It is interesting to try to qualify acute psychosis not by using atomized, randomly intertwining symptoms, but by recognizing a regular shift of more holistic states. At the same time, impaired consciousness ceases to be a symptom only of mental confusion, and it is given a large place during “crazy flashes” and even with purely affective ones. As for the general assessment (from a clinical point of view) of the concept of acute psychoses of Ey, its weakest place is excessive schematization and psychologisation of mental diseases, an attempt to “break the deadlock” with the help of exclusively psychological and philosophical concepts. General pathological, biological basis of psychosis is bracketed, actually turning into a group of causes divorced from the nature of the phenomena they cause.

Ey is almost not concerned with the relationship of catatonic disorders with oneiric, individual acute psychosis or syndromes, where fear affect and nonsense prevail. The place of delirium, which seems to be dissolved in the concept of “amentia” (mental confusion), remains unclear. Having noted the weak points of the old approaches to the description of many acute psychosis, and in part using the new achievements of clinical psychiatry, Ey still bases his psychopathological synthesis on the materials of the clinical analysis of the past and only proposes his own scheme for them. Regarding the course of these acute psychoses, EU also allows a transition to schizophrenia or other chronic delusional states, although in most cases he considers the course of the disease favorable.

In German psychiatry, three main approaches to acute atypical psychosis were defined. Unlike French psychiatry, the answer to the question about the relationship of these psychosis to schizophrenia and manic-depressive psychosis often constitutes the main task. For one group of psychoses, although the atypical nature of their clinic is beyond doubt, it is still considered possible to classify them as either schizophrenia or manic-depressive psychosis. Loyalty to the dichotomous division of endogenous psychosis according to Krepelin and at the same time some deviation from it towards their typological understanding is expressed by these authors in that they admit the existence of mixed, or intermediate, psychosis.

Schneider (1957, 1967) divides the intermediate psychosis into 3 groups: in the first picture of the disease contains both schizophrenic and cyclothymic symptoms, in the second attacks of manic-depressive psychosis and schizophrenia alternate. The third group includes psychosis, the clinical picture of which is mainly schizophrenic, but at the “height” has a “manic-depressive tone” and vice versa. Schneider’s cycloid psychosis (see below) is atypical autochthonous psychosis related to manic-depressive psychosis.

Another major representative of classical German psychiatry — Mayer-Gross (1960) also attributed atypical psychosis mainly to schizophrenia and manic-depressive psychosis. Thus, in the manic-depressive psychosis, the author included a form with catatonic manifestations, a hereditary and familial form sui generis, and true mixed psychosis (with two pathological heredities). True, the author acknowledged the existence of forms that can not be attributed either to schizophrenia or to circular psychosis.

Questions of clinical description, classification of acute endogenous psychosis for many years have been the subject of a large German psychiatric school, the leading representatives of which are Kleist and Leonhard.

In Leonhard’s classification (1957), acute atypical psychosis is included in phase psychoses, in cycloid psychosis, in unsystematic schizophrenia. In phase psychoses described:

a) pure depression (suspicious depression, or depressive psychosis of a Kleist relationship);

b) pure euphoria (confabulatory euphoria, or acute expansive confabulous disease according to Kleist);

c) dreamy euphoria. Non-systematic schizophrenia includes affectively saturated paraphrenia, schizophasia, and periodic catatonia.

Of greatest interest is the group of cycloid psychoses, which, according to Leonhard, are bipolar positively flowing psychosis. This group includes the psychosis of fear — happiness, agitated-inhibited confusion, and hyperkinetic-akinetic psychosis. The psychosis of fear — happiness is characterized at one extreme by the presence of fear with distrust and ideas of relationship. The other pole (happiness) is determined by the experience of bliss with delusions of grandeur. There may also be pseudo-hallucinations, ecstatic stupor, delusions of physical influence, confabulation, incoherence of thoughts, etc.

In the case of another cycloid psychosis – “agitated inhibited confusion”, thinking disorder is a determining disorder according to Leonhard. When excited confusion there is incoherence of thoughts, which leads to the formation of abnormal ideas (false recognition, ideas of relationship). Auditory illusions are observed, and less often visual ones. With inhibited confusion

thinking is “still”, and this gives rise to ideas of attitudes, meanings, pronounced confusion, etc.

Finally, hyperkinetic-akinetic psychosis is characterized by the presence of “pure psychomotor arousal” or “inhibition”, independent of thinking disorder or affective disorders. In the hyperkinetic pole, expressive and reactive movements are observed. In the pole of akinesia, posture and facial expressions are noted, patients do not perform the simplest proposed movements, they offer resistance. Akinesis is often accompanied by confusion, and sometimes incoherent arousal with a frozen posture and facial expressions.

Ecstasy, ideas of the relationship can be observed, and sometimes the picture resembles mania or melancholy (most often this is observed when the motor psychosis increases or decreases).

Leonhard distinguishes clinical forms on the basis of a grouping of disorders around one core disorder: in one case of affective, in the other – thinking disorders, in the third – psychomotor. The remaining symptoms are more or less optional and most often “secondary”. It is interesting to note that neither the semiotics nor the role of the disturbance of consciousness is discussed in detail by the author. It is only mentioned that at the height of cycloid psychosis, disorders of consciousness can easily arise, and they can determine the scenic nature of false recognition. When describing periodic catatonia (in the group of non-systematic schizophrenia), the author does not include oneiroid disorders in its clinical manifestations.

In the literature, the nosological assessment of cycloid psychosis, proposed by Leonhard, meets many objections. Separate from psychoses, isolated from Kleist and Leonhard, are recognized by many psychiatrists as forms of acute “attacks” (motor psychosis, expansive confabulous disease).

The works of Kleist, Leonhard, and their numerous students allowed them to describe clinical contours in a new way and to describe in part the content of many acute psychoses. The work of this school, however, shows how important methodological principles are for the successful clinical description.

