychology, there are many definitions of the concept of “personality.” However, in such medical disciplines as psychotherapy, psychological correction, psychological diagnostics, personality terminology is widely used from the perspective of the “psychology of relationships” created by psychiatrists and psychologists A. F. Lazursky and V. N. Myaschischev, according to which this term is interpreted as system or a set of relations to the surrounding world, primarily the social, as well as to itself.

The basis of the personality is the character, which is determined by the hereditary predisposition, however, it is finally formed under the influence of education and can be distorted by the adverse effects of various factors (from chronic mental trauma to the individual to organic brain lesions).

Premorbid personality types

A premorbid personality type determines its basic traits, the type of character until the moment the mental disorder occurred. This type is described from the words of the patient or his relatives in the presentation of the history of life. Assessment of the premorbid type is extremely necessary for the diagnosis, prognosis and selection of methods of psychotherapy and rehabilitation of various mental disorders, since the risk of development of individual psychopathologies is not the same for different types.

The most famous of the developed systems of personality types, convenient for assessing premorbid traits, is the classification of “accentuated personalities” of the famous German psychiatrist Carl Leonhard. The basis of this typology of personalities lies in the variants of character accentuation, namely, excessive strengthening of its individual features, as a result of which a selective vulnerability is revealed with respect to a certain kind of psychogenic influences with good and even increased resistance to others. Unlike psychopathies and personality disorders, accentuated personalities are regarded as extreme variants of the norm. In most developed countries, they include more than half of the population.

According to K. Leonhard and A. E. Lichko, there are the following main types of accentuated personalities and character accentuations.

Hyperthymic type. Persons with this type of accentuated personality are almost always distinguished by high spirits, high vitality, activity, and unlimited energy. Short flashes of irritation and anger in patients cause opposition from others, the suppression of their violent activities, the desire to interfere in everything. Such people strive for independence and independence, however, loneliness and forced idleness, they are extremely resourceful, they know how to dodge and trap, while at the same time they do not tolerate strict discipline and a regulated regime; illegible in the choice of dating. Carried away by something new, they do not bring it to the end. Such individuals tend to overestimate their capabilities and abilities, are unjustifiably optimistic about the future, poorly cope with work that requires perseverance and accuracy.

Cycloid (affective-labile) type. This type of personality is characterized by a change in periods of recovery, when patients behave like hyperthyms, periods of decline in mood and tone. During the latter, the patients show lethargy, fatigue, a decrease in working capacity, they become unsociable and inactive. The most minor troubles during these periods are experienced very hard. Between ups and downs there can be long periods of even mood. The duration of the periods – from several days to several months.

Emotionally labile (emotive, affectively exalted) type. The main feature of people with this type of personality is the extreme variability of mood, the differences of which occur even from an insignificant cause. Well- being, working capacity, sociability and attitude to everything depend on the mood. Patients are experiencing trouble, prone to neurotic reactions, sincerely attached to those people from whom they see care and understanding. There is a great need for emotional contact, empathy.

Sensitive (alarming) type. Characteristic features of such personalities are great impressionability and a sense of inferiority. In unfamiliar surroundings, among strangers, they are timid and shy and, on the contrary, sociable and open only to those they are used to. They have a strong sense of duty and responsibility. In this connection, such personalities notice many shortcomings in themselves, then they strive to overcome them, claiming themselves not where their real abilities can unfold, namely in the area where they are weak, for example, shyness and shyness are trying to overcome by taking public office . Anxiety is most affected by the fear of making an adverse impression on others. Patients are experiencing a hostile attitude towards others.

Psychasthenic (pedantic) type. Persons with this type of personality combine indecision, tendency to rationality with anxious suspiciousness in the form of fears for their future and the future of their loved ones. Pedantry and formalism become a defensive reaction from constant internal anxiety. Invented signs and rituals become another defensive reaction. Indecision is combined with impatience when the decision has already been made. Patients are prone to introspection and self-digging. A heavy burden for them is responsibility, especially when it is necessary to answer not only for themselves, but also for others.

Schizoid (introverted) type. This type of personality is known as a pattern of closure. Although formal contacts with people of this type are usually not difficult, however, emotional contacts usually prove to be an impossible task for them. The isolation of such personalities is accompanied by external restraint, and sometimes coldness. The lack of empathy manifests itself in the inability to respond to the joy, sadness or fear of another person. There is also a lack of intuition – the inability to understand the experiences of others, to guess about the unspoken desires or concerns of others, to feel sympathy or hostility towards oneself. The inner world filled with hobbies and fantasies becomes a native element for such people. Patients fantasize about themselves, they do not share their fantasies with others. They also differ in independence and propensity to non-conformism.

Epileptoid (explosive, excitable) type. For such types of personality, a tendency toward short periods of angry, dreary mood with boiling irritation and, as a result, a necessary search for an object on which to “disrupt evil” is characteristic. During these periods, affective explosiveness is particularly pronounced. Affects are strong and long lasting, patients during them are able to reach unrestrained rage. Also strongly expressed are instincts, in particular, sexual attraction, which is combined with strong jealousy, and sometimes with sadistic and masochistic inclinations. With respect to others manifest imperiousness. All the behavior of such people is distinguished by heaviness, retardation, inertness. Petty accuracy, meticulous observance of the rules, and pedantry that bothers others, are combined with thrift, prudence and rancor.

Hysteroid (demonstrative, histrionic) type. Persons with this type of personality draw attention to themselves with an insatiable thirst to be in the center of attention. This is served by deceit and fantasy, the propensity to portraying and posturing, a mock-exaggerated expression of emotions, excessive dramatization of events. Related to this is the claim to an exceptional position among others, as well as a high level of aspirations for their future. Good acting skills allow you to mislead gullible people. The suggestibility often attributed to hystericals is highly selective — it only applies to what can attract the attention of others and show off in front of them. Patients like to change the company of friends, assuring that they “have given up on” the former.

Unstable type. For individuals of this type is characterized by continuous increased craving for pleasure, entertainment, idleness, idleness. They strive to evade any labor, duty, and duty. They live today, they do not set any long-term goals. Any hard work pushes them away. Real attachments are never felt for anybody – neither for relatives, nor for friends. Nobody falls in love – sex life is just one of the ways to get pleasure. They are attracted to any antisocial companies that promise entertainment. Cowardice and lack of initiative condemn them to a subordinate role. They often begin to abuse alcohol and other intoxicating substances, thereby trying to escape from difficulties, troubles and trials.

Conformal type. This type is represented by people of “their environment”. Their life rule is to think, act, live as their usual environment. In this connection, they are completely the product of their microenvironment, in a good environment they are not bad people, in an unfavorable environment they can easily drink themselves and take the road of crime. Conformity in everything to their surroundings is combined with conservatism, due to the difficulty of adapting to new conditions, unusual environment, new trends, lack of personal initiative, preference to always go the usual way, to act on hardened stencils. Another feature is striking noncriticality: everything that comes through the usual channels of information is perceived as truth. Patients lose composure with drastic changes in life when they lose their familiar society.

Mixed types are quite common. They can be intermediate when features of two types can be traced from a young age, sometimes from childhood (for example, a mixed hysteroepileptoid type), or amalgamic, when features of a different type are layered on the basis of one type due to prolonged adverse influence of the environment cruel relationships in the environment contributes to the attachment of some epileptoid traits on the basis of other types).

