Does dementia occur in schizophrenia? Simple form of schizophrenia

Chapter 19 discusses disorders classified in ICD-10 class F2. Although the symptoms of these diseases are varied, their main manifestation is delirium and related psychopathological phenomena. Despite the similarity of symptoms, the described disorders differ significantly in course, outcome, and degree of social maladjustment of patients. The main disease in this class is schizophrenia.

Schizophrenia

Schizophrenia- a chronic mental endogenous progressive disease that usually occurs at a young age. Productive symptoms in schizophrenia are very diverse, but the common property of all symptoms is schizis (internal inconsistency, disruption of the unity of mental processes). Negative symptoms are expressed in a violation of the harmony of thinking and progressive personality changes with loss of interests and motivations, emotional impoverishment. At late stages of the disease, if not favorable course a deep apathetic-abulic defect (“schizophrenic dementia”) is formed.

The basis of the doctrine of schizophrenia is the work of E. Kraepelin (1896), who united under the name dementiargaesoh(dementia praecox) several psychoses that begin for no apparent reason in at a young age and characterized by an increasing (progressive) course and the formation of a deep personality defect - hebephrenia [Hecker E., 1871], catatonia [Kalbaum K., 1890] and chronic delusional psychoses [Manyan V., 1891]." Early onset of these psychoses and similarities symptoms observed in the outcome of the disease allowed E. Kraepelin to consider the listed disorders as forms of the same disease.Later, various authors proposed to distinguish, in addition to the main forms of schizophrenia, other less typical variants - circular, recurrent, psychopathic, latent, sluggish and etc. The selection of these options cannot be considered unreasonable: in many psychiatric schools

Somewhat later, a simple form of schizophrenia was included here [Dim O., 1903].

Table 19.1. Predictors of prognosis for schizophrenia

Bad prognosis

Onset of disease before age 20

Cases of schizophrenia in the family (hereditary history of schizophrenia)

Distinct signs of constitutional predisposition (withdrawnness, autism, etc.)

Asthenic or dysplastic body type

Slow gradual start

Impoverishment of emotions

Spontaneous causeless start

Lack of family and profession

No remissions for 2 years

Predominance of negative symptoms

Relatively favorable prognosis

Late onset of the disease

No hereditary burden

Lack of constitutional predisposition (sociability, having friends)

Picnic body type

Acute onset of the disease

Vivid, heightened emotions (mania, depression, anxiety)

The onset of psychosis after the action of exogenous factors or psychological stress

State V marriage; having a profession

History of prolonged remissions

Predominance of productive symptoms

With a paroxysmal course, there is an alternation of attacks of the disease with the onset of remission. Light intervals - remissions can be complete or incomplete. With complete remission (intermission), a stable state is observed with the absence of obvious mental disorders; with incomplete remission there are mild residual mental disorders.

With a paroxysmal course, changes in the personality of patients are usually less pronounced. But this can only be judged in the interictal period, since during an attack personality changes are masked by acute manifestations of psychosis. As the number of attacks increases, personality changes intensify. Residual symptoms also increase in the interictal period. The nature of the course of the disease is not always strictly preserved in the same patient throughout the entire period. Transitions from continuous to paroxysmal, as well as paroxysmal to continuous, are possible. However, the general trend in the course of the disease often persists.

In Russia, the classification of schizophrenia according to the type of course of the disease is actively used [Snezhnevsky A.V., 1960, 1969]. In ICD-10 it is proposed to encode the type of disease with an additional 5th character.

Continuous type The course is characterized by the absence of remissions. Despite fluctuations in the patient's condition, psychotic symptoms never disappear completely. The most malignant forms are accompanied by an early onset and rapid formation of apathetic-abulic syndrome (hebephrenic, catatonic, simple). With a late onset of the disease and the predominance of delusions (paranoid schizophrenia), the prognosis is more favorable; patients remain in society longer, although complete reduction of symptoms is also not possible.

Patients with the mildest forms of schizophrenia (senestopathic-hypochondriacal form) can remain able to work for a long time.

Paroxysmal-progressive (fur-like) type The course is characterized by the presence of remissions. Delusional symptoms occur acutely. The manifestation of delirium is preceded by persistent insomnia, anxiety, and fear of going crazy. Delirium in most cases is unsystematized, sensual, accompanied by severe confusion, anxiety, agitation, sometimes combined with mania or depression. Among the plots of delirium, ideas of relation and special meaning predominate, and delusions of staging often arise. An acute attack of schizophrenia lasts several months (up to 6-8 months) and ends with a clear reduction of delusional symptoms, sometimes with the appearance of criticism of the psychosis suffered. One

However, from attack to attack there is a stepwise increase in the personality defect, ultimately leading to disability. In the final stages of the disease, the quality of remissions progressively worsens and the course approaches continuous.

Periodic (recurrent) type course - the most favorable variant of the course of the disease, in which long clear intervals without productive symptoms and with minimal personality changes (intermission) can be observed. The attacks occur most acutely, the symptoms are affectively intense (mania or depression), and at the height of the attack, confusion may be observed (oneiric catatonia). A personality defect, even over a long period of time, does not reach the level of emotional dullness. Some patients experience only 1 or 2 attacks throughout their lives. The predominance of affective disorders and the absence of gross personality defects make this variant of the disease the least similar to typical forms of schizophrenia. ICD-10 proposes to classify these disorders not as schizophrenia, but as acute transient or schizoaffective psychoses (see sections 19.3 and 19.4).

End states in schizophrenia

Final states with sluggish-apathetic dementia and pronounced personality changes often develop in patients with simple schizophrenia. The clinical picture of these conditions is characterized by a predominance of pronounced schizophrenic personality changes with extremely slightly expressed positive psychopathological symptoms. The latter is more often presented in the form of rudimentary and unstable catatonic symptoms. Almost dominant complete absence active motives and interests. The behavior is extremely monotonous. Patients are lethargic, inactive, passive. Their facial expressions are also poor and monotonous; Sometimes smiles and grins are observed for no apparent reason. Motor skills are disharmonious. Mannered movements and loss of plasticity are noted. Speech is monotonous, poorly modulated, there is no expression. Patients can answer simple questions, but in most cases their statements are absurd, random, and not related to the topic of the question. Stereotyped automatisms, torpidity and rigidity of thinking, reasoning, paralogicality, etc. may be detected. Sometimes patients can be involved in simple work, which they perform without interest, slowly, requiring active stimulation from the outside to continue it. Sometimes patients experience episodes of lethargy, grimacing, in other cases - impulsiveness: patients may

laugh expectantly, make some sudden movement, perform an unexpected act.

Final akinetic catatonic And negative states, unlike the previous group, are characterized not only by a deep regression of behavior, but also by a significantly greater severity of productive disorders with a predominance of akinetic catatonic disorders or negativism. Patients are inactive, indifferent, and hardly take care of themselves. Their facial expressions are poor, their gaze is absent. Usually there is a tendency to maintain a monotonous posture, passive submission, partial or complete mutism. Almost complete immobility is at times replaced by monotonous rhythmic swaying of the body, stereotypical movements of the limbs, and catatonic-foolish excitement. Upon careful examination, in addition to catatonic ones, other productive disorders are also identified: stereotypical verbal pseudohallucinations; fragmentary, sometimes fantastic visual hallucinations, delusional ideas of absurd content. In other cases, the phenomena of negativism come to the fore in the form of active opposition to instructions. Possible agitation with aggression in response to persistent orders.