After identifying a definitive core disorder in these complex psychoses, the rest of the symptoms turned out to be very weakly associated with it. As a result of this approach, the oneyroid series of symptoms and other signs of disorder of consciousness fall out. Another weak point in the classification of these psychoses (reaching the level of nosological synthesis) is the recognition of phase as the defining and obligatory feature. How risky it can be seen from the results of the follow-up check 10 and more years after the first attack, 29 patients diagnosed with expansive confabulese (Giebner, 1961). Benign phasic course of the disease took only 14 patients. In 13 patients, a follow-up check established schizophrenia (paranoid or hebephrenic form), in 2 patients — organic psychosis (progressive paralysis, arteriosclerosis).

In German psychiatry, more and more supporters are finding a more extreme, purely typological assessment of acute anti-acute psychosis within a single psychosis.

So, Janzarik (1962), believing that with the current level of knowledge in psychiatry it is impossible to strive for the nosological distinction between endogenous psychosis, proposes to distinguish only psychopathological types. Within a single psychosis, he distinguishes between 4 types of dynamic psychopathological disorders that correspond to the clinical concepts of depression (“dynamic reduction”), mania (“dynamic expansion”), acute schizophrenic psychosis (“instability”), and schizophrenic defect (“emptying”). Conrad (1958), also a supporter of a single endogenous psychosis, divided it into 4 types depending on the severity:

1) the type of pure cyclothymic psychosis;

2) type of phase psychosis with delirium, a sense of change (schizoaffective psychosis, catatonia with “release of fantasy”, etc.);

3) the type that proceeds with seizures, but with residual effects in the states of remission, which makes it possible to speak of a fur coat, and not a phase;

4) the type of schizophrenic process in understanding Kraepelin early dementia.

The existence of typologically intermediate phase psychosis (between manic-depressive psychosis and schizophrenia), their interpretation from the standpoint of a single endogenous psychosis we find in recent years in the works of a number of leading German psychiatrists: Kranz (1969), Pauleikhoff (1969), Weitbrecht (1969), Petrilowitsch 1969, 1972). These authors did not specifically engage in the clinical study of individual forms of the psychoses in question, but even with a summary of the division of endogenous psychoses, they recognize a special clinic of acute atypical psychosis.

Portuguese psychiatrists have shown great interest in acute atypical psychosis for many years. Polonio (1954) called “cycloid psychosis and reactions” described acute psychosis, which divides into two groups: paranoid and incoherent. For both groups, the author considers as characteristic the occurrence on the background of “super clear” (“hyperlucidic”) or dimmed consciousness, an increase or decrease in mood and psychomotor activity. The beginning is usually sudden. The prognosis is favorable, personality changes do not occur. The author believes that these types of reaction are more likely than nosological units. According to the features of the clinical picture, Polonio distinguishes between: confabulous, hallucinosis, neurotrophy, paranoid expansive psychosis, paranoid attitudes towards oneself, paranoids of suggestion and influence, incoherent hyperkinetic and akinetic psychosis.

In addition to these “reactions,” Polonio described occasional schizophrenia. He referred those cases at which it was observed not less than three attacks divided by remissions to the last. He distinguishes paranoid, hebephrenic and catatonic forms (the latter is the most frequent). With all these forms, the pyknic constitution was more common, exogenous hazards before attacks. The most frequently observed were catatonic states of excitement and stupor, manic-disjointed, expansive delusions or delusions of persecution and hallucinosis. Often there is confusion, change of mood. The remaining symptoms are the same as for other (nuclear) forms of schizophrenia. Personality changes are not very pronounced and consist in the superficial nature of emotions and the absence of a clear sense of reality. The average duration of attacks in the absence of treatment – 7 months.

Barahona Fernandes (1959) identified a group of holodisfrenia, which includes several clinical types of psychosis: paranoid, hallucinatory, incoherent, motor, as well as twilight states and delirium. The author considers the main disorders of the global disorder of consciousness, attention and incoherence of thinking. There are disorders of sleep, instincts and affect, feelings of time, orientation. In the occurrence of these psychoses, constitutional, exogenous and psychogenic factors play a role. The course of the disease is acute, complete remission, without defect. Holodisfrenia differs from schizophrenia, according to the author, by the absence of a real discrepancy between behavior and frustrated functions. Nosologically, these psychoses are unclear, located between schizophrenia and manic-depressive psychosis.

As you can see, Polonio and Fernandes, adhering in terms of the clinical division of these psychoses of similar views with the Kleist and Leonhard schools, emphasize the special role of the disorder of consciousness. This brought them closer to the concept of Ey, which was reflected in the work of Goncalves (1961), an employee of their clinic.

When studying 45 patients (at the onset of the disease and at remote stages of the course), Goncalves came to the conclusion that the clinical picture of holodisphrenia is not always clear (as in the case of Leonhard’s cycloid psychosis), and he draws on the concept of disruption of Ey consciousness to explain this phenomenon. The author believes that with these psychosis, consciousness is almost always disturbed. The clinical picture may vary from attack to attack. Noting that the development of an attack goes through a regular change of syndromes, and recovery through a reverse change of states, Goncalves tries to concretize this situation. Acute delirium (delirium acutum), in his opinion, may be the final stage of these psychoses. In terms of nosology, Goncalves believes that a global disorder of mental functions distinguishes these psychoses from schizophrenia.

In the clinical evaluation of acute atypical psychosis, French psychiatrists do not raise the question of their relationship to schizophrenia. This is explained by the fact that schizophrenia is regarded by them only as a purely psychopathological concept. This is “chronic discordant psychosis”, the essence of which lies in a peculiar personality change, “total modification of human existence”, etc. (Follin, 1958; Ey, 1958). Discordance and autism are considered to be determining disorders (Ey adds nonsense). Clinically, schizophrenia includes 4 nuclear forms according to Kraepelin’s classification and some cases with a sluggish course (Eue et al., 1967).