Personality disorders

Psychopathy, or the pathology of the person, is described in more detail in Part 3 of Section 4 of this book, and also provides characteristics for each case, in particular, for various mental disorders. Such disorders are constitutional – predisposed to heredity, or are formed due to the long-term adverse effects of the environment in childhood or adolescence.

Pathological personality development is characterized by its increasing changes in a certain type due to mental trauma, manifested in the “place of least resistance” of this type of character accentuation. In more rare cases, changes in personality during such development can grow to the level of psychosis. Only then is the ability to report and act on one’s actions lost.

A separate group is the pathological development of the personality, due to severe physical defects, such as blindness, deafness, and congenital paralysis.

Personal defects can be characterized as the consequences of severe mental illness or organic brain lesions, and the changes that are evolving are persistent. There are several types of personality defects, namely: schizophrenic, epileptic, organic and others.

Pathology of the Hippocampus in schizophrenia. Part 1

The hippocampus is a key element in the organization of subjective perception-action, ensuring the switching of conscious attention.
Hippocampal neurons serve all possible emotional contexts, because specific to all types of neurotransmitters.

This means that at different concentrations of neurotransmitters, only those connections in the hippocampus that are specific to these neurotransmitters will be included, which, at this level, ensures that the perception-response style is highlighted.

The pathology of the hippocampus in schizophrenia has begun to attract the particular attention of researchers over the past two decades. This is primarily due to the progress in the development of methods for intravital studies of the brain (computer, magnetic resonance imaging, etc.), allowing to identify violations of the structure and functions of the hippocampus in the brain of patients with this disease. In addition, these data have given particular importance to the results of morphological and neurochemical studies of autopsy brain, which revealed structural and functional changes in the hippocampus during schizophrenia. The hippocampus attracts the attention of researchers also due to the fact that its structure and functional organization are well studied, which allows you to come closer to establishing parallels between the clinical manifestations of the disease and its pathology.
This review presents a modern understanding of the structure and functions of the hippocampus in terms of studying its role in the pathogenesis of schizophrenia according to the literature of the past two decades.

The main sections of the review contain the results of intravital structural and functional studies of the hippocampus in schizophrenia; data from neurochemical studies concerning predominantly alterations of glutamate and GABAergic neurons of the hippocampus in schizophrenia; analysis of evidence of synaptic contact impairments, including the results of synaptic marker studies and ultrastructural research data. These sections are prefaced with basic information about the anatomy and physiology of the hippocampus.
Structure and main functions of the hippocampus
The hippocampus enters the hippocampal formation, which includes, in addition to it, the dentate fascia, subicle, presubiculum, and entorhinal cortex, and is a key structure of the limbic system of the brain.

The hippocampus itself (or Ammon’s horn) is a dense ribbon of cells that stretches in the anteroposterior direction along the medial wall of the lower horn of the lateral ventricle of the brain. The main nerve cells of the hippocampus are represented by pyramidal neurons and polymorphic cells, most of which are intercalated neurons with processes that do not extend beyond the limits of the hippocampus.

Being an ancient cortex, the hippocampus consists of 3 main layers: a polymorphic layer (stratum oriens), a layer of pyramidal neurons (stratum pyramidale) and a molecular layer (stratum radiatum and stratum lacunosum-muslare)

The layer lying on the ventricular surface, alveus, consists mainly of horizontally myelinated axons of the pyramidal neurons of the hippocampus. The basal dendrites and initial axon segments are located in the stratum oriens. This is followed by a layer of pyramidal neurons, and then a stratum radiatum, containing the trunks of the apical dendrites, and the stratum lacunosum-muslare, where the terminal terminal and terminal branches of the apical dendrites are located. The precise organization of the cytoarchitecture of the hippocampus is preserved throughout its front-uterine course, which suggests its laminar organization.

The peculiarities of the cytoarchitecture of the pyramidal layer of the hippocampus served as the basis for its division into 4 main fields, oriented in the mediolateral direction and designated as CA1 – CA4. The main fields of the hippocampus itself are CA1 and CA3. The CA1 field is distinguished by small pyramidal neurons that are tightly arranged in 2 layers, the cells of this layer in the CA3 region are very large, not so densely arranged. Apical dendrites of the CA1 pyramids run at a considerable distance from the cell as a single stem and do not have large spiny outgrowths. Powerful apical dendrites of the CA3 pyramids of the region give bifurcation near the cell body and are covered with giant spike outgrowths (thorny excrescences). These giant spines of the CA3 pyramidal neurons form synaptic contacts with axons of granular neurons of the dentate fascia, mossy fibers. Axons of the CA3 pyramidal neurons give the so-called Schaffer collaterals in contact with the apical dendrites of the CA1 pyramids. The above links are the two main associative pathways of the hippocampus, connecting together its main elements, and constitute the so-called trinsynaptic pathway. Both the mossy fiber system and the main afferent entrance of the dentate fascia (perforating path) are characterized by strict topical organization. Thus, the hippocampus can be represented as a set of consecutive morphofunctional segments that can function relatively independently.

Laminar organization is also characteristic of the terminal fields of afferent inputs and commissural connections with the contralateral hippocampus [68]. The most important afferent inputs, from the septum and the entorhinal cortex, end up mainly in the CA3 region of the hippocampus, whereas the pyramidal neurons of the CA1 region receive the afferent input directly from the entorhinal cortex. The entorhinal cortex in turn receives afferent inputs from the limbic cortex and polymodal associative zones of the neocortex. Direct efferent connections from the hippocampus to the temporal region of the neocortex and the prefrontal cortex were also detected. Septum is connected to the hippocampus by bilateral ties and is an extremely important relay link on the paths between the hippocampus and the structures of the brain stem and the hypothalamus. Other efferent pathways of the hippocampus are directed mainly to the structures of the limbic circle. Thus, the CA3 region of the hippocampus is the point of convergence of information flows from the associative cortex and phylogenetically ancient structures of the brain stem.

The basis of the functioning of the hippocampal neural ensembles is glutamatergic neuromediation, since both the pyramidal neurons and the granular cells of the dentate fascia are glutamatergic. However, almost all known neurotransmitter systems play a significant role in the regulation of the functional activity of the hippocampus. GABA and cholinergic afferents are important modulating inputs from septum. The CA3 region of the hippocampus receives direct inputs from the noradrenergic blue spot and serotonergic suture nuclei. The entrance from the nuclei of the reticular formation of the brainstem is carried out indirectly through the cholinergic nuclei of the forebrain.

Inside the hippocampus, the brake control of glutamatergic pyramidal neurons is carried out by polymorphic intercalated neurons, most of which are GABAergic. The latter are subdivided into several subtypes according to the content of calcium-binding proteins in them: parvalbumin-, calbindin- and calretinin-containing interneurons. Parvalbumin neurons innervate mainly (but not exclusively) the bodies of pyramidal neurons]. A special subclass of parvalbumin-containing neurons, the so-called “candelabra cells”, innervate the initial axonal segments of the pyramidal cells of the hippocampus. Kalbindin-containing neurons form synaptic contacts primarily on the proximal apical dendrites of pyramidal cells. Calretinin-containing interneurons mainly specialize in inhibitory control of other GABAergic neurons.