Final hyperkinetic catatonic states(including “mumbling dementia”) develop in patients with hebephrenic form of schizophrenia. Patients are constantly in a state of stereotypical motor restlessness, grimace, and make elaborate movements. Various motor stereotypies and rituals are observed. Some patients behave foolishly, childishly, use a lot of diminutive words, others constantly express various affects with the help of grimaces and gestures: fear, curiosity, bewilderment, embarrassment, etc. In some cases, there is a senseless desire to touch surrounding objects and people. At the same time, the desire for touching, as a rule, is accompanied by symptoms of increased distraction of attention: patients react to any noise, turn to the sound of a slamming door, look at those entering, etc. All of the disorders described above are usually not permanent. Mutism, food refusal, and episodes of catatonic agitation may occur. In some cases, constant speech excitation comes to the fore in the clinical picture in the form of monotonous and inarticulate muttering that occurs without external prompting (“mumbling dementia”). Not paying attention to those around them or interrupting their muttering to answer, patients monotonously and indistinctly pronounce separate, unrelated phrases, fragments of sentences, individual words (often their speech is a verbalization of only individual words).

Final hallucinatory-delusional states represent a combination of signs of a pronounced schizophrenic defect with preserved and stabilized productive hallucinatory-delusional symptoms. As a rule, rudimentary and intermittent catatonic disorders are also observed. In some cases, fragmentary delusional ideas of greatness and persecution, having a fantastic, often absurd content, are predominant. In other cases, auditory pseudohallucinations and other manifestations of mental automatisms (“voice carriers”) predominate. The behavior of patients is often not sharply disturbed, and only a thorough examination makes it possible to identify productive hallucinatory-delusional disorders. Over time, they become increasingly scarce and fragmented. Thinking disorders are very characteristic: there is a complete lack of meaning while maintaining the correct grammatical structure and intonation - schizophasia. Unlike other types of final conditions, in these patients the emotional-volitional defect and personality changes are much less pronounced.

The main forms of schizophrenia were described above, for which there is the greatest agreement among psychiatrists of various psychiatric schools, and similarities between various national psychiatric classifications. These are, as a rule, quite pronounced disorders characterized by an unfavorable course, which makes it possible to find a certain compromise in the opinions of psychiatrists who adhere to different principles for diagnosing schizophrenia. Socio-pragmatic considerations also contributed to the tightening, so to speak, of the criteria for the diagnosis of schizophrenia: doctors strive to avoid diagnosing many patients with endogenous mental disorders with schizophrenia, which in the eyes of society is a label of a severe and incurable mental illness. Other mental disorders included in this block may have genetic similarities with schizophrenia and often exhibit psychopathological symptoms similar to it. However, the clinical picture of each of the diseases listed below has its own characteristics.

Schizotypal disorder (sluggish schizophrenia)

Schizotypal disorder (sluggish schizophrenia) is a fairly common pathology. According to statistical indicators obtained from diagnostic

According to ICD-9 criteria (in the previous classification, schizotypal disorders were included in schizophrenia as a low-grade form), schizotypal disorders accounted for 40% of the entire schizophrenia population. Schizotypal disorder is characterized by inadequacy and impoverishment of emotional manifestations, eccentricity and strangeness of behavior, delusional mood, originality of thinking, speech, etc. These personality changes occur more slowly and are not as pronounced; productive psychopathological symptoms appear in a reduced form. These disorders include obsessions, hysterical, asthenic, senestopathic, and depersonalization disorders.

Neurosis-like variant in many of its manifestations it resembles neurosis (see section 21.3). In the presence of obsessions (obsessions), the diagnosis of schizotypal disorder (sluggish schizophrenia) is indicated by the following features: the appearance of obsessions in a patient whose personality structure does not predispose to the emergence of obsessions (lack of anxiety and suspiciousness), the occurrence of obsessions without an external reason (without psychogenicity), and also rapid complication and expansion of psychopathological manifestations (progression). In case of predominance hysterical manifestations Also noteworthy is the spontaneous, outwardly unprovoked occurrence of hysterical symptoms. Most often, the patient was not previously characterized by appropriate forms of behavior. In the presence of provoking factors, one can notice a clear discrepancy between the significance of the traumatic situation and the strength of painful reactions.

The patient is 40 years old, disabled group 11.

There is no hereditary history of mental illness. Born the first child in the family. Pregnancy and childbirth proceeded normally. Early development is correct. In childhood, I did not suffer from serious somatic diseases. He grew up sociable, friendly, and cheerful. I studied well. After the 8th grade I entered the radio-mechanical technical school. Later, working in his specialty, he graduated from the evening department of the Moscow Institute of Radio Electronics and Automation. He loved his profession very much, at home he was constantly soldering and making something, collecting various radio components. He successfully served in the ranks of the Soviet Army. Was married. Now divorced; has a daughter from this marriage. After a divorce, he lives alone with his wife.

The present disease began at the age of 20. “Pre-fainting” states appeared: fear of fainting in the wrong place (in the subway, store, while crossing the street, etc.), accompanied by increased blood pressure, increased heartbeat, and a feeling of “wooliness” in the legs. He became fearful and inert. The circle of interests and communication has narrowed. Later, the fear of crowded places intensified, as several times “I got seized in transport” (fear of death, palpitations, profuse sweating arose). He was repeatedly admitted to psychiatric hospitals. Made complaints about various countries

hee, lethargy, increased fatigue. I had little contact with other patients, but in the evening I felt better. He received treatment with neuroleptics and antidepressants. After his stay in the hospital, he noted some improvement, although his apprehensions and fears did not completely go away. Another deterioration occurred for no apparent reason. Over the years of illness, he became passive, stopped tinkering, and threw away all the accumulated radio components. He treated his ex-wife and daughter with indifference. He accepted their concern for himself (“I can’t go to the store myself!”), but did not tolerate the long presence of strangers in his apartment. He constantly took maintenance doses of medications, but his condition continued to worsen, and his fears and vegetative crises intensified. Disability was registered (group 11). Lately, he has been hospitalized 2 times a year, each time spending 3-4 months in the hospital. Outside the clinic he does not leave the house. Notes an increase in the number of situations that cause fear. Some fears are quite abstract and meaningless (for example, “fear of an empty refrigerator”).

There are no pathological changes in the somatic and neurological condition.

Mental state: the patient is passive in conversation, monotonous, his face is hypomimic. The background mood is reduced. Complains about various fears. Understands their groundlessness, but cannot cope with them. He notes that the hospital environment has a favorable effect on him (“You feel calmer around the doctors”). He behaves correctly in the department. He communicates little with patients and spends most of his time alone. Almost unoccupied. He explains this by a lack of desire and difficulty concentrating, for example, on reading books. Shows no real interest in his daughter's life. Has no plans for the future. “I live one day at a time; It’s scary to think about what will happen tomorrow.”

Diagnosis: schizotypal disorder (sluggish schizophrenia), neurosis-like form with affective fluctuations.