Understanding schizophrenia as a purely psychopathological phenomenon, the content of which is personality change, it is assumed that a variety of illnesses can cause schizophrenia, including acute delusions and confusion. Acute psychoses (“syndromes”) are considered nosologically free, mobile. So Laboucarie and Barres (1959) with the clinical and follow-up study of 400 patients with acute psychosis (follow-up period 5–20 years) obtained the following results: in 100 patients, mental confusion or manic-depressive psychosis was determined after analysis of the first attack. The remaining 300 patients were divided into two groups according to the characteristics of the clinical picture of the first attack: a) with the state of the polymorphic structure (170 patients) and b) with acute depersonalization syndromes (130 patients).

For the states of the polymorphic structure, the authors consider the characteristic: a sudden onset without prodrome (as a rule, after psychogeny); global disorder of consciousness of the type of true oneiroid with fluctuations of its degree; affective disorders (most often of the type of purely manic or with elements of disturbing melancholia); polymorphic nonsense without systematization.

The first attack ended in complete remission after a few weeks or (less) months. The further course of the disease according to the follow-up was estimated as follows: in 30% of cases, remission after the first attack was stable, and there was no recurrence of the disease; 50% of patients had relapses, either with the same picture of the attack, or in the form of phases of manic-depressive psychosis. In 15% of patients, the disease took the form of chronically current schizophrenia.In conditions of acute depersonalization, the first attack was almost always preceded by a prodromal period, such as neurotic changes with elements of autism.

Psychosis often began spontaneously, and, if psychogeny occurred, it was rather a prolonged conflict situation in the family. The attack itself was characterized by ambivalence, an abundance of senesthopathic and catatonic symptoms against the background of unexpressed consciousness disorder (such as a reduced one-neuroid). The attack lasted from 3 months to 1 year, regardless of treatment.

The follow-up history of this group of patients revealed the following course options: “recovery” after the first attack in 20% of patients; rapid transition to classical schizophrenia in 30% – (the disease has taken a particularly malignant course); 50% of patients had relapses. In some of these patients, recovery from the defect sometimes occurred after many attacks. In other patients, after many years of almost complete recovery, there were bouts of melancholia, which are easily treatable. In other cases, relapses retained a schizophrenic nature, including the type of periodic catatonia.

The schizophrenic or affective structure of seizures depends, according to the authors, most of all on age. It is assumed that, despite the apparent schizophrenic structure of the first attacks (at a young age), the course of the disease in later periods proceeds very often in the manner of manic-depressive psychosis.Lacassin (1959), on the basis of a study of 180 patients with acute schizophrenia (the disease was at least 5 years old), concluded that the clinical picture of the initial period does not have the characteristic features that allow one to predict the course and even make a diagnosis. Regarding the psychopathological structure of these psychoses, Lacassin joins Ey’s point of view, considering them to be a manifestation of a particular level of consciousness destructuring, namely the oneiric level (see below).

Of the post-war works of French authors, the most significant in volume, depth of analysis and original views are the works of Ey. Most fully the views of this author are set forth in a large monograph on the structure of acute psychosis (1954). In this work, Eu expresses a special point of view on the question of the psychopathological structure and pathogenesis of all acute psychoses (manic-depressive psychosis, symptomatic affective psychoses, acute toxico-infectious, organic, epileptic psychoses, delusional outbreaks).Staying in terms of the clinical division of the true traditions of French psychiatry, Ey tries to explain the existence of many clinical options from the perspective of a special understanding of the whole of psychopathology.

In terms of psychopathology, in which, according to the author, the classification of psychosis is only possible, all psychotic states are divided into two groups: acute psychosis, which is caused by a pathology of consciousness (especially understood by him), and psychosis associated with personality pathology. The author refers to the first group:

1) manic and depressive seizures (endogenous or symptomatic, mono- or bipolar),

2) acute delusional and hallucinatory outbreaks and one-iroic states (also regardless of their etiology)

3) confused-onyric psychosis (delirious and amental structure).

Three groups of acute psychosis represent, in Ey’s view, the clinical expression of the three levels of consciousness destructuring. In the first degree of consciousness destruc- tion, a manic and depressive state arises; with a deeper disturbance of consciousness, acute delusional and hallucinatory flashes and oneiric states arise, and finally, the third, deepest degree of consciousness destruc- tion corresponds to psychosis, designated as exogenous delirium, exogenous confusion, amentia, etc. This understanding and classification of acute psychosis follows from general theoretical positions of the author, defending the need for an application to the psychiatry of the Jackson concept.

Ey understands consciousness as a form (“layer”) of psychic life, which “organizes in the field of the presenting present” sensually experienced at the moment (including data of perception, part of past experience and ideas about the future). In the “field of consciousness” at each moment the subjective and objective are presented, which are ordered by consciousness. The main content of consciousness is ordered sensory experiences. Hence the concepts of “phenomenal field”, “scene”. This field has a dynamic structure and organization. Consciousness has its own structure, reflecting the stages of evolution during life. The first, least profound degree of impairment of consciousness is “temporarily ethical destruction”.

Clinically, this is expressed in manic and depressive syndrome.In the manic state, only the direction of the stream of consciousness, its “ethical-temporal” orientation, changes. The consciousness of a maniacal patient is a “propulsion movement”, thanks to which the subject “breaks away from the forms of the present and eliminates them as rules of behavior”. Subjectively, this disorder is experienced by the patients as “endless striving forward”, as “celebration”, in which “all impulses of mastering the world are satisfied”, and clinically it is ecstasy, enchantment, etc. With melancholy, the negative structure consists, on the contrary, “to stop and retreat in the face of the requirements of the present. ” The positive structure of melancholia is expressed in tragedy or anxiety, in which all sorts of fears are actualized.

Both the manic and the depressive patient are characterized by “impossibility to balance with the present” and to keep in it. This ability, according to the author, is part of the functions of consciousness and is upset in the first place.With the next, deeper level of consciousness destruc- tion, except for a temporary ethical disorder, that is, a violation of the direction and purpose of consciousness, the sensory representation in the field of consciousness of reality itself is also disturbed.