As already mentioned, the CA3 region occupies a special place in the structural and functional organization of the hippocampus, since it is precisely the neurons of this hippocampus region that receive the main information flows from the higher associative cortical zones, as well as from the stem and subcortical structures of the brain. The functional organization of neural ensembles in the CA3 region of the hippocampus has a number of specific features. The CA3 pyramidal neurons are connected to each other through a set of reciprocal links, with the result that each of them is able to influence the discharge of many other neurons. The GABAergic CA3 interneurons also receive a glutamatergic stimulating entry from the pyramidal neurons of this region and from the collaterals of mossy fibers (axons of the granular neurons of the dentate fascia) that innervate the apical dendrites of the pyramidal neurons. Thanks to this system of connections, the inhibitory neurons of the hippocampus are capable of performing both direct and reverse inhibition of pyramidal neurons. This complex network can control pyramidal neurons and provide the time structure needed to coordinate the activity of hippocampal neuronal ensembles. Since inhibitory interneurons modulate both afferent inputs and efferent activity and the excitability of pyramidal glutamatergic neurons, they are able to synchronize large cell populations. It is believed that, being the main target of the subcortical pathways, it is inhibitory interneurons that are able to exercise motivational, emotional, and autonomous control of the activity of the hippocampus. Braking control of glutamatergic pyramidal neuron activity is also the basis of memory acquisition and reproduction processes.

The exclusive role of the hippocampus in the processes of memory and learning in humans and animals is currently a proven fact, largely due to the work of domestic researchers. After the emergence of such methods as recording the electrical activity of single neurons, local microdestruction, etc., it became possible to study the role of individual areas and even individual types of hippocampal neurons in the processes of acquisition, storage and reproduction of memory. Summarizing the data of numerous clinical observations of patients with a destroyed hippocampus, Vinogradov concluded that the destruction of the hippocampus leads to violations of the so-called general (supmodal) memory factor.

To understand the role of the hippocampus in brain activity, it is important to emphasize that the hippocampus has powerful links with the associative cortex. Neocortical-limbic projections from individual sensory areas of the cortex are duplicated by connections from the higher convergence areas of all modalities (the lower tempered region and the upper part of the superior temporal gyrus in the posterior part of the hemispheres, as well as the frontoorbital cortex, arcuate sulcus and frontal poles in the front part of them). The posterior associative and convergent regions are believed to be associated with gnosis, i.e. “Objective” reception of external information, its processing and storage, whereas the pre-frontal areas – not only with praxis, but also with a subjective attitude to external information, to their own actions and their results. Such a two-way connection of these areas with the limbic system is necessary for the normal functioning of the fixation system of the new experience and the reproduction of the old.

Thus, the hippocampus is a structure that plays a large role in the implementation of cognitive functions. In this regard, it attracts the attention of researchers in cases of cognitive deficits, especially in Alzheimer’s disease and other neurodegenerative diseases, as well as in the development of such deficits in endogenous psychosis, including schizophrenia.

Schizophrenic Spectrum Disorders

To schizophrenic spectrum disorders include mental illness, their symptoms are similar to schizophrenia but by the severity is not equal   her. Sometimes they have such a blurred picture that they don’t only relatives of the patient, but sometimes and   health workers “look through” symptoms, such as schizotypal personality disorder, in the power of which help is not turns on time. Thats   same may apply to acute transient endogenous disorders of the schizophrenic spectrum when symptoms (for example, delusional and hallucinatory ) lasts a short time, and then disappears. However, being not treated on time, she can return again, leaving her negative consequences.

Probably in   Based on the origin of all such disorders, a common basic genetic vulnerability has been established. And usually in schizophrenia, and with schizophrenic spectrum diseases in   prodromal period (n and   dosymptomatic stage) already marked the special features of a person. So, teachers in   school may point to   some features of the memory, thinking of the child, his communicative features and   emotional reactions, “weirdness” in behavior.

To Unfortunately, the opinion of the average man and   on   Today it remains such that all mental disorders are commonly referred to as  schizophrenia which is considered a little whether or not   contagious disease. This leads to   stigmatizing disorder so much so that   patients and   their  Relatives sometimes even when doctors are embarrassed to make a diagnosis, replacing its wording with the phrase:   I’m sick on   the letter Sh . None   less with adequate treatment of schizophrenia and   diseases of the schizophrenic spectrum, the prognosis can be very favorable. BUT  speaking of   the latter, it can be noted that sometimes their   the symptoms are so erased (for example, in schizotypal disorder) that certain moment not attracted to attention, since pronounced social maladjustment can and   not   be as well   with successful and   timely treatment of a person remains workable and   socially adapted to throughout life.

The very prevalence of schizophrenia is sometimes greatly exaggerated (by according to statistics, it is 1% of population in   any region of the world). However, this number may vary, but   not at all by the cause of the beginning of the “epidemic” of schizophrenia and   disorders of this spectrum, and at mind overdiagnosis of this group of diseases.

Since the etiology of this group of disorders is not yet   before   the end is understandable only terminological confusion (for example, there are certain differences in two large medical classifiers of diseases   – ICD adopted in   Russia and   European countries, and   DSM used in   countries of America).

However , if the origin of this group of disorders causes controversy, and mankind is still looking for the causes of these diseases, there are statistics that can disprove the myths about total severity of schizophrenic spectrum disorders. In   worldwide treatment   Is a way of qualitatively stopping the acute condition of patients, and subsequent socio-pedagogical, cognitive, labor rehabilitation and psychotherapy, in including family, give opportunity recovery, in including full, for a certain percentage of patients.

Thus, schizophrenic spectrum disorders, including schizotypal personality disorder, and schizoaffective disorders are amenable to correction and   treatment, especially in   In cases where the disorder is diagnosed on time, the diagnosis is established correctly, and   treatment is prescribed adequately.

Although often we hear the question: if symptoms of schizotypal disorders do not so pronounced then worth do worry at all and “Pull” a person along   to doctors? The answer can be only one: worth it. At a minimum, differential diagnosis and   accurate diagnosis. In the study of schizophrenic spectrum disorders it is always very important to separate from   schizophrenia itself. Only then will it be possible to assign adequate treatment, and   therefore, the possibility of high-quality rehabilitation, significant assistance to the patient’s family and   guarantees that his life will be in   further full and   quality.

Residual schizophrenia

Residual is called schizophrenia , which continues to bother the patient (and more – his relatives) one year after the successful treatment of acute psychosis. Term in one year is a fairly conventional unit for determining the diagnosis of “residual schizophrenia”. Span can last from nine to  fourteen months old that lets talk about chronic schizophrenia.

Symptoms residual schizophrenia

•           Negative symptoms predominate (a scientific term for this symptom complex   – “affective flatness”):

  1. Lack of will.
  2. The absence of any initiatives .
  3. Persistent indifference .
  4. The absence of significant reductions in facial muscles of the face.
  5. Overall
  6. Indifference to   need self catering. This is what causes the most problems for people surrounding a patient with residual schizophrenia.
  • There are no signs of organic damage to the central nervous system.
  • Not  detected
  • Notsigns depressed.
  • Productive symptoms (hallucinosis , delusions) in   this period is quite rare and expressed weakly.
  • The patient himself is not pays attention to listed manifestations of the disease but they disturb his relatives and surrounding
  • A prolonged form of schizophrenia (residual schizophrenia) turns the patient off active forms of social life.