The disease in this patient arose without any apparent reason in adolescence. The leading mental disorder was phobic syndrome, occurring against the background of emotional disturbances. As the disease progressed, the psychopathological structure became more complex: in addition to fears of fainting, fear of dying and absurd fears (“of an empty refrigerator”) appeared over time. The range of interests narrowed, emotions became scarce, and changes in thinking appeared. Thus, in addition to the symptoms characteristic of obsessional neurosis, in this case there are pronounced personality changes similar to those in schizophrenia. However, they are much less pronounced, and the patient’s clinical picture does not contain psychotic disorders typical of schizophrenia. Nevertheless, it should be noted that socially and professionally the patient is grossly maladjusted.

Psychopathic variant its manifestations are similar to mental disorders in psychopathy (see Chapter 22). However, in these patients, in addition to pathocharacterological

Such violations also reveal noticeable personality changes: emotional and volitional disorders (callousness, sometimes hostility towards loved ones, paradoxical affect, unmotivated mood swings, eccentric behavior), thinking disorders (tendency to reflection, introspection, unusual, pretentious interests, etc. ). One of the characteristic manifestations of psychopathic behavior in schizophrenia is heboid syndrome(see section 13.3.1) with disinhibition of drives, antisocial behavior and uncontrollability.

As the disease develops, a complication of symptoms is noted in the form of the appearance of rather long-term affective fluctuations, overvalued and unstable paranoid ideas. Some paranoid mood can be observed at the level of not only overvalued, but also delusional disorders (for example, stable delusions of jealousy in a patient without a clearly growing personality defect over many years). Sometimes the diagnosis of schizotypal disorder (sluggish schizophrenia) has only a stage significance, since subsequently conditions characteristic of typical paranoid schizophrenia develop.

“In general, schizotypal mental disorders are quite favorable. Most patients remain able to work. Schizotypal disorders can occur continuously or in the form of erased attacks. With a continuous course, neurosis-like or psychopath-like symptoms remain stably with a gradual complication of psychopathological manifestations and an increase in personality changes. Patients become deceitful, make ridiculous adventurous plans, sometimes leave home, get involved in criminal companies, and become involved in taking drugs and alcohol. With a paroxysmal course, attacks of hypochondriacal or apathetic depression may be observed. Often the longest attack occurs during puberty. Since passivity and indifference increase with age, in some cases patients become more obedient, lose contact with asocial company, and find simple work. This allows them to maintain relative adaptation (at a low social level) for a long time without special help from a doctor.

All of the above features make it possible to distinguish schizotypal disorders, on the one hand, from schizophrenia, which occurs with obvious psychotic disorders, and on the other, from psychopathy and neuroses, where there is no progression of the disease and changes in the patient’s personality.

Chronic delusional psychoses

Mental disorders, manifested by persistent delusional ideas of various contents, usually differ from schizophrenia in the absence of obvious dynamics and a high degree of systematization of delusions. Such psychoses are characterized by delusions of persecution, jealousy, hypochondriacal and dysmorphomanic ideas. Delusions of influence and automatism (Kandinsky-Clerambault syndrome), on the contrary, almost never occur. There is also no emotional-volitional personality defect observed. Delirium can be combined with depression, individual visual, olfactory or tactile hallucinations.

Involutionary paranoid- psychosis of involutionary age, manifested by delirium of everyday relationships (“delirium of small scope”). Occurs after 45-50 years, more often in women. The delusion is paranoid in nature and has no tendency to expand and become more complex. Patients claim that those around them cause them material harm (spoil and steal things), annoy them with noise and unpleasant odors, and try to get rid of them, hastening their death. Delirium is devoid of mysticism, mystery, and is specific. Along with delusional experiences, individual illusions and hallucinations can be observed (patients smell “gas”, hear insults addressed to them in outside conversations, feel signs of ill health in the body caused by persecution).

Usually patients are quite active and optimistic, but sometimes an anxious and depressed mood is observed. K. Kleist (1913) describes the premorbid characteristics of such patients. They are characterized by a narrow range of interests, conscientiousness, frugality along with modest requests. They love independence in everything and therefore are often lonely in old age. Deafness and blindness also predispose to the disease.

The most typical statements are from patients that their neighbors or some other persons enter a room or apartment without their knowledge, damage things, furniture, add poison to food, etc. Typically, patients try to protect themselves from persecution with additional locks; hide food in special hiding places; often ventilate the room “from gases”; They try not to touch objects with their hands that, in their opinion, are “poisoned” or “infected.” Some of their statements seem plausible and mislead others. Thus, one woman told her relatives and friends that neighbors, having picked up the keys to her apartment, were stealing food, things, etc. The relatives, together with the patient, contacted the police so that the

investigation, until, once again talking about neighbors breaking into her apartment, the woman said that the neighbors had cut her carpet in order to harm her. Only then did the illness become obvious.

Here is one typical observation for this group of psychoses.

Patient 60 years old.

Heredity: Mother suffered from mental illness. The patient herself grew and developed normally. Graduated from 6th grade. For most of her working life she worked at a plant as a quality control inspector. She was kind and sociable by nature and had many friends. Married, has 2 adult children. At the age of 48, she began to complain to her husband that her neighbors in her apartment treated her badly and wanted her to survive in order to occupy the apartment. She cited facts of persecution. Recently I began to notice that in her absence someone breaks into the apartment, rearranges the furniture, and spoils things. She discovered in her closet a piece of material that supposedly did not belong to her; decided that he was deliberately planted in order to accuse the patient of theft. Regarding this, she contacted the police, where she demanded to “call the persecutors to order.” Subsequently, she repeatedly changed the locks on the front door and sprinkled dust on the floor to “catch the criminals.” She blamed the neighbor living in the adjacent apartment for everything. She decided to “scare” her and, meeting her on the landing, threatened her with a knife. In the ensuing struggle, she wounded her neighbor. She was prosecuted.

Mental state: in a conversation with a doctor at first he is somewhat wary. Upon persistent questioning, she confirmed that she was being “harassed” and “pursued” by her neighbors. For more than a year, according to the patient, her neighbors have been constantly defaming her and slandering her in order to achieve eviction, expressing their intentions with “winks and glances.” I am confident that I am right.

Taking into account the presence of severe mental disorders in the patient, due to which she could not account for and control her actions, she was declared insane by the forensic psychiatric commission.

The prognosis for involutional paranoid is unfavorable. Atherosclerotic changes in cerebral vessels contribute to the inertia and persistence of psychopathological manifestations. Over time, anxious and delusional manifestations become monotonous. Patients report in similar terms about their complaints, worries and delusional fears. Over time, a significant weakening of the relevance of painful experiences is possible, but complete recovery, as a rule, is not observed. Patients exhibit peculiar personality changes: a narrowing of the range of interests, monotonous activity, distrust and suspicion.

Paranoia- chronic delusional psychosis, in which delusion is the leading and, in fact, the only one

manifestation of the disease. Unlike schizophrenia, delusions are persistent and are not subject to any pronounced dynamics; it is always systematized and monothematic. The predominant plots are persecution, jealousy, hypochondriacal ideas, and often querulant tendencies (“delirium of complainers”). Hallucinations are not typical. There are no pronounced personality changes and emotional-volitional impoverishment. Particularly distinguished are patients with delusional forms of dysmorphophobia (dysmorphomania), which are characterized by a false belief that they have physical handicap or deformity.