This level of destructiveness corresponds to “delusional flashes”, epileptic twilight states, intoxication hallucinatory-delusional psychosis without confusion, oneiric syndrome, etc. With such a disorder of consciousness, there is a destruc- tion of the perception itself, which leads to a change in the temporal-spatial structure of the relationship between “I” and “peace”.

With a mild degree of disturbance of the temporal-spatial “layer” of consciousness, a disorder in the perception of the body arises, that is, the “bodily space” is upset (depersonalization, violations of the body pattern and senestopathy). If the violation is more profound, depersonalization reaches the depth of the “thinking person” and this is experienced by the patient as penetration, seizure, parasitism in thinking (mental automatisms and hallucinations, “experiencing hallucinatory splitting or acute states of mental automatism”).

With a somewhat deeper destruc- tion, the “fantastic encompasses the whole consciousness”, a “complete overturn of the space” sets in and a one-way state arises.Thus, Ey divides this second level of consciousness destruction into several degrees, with each of which connects groups of symptoms.When, finally, the destruction of consciousness encompasses “the ability to create a field,” the ability to “present,” there is a syndrome of mental confusion (amentia), in which clinically there is the impossibility of differentiating mental processes, deep obscuration, disorientation in space and space, and the world almost completely ceases. ” introduce myself. ”

According to Ey, each subsequent level of consciousness destruc- tion includes the violations of the previous level and therefore the clinic has affective disorders, for example, in the oneiric state, and affective disorders and symptoms inherent in the oneiric state in the amential state.In terms of clinical classification, Ey does not deviate from the traditional clinical division characteristic of French psychiatry, and proposes only with regard to psychoses of the “second level of destruction”, i.e. hallucinatory-oneiric, to distinguish two thematic modalities: the theme of happiness (ecstasy) and the theme of unhappiness (disaster, torment).

The concept of Ey represents, therefore, an attempt to more modernized the rationale for the traditional division of acute psychosis into large syndromes.Интересной является попытка квалифицировать

Alcohol is the most widely used psychoactive substance in the population. Due to the fact that not all cases of abuse are in the field of medical observation, epidemiological data on the alcoholization of the population, in addition to the number of patients with relevant diagnoses undergoing treatment, are obtained in a variety of ways: per capita consumption, life expectancy, suicide rate, germinal alcoholic the syndrome, the prevalence of cirrhosis of the liver, the cost of treatment for somatic diseases caused by alcoholism, the cost of lost as a result of alcoholism What time is it?

Morbidity varies greatly depending on geographical and socio-cultural conditions. In some countries, alcohol consumption is considered high (Russia, France, Scandinavia, Ireland, Korea), in some – low (China, countries of the Islamic world and the Mediterranean basin).

Mostly alcohol problems are typical for men; there are also significant transcultural differences. In women, pathological alcoholism begins later, spontaneous remissions are less likely. Pathology is most common at a young age (15-30 years), in individuals divorced or single, with lower levels of education and antisocial tendencies in adolescence. There is no systematic data on the role of the profession in the occurrence of the disease, however, there was a significant predominance of cases of liver cirrhosis in the service sector and literary circles.

Alcoholization is associated with 50% of road accidents, 50% of homicides, 25% of suicides. As a result of cirrhosis of the liver and a number of generalized somatic diseases provoked by alcoholism, the average life expectancy of patients is shortened by 10 years compared with the healthy population. Patients with alcoholism have the same risk of suicide as depressive patients – 15% of them complete their lives in this way.

Etiology. The disease is apparently the end result of a complex interaction of the biological vulnerability of the body and the influence of environmental factors. Hereditary burden plays an absolute role, although the mechanism of genetic transmission is still unknown. Children of alcoholics are 4 times more likely to get sick than non-alcoholic children, even if they were not brought up by their biological parents. In the presence of hereditary burden, the clinical picture is characterized by a more severe course.

The concordance of alcoholism among identical twins is twice as high as that of opposing people of the same sex. Neuropsychiatric pathology in childhood contributes to the development of the disease, for example, behavioral disorders (F91) or tic disorders (F95). A number of metabolic products when exposed to alcohol causes a change in the neurochemical adaptation of the brain at the cellular level. Perhaps this makes the body dependent on alcohol to maintain established pathological homeostasis. Alcohol can also lead to increased activity of endorphins or morphine-like substances.

The theory of learning was also used to explain the emergence of dependence. Temporary relieving of internal tension, fear, and the concomitant feeling of success in one’s social behavior during the first episodes of alcohol abuse can play the role of positive reinforcement, fixing a behavioral pattern dependent on alcohol.From the point of view of psychoanalytic theory, alcohol addiction predisposes excessively expressed, learned in the course of upbringing, excessive demands on moral attitudes and social behavior (“Super-I”). Stress arising from the inconsistency of the patient with these standards, decreases with alcoholism (“Super-I dissolve in alcohol”). Psychological features formed in early childhood that are generally typical for the personality of an alcoholic are described. It is characterized by timidity, difficulty in establishing contacts, insufficient self-assertion, impatience, irritability, anxiety, hypersensitivity and taboo in the course of education sexuality. An increased level of aspirations is combined with insufficient opportunities to achieve goals. Alcohol can give an illusory feeling of inner strength and success.

F10.0 Acute alcohol intoxication

Clinic, The state develops soon after taking an excessive (different depending on individual tolerance, rate of absorption and metabolism) amount of alcohol. A variety of clinical manifestations include disorders of social behavior, intellectual functions, motility, affect, vegetatics. In some cases, there is an increased talkativeness and sociability, in others – the desire for solitude and dysphorically suppressed background mood. Affective lability can reach the level of intermittent episodes of laughter and crying.

Symptoms increase as the level of alcohol in the blood increases, but they can also decrease with a sufficiently high tolerance, despite continued administration.

Depending on the dosage, the clinical picture changes, ranging from a state of mild euphoria (0.3 mg% in blood with normal tolerance) to impaired coordination, ataxia (1 mg%), confusion, constriction of consciousness (2 mg%), coma, suppression respiration and, occasionally, death (at a level in excess of 4 mg%).