Diagnosis of residual schizophrenia

At  currently, there are disputes over about the criteria for this diagnosis. At the presented material contains the most accepted signs of residual schizophrenia by the scientific world. A clear diagnosis should be made for a differentiated approach to treatment, the development of uniform standards of therapy. Decisive role in accurate diagnosis is played by a competent psychiatrist.

Treatment of residual schizophrenia

Often, treatment is possible only when   foreground psychotherapy and   social rehabilitation . Without them, drugs (even prescribed in maximum doses) may have little effect on   symptoms of the disease. Requires a careful individual approach to each individual patient for his successful adaptation in family and society. The patient must constantly explain the details of his condition, which are visible only to an outside observer. Rehabilitation success is possible only with full confidence in   psychiatrist with patient side and   his relatives or guardians. Of great importance isgroup psychotherapy . If in the collective of patients with residual schizophrenia develops mutual support, which continues after the inpatient course, then This group has good prospects for   full social adaptation. Higher stage – professional adaptation, which is possible with perfect compliance with the recommendations of the attending physician.

Passive-aggressive personality disorder

Passive-aggressive personality traits stood out in the DSM classification, starting with its first version. The core line of patients is a permanent installation to a hidden obstruction, passive resistance to the leadership, behind the facade of which there is aggression not allowed to manifestexpression. They have a low level of self-affirmation, they cannot stand up for themselves, directly talk about their needs and desires. At the same time, they are always dissatisfied, annoyed and disappointed with someone or something. Patients are constantly looking for flaws in the authoritarian figures to which they are subordinate, and at the same time make no attempt to break free from their dependent position. Delays in the work are plausible excuses in varying degrees. At the same time, patients believe that they work much better than others think about it, reacting with indignation to the assumption that their productivity could be higher.

When forced to achieve success in work, or when, for some other reason, their internal aggression loses ground, they are clearly worried. They have a specific, hostile-subordinate character of communicative behavior, which manifests itself not only in work, but also in communication in general.They impose on others the position of their own dependence in such a way that it is perceived by others as punishment and manipulation. Those with whom the patients are in a relationship, are rarely calm and happy. Patients can, for example, spoil the party with their complaints and claims, without making any excuses without making their positive contribution to it.

Others eventually have to fulfill instructions for them and take their share of responsibility. Friends and relatives have to intervene in the process of therapy, expressing those claims to the wrong, in the opinion of the patient, treatment that he himself does not make to the doctor. Since patients are constantly focused on the presentation of claims, it is often difficult to formulate how the situation in which they would be satisfied should look like. Naturally, negative reactions of others to the behavior of the patient close the vicious circle, being for patients a subjective confirmation of the validity of their pessimism and negativism. Suicidal threats are common, but rarely accompanied by suicidal attempts.

High comorbidity with alcoholism, depression and somatization disorder. High level of employment and maladjustment: less than half of patients with a longitudinal observation catamnesis retain manufacturing jobs or domestic work.

To diagnose a passive-aggressive disorder, the condition must meet at least five of the following criteria: 1) non-compliance with the deadlines, delaying and postponing the completion of the daily tasks performed, especially when the completion is stimulated by others; 2) unreasonable protest against just demands and comments of others, statements about the illegality of these claims; 3) stubbornness, irritability or conflict with the forced need to perform undesirable tasks for the patient; 4) unfounded criticism or contempt for the authorities, responsible persons; 5) intentionally slow or bad work when performing unwanted tasks; 6) hindering the efforts of others due to the non-performance of their part of the work; 7) Avoiding fulfillment of obligations with reference to forgetfulness.

Differential diagnosis. Despite the known external similarity, the behavior in passive-aggressive disorder is less spectacular, dramatic, emotional and aggressive than in cases of hysterical and borderline disorders.

Treatment. Patients of this type rarely see the cause of their social maladjustment within themselves and, therefore, have no motivation for treatment. The structure of the personality makes the patient, who wants to get help, outwardly fight against this as against an imposed, degrading task. In any case, they bring their own communicative style into communication with the doctor. Maintaining psychotherapeutic contact with patients of the passive-aggressive type is extremely difficult: concessions to their requirements are anti-therapeutic , and refusal of them threatens the loss of contact.Psychotherapy therefore runs the risk of degenerating into the constant presentation of claims to the doctor for not wanting to accept the addiction of the patient.

A suicidal threat, as a rule, should not be interpreted as a depressive reaction to the loss of love, but as an indirect expression of anger. Nevertheless , a sufficient severity of melancholic affect is an indication for the appointment of antidepressants.

Cognitive- behavioral techniques that confront the patient with the social consequences of his behavior are more effective than correct interpretations of his mechanisms. It is more productive to focus on cognitive techniques; pure coping training programs come up against the evading reactions of patients in which they are very skilled. Purely behavioral techniques of group therapy and social skills training are also successful here. The constant opposition of patients can be used in the paradoxical methods of managing them, when the doctor deliberately suggests doing the opposite of what he wants from the patient.

Dissociative (conversion) disorders

Common to this category of disorders are transient disturbances in the integration of functions of memory, consciousness, self-identity and motility, including the loss of some part of these functions. These disorders are known to mankind from time immemorial. Similar conditions are described in ancient Egyptian papyruses about 2 thousand years BC, where their appearance in women was associated with the “wandering of the uterus” (hence the term hysteria). Hippocrates and Galen linked them to sexual abstinence. In the 19th century, the French physician Briquet first identified them as dysfunction of the nervous system as a result of psychological stress. Charcot considered hysteria a consequence of hereditary degenerative changes in the central nervous system and, despite such an organic interpretation, he successfully treated her psychologically – with hypnosis. Janet (1989) advanced the theory of psychic dissociation, according to which, as a result of constitutional genetic causes, the synthetic activity of the psyche may decrease, while certain ideator and affective components are no longer recognized, manifesting themselves in sensory-motor effects through unconscious mechanisms. Breuer (1985), unlike Janet , considered the process of dissociation not as passive, but as initiated by the patient himself. He called this special state of only partial awareness of disintegrated mental processes autohypnosis .

Freud’s discovery of the basis of the mechanism of dissociation — the active process of psychological defense, the phenomenon of repressing threatening or undesirable content elements from consciousness — was extremely important . The emotion that could not be expressed turned out to be turned into a physical symptom, thus representing a compromise between an unconscious desire to express a thought or feeling and the fear of possible consequences. The symptoms, as it turned out, allowed not only to mask unwanted emotions, but also represented a kind of self- imposed punishment for forbidding the desire or removing oneself from a frightening situation. The same symptoms were responsible for obtaining secondary benefits from the role of the patient. The “somatic language” of symptoms can also be used as a means of communication when the latter is obstructed by unconscious, conscious, or socio-cultural factors. This way of communication is especially characteristic of infantile, immature, dependent individuals with a low level of education and intelligence. The communicative effect of the symptom is also manifested in the fact that, by transforming the conflict in different spheres of a person’s relationship into a physical disease, it allows the patient to manipulate the social environment, to some extent reducing the painfulness of the conflict situation.