The disease begins at a young and mature age. The persistence of delirium determines the low effectiveness of existing treatment methods. Drug therapy is prescribed to reduce the affective tension of patients. It is especially necessary in the presence of aggressive tendencies, which are often the cause of crimes. Most patients retain their social status and ability to work for a long time.

The nosological independence of paranoia is disputed by some authors, who consider it as a variant of low-progressive schizophrenia.

Acute and transient psychotic disorders

The symptoms of psychoses included in subclass F23 are characterized by extreme polymorphism, severity and variable duration (from several days to several weeks). The set of symptoms includes different kinds affective disorders, paranoid and hallucinatory manifestations. There are psychotic attacks without symptoms of schizophrenia, schizophrenia-like and attacks with symptoms of schizophrenia. In the latter case, if the duration of the attack is more than 3 months, it is recommended to make a diagnosis of schizophrenia. If a delusional attack lasts more than 3 months, but there are no characteristic schizophrenia symptoms, a diagnosis of chronic delusional disorder is recommended. The onset of the disease with acute and transient attacks is possible in childhood, adulthood and late age. Characterized by extremely rapid development of psychosis (within 48 hours).

In a number of patients, the onset of an attack is preceded by external unfavorable factors, severe emotional stress (court proceedings, loss of loved ones, military action, etc.). IN domestic psychiatry in such cases a diagnosis is made reactive paranoid(see section

Since the differential diagnostic criteria that distinguish reactive paranoid from other transient delusional psychoses, not sufficiently developed, in ICD-10

Such psychoses are combined with other acute paranoids. The presence of previous psychological trauma is indicated by the fifth character in the code.

Induced delirium(folie a deux) is also formed under the influence of psychogenic influences. But such influences come from a mentally ill person. A person suffering from delusional ideas seems to impose his painful ideas and views on another person. This happens, as a rule, during close communication with him, and the active carrier of delusional ideas (inducer) occupies a dominant, leading position in relation to the partner with induced delusions (inducible). Such nonsense is usually unstable. Persons with intellectual disabilities, infantility, suggestibility, etc. are predisposed to it. (see also section 5.2.1).

It is extremely rare to experience acute psychotic states with a clinical picture of severe toxicosis, previously described as febrile schizophrenia(hypertoxic schizophrenia, fatal catatonia). Patients have a high temperature. Outwardly, they look like patients in a state of severe toxicosis. Consciousness is impaired according to the type of oneiroid or amentia, chaotic excitement (yactation) is observed. Simultaneously with mental disorders, somatic disorders increase (tachycardia, dehydration, hemorrhages on the skin and internal organs). Failure to take appropriate therapeutic measures may result in death (see section 25.6). In some patients, such attacks are repeated in the future, which makes them similar to manifestations of periodic (recurrent) schizophrenia.

Clinical qualification of acute transient psychoses and determination of their nosological affiliation are very difficult. The term "acute psychotic disorder" is considered the most appropriate. These disorders can manifest as oneiric, affective-delusional and hallucinatory acute states. The more acute a psychotic disorder occurs, the shorter its duration.

The patient is 40 years old. There is no hereditary history of mental illness. Born as the first child in the family, he has two younger brothers. My parents always worked. Relationships in the family were very good and warm. Early development without features. I went to school at the age of 7. I studied well. By nature he was cheerful, active, “always became a leader in the company, although he did not strive for leadership.” After school he served in the army. Then he graduated with honors from the institute. Then he defended his dissertation and after his defense he works at one of the institutes of the Russian Academy of Sciences. Doesn't drink or smoke. Married and has two children. Family relations are good.

By nature he was always very energetic and active. “At work I shouldered everything on myself and didn’t take a vacation for 6 years.” The mood was usually high. I've always been very confident

stubborn, tried to achieve his goal; was distinguished by restraint in the expression of feelings. According to his wife, “with external openness, he always remained a thing in itself.” In the fall he was offered to head the department. I was very pleased. He began to work on it, without leaving his previous place. “I spent days and nights at work.” However, he was unable to carry out his plans and resigned from the position of manager. I was worried for a week, my mood was low, I couldn’t sleep at night. Then my health seemed to return to normal. With renewed energy he fulfilled his previous duties as the scientific secretary of the institute.

Once I took my son to my office to show him computer games, and that same day in the evening my wife and I went to visit. There he behaved as usual: he laughed and joked. At night I woke up and saw in front of me, like in a movie, a computer screen with an inscription in an unknown language. I immediately realized that this inscription was in Slovak. It said that he got into a “paid file” and had to pay a huge amount of money for it. It became clear to him that not only he, but also the institute would not be able to pay this amount. He decided that his institute would be closed, employees would be fired, and unemployed people would begin to take revenge on his family; and since the state cannot pay this huge amount of money, the third world war may begin. In the morning I went to work and rushed to the computer, but could not find the inscription that I saw at night. He turned to the programmers, but they convinced him that they could not find anything in the computer. After that, he decided to commit suicide: he tried to drown himself in the bathtub and put a plastic bag over his head. Suddenly he heard the “voice of God,” informing him that he had become the center of the world in the struggle between God and the devil, that black forces had made him an extraordinary creature called to destroy all people on earth. According to his wife, he looked stunned outwardly; did not answer questions; started doing something; suddenly froze in one position. Without explaining anything to his family, he left home and wandered the streets for several hours. At this time, his wife, starting to rummage through his things, found notes about the suicide attempt and called friends to look for the patient. They found him only late in the evening. When he was brought home, he told everyone about the story with the computer, after which it was decided to see a psychiatrist. Upon admission to the hospital he was active and talkative. He considered himself an extraordinary person who would cause the destruction of the world. He expressed thoughts that the people around him were messengers of God and the devil in disguise. Periodically froze in unusual positions and did not answer questions.

This state lasted for about a week. All this time he received large doses of haloperidol intramuscularly. After another week he became calmer, more restrained; consulted with the doctor whether he should go and report everything to the Prosecutor General's Office. After much persuasion, he reluctantly admitted that perhaps all the inscriptions he saw on the computer were his imagination. After discharge, he continues to receive maintenance therapy. The previous state of mental health was completely restored. He returned to his previous place of duty and continues to work successfully. Refers to the psychosis suffered with criticism.

In the example given, psychosis occurred without an obvious cause, acutely, within a few hours. Unsystematized delusional ideas of relation and staging predominated.

At the height of psychosis, an oneiric-catatonic state developed. The rapid resolution of psychosis and the absence of personality changes after the acute attack of the disease has passed make it possible to refrain from establishing a diagnosis of “schizophrenia” and to state “acute oneiric-catatonic transient psychosis.”