Diagnosis.

In addition to signs common for acute intoxication, the condition should meet the following criteria: 1) the presence of at least one of the following behavioral and cognitive impairments: a) disinhibition, b) conflict, c) aggressiveness, d) affective lability, e) concentration disorders, f) narrowing of mental abilities, g) decrease in mental and productive productivity; 2) the presence of at least one of the following neurological disorders: a) unsteadiness of gait, b) negative Romberg test, c) signs of dysarthria, d) nystagmus, d) impairment of consciousness (for example, somnolence, coma).Differential diagnosis is carried out with soporous comatose states of a different etiology: injuries of the skull and spine, diabetic and hepatic coma, cardiac arrhythmia, myasthenia, overdose with a combination of use with other psychoactive substances.

F10.07 Pathological intoxicationThe etiology is unknown.

Predisposing factors are organic brain damage (especially in connection with encephalitis and injuries), old age, general fatigue, and alcoholism while taking sedatives and hypnotics. Since this rare violation is more common in people with an increased level of anxiety, for whom aggressive behavior is generally not characteristic, it is assumed that alcohol, causing disorganization of mental processes and loss of self-control, may contribute to the release of aggressive impulses.

Clinic.

The condition is characterized by behavioral disorders that suddenly appear shortly after drinking small amounts of alcohol (the level in the blood is usually below 1.5 mg%). Behavior is characterized by impulsive aggressiveness with tendencies that are dangerous for others or, more rarely, for oneself against the background of confusion, disturbances of orientation and perception (illusions, transient visual hallucinations and delusions). The condition lasts up to several hours, ending with a long sleep, followed by amnesia of the episode.

Diagnosis.

In addition to the fact that pathological intoxication occurs after taking a dose that does not cause a state of intoxication in most people and the signs common to Flx.0 are observed, the following criteria must be met: 1) the presence of verbal and / or non-verbal aggression towards others, which is atypical for a person sober condition, 2) the condition develops very quickly, usually within a few minutes after taking alcohol, 3) there is no data on the presence of any other cerebral or mental disorders.The differential diagnosis is carried out with episodes of sudden behavioral changes in temporal epilepsy.

Treatment.

The focus is on preventing the consequences of allo- and auto-aggressive behavior. Motor restriction may be necessary, but difficult because of the suddenness of development of the state. Plegiruyuschiy effect (if possible) is achieved by injection of antipsychotic (haloperidol).

F10.1 Harmful use of alcoholClinic.

Massive use of alcohol causes reversible fatty infiltration of the liver – the center of alcohol catabolism. It is not yet known exactly how this infiltration contributes to the occurrence of cirrhosis of the liver. Inflammation and, then, destruction of liver cells in cirrhosis is fatal in 10–30% of carriers of this disease.

Alcohol dissolves the gastrointestinal mucosa, causing irritation and bleeding, and contributes to achlorhydria, gastritis, and stomach ulcers. Diseases of the small intestine, pancreatic insufficiency and pancreatitis are also associated with alcoholism (75% of patients with pancreatitis are alcoholics). Alcohol interferes with the normal processes of digestion and absorption of food, reducing the intestinal absorption of a number of important nutrients, including vitamins and amino acids.

Chronic alcohol consumption violates the performance and rhythm of the heart, myocardial oxygenation, causing cardiomyopathy after 10 years or more of alcohol abuse. Chronic alcoholism due to a decrease in the number of leukocytes reduces the body’s resistance to infectious and oncological diseases, adversely affecting the body’s immunity.

As a result of direct effects on testosterone levels and testicular atrophy, alcohol reduces sexual and reproductive functions in men. Increasing the level of female hormones leads to female type of hair growth and an increase in the mammary glands in 50% of alcoholics. The indirect toxic effect of alcohol in the zone of limbic structures and the hypothalamus, as well as the neuropathy of the peripheral parasympathetic nerves involved in erection, also plays a role in impaired sexual function. In alcoholic women, there are dysfunctions of the sex glands, accompanied by insufficient production of female hormones, changes in secondary sexual characteristics, extinction of the menstrual cycle, infertility.

Alcohol use during pregnancy is fraught with the emergence of the so-called fetus in the fetus. fetal alcohol syndrome (slow growth before or after childbirth, abnormal configuration of the face and skull with a decrease in head circumference and flattening of facial features, signs of mental retardation and behavioral disturbances).

F10.2 Alcohol addiction syndrome

Clinic.

In addition to common for F1x. 2 manifestations of the syndrome of addiction should be mentioned that the specificity of chronic alcoholism includes various stereotypes of alcoholism. Drinking significant amounts of alcohol can be daily or limited to weekends. Alcohol abuse for several days / weeks / months (binges) can be interrupted by long periods of abstinence (dipsomanic stereotype). Daily alcoholism during off-hours can be accompanied for a long time by relatively safe professional status and lack of awareness of uncontrollable abuse.Binges can also be of a different nature, ending either spontaneously or involuntarily as a result of the corresponding complications of the social situation or physical condition (the latter is called “gamma-alcoholism” in the USA).

Characteristic signs are also episodes of complete or partial amnesia (the so-called palimpsests) of the period of intoxication, during which the patient could make the impression of a person with a safe mind on others.Amnestic manifestations generally correlate with the severity and duration of the disease.

The tendency to the use of non-food alcohol (technical alcohol, polish, brake fluid, etc.) is quite typical, increasing with the social degradation.Diagnosis. Diagnosis of addiction syndrome, especially in its initial stages, as a rule, complicates the tendency of patients to reject alcohol abuse. Sometimes the family of the patient takes the same position. The clinician should pay attention to such signs of early problems associated with alcoholism, such as difficulties in communicating with the spouse partner, loss of contact with children, loss of interest in family problems, frequent outbreaks of irritability.