The elimination of the blockade in the way of emotion, the subsequent emotional unloading (catharsis) and, consequently, the disappearance of the physical symptom, deprived of its unconscious emotional support, was the original basis of the psychoanalytic method. Unfortunately, the relationship between the extensive phenomenology of dissociative disorders and the laboratory study of dissociation is still far from being a clear concept.


Paranoid personality disorder

There is no accurate data on the prevalence of paranoid personality disorder. Patients rarely ask for help themselves and, when talking to a doctor, deny manifestations of personality disorder if they are sent by their relatives. Among the relatives of patients with schizophrenia, more cases of disorder than in the population. In men, it is more common than in women; individuals at high risk are those who have been formed in situations of various kinds of communicative restrictions (members of national minorities, residents of states with a ollitarian regime, emigrants, deaf people).

Clinic. Paranoid personality disorder is characterized by constant suspicion and distrust of people in general, a tendency to shift responsibility from themselves to others. This is an easily recognizable from fiction collective image of a collector of petty offenses and injustices, hypocrites, jealous husband, litigies . AT all kinds of situations they feel used in the interests of others, betrayed or offended. They are full of prejudices and often ascribe to others those thoughts and promptings that refuse to recognize in themselves. Transit ideas of a relationship are common, the wrong premises of which are purposefully and logically justified. At the same time, patients are convinced of their own objectivity and rationality. Their affective repertoire is limited, they lack humor, spiritual warmth, they often seem to be unemotional. The manifestations of power and authority are highly valued, all that is weakly and impairedly causes their contempt.

  1. Gannushkin considered the main feature of this type to be the tendency to form overvalued ideas, the most important of which “is the thought of the special meaning of … self.”In business, they can make an impression of energetic and active people, but others, as a rule, evoke negative feelings.

The conversation draws attention to muscular tension, inability to relax, and extreme suspicion of the doctor’s interpretations that may be unfavorable to them. Sometimes the disorder is a precursor to schizophrenia. In most cases, it lasts a lifetime, accompanied by problematic situations at work and in the patient’s family. As maturity is achieved and with low life stress, a psychological defense mechanism can act – the formation of reactions when patients become stressed by altruists.

In order to diagnose a paranoid personality disorder, a condition other than personality disorders (F60) must correspond to at least four of the following qualities or behavioral stereotypes: 1) excessive sensitivity to failures and failures; 2) constant dissatisfaction with other people, a tendency not to forgive insults, neglect, damage caused; 3) suspicion and a persistent tendency to distort the experience, when the neutral or friendly attitude of others is wrongly interpreted as hostile or dismissive; 4) laxity, selfishness, quarreliness and persistent, inadequate defense of one’s own rights;5) frequent unjustified suspicions of infidelity of marital or sexual partners; 6) increased self-esteem with a tendency to take what is happening to your account; 7) frequent unsubstantiated thoughts of conspiracies that subjectively explain events in a close or broad social environment.

Differential diagnosis. In the case of paranoid personality disorder, delineated delusional structures characteristic of delusional psychosis, as well as hallucinations and formal thinking disorders inherent in paranoid schizophrenia, are absent. Patients with a borderline type of emotionally unstable personality disorder are distinguished from this type by their ability to establish, albeit saturated with suspicion and heightened vulnerability, but extremely emotional relationships with others. Paranoid psychopaths are distinguished from antisocial lack of a chain of antisocial behavior in the anamnesis. With schizoid psychopaths, they are brought together by limited emotionality, but they are distinguished by their characteristic trait of intense suspicion and distrust. The most difficult to distinguish between paranoid and schizotypal disorder (F21), for which suspicion is also a feature.

In contrast to schizotypical , patients of this type do not have such a bizarre complex of behavioral, sensory and mental disorders, they are characterized not so much by the absence of distortions of communication skills, but by their characteristic orientation (eccentricity, eccentricity).

Treatment. The best approach is supportive individual psychotherapy. These patients do not tolerate group therapy, and behavioral seems to them too compulsory. Cognitive -behavioral programs aimed at reducing the background level of anxiety and improving the skills of problem-solving behavior achieve greater success . The physician should strive to be as open as possible, consistent and authentic, honest recognition of something here is always preferable to defensive reasoning. The doctor’s statements should be clear, unambiguous, the style of treatment should be professional, respectful and somewhat distant , given that trust and closeness of relationships are the problem areas of these patients.

One should not be overly zealous with the interpretation of dependency and the lowered self-esteem of patients, hiding behind the protective facade of mistrust and hostility. The basic setting of an unbiased and benevolent assistant helps the patient to adopt alternative explanations for what is happening. It is more productive not to rush into correcting such defense mechanisms as the negation of reality and the projection of guilt on others. It is better to just attentively listen to the accusations and complaints of the patient, avoiding standing on someone’s side.

These patients take drug therapy with an excessive amount of suspicion and the effect of it is usually not noted. Although the direct effect is indeed problematic, nonetheless, during episodes of alarming agitation, short-term administration of benzodiazepines is possible ; Delusionalinterpretations are an indication for prescribing small doses of Sonapax or Haloperidol .

Disorders of personality and behavior due to illness, damage or dysfunction of the brain

A common cause is a variety of structural brain damage, among which the most common trauma to the skull . The most etiologically significant are damage to the temporal and frontal areas.

Clinic. The syndrome is characterized by sharpening (strengthening) premorbid personality traits or the appearance of pathological personality traits. Control of impulses and expressions of emotions decreases, the latter become labile and superficial with a predominance of euphoria or apathy.Euphoria is devoid of true fun, which can be recognized by the patient. On the euphoric background, especially when the frontal lobes are damaged, there is a characteristic tendency to flat jokes.

The frontal syndrome as a whole is characterized by indifference, apathy, lack of involvement in what is happening in the immediate environment. There are frequent outbursts of rage on minor occasions, especially during alcoholism, accompanied by aggressive behavior. The generally accepted norms of behavior are not observed, sexual disinhibition and law conflicts are frequent. Typical is the inability of patients to anticipate the consequences of their actions, to understand the problems that they create to others. Blaming others is the most frequently used technique for solving their problems.

In cases of temporal epilepsy, there is often a loss of a sense of humor, viscosity (a tendency to pseudo-philosophizing , entrapped stuck on serious topics, ignoring the lack of interest in the interlocutor) and pronounced aggressiveness beyond convulsive manifestations. For such patients, characterized by a triad: the hypergraph (the endless diary writing, texts), increased religiosity (or preoccupation with a sublime idea) and hy about – or hypersexuality. Possible slight cognitive impairment (reduction of short-term memory) does not reach the degree of intellectual decline.

In the presence of structural morphological changes, the syndrome is persistent. The growth of an organic lesion (brain tumor, Huntington’s disease ) can transform the syndrome into dementia. In some cases, with the successful treatment of a primary disorder or cessation of intoxication, the syndrome may be reversed.