Schizoaffective disorders

Subclass F25 occupies an intermediate position between schizophrenia and affective psychoses (see Chapter 20). A sign of these disorders is a combination in the manifestations of a psychotic attack of intense affect (mania or depression) and symptoms characteristic of schizophrenia. In the presence of emotional disorders of the manic type, patients may express increased self-esteem and ideas of grandeur, often combined with irritability and aggressiveness. In depressive states, there is a decrease in interests, sleep disorders, ideas of self-blame, and a feeling of hopelessness. The duration of psychosis ranges from several weeks to several years. Repeated attacks are often observed. In some patients, each attack is provoked by exogenous or psychogenic factors (symptomatic lability). The attacks are generally characterized by intense effectiveness, the presence of acute sensory delirium, and catatonic symptoms are less common. Remissions are of high quality. The absence of changes in the patient's personality after the first attacks allows us to talk about intermissions. Gradually, after repeated attacks, patients experience personality changes, characterized by asthenia or hypersthenia, increased performance with a simultaneous decrease in creative activity and a slight depletion of emotional manifestations. Usually these changes are observed after the third or fourth attack. Then the activity of the process decreases: attacks become less and less frequent, personality changes seem to freeze at the same level. Patients have a critical attitude towards the psychotic state they have suffered, and they clearly distinguish between health and illness. The performance of such patients outside of attacks usually does not decrease (with the exception of a slight drop in patients with asthenic personality changes). The prognosis is quite favorable, but it should be borne in mind that such patients, against the background of severe depression, often experience suicide attempts. In this case, special supervision is required. Given the severity of psychotic symptoms during acute attacks, treatment of acute schizoaffective psychoses should be carried out in a hospital.

Patient B., 35 years old.

The patient's mother suffered from emotional disorders: she periodically experienced subdepressive and hypomanic states. She was treated in psychiatric hospitals with a diagnosis of cyclothymia. The patient was born at term from a normal pregnancy. Early development without any deviations from the norm. I studied well at school, after graduating I entered the economics department of the university, which I successfully completed. After graduation, he organized and headed the company. Has business connections with foreign countries. By nature he is sociable, active and purposeful. Married, has a 10-year-old daughter. Family relationships are good.

Real illness: according to the patient and his wife, about 5 years ago he felt a special surge of strength and energy. Everything was easy, I slept 3-4 hours a day without feeling any fatigue. At the same time, he was often harsh and rude to his relatives and subordinates. Suspicion arose: he wrote down the license plates of cars that were parked near his house. He believed that there might be people from competing companies watching him. He was admitted to the clinic at the insistence of his wife after he, without sufficient grounds, organized a grandiose banquet in a restaurant for company employees and acquaintances, wasting a large amount of the company’s money on it.

Mental state: clear consciousness, oriented in time and environment. He knows that he is in a psychiatric hospital. He does not consider himself sick. He explains that he entered the clinic by saying that he does not resist his wife’s persuasion. He also thinks that maybe he needs more sleep. verbose; talks about his extensive plans, fears persecution by competitors. Declares that he has enough strength and understanding of the situation to thwart the plans of his enemies.

The patient was treated with teralen and stelazine. He was discharged from the hospital in a state of complete remission. Refers to the psychosis suffered with criticism. Behavior and emotional state were streamlined, sleep normalized. He returned to his duties as head of the company. He went on business trips to negotiate with his partners. After 4 years, a relapse of the mental disorder occurred: sleep deteriorated, motor agitation appeared, increased desire for activity and distractibility: having started something, did not complete it, the background mood was inappropriately elevated; expressed grandiose plans for the reorganization and expansion of the company’s activities. At the same time, he was concerned about the allegedly renewed persecution by competitors. According to him, they not only organized constant surveillance of him, but also tapped his phones. His attitude towards his loved ones changed: he became harsh, tactless, and did not show his previously characteristic care and attention to his daughter.

In the clinical picture of the disease one can see the coexistence of two psychopathological manifestations - hypo- manic states and delusional ideas that do not arise directly from existing affective disorders. Personality changes unusual for affective psychoses are also observed in the form of an increasing emotional defect characteristic of schizophrenia.

Etiology and pathogenesis of schizophrenia, schizotypal and delusional mental disorders

As already noted, in a number of national classifications, all these mental disorders were previously considered mainly within the framework of schizophrenia, so that the basic data obtained from studying the biological foundations of schizophrenia, with a certain correction, can be applied to assessing the etiology and pathogenesis of this entire group of mental disorders.

The etiology and pathogenesis of schizophrenia became the subject of special study soon after the disease was identified as a separate nosological unit. E. Kraepelin believed that schizophrenia occurs as a result of toxicosis and, in particular, dysfunction of the gonads. The idea of ​​the toxic nature of schizophrenia was developed in some further studies. Thus, the occurrence of schizophrenia was associated with a violation of protein metabolism and the accumulation of nitrogenous breakdown products in the body of patients. Several decades ago, the idea of ​​the toxic nature of schizophrenia was introduced by an attempt to obtain a special substance in crevi serum from patients with this disease. However, the idea that patients with schizophrenia have some specific substance, for example taraxein [Hiss R., 1958], has not received further confirmation.

Toxic products are present in the blood serum of patients with schizophrenia, but they are not particularly specific, characteristic only patients with schizophrenia, and are also present in other mentally ill people and in some conditions in healthy individuals. At the same time, the toxic theory contributed to the development of biochemical and immunological research. Experiments revealed an inhibitory effect of blood serum from patients with schizophrenia on the development of the nervous tissue of the embryo. Disturbances in the development of the central nervous system have also been noted in embryos obtained through artificial termination of pregnancy in women suffering from schizophrenia. These data supported the presence of membranotropic toxins in the blood of patients with schizophrenia. A correlation was shown between the severity of the toxic factor and the malignancy of the schizophrenic process. The same idea was developed in the immunological hypothesis of schizophrenia. The damaging effect of the so-called active factor in schizophrenia on cells nervous system leads to the formation of autoantigens and autoantibodies, which in turn can damage brain tissue. Their number corresponds to the malignancy of the disease process. These data indicate certain biological disturbances that occur in the activity of the body of patients with schizophrenia.

However, there is not enough clarity in understanding the mechanisms that form these disorders and the conditions that contribute to their occurrence.

In recent years, the most interesting data have been obtained in connection with the study of the activity of biogenic amines in endogenous diseases (see section 1.1.2). Special studies and experience in the use of modern psychotropic drugs confirm the participation in the pathogenesis of schizophrenia of metabolic disorders of the main CNS mediators (dopamine, serotonin, norepinephrine). This served as the basis for the creation of the so-called catecholamine and indole hypotheses. The first are based on the assumption of the role of an imbalance of norepinephrine and dopamine in the mechanisms of disruption of neurobiological processes in the brain of patients with schizophrenia. Proponents of the indole hypothesis associate the manifestations of schizophrenia (especially negative symptoms) with an imbalance of serotonin and other indole derivatives. In essence, the idea of ​​a connection between the schizophrenic process and dysfunction of enzyme systems involved in the metabolism of biogenic amines is also close to the concepts described above.

Role installed hereditary factors in the occurrence of schizophrenia (see section 1.1.1). The frequency of schizophrenia in close relatives of patients is several times higher than the average in the population, and the frequency of hereditary complications directly depends on the degree of relationship. In persons raised by adoptive parents, the likelihood of developing the disease depends on the health of the biological parents, while the character and health of the adoptive parents are not significant factors. A certain connection has also been established between the form of schizophrenia in the proband and his relatives, including parents. Besides, modern research some general characteristics have been established metabolic processes and intellectual characteristics of patients with schizophrenia and their close relatives, especially parents.