Alcohol can be used both to relieve sexual lethargy and to avoid sexual contact. Late arrivals, inability to properly organize work, and meet the deadlines become typical for professional activities. Morning vomiting, diarrhea, gastritis, liver enlargement, cigarette burns on the fingers can be early somatic stigmas.

Treatment.

Central is the problem of abstinence from alcohol. Due to the fact that the so-called. controlled use still represents a high risk of relapse, the patient should be offered complete and lifelong abstinence, on the assumption that there is no condition: “recovered alcoholic”.The formation of motivation for total abstinence determines the overall success of treatment and depends on the proper use of intrapsychic and social factors that are important for motivation. Here, a proper assessment is needed in each case of an individual complex system of hereditary factors, conditions for early development, personal structure, socio-cultural and family influences, and concomitant psychiatric pathology.

The pessimistic conclusion about the lack of motivation for treatment too often hides the inability of the doctor to find an individual approach to the patient, to establish a therapeutically productive relationship with him.

At the initial stages, individual psychotherapy sets the tasks of emotional support for the patient with a gradual analysis of the mechanisms of dependence on others, lack of self-esteem, aggressive impulses, and such maladaptive psychological defenses as lies and denial. The most successful is a combined psychotherapeutic approach, which includes both identifying the internal causes of alcoholism (lack of resistance to social stress, low self-affirmation, etc.) with the development of more effective strategies for resolving behavior, and connecting with emotionally stimulating social influences that are important for the patient ( family relations, goal-setting behavior in the professional sphere).

Here, various group and matrimonial therapy programs are very effective, carried out both in inpatient conditions and for the purpose of long-term supportive psychotherapy in outpatient settings, including self-help groups (the most famous of them is the Alcoholic Anonymous program).

f it is impossible to correct the pathogenic influence of the family and close social environment, it is advisable to temporarily place the patient after the inpatient treatment in specially structured conditions of out-of-hospital residence.

The latter have not yet received practical distribution in Russia.Of the drugs, the most widely used is antabuse (disulfiram), the metabolism of which is accompanied by the accumulation of acetaldehyde in the blood when even small amounts of alcohol are consumed. The toxic reaction caused by a daily dose of 250 mg of antabus includes facial flushing, feeling of heat in the sclera, upper limbs and chest, nausea, dizziness, marked malaise, blurred vision, tachycardia, feeling of suffocation, numbness of the extremities.

The most serious consequence is a pronounced decrease in blood pressure. The reaction usually lasts 30-60 minutes. At higher doses of antabus, impaired consciousness and memory disorders may develop. The success of therapy depends on the motivation of the patient to regularly receive antabus.

At the initial stages of withdrawal symptoms of anxiety, anxiety, sleep disturbances dominate, which are controlled by anxiolytics; the clinical severity of depression during this period necessitates the use of antidepressants, lithium.

To relieve anxiety, behavioral therapy techniques can be successfully used (relaxation programs, self-control, self-affirmation enhancement). Chemical observational conditioning (apomorphine, against the background of which alcohol intake causes vomiting), as well as various suggestive methods (acupuncture, shock psychotherapy, coding, therapeutic vows, etc.) have a long-term effect only in a narrow category of highly motivated to treatment. patients, by virtue of which they are not funded by the insurance system, and they find much more limited use in world narcology than in Russia.

F10.3 Cancellation status due to alcohol use

Clinic. The condition is characterized primarily by a variety of vegetative symptoms, gross rapid-frequency generalized tremor, aggravated by movement or excitement. Due to the reduction in alcohol by the convulsive threshold, often within the first day, large convulsive seizures may develop, especially if they are in history. Usually disturbed sleep, accompanied by vivid nightmare dreams. Symptoms are enhanced by prolonged use of significant doses, dipsomanic alcoholism stereotype, general weakening of the body as a result of overwork, malnutrition, concomitant physical illness or depressive state.

The syndrome develops in 24–48 hours after stopping the intake and does reverse development within 5–7 days (including without treatment), although irritability and sleep disturbances can last even longer. In some cases, the development of symptoms leads to the resumption of alcohol intake for its removal.

Diagnosis.

In order to make a diagnosis, in addition to meeting the general criteria for withdrawal syndrome (Flx.3), at least 3 of the following symptoms should be observed: a) tremor of the fingers of the hands extended in front, the tip of the tongue or the eyelids, b) sweating, c) foul condition, nausea, vomiting, d) tachycardia or hypertension, e) psychomotor agitation, e) headaches, g) insomnia, h) malaise, weakness, and) transient visual, tactile or auditory hallucinations or illusions, j) large convulsive seizures.

Symptomatic treatment with bed rest, rehydration with severe fluid loss (sweating, vomiting, low-grade fever), elimination of vitamin B12 deficiency and folic acid. With reduced nutrition, thiamine is injected parenterally (before glucose, since the latter can impede the absorption of thiamine). If there is information about convulsive seizures in the history, magnesia sulphate is prescribed (2.0 50% w / m 4 times a day for two days). In general, anticonvulsants are less effective in preventing and treating convulsive manifestations with withdrawal syndrome.

In this regard, as well as to relieve hyperactivity of the sympathetic nervous system, benzodiazepines (diazepam, chlordiazepoxide) are more effective.

F10.4 Cancellation status with delirium due to alcohol use

Clinic.

The condition is also known as delirium tremens (delirium tremens). This is the most severe manifestation of withdrawal syndrome; it develops within a week after stopping or reducing doses, most often at the age of 30–40 years after 5–15 years of consuming significant doses. It develops in about 5% of alcoholics who are on a permanent basis, often being the first sign of alcoholism not previously diagnosed. Dipsomanic stereotype of alcoholism and concomitant somatic pathology contributes to the emergence.

Vegetative disturbances (tachycardia, sweating, hypertension), low-grade fever, wakefulness of perception (often visual and tactile, in the form of insects, small animals) and rudimentary delusional ideas defining the patient’s behavior, often dangerous, join signs common for delirium (F05). for myself and others. Large convulsive seizures are common, usually anticipating the onset of delirium in a third of patients with convulsive syndrome, most likely due to the deficiency of pyri-doxin (vitamin B6). Increases the pressure of the liquor and the level of globulin in it. In half of the cases transient albuminuria is noted.