Diagnosis. The ICD-10 formulates the following diagnostic criteria common to the group of disorders F07: 1) objective data on the presence of organic cerebral disease, brain damage; 2) the absence of impaired consciousness or pronounced memory impairment; 3) the lack of convincing data on the presence of a different cause of personal and behavioral disorders characteristic of group F07.

Differential diagnosis. With dementia, personality disorders are only one aspect of global intellectual decline. The presence of an organic etiological factor distinguishes this syndrome from other mental illnesses accompanied by personality changes.

Treatment. The main is the impact (if possible) on the primary organic violation. Symptomatic treatment with various (depending on the target of therapy) drugs is variously effective: antipsychotics, anxiolytics , lithium, hormones, beta-blockers, non-tricyclic anti-depressant trazodone , anticonvulsants. In the presence of aggressive behavior in cases of temporal epilepsy, carbamazepine therapy is indicated . Should strive to avoid alcoholism. The participation of social workers contributes to the improvement of social accommodation of patients. Family counseling should provide emotional support for the patient’s family members and specific advice to help minimize unwanted patient behavior. Antisocial inclinations often make it necessary to keep these patients in specialized closed medical institutions.

Paranoid schizophrenia

Paranoid schizophrenia is the type of disease that occurs most often. Sometimes mistakenly called paranoid schizophrenia. Manifested by the presence of delusions of persecution, obsessive ideas, conversations with non-existent interlocutors, while there are problems with self-identification. Sometimes paranoid schizophrenia is accompanied by hallucinations and catatonic symptoms (mild).

The exact causes of the disease are still not fully determined. Possible causes that can cause hereditary mental disorders are: the influence of the environment, family education, prenatal and stressful factors, alcoholism, drug addiction and disorders in the brain (neurobiological factors), age crisis.

Prevention of paranoid schizophrenia

Schizophrenia affects about 1% of the population. The first, pronounced attack often comes to 30 years. But the early signs and symptoms of paranoid schizophrenia can occur as early as adolescence / adolescence. During his life, anyone can get schizophrenia (the probability of developing the disease is 1-2%). In the course of the development of the disease, the social aspects of life and the functioning of a person in society suffer, which causes a person to have a strong mental discomfort.

Diagnosis of paranoid schizophrenia

In the Center for Psychiatry and Psychotherapy “Transformation Clinic”, clients will receive comprehensive medical care:

  • diagnostics and detection of mental disorders;
  • determining the risk of schizophrenia;
  • detection of symptoms of the disease;
  • selection and appointment of optimal methods of recovery and treatment;
  • determination of the effectiveness of treatment;
  • the use of methods to prevent the occurrence of recurrence of schizophrenia;
  • the use of rehabilitation methods for the return of a person to a full life.

Signs and symptoms of paranoid schizophrenia

The main symptom of paranoid schizophrenia is nonsense. These are persistent similar installations that lead to a misconception about the world. With this mental pathology, delusions are mixed. This and the feeling of persecution, when the patient feels that he is involved in some business for which he can be punished. Brain of high origin: a person appropriates non-existent regalia. Hypochondriac delirium in paranoid schizophrenia is an artsy character and has little to do with reality. For example, the patient claims that they introduced computers inside the body, which disrupt the work of the organs. In addition, there can be love delusions, jealousy, dysmorphophobia (non-existent physical deficiency) and others. With the progression of the disease nonsense is built up in a clear systematic chain.

Hallucinations can join delusions. This is a distortion of perception when a person perceives something that is not in the real world. Auditory hallucinations are most common: voices that only a person hears. They criticize the patient, argue among themselves, are threatening, forcing a person to do what he does not want. If visual hallucinations join, the patient is even more detached from reality.

Among other disorders of paranoid schizophrenia, note:

  • senesthopathy- bodily sensations, not having a physical justification;
  • depersonalization – a disorder of perception of oneself, with the alienation of one’s personality;
  • social fenced off and care in your inner world;
  • emotional inadequacy, anxiety, sleep disorders, and other common mental disorders.

In paranoid schizophrenia, thinking remains safe for a long time. Just a small degree develops negative symptoms: rarely suffers will and emotional devastation is almost not expressed. Therefore, this group of patients for a long time maintains efficiency and commitment to socially approved actions: the creation of a family, the birth of children and others.

Most often, schizophrenia begins with auditory hallucinations, which are subsequently supplemented by visual. Brad is characterized by a distorted reflection of the surrounding world, which becomes a reason for misunderstanding of situations and a source for the development of false judgments and assessments.

Differential diagnosis

For the correct diagnosis of paranoid schizophrenia, it is necessary to exclude the likelihood of developing delusional disorder, acute transient psychotic and schizoaffective disorders, dementia and other organic personality disorders.

Medical history of a famous scientist

In 1958, at the age of 30, the first signs of illness appeared in the famous mathematician John Nash. In the same period of his life, Nash made several discoveries in the field of mathematics. During his life he was treated several times in psychiatric clinics. When his health condition improved at age 34, he got a job at Princeton University.

At the age of 66, John Nash received the Nobel Prize in Economics. Thanks to the research of John Nash in mathematics, a new scientific approach.

The scientist learned to live with a diagnosis of paranoid schizophrenia. And this did not prevent him from achieving success. The story of his life became the basis of the film “Mind Games”.

How to beat schizophrenia?

Treatment of schizophrenia is the use of a whole range of methods: drug treatment, psychological support, the use of psychotherapy and social rehabilitation.

Treatment of paranoid schizophrenia

The first attack may mean the beginning of a long-term mental illness, and may never happen again. The success of treatment depends largely on the time of detection of the disease: the earlier signs of schizophrenia are detected, the faster the treatment begins, the greater the likelihood for a positive prognosis and the greater the chances of long-term remission.

Paranoid schizophrenia – fully stopped by modern means!

Anyone who wants to recover and gets the support of loved ones and caring people have all the chances to cure mental illness. According to general statistics, every fifth person in the world who suffers from schizophrenia, with the right approach to treatment, achieves a prolonged remission of 5 years or more. These people become full-fledged members of society and a reliable support in their family.

Studies show that if a patient participates in a special psychotherapy program, the likelihood of a patient’s long-term remission increases dramatically.

Treatment of schizophrenia takes place under the supervision of a psychiatrist with the use of medicines (neuroleptics), psychotherapeutic methods under the guidance of a psychotherapist and a clinical psychologist. During treatment, the client undergoes a compulsory rehabilitation course in the hospital and after discharge.

Prognosis in the treatment of schizophrenia

90% of patients achieve a high degree of remission and can live and work on minimal doses of drugs supporting drug therapy. Even in the case of long-term medication, patients can lead a normal life and fully realize their potential. For this, a rehabilitation course is needed, in which the patient and his relatives participate. Statistics show that very often people who have suffered a disease, can return to a rich life and become even more productive than the average person.

City provokes schizophrenia

The brain of the townspeople and people living in the village reacts differently to stressful situations, scientists from Canada and Germany write in an article published Thursday in the journal Nature.

Life in the city, on the one hand, increases the risk of various diseases, but it also has advantages: inhabitants of policies usually earn more living in rural areas, here modern methods of treatment are more accessible. However, from the point of view of mental health, citizens are much more vulnerable than the villagers: neurotic and mental disorders, in particular, schizophrenia, are much more common among the former.