A point of view is also expressed about the etiological heterogeneity of these diseases. In particular, forms of the disease with periodically recurring attacks are more associated with pathological heredity. Early childhood and adolescent malignant variants of schizophrenia show a high frequency of comorbid organic pathology; These patients often show clear signs of ontogeny disorders in the early stages of development (abnormalities in the structure of the brain, dysplastic physique, special character of dermatoglyphics).

Although the above data are certain biological prerequisites for understanding the nature of schizophrenia and related mental disorders,

However, to date, a reliable concept of their essence has not yet been formulated.

The absence of specific characteristics that determine the occurrence and formation of biological and psychopathological changes in schizophrenia creates the opportunity to construct various speculative concepts about its nature. The concept of psychogenesis can also be classified as such. From the perspective of this concept, schizophrenia is considered as one of the forms of disturbance of the individual’s adaptation to life. The impossibility of full adaptation is explained by a special personality defect formed as a result of incorrect interpersonal relationships within the family in early childhood.

Information about children with schizophrenia, raised from early childhood by adoptive parents, refutes this point of view. At the same time, it is impossible to completely ignore the participation of psychogenies in the occurrence of attacks of schizophrenia, since in some patients psychotraumatic situations can play the role of trigger factors contributing to the implementation of pathological heredity.

„ Thus, the present data suggest that schizophrenia and similar mental disorders are diseases of a multifactorial and, possibly, polygenic nature. At the same time, a hereditarily acquired predisposition in each individual patient can only be realized through the interaction of internal and environmental factors.

Differential diagnosis

Schizophrenia has a wide range of clinical manifestations, and in some cases its diagnosis is very difficult. The main diagnostic criteria for the disease are the so-called negative disorders typical of schizophrenia or peculiar changes in the patient’s personality: impoverishment and inadequacy of emotional manifestations, apathy, autism, disorders of the harmony of thinking (mentism, sperrung, reasoning, fragmentation). Schizophrenia is also characterized by a certain set of productive syndromes: a feeling of putting and taking away thoughts, an echo of thoughts, a feeling of openness of thoughts, delusions of influence, catatonia, hebephrenia, etc. The differential diagnostic assessment of schizophrenia has to be carried out mainly in three directions: to distinguish it from organic diseases (traumas, intoxications, infections, atrophic processes, tumors), affective psychoses (in particular, manic-depressive psychosis) and functional psychosis

gene disorders (neuroses, psychopathy and reactive states).

Exogenous psychoses begin in connection with certain hazards (toxic, infectious and other factors). The personality defect that develops in organic diseases is significantly different from schizophrenic (see section 13.3.2). Productive symptoms are also unique; the exogenous type of reaction predominates (see section

: delirium, hallucinosis, asthenic syndrome - all these disorders are not typical for schizophrenia.

At affective psychoses(for example, with MDP), personality changes do not develop even with a long course of the disease. Psychopathological manifestations are limited mainly to affective disorders (see Chapter 20).

When diagnosing persistent delusional disorders, acute and transient psychoses, it should be taken into account that, unlike schizophrenia, these diseases are not accompanied by a specific schizophrenic personality defect; the course of these diseases does not show progression. In their clinical picture, with some exceptions, there are no signs characteristic of schizophrenia (schisis, delusional ideas of influence, automatism, apathy). The clear connection of all manifestations of the disease with previous psychotrauma, the rapid reverse development of psychosis following the resolution of the traumatic situation, testify in favor of reactive psychosis (see section 21.2). When delimiting schizoaffective psychoses from other disorders considered in this block, one should focus on the presence in patients with schizoaffective pathology of psychotic attacks, manifested simultaneously by severe emotional disorders and hallucinatory-delusional experiences typical of schizophrenia (pseudohallucinations, ideas of influence, ideational automatism).

Delimitation schizotypal disorders from schizophrenia and other psychotic disorders discussed here does not present any particular difficulties, since they are not characterized by pronounced psychotic level disorders (delirium, catatonia, pseudohallucinations, etc.). The symptoms of schizotypal disorders are more similar to the psychopathological manifestations of neuroses (see section 21.3) and psychopathy (see chapter 22). In contrast to low-grade schizophrenia (schizotypal disorders) neuroses are non-progressive psychogenic diseases and arise as a result of long-existing intrapersonal conflicts. A psychotraumatic situation in this case is a condition for decompensation of personality traits that were initially characteristic of the patient, while with sluggish schizophrenia one can observe a transformation, modification of the original personality traits

ity and an increase in character traits typical of schizophrenia, such as lack of initiative, monotony, autism, indifference, a tendency to fruitless reasoning and separation from reality. Unlike schizotypal disorders psychopathy are characterized by stability, their manifestations are formed in early childhood and persist without significant changes throughout life.

Therapy with psychotropic drugs is now the mainstay of treatment for patients with severe mental disorders (see section 15.1). According to observations, the therapeutic effect of the use of psychotropic drugs mainly depends on the mechanism of action of the drug, the characteristics of the structure of mental disorders in the patient and (to a lesser extent) on the causes of their origin.

In case of severe mental disorders with a predominance of delusional, hallucinatory manifestations, states of excitation, neuroleptics are mainly used - haloperidol, aminazine, triftazine, azaleptin, etc. In the presence of catatonic symptoms - etaprazine, mazeptil, frenolone, eglonil. In schizophrenia and chronic delusional disorders, there is a need for long-term maintenance treatment. In this case, long-acting neuroleptics are used - moditene depot, haloperidol decanoate (injections are carried out once every 3-4 weeks). It should be noted that there is no differentiated, exclusive, selective preference in the action of specific psychotropic drugs on psychopathological syndromes. Doses are selected individually and may vary significantly depending on individual sensitivity (see Appendix 2).

Patients receiving antipsychotics, especially in high doses, often experience neurological side effects - neuroleptic syndrome, drug-induced parkinsonism, manifested by general muscle stiffness, tremor, spasm of individual muscles, restlessness, hyperkinesis. To prevent these disorders, patients are prescribed antiparkinsonian drugs (cyclodol, akineton), diphenhydramine, benzodiazepine tranquilizers and nootropics.

In cases where negative mental disorders predominate, it is recommended to use antipsychotic drugs with a stimulating effect and psychostimulants in small doses. If the symptoms of depression, hypochondria, senestopathies and obsessions predominate, antidepressants are prescribed - amitriptyline, melipramine, anafranil, ludiomil, etc. It should be borne in mind that the prescription of antidepressants is

In patients with depression, it may contribute to the exacerbation of delusional symptoms. For complex psychopathological syndromes (depressive-paranoid, manic-delusional), a combination of drugs is possible, including various antipsychotics, antidepressants and other drugs. You should always be aware of the possible somatic side effects of psychopharmacotherapy. The most dangerous complications include agranulocytosis when prescribing azaleptin, urinary retention and cardiac arrhythmias when using TCAs, and neuroleptic malignant syndrome (see section 25.7).

A common problem in the treatment of schizophrenia is the emergence of drug resistance (see section 15.1.9). To overcome it, intravenous drip administration of psychotropic drugs, sudden withdrawal of the drug after increasing doses, or a combination of psychopharmacotherapy with pyrotherapy (pyrogenal) are used.

In patients with acute affective-delusional attacks (especially during the first or second attack of the disease), a good effect can be achieved by using such traditional methods as insulin shock And electroconvulsive therapy(EST). ECT is especially effective for depression and oneiric-catatonic attacks.