The syndrome differs from delirium of non-alcoholic genesis by more severe impairments of consciousness and behavior, deeper amnesia of the episode at the exit from it, and greater vestige-related concomitant delusions.In the absence of complications, death is relatively rare (3-4%). The presence of auditory hallucinations is a prognostic sign of a more protracted course. In the absence of recovery, the state progresses to the formation of Korsakov syndrome in 15% of cases. If untreated, as a result of concomitant somatic pathology (pneumonia, fat embolism, renal, hepatic or heart failure as a result of hypohydration and hyperkalemia) delirium can be fatal in 20% of cases.

Treatment.

The most reliable way of dealing with delyriya is its prevention. 25-50 ‘mg of Elenium (chlordiazepoxide) every 2-4 hours during the most dangerous period of the withdrawal syndrome usually prove to be sufficient. If delirium could not be prevented, the dose is increased to 50-100 mg every 4 hours. The use of phenothiazine preparations should be avoided due to the fact that they lower the threshold of convulsive readiness, and may also contribute to a further reduction in liver function.Important is a high-calorie diet rich in carbohydrates and vitamins, if necessary – measures for rehydration.

The physical limitation of agitated patients is impractical, since they usually do not stop their attempts to free themselves, continuing to complete exhaustion. Skillful sedative psychotherapy may be important.

F10.5 Psychotic disorders as a result of alcohol

Manifestations of alcoholic hallucinosis (usually auditory) usually begin within 48 hours after the cessation of alcoholism and persist after the withdrawal of withdrawal syndrome, while not being a component of possibly accompanying delirious symptoms. The content of votes is usually unpleasant for the patient, causing reactions of fear and anxiety, sometimes defining behavior and making it dangerous. This is usually a critical, threatening or offensive comment, where the patient is mentioned in the third person. Auditory deceptions can take on the character of elementary sounds (for example, calls).

The disorder is relatively rare, more common in men; the syndrome appears at any age, but against the background of an already formed dependence on alcohol. Its duration is varied – from several weeks to several months.Psychotic disorders can take on the character of paranoiac symptoms or systematized delusions, the most famous of which is the alcoholic delirium of jealousy.

The diagnosis of the latter can be complicated by the existence of real justifications for jealousy due to the sometimes existing decline in sexual function and the loss of the patient’s interest in family matters.

From schizophrenia and affective disorders, these conditions are distinguished by the lack of relevant data in history, a temporary connection with the abolition of alcohol, the relative short duration of the course, the characteristic content of votes. The syndrome differs from alcoholic delirium by preservation of consciousness, the preferred appearance of hallucinations not at night.Treatment includes primarily activities carried out with withdrawal syndrome. In the absence of effect, small doses of high-potency neuroleptics can be used with discontinuation after the symptoms have been eliminated.

F10.6 Alcohol-based Amnesia Syndrome

Wernicke’s encephalopathy (delirium, ataxia, nystagmus, ophthalmoplegia), acutely developing amid perennial alcohol abuse with concomitant tiamin deficiency due to nutritional deficiencies and vitamin B1 absorption, in 85% of cases without treatment ends with amnestic syndrome (psychosis) of Korsakov, nature a feature of which is a violation of short-term memory (but not direct memorization) against the background of an unbroken consciousness with the impossibility of transition of short-term memory into long-term yu Both disorders sometimes designate Wernicke-Korsakov syndrome.

The syndrome in recent years has become increasingly rare due to the routine use of thiamine during detoxification. The common amnesia disorder can be accompanied by the usual somatic and neurological consequences of alcohol abuse. With daily use of 50-100 mg of thiamine chloride, it is possible to achieve different degrees of recovery, but in most cases, Korsakov’s syndrome remains irreversible, despite withdrawal and continued administration of thiamine. Structural deficiency of the trunk and diencephalic brain regions is determined pathologically.

As an in-depth psychopathological study of early dementia, the concept of “schizophrenia” appeared and was recognized. However, the solution to the problem of acute atypical psychosis has not progressed significantly. The clarification of the clinical forms of schizophrenia, made somewhat later by Kraepelin (1913), did not lead to the final solution of the question. As you know, Kraepelin recognized the existence of circular schizophrenia, schizophrenia with a depressive-delusional clinical picture, the possibility of recovery from schizophrenia, its periodic course. For all these reasons, by the end of the 10s and especially in the 20s of our century, the controversy surrounding atypical psychosis intensified.

There were again points of view about the impossibility of reducing many forms of psychosis to one of two endogenous diseases according to Kraepelin’s classification. In France, many psychiatrists again put forward, with minor amendments, the teaching of Magnan on acute polymorphic attacks.

In Germany, by this time, even more attention began to attract direction, whose supporters viewed acute atypical psychosis as a group of endogenous diseases (along with manic-depressive psychosis and schizophrenia). Representatives of the Kleist school in the 1920s proposed a new clinical classification of acute atypical psychosis. This direction has many supporters. Other psychiatrists (Kretchmer, Mautz) have suggested the genetic or constitutional conditionality of the mixed clinical picture of acute atypical psychosis.

A point of view emerged that many of the schizophrenic manifestations of psychosis are “schizophrenic reactions” and their occurrence is associated with the presence of a special form of degenerative background (Popper, 1920), with a schizoid predisposition (Kahn, 1921).

Thus, in the 1920s, the following clinical guidelines for assessing acute atypical psychosis were already determined:

1. The classical dichotomous direction, which has many supporters at the present time, according to which all atypical psychosis, including acute, can be attributed either to manic-depressive psychosis or to schizophrenia. It may be noted that for supporters of this point of view it was still a controversial question as to which of these two psychoses one should nevertheless refer certain variants of acute atypical psychoses.
2. The direction according to which acute atypical psychosis should be considered as a special group of endogenous psychosis (Kleist and his school).
3. The direction that treats atypical psychosis as mixed as a result of combining different constitutional radicals or as reactions when they are especially ready.