Group led by Andreas Meier-Lindenberg from the University of Heidelberg (Germany) decided to investigate the biological mechanisms that are behind the increased mental vulnerability of citizens.

To do this, scientists with the help of functional magnetic resonance imaging investigated how the brains of people with varying degrees of “urbanization” react to stress – from those born in the city to those who arrived there at a mature age.

In the course of the experiment, 32 volunteers had to press the buttons to choose the correct answers to the arithmetic problems that appear before their eyes on the displays of special glasses, under severe time constraints. The researchers at the same time through the headphones “criticized” them for poor performance of the task.

The stress level of the subjects was monitored at different stages of the experiment by measuring the content of the hormone cortisol in saliva, as well as pressure and pulse.

It turned out that in people with varying degrees of urbanization, different parts of the brain are activated in response to stress. For subjects currently living in the city, the stress “included” the amygdala in the brain, with the degree of activation increasing, from low in those living in small towns to much higher in those living in megalopolises.

In subjects who grew up in the city, but moved to the countryside, the center of activity under stress was located in another area of the brain – the cortex of the gyrus, which controls the emotional state.

“This discovery means that different regions of the brain are sensitive to the experience of living in a city at different periods of life,” says one of the authors of the study, Jens Prussner (Jens Pruessner) of Canadian McGill University.

According to him, this work allows us to better understand the risks that the urban environment poses to people’s mental health. Scientists intend to further explore the relationship between the observed effect and mental disorders.

The brain of the townspeople and the village reacts differently to stress

Life in the city is associated with an increased risk of increased anxiety, depression and schizophrenia, reports Live Science. Testing the brain of students who grew up or live in large cities allowed scientists from the University of Heidelberg (University of Heidelberg), Germany, to determine which parts of the brain are responsible for the stress response to the urban environment and lifestyle. Their article was published on June 22 in the journal Nature.

It has long been known that life in the city as a child two or three times increases the likelihood of developing schizophrenia, and a person who migrates to the city as an adult increases the risk of heightened anxiety and other personality disorders by 21% compared with rural residents.

To establish how the city changes the human brain, scientists scanned German students at a time when they were under severe stress: they were asked to decide an exam in which they could give no more than a third of the correct answers. The students were informed that they had passed the worst exam, and they also put pressure on them, constantly reminding them how important it is to pass the exam well.

It turned out that students who lived in urban conditions, in response to stress, increased activity in the anterior part of the cingulate gyrus of the cerebral cortex, and those who lived in cities in early childhood, increased activity in the amygdala. Both of these sites are responsible for the reaction to stress and in many ways help each other work. The researchers considered the behavior of the brain of a rural resident to be normal.

Now scientists want to establish what the urban environment should be so as not to cause a stress reaction in the brain. Their theory is that increasing the number of green areas and a more environmentally friendly environment can significantly reduce the pressure on the urban dweller, and thus improve his mental health.

However, the environment in which a person is located only increases the risk of developing mental illness. The causes that cause these diseases are most likely related to genetics. According to Around the World, a team of scientists led by Professor Douglas Blackwood (Douglas Blackwood) from Edinburgh University (University of Edinburgh) Scotland allegedly found a gene responsible for mental illness

It turned out that people suffering from schizophrenia, clinical depression or bipolar disorder, “silent” gene ABCA13. Two years ago, scientists from the Institute of Neurology in London (Institute of Neurology in London) and their colleagues discovered the genes responsible for the occurrence of dementia (dementia). This common disease is caused by damage to the GAB2 gene, which is usually associated with the APOE4 gene.

Brain electrical stimulation can cause symptoms of schizophrenia

Simple electrical stimulation of certain parts of the cerebral cortex can cause obtrusive hallucinations in a patient, resembling the symptoms of schizophrenia. An unusual effect was discovered and described by the staff of the Swiss State Polytechnic School. A study report published in the journal Nature.
A strange side effect was observed in the treatment of a 22-year-old woman who suffered from epilepsy and who had no previous mental health problems. The patient was trained for surgery to remove the epileptic seizure-causing scar tissue formed after a brain injury.

Trying to determine the center of epileptic activity as precisely as possible, the doctors applied electronic impulses to the patient’s brain. During the examination, the electrode accidentally touched the temporal-parietal region of the cortex, which is responsible for coordinating the body data in space to the brain. As a result, the patient had a steady feeling of the presence of a dark figure behind her back, copying the movements of her body.

The doctors who treated the woman decided to understand what was happening and repeated electrostimulation of the temporal-parietal region several times. Every time the impact caused the illusion of the presence of the “alien” figure in the patient. When the lying patient was asked to hug her knees, she had the impression that the dark figure was trying to hug her. Despite the fact that the patient was fully aware that what was happening was an illusion, her feelings were very realistic and frightening.

The patient “stranger” standing behind his back and copying the movements seemed to her to be a completely independent person, in no way connected with her body and consciousness.
According to the coordinator of the research project, the illusion recorded during the research can be explained by the projection of information coming in to the brain about the position of the patient’s own body under the influence of electrical impulses.

Observation results clearly indicate that relatively simple switching of electrical signals in the brain can cause complex psychiatric symptoms in mentally healthy people, notes Dr. Blanque. It is possible that a similar mechanism underlies such symptoms of schizophrenia as a split personality, an obsessive sense of subordination to someone else’s will, the perception of members of their own body as belonging to others, etc.

In the near future, scientists are going to reproduce the observed effect in clinical studies involving several healthy volunteers.

Functional neuroanatomy of schizophrenia

At this point in time   The diagnosis of “schizophrenia” today is made on the basis of subjective data that rely on the patient’s observations and research on his experiences – that is,   phenomenological level.

Brain tests after smith patients show that in schizophrenia there can be various   neuropathological processes. But new methods used in the practice of neuroimaging are not yet effective enough to reveal such a pathology in this disorder.   At   their use   not fixed and   functional,   and morphological changes in the brain.

Some functional neuroimaging techniques identify specific changes in the frontostriatal and frontolymbic regions of the brain in schizophrenia. Moreover, these changes were detected at the beginning of the disease, and during the manifestation during the first episode of psychosis.

Neuronal dysfunction underlies cognitive impairment in schizophrenia.

  • Dysfunction of the prefrontal cortex in schizophrenia

Many symptoms of schizophrenia   associated with the defeat of various areas of the prefrontal cortex. For example,   deterioration of working memory and other test scores are associated with insufficient activity   dorsolateral prefrontal cortex.

Functional neuroimaging in schizophrenia, confirming a decrease in the activity of the prefrontal dorsolateral locus, which is confirmed by special tests (Perlstein et al., 2003).

Numerous studies indicate increased activity in the dorsolateral prefrontal cortex in patients with schizophrenia. When performing complex tests, for example, split ringtones that require some effort, these changes become more pronounced. With simple tests, an increase in the activity of the cortex of the dorsolateral prefrontal region of the brain is observed;   Complicated tests decrease activity of this department, if schizophrenic patients do not perform these tests. (Callicot et al., 2003).

Reduction   activity of the dorsolateral prefrontal cortex leads to an executive response deficit   in patients with schizophrenia. And the deficit in selecting answers with a corresponding sense of success, with concomitant reward, is associated with the ventral and orbitofrontal areas of the prefrontal cortex.    (Chemerinski et al., 2002).