Psychiatrists play an important role in returning patients to a full life social and labor rehabilitation. The general system of organizing psychiatric care provides for various forms of occupational therapy and social support for patients. A psychiatrist selects types of work for the patient, taking into account his mental state and previous professional training. The relative safety must be taken into account intellectual sphere in patients with schizophrenia, which allows them to engage in mental work even with a long duration of the disease. If it is impossible to carry out the previous job, the patient can undergo vocational training and master a new specialty.

Prevention

Issues of prevention of schizophrenia and other mental disorders constitute one of the most important tasks of psychiatry. Insufficient knowledge about their etiology does not allow the development of effective measures for primary prevention of the disease. Primary prevention currently limited mainly to medical genetic consultations. Patients with schizophrenia and their partners should be warned about the increased risk of the disease in their unborn children. For secondary and tertiary prevention it is used as

medicines and social rehabilitation methods. With early identification of the patient, timely treatment and subsequent long-term maintenance therapy, it is often possible to prevent the development of severe mental disorders and keep the patient in society and family. Drug treatment is effective only in combination with social rehabilitation measures and adequate career guidance.

The approach to the rehabilitation of patients must be individual and differentiated. Depending on the patient’s condition, rehabilitation measures are carried out in a hospital or out-of-hospital setting. Options for hospital rehabilitation primarily include occupational therapy in hospital workshops, cultural therapy, intra-departmental and hospital-wide social activities. A further possible step in inpatient treatment is to transfer patients to light-security units (such as sanatoriums) or to day hospitals. An important condition for the success of rehabilitation is continuity in the actions of doctors, psychologists and social workers in hospitals and mental health centers.

BIBLIOGRAPHY

Clinical psychiatry: Transl. with him. / Ed. G. Grule, K. Jung, W. Mayer-Gross. - M., 1967. - 832 p.

KraepelinE. Textbook of psychiatry for doctors and students: Trans. with him. - T. 1-2. - M., 1912-1920.

Kutsenok B.M. Recurrent schizophrenia. - Kyiv: Health, 1988. - 152 p.

Lichko A.E. Schizophrenia in adolescents. - JI.: Medicine, 1989. - 216 p.

Early diagnosis of mental illness / Under the general. ed. V. M. Bleikher, G. L. Vorontsov. - Kyiv: Health, 1989. - 288 p.

Management in Psychiatry / Ed. A.V. Snezhnevsky. - T. 1-2. - M.: Medicine, 1983.

Management in Psychiatry / Ed. G.V. Morozova. - T. 1-2.- M.: Medicine, 1988.

Smulevich A.B. Low-progressive schizophrenia and borderline states. - M.: Medicine, 1987. - 240 p.

Smulevich A.B., Shchirina M.G. The problem of paranoia. - M.: Medicine, 1972. - 183 p.

Tiganov A.S. Febrile schizophrenia. - M.: Medicine, 1982. - 228 p.

Schizophrenia/ Under. ed. I.A. Polishuka. - Kyiv: Health, 1976. - 262 p.

Schizophrenia: Multidisciplinary research/Ed. A.V. Snezhnevsky. - M., 1972. - 400 p.

BleulerE. Guide to psychiatry: Trans. with him. - Reprint edition, 1993.

Psychogenic false dementia (pseudo-dementia, Wernicke C., 1900; Stertz G., 1910).

This type of dementia is one of the clinical forms of hysterical psychoses. The conditions for the occurrence of pseudodementia are acute psychotrauma and the presence of mild premorbid mental disability (G.A. Obukhov). According to N.I. Felinskaya, most often inferiority is characterized by features of hysterical or epileptoid, less often - schizoid or cycloid accentuation or psychopathy.

Phenomenologically, pseudodementia refers to a transient type of dementia. Symptoms occur acutely, usually against a background of depressed mood and anxiety. Orientation is lost, patients experience a feeling of fear and anxiety: they tremble, look around in fear, huddle in a corner, sometimes silently cry. Their statements often contain elements of paranoid experiences, also colored by an affect of fear (“they will come, kill, slaughter, quarter…”). Patients experience vivid hypnagogic hallucinations of a frightening nature (they see “scary faces with knives in their teeth,” angry dogs, devils, hear barking dogs, footsteps, feel that they are being strangled, bitten, etc.). Then the clinical manifestations become more specific. In the behavior of patients, confusion comes to the fore, which manifests itself in the whole appearance, gestures, in a characteristic lack of understanding of what is happening, in a frightened and anxious gaze that does not fixate on objects and faces. Patients stare, try to climb the wall, bump into objects, pull socks on their hands, do not know how to sit on a chair, pick up certain objects and look at them in surprise, crawl on all fours on the floor, etc.

Left to their own devices, patients lie on the bed or sit, not communicating with anyone. When contacting patients, they only answer questions and carry out actions as directed. At the same time, attention is drawn to the contrast between the usual lethargy of patients and fussiness and haste while performing tasks.

The symptom of passing speech, passing speech is very characteristic (Ganser S.J.M., 1898). Its essence lies in a certain correspondence between the content of the incorrect answer and the meaning of the question posed. Patients incorrectly name the time of year or year. The floor is called the table, and the table is called the floor. The counting is done slowly, using fingers, moving lips 5+5=8, 7-3=5. In response to the question of how many fingers there are on their hands, patients often begin to look at the splayed fingers, count them with errors, or answer “I don’t know.”

In some cases, the answers are similar to amnestic aphasia; when asked to name this or that object, the patient describes their function (“glasses - to look”, “key - to open the door”). Patients respond with long pauses and slowly. You have to repeat the questions. The answers may be of the nature of echolalia: when asked how old you are, the patient answers “how old are you.” Phrases are sometimes constructed ungrammatically. The content of the speech is poor and unreliable. Sometimes hysterical phantasms are observed.

No less characteristic are “mimic actions” (“motor pseudodementia” - G. Stertz), when patients, when asked to touch their nose with a finger, take themselves by the ear; when asked to show their teeth, they open their mouth with their fingers. In this case, helpless fussiness, incomplete attempts at certain actions, and lack of coordination of movements are typical. This is similar to “apraxia”, but it is pseudoapraxia (G.A. Obukhov).

The clinical picture of pseudodementia usually includes elements of puerility, manifested in capriciousness, in naivety of answers, in children's intonations of speech, in children's games with sticks, with balls made of bread, etc. Symptoms of “running wild” may be observed: patients eat with their tongue (lapped) from a plate, crawl on the floor on all fours, and make sounds reminiscent of a dog barking.

In some cases, manifestations of pseudodementia appear against the background of severe depression: patients are motorally inhibited, often cry, and their responses sound hopeless and melancholy.

Depression and asthenic-depressive manifestations are observed in most patients at the exit from a psychotic state. At the same time, the symptoms of pseudodementia gradually smooth out: confusion and anxiety decrease, orientation in the place and then in the situation appears. The answers are becoming more correct, patients are becoming more accessible.

The acute psychotic period is usually completely amnesic, but some vague memories may remain, most often images of hypnagogic hallucinations are remembered.

Pseudo-dementia is also observed in the structure of Ganser's syndrome (Ganser S.J.M., 1898).