In the following decades, up to the 1940s, the central issue regarding acute atypical psychosis remained the issue of their nosological affiliation in numerous discussions on schizophrenia. True, the view was increasingly expressed that it was necessary to consider the possibility of their exogenous conditionality in their nosological assessment. A similar point of view arose after psychiatrists considered “endoform pictures” and began to allow for exogenous mental diseases. Many psychiatrists, supporters of the nosological direction, began to describe various types of acute psychosis, the clinical picture similar to manic-depressive psychosis and schizophrenia. In particular, psychogenic delusional psychosis (acute paranoids, prison psychosis), various catatonic and delusional psychosis in infectious, somatic diseases, etc. were described.

A broader understanding of somatogenic and reactive psychoses led to the “dissolution” of a large number of acute atypical psychoses in them. Nevertheless, the study of acute psychosis from the standpoint of “exogenesis” made it possible to find out a number of important aspects of acute atypical psychosis, in particular, to establish a close connection between the onset of seizures and certain harmful factors.

The literature data on the development of views on acute endogenous psychosis show how difficult they have been for clinical analysis for many decades. As is known, up to the present, these psychoses remain one of the most difficult problems of clinical psychiatry. The extensive literature is devoted to them, in which questions of clinic, psychopathology, systematics, nosological assessment are considered. There are numerous disagreements about these issues. This fact determined the direction of our analysis of the main modern works devoted to the psychoses under consideration. It seems to us important to identify the main sources of still existing difficulties and disagreements regarding the most important clinical aspects of acute endogenous psychosis. Such an analysis of modern literature, together with the historical data, should, in our opinion, facilitate the development of approaches to overcome the difficulties of the clinical evaluation of acute endogenous psychoses.

In determining the scope of the literature to be analyzed, the following provisions were taken into account, arising from the state of clinical psychiatry.

1. The most clinically clear and generally accepted acute endogenous psychosis are typical manic-depressive psychosis and seizure-like remitting schizophrenia with a fairly pronounced schizophrenic seizure pattern and characteristic schizophrenic personality changes (dissociative defect type). For these two psychoses, the classic differences between manic-depressive psychosis and schizophrenia remain true.
2. Difficult for clinical evaluation are those acute endogenous psychosis, which are referred to as atypical circular psychosis, schizoaffective psychosis, acute atypical psychosis, recurrent schizophrenia.

In French psychiatry, acute atypical psychosis is currently included in manic-depressive psychosis, in the syndrome of mental confusion (confusion mentale) and in the group of delusional flashes (bouffees delirantes) singled out by Magnan.

In the understanding of French psychiatrists, mental confusion, or “states of confusion,” is a psychopathological syndrome characterized by stupefaction, irregular thinking, disorientation, false recognition (not always), oniric (dreaming) nonsense. Considering the main, determining disorder of confusion (simple or with hallucinatory-delusional phenomena), the syndrome of mental confusion can be understood very broadly.

Along with delirious states (such as delirium tremens), with Korsakov’s psychosis, with various acute infectious and intoxication psychosis, the concept of mental confusion also includes acute delirium (delirium acutum, febrile catatonia), and acute catatonic psychoses (non-febrile) and even psychoses with frustrated mind. leading to organic dementia.

All acute psychoses with catatonic symptoms and disorders of consciousness (including delirium acutum) are practically included in mental confusion as a syndrome of toxic-infectious genesis. Other acute, schizophrenia-like hallucinatory-delusional psychoses are combined by Magnan, the common term “delusional outbreaks”. True, at present (unlike Magnan), this group does not include catatonic psychoses. The delusional outbursts themselves are considered as a syndrome of different etiology, which is not only found in “degenerants”. Clinical and psychopathological description of such psychosis, made by Magnan. remains classical and almost generally accepted. Thus, the main clinical features of these psychoses are: the suddenness of the appearance of delirium (“instant illumination”), polymorphism and instability of delusional stories, massive affect (elevation or decline of mood), clarity of consciousness (at least apparent), and most often a sudden end of an attack. Although relapses are allowed and considered frequent, there is usually no personality change after an attack. The classic clinical forms of these delusional outbreaks are as follows:

1. Acute fantastic psychoses described by Dupre (1925). We are talking about acute psychosis, the clinical picture of which is determined by the acute fantasy that has arisen, more often such as delusions of grandeur and less often self-incrimination with the nature of immensity.
2. Acute interpretative psychoses (described by Serieux, Capgras, 1909) and later designated as “acute interpretative states” . These psychoses are delusional syndromes such as acute paranoid with fear and anxiety.
3. Acute hallucinatory outbreaks and acute hallucinatory psychoses with a predominance of auditory, verbal hallucinations, pseudohallucinations, and impact ideas;
4. True polymorphic forms, under which the systematization of delusional ideas does not occur.

Many of the acute transient psychoses are considered by French psychiatrists as atypical attacks or equivalents of manic-depressive psychosis. A catatonic equivalent (replacement of one or more affective attacks with catatonic attacks), episodic delusions of exposure, a senestopathic equivalent (an acute senestopathic attack), intermittent hebephrenia, acute paranoids, pseudo-paired melancholia are described; schizoform melancholia, pseudoshizophrenic postpartum psychosis of catatonic structure.

Recently, new terms have appeared and continue to appear to denote individual acute psychosis or whole groups. Baruk distinguishes postpartum hallucinatory delusions and postpartum delusions of persecution. Courchet et al. described acute psychosis in men and called it “transient mania” (according to Krafft-Ebing). According to the authors, this psychosis is a suddenly beginning state of motor excitation or confusion with disorientation, deep anxiety, mutism, without delusions and hallucinations. The psychotic state lasts 2–3 days, followed by a short phase of asthenia, and then recovery occurs. The acute period is completely amnesized. Attacks are not associated with any exogenous factors.

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.

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.

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.

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.

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 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.