Reduced prefrontal activity associated with reduction   responses to stimuli that enhance motivation, as the neural networks of the amygdala, which are projected, are suppressed   on the prefrontal region (Paradiso et al., 2003).

Strengthening the motivational aspect when choosing an answer is associated with the lower or orbitofrontal region, which play a role in the process of choosing one or another solution of problems associated with tests for inappropriate behavior.

Healthy people   The interaction between the dorsolateral and ventral and prefrontal cortex provides a balance between test responses based on choice and the motivation to inhibit inadequate responses. And in schizophrenic patients, this interaction is destroyed.

In patients with schizophrenia   interaction   between the lower and dorsal foci of the prefrontal area   affects pathological activity in the anterior cingular region, which is also involved in monitoring responses.

These data suggest that dysfunction of the prefrontal cortex is observed in schizophrenia, which leads to clinical and cognitive symptoms.

  • Dysfunction of the temporal cortex

Reduced activity of the temporal cortex   schizophrenia revealed by many scientists. This is established both by functional neuroimaging ,   and electrophysiological studies, as well as in the process of conducting auditory tests for selective attention.

A progressive deficit in the activity of the temporal cortex has been identified in schizophrenia by many researchers. Functional neuroimaging and electrophysiological studies also revealed pathological foci. The research results revealed a decrease in ties   between the frontal and temporal cortex of the brain that was associated with   results of the auditory test.

Functional deficiency of the limbic cortex and pathology of the midbrain

The limbic system of the brain is represented by the area of the cortex on the medial side of both hemispheres of the brain, and includes the amygdala and hippocampus . Limbic system   involved   in the cognitive process, and also associated with taste, eating behavior, aggression, expression of emotions, sexual behavior.

In patients with schizophrenia, the content of dopamine in the limbic system is increased , especially in the left amygdala of the brain.

Dopamine receptor increase   also found in patients with schizophrenia in the area of the visual mound. Based on these data, it can be said that diagnostic methods based on phenomenological   level, will soon be a thing of the past.

Hallucinations and delusions as symptoms of schizophrenia

Hallucinations and   rave   – it is alone of major signs acute frustration psyche . Wrong to call them   only signs of schizophrenia, since they can accompany and   other mental illnesses. Exactly so at treatment patient having similar symptoms , extremely is necessary thorough medical survey and   differentiated diagnostics .

But   here we   will consider these phenomena exactly in   framework given disease, where they are positive ( productive ) symptoms schizophrenia . Thats   there is   the picture diseases appears   what not   can be at   man in   normal.

Let’s start with   that hallucinations and   delirium in schizophrenia   These are signs of acute psychosis that require immediate treatment.   qualified psychiatric care. Need to remember that on   further course of the disease affects   how timely and   its acute manifestation was stopped. The faster the patient’s relatives take care of   rendering assistance, the more favorable the prognosis. A gross mistake is   what   for some reason, relatives expect that the symptoms of schizophrenia will disappear   yourself, or about   there is simply no one to take care of the patient, and   then the acute psychotic state continues to progress. Naturally in   In this case, it is becoming increasingly difficult to stop it.

Hallucinations in schizophrenia

When diagnosing schizophrenia, auditory hallucinations are most often detected when a person hears those   or other sounds or voices that are not in   objective reality. Voices most often first comment on a person’s actions, then they can begin to criticize him, threaten him, and   by   as psychosis unfolds, even ordering to commit those   or other actions. It is very dangerous, in   first of all, for the patient himself, since he   can harm itself or people surrounding it, trying, for example, to be protected from   not   existing objectively but   available in   his distorted picture of the world, danger.

Signs of hallucinations :

  • the man suddenly becomes silent, starts toto listen to anything
  • talking tomyself (here, naturally not include man’s thinking out loud or comments on about anything he perceives or experiences in currently in reality, for example, “Where did this book disappear … “),
  • sudden,causelesslaughter,
  • increasing closure, inability to focus on

Delusional disorder in schizophrenia

Rave   – one more of   acute signs of schizophrenia. These are certain beliefs of a person or his conclusions that are not   match what surrounds it in   reality. This is the most inconsistency of reality   – one of   The first signs that an idea, a belief are delusional. The second feature of delirium   – her   sustainability and   the fact that no third-party reasonable counterargument given ideas   give in

According to statistics, order   80% of people with schizophrenia? suffer from various kinds of delusions.

By   Crazy ideas can be different in their content. So, classified:

  • Delusion of relationship (observed most often). The person feels like the center of all the phenomena around him and   events: the actions of all, even completely unfamiliar and   randomly passing people expressing them   persons driving past cars and   other things.
  • Brad of pursuit when the patient is sure that certain people / people / organizations intend to cause him some damage, are watching or are already causing some harm (neighbors are poisoned by gas, relatives pour in   food poison   and   other).
  • Nonsense effects (mental or physical), when a person is convinced that his thoughts, actions, experiences are not connected with   his inner personal motives as well   are the result of the influence of some external force: witchcraft, hypnosis, cosmic rays.

Less common but   So   other types of nonsense can occur.

The productive symptoms of schizophrenia may increase gradually or appear suddenly. Regardless   the rate of unfolding of such an acute condition in schizophrenia, you must immediately apply for   medical care. Remember: a person with such manifestations of the disease is often not   able to ask about   aid because the picture of the world and   perception of his own state for him is very much distorted. Especially if this is the first attack, the manifestation of schizophrenia.

High-quality relief of such conditions is impossible outside the hospital. The sooner assistance is provided, the more favorable the further forecast will be.

State of the Vegetative Nervous System in Schizophrenia

In patients with schizophrenia, especially before the period of psychosis and in the subacute period, there are changes in the vegetative nervous system. This requires attention during the diagnosis and treatment of a mental disorder.

The first sign of the development of schizophrenia is a dysfunction of the autonomic nervous system. This is manifested in the presence of pathological processes in the cardiovascular system, gastrointestinal tract, sleep disturbance, sleep cycle disturbance – sleep / wakefulness, etc. Therefore, when psychosis occurs, it is necessary to prescribe medications that affect the autonomic nervous system.

The results of studying the parameters of the autonomic nervous system in patients with schizophrenia indicate that they have a predominant parasympathetic system over the sympathetic one.

Of course, the appointment of substances toning the sympathetic nervous system should reduce the symptoms of schizophrenia, however, at the peak of psychosis, fluctuation in tone and predominance of the sympathetic nervous system over the parasympathetic with affective-delusional symptoms, also increased parasympathetic nervous system – with catatonia, which reduces the effectiveness of sympatomimetic drugs and prompts the use of drugs that stimulate the parasympathetic system.   It follows from this that the use of sympathicotonics during remission of schizophrenia may occur with the aim of preventing the recurrence of psychosis. It is known that medications of the vagoparalytic group, in particular atropine, were previously used in the treatment of neurosis-like , sluggish forms of schizophrenia, and pilocarpine could provoke a relapse of psychosis.

Observations on patients with schizophrenia during remission showed that the duration of remission can be predicted by the severity of the tone of the sympathetic nervous system.