Schizophrenic dementia phenomenologically belongs to the transient type. I.F. Sluchevsky, justifying the identification of transient dementia, wrote: “patients with schizophrenia can exhibit deep dementia for many years, and then, unexpectedly for those around them, including doctors, discover relatively well-preserved intellect, memory and the sensory sphere” (1959). In this regard, the views of Gruhle (H.W., 1929) are of interest, according to whom intellectual failure in schizophrenia depends on mental characteristics, lying outside the intellect: violation of initiative, resourcefulness, ingenuity, perseverance, determination, etc. Grule and Berze argue that a person with schizophrenia “possesses the instrument of formal intellect until the end of his days, but for a long time he cannot use this instrument, since he has no interest in using it” (1929). In their opinion, we should rather talk about a special different manner of thinking in patients with schizophrenia, so unusual that the thought of dementia appears. A.N. wrote about the incomprehensibility and alienness of mental structures, consciousness and logic of patients with schizophrenia to ordinary (normal) people long before Grule. Bernstein (1912) in Clinical Lectures on Mental Illnesses.

According to M. Weisfeld (1936), intellectual deficiency in schizophrenia is caused by “distraction” (delusional experiences, hallucinations, etc.), “insufficient activity” (a property of a premorbid personality), “the influence of acute psychotic states” and “lack of exercise” ( M. Weisfeld cites the judgments of Leonardo da Vinci on this matter, who, referring to the fact that a razor becomes covered with rust through disuse, notes: “the same happens to those minds that, having stopped exercising, indulge in idleness. Such as the above-mentioned razor , lose their cutting subtlety and the rust of ignorance eats away their appearance." However, incorrect behavior, absurdity in actions, inadequacy of intellectual reactions, their inconsistency with social stimuli in patients with schizophrenia indicate the presence of dementia. An important sign of schizophrenic dementia is Berze (Berze J ., 1914) considered “hypotonia of consciousness,” which a number of authors compare with the state when falling asleep (K. Schneider, A.S. Kronfeld, O. Bumke, etc.), which is very close to the pathophysiological interpretations of I.P. Pavlov, who considered schizophrenia to be a chronic hypnoid state. However, this is not enough to understand the clinical structure of schizophrenic dementia. As numerous studies have shown, in schizophrenia there is a disruption in the systemic functioning of the intellect while its individual elements are preserved. In particular, this is manifested in the asynchrony of thinking processes, which acquires a special character of pretentiousness, symbolism, formality, mannerism, mosaic. The cognitive apparatus is preserved, but associative connections are significantly modified, narrowed and disordered. Disunity, “piece-like” work of the intellect and individual apparatuses of the “I”, fragmentation in perceptions and ideas, mosaic of experiences, along with the paralogical structure and “affective attenuation of the personality” (Vnukov V.A., 1934) form the basis of schizophrenic dementia.

It should be added that in patients with schizophrenia, orientation in time, place, surroundings, as well as basic memory processes, are satisfactorily preserved for a long time. Only their memorization turns out to be worse due to a drop in interest and impaired ability to concentrate. E. Bleuler (1911) refers to the combination of psychotic symptoms with individual normal intellectual abilities in schizophrenia as manifestations of “double-entry bookkeeping.”

A destructive influence on intellectual activity is exerted by perverted, incorrect, symbolic perception, the phenomena of derealization and depersonalization, and most importantly, disturbances in thinking caused by the “driving around”, “sliding”, “pulling apart” of thoughts described by Kraepelin. Disconnection occurs, disruption of the flow of associations, loss of individual links of the associative chain; during the associative process, extraneous ideas and ideas burst in atactically (embolically), which is due to the absence or lowering of goals, a decline in the processes of concentration and interest, and a violation of the harmonious relationship between cognitive processes and emotional response . This determines the features of ataxic speech confusion, characterized by the presence of the correct grammatical structure of phrases with a violation of the semantic content in the form of distorted thought formation, “slipping”, “driving around”, pseudo-concepts and neologisms, contamination, symbolic understanding and interpretation, “substitution”, described by B.Ya . Pervomaisky (1971) of the phenomenon of “displacement” (temporary asynchrony), perseverations, emboli, absurd answers, paradoxical conclusions and statements, combination of the incongruous and separation of the indivisible. In the structure of schizophrenic dementia, schizophasia may occur, which is a degree of ataxic speech confusion in which intellectual communication is impossible. Speech in these cases is devoid of emotional expressiveness, monotonous, and sometimes takes on the character of indistinct, meaningless muttering. The voice is usually quiet, but at times there may be loud cries.

As the disease progresses, dementia increases, which manifests itself in an increasingly sharp decline in intellectual productivity, intelligence, loss of a critical attitude to the environment and to one’s condition, and an increase in absent-mindedness, apathy, autism, and associative ataxia.

With deep schizophrenic dementia, patients sit motionless or lie in bed, completely indifferent to what is happening around them and to their own needs, not even showing purely physiological desires: they are unkempt, they have to be spoon-fed. All social and personal connections disintegrate, verbal communication with patients turns out to be impossible. For some time, some familiar gestures are retained.

Dementia can be of a simple nature, in which productive psychopathological symptoms are reduced and more or less pronounced intellectual failure comes to the fore, including not only a decrease in the level of cognitive processes, but also an impoverishment of the intellectual thesaurus.

A.O. Edelstein (1938) proposed to distinguish variants of the initial states of schizophrenia depending on the degree of personality destruction: the syndrome of “apathetic” dementia (“dementia of impulses”); “organic” type of dementia, which is characterized by a disorder of criticism, primitiveness and banality of judgments, poverty of thinking, mental exhaustion; “ruining” syndrome – a total collapse of the intellect and personality while maintaining only lower mental functions; “personal disintegration” syndrome.

The initial conditions in schizophrenia can be of the nature of dementia, in which some traces of the clinical form are preserved: hebephrenia (defect hebephrenia), catatonic manifestations (negativism, stereotypies), some extremely monotonous, stereotypical delusional statements devoid of emotional coloring.

V. Kerbikova, it belongs to dementia, in which there are no deep organic changes. According to I.F. Sluchevsky, it belongs to transient dementia. On this occasion he wrote:

There was a debate whether dementia in schizophrenia could be considered dementia itself. Thus, Kurt Schneider believed that in these cases, strictly speaking, dementia is not observed, since “general judgments and memory and other things that can be classified as intelligence do not undergo direct changes,” but only some disturbances in thinking are observed. A.K. Anufriev noted that a patient suffering from schizophrenia may simultaneously seem during a conversation with him to be both feeble-minded and not feeble-minded, and that the term “schizophrenic dementia” is quite justifiably put in quotation marks. According to G.V. Grule (German) Russian. , intellectual disorder in schizophrenia depends on the characteristics of mental activity that do not directly affect intelligence and are volitional disorders such as apato-abulia and thinking disorders. Therefore, we cannot talk about changes in intelligence in schizophrenia as classic dementia. With schizophrenic dementia, it is not the intellect that suffers, but the ability to use it. As the same G.V. Grule said:

Other authors compare intelligence in schizophrenia to a bookcase full of interesting, smart and useful books, to which the key has been lost. According to M.I. Weisfeld (1936), schizophrenic dementia is caused by “distraction” (delusions and hallucinations), “insufficient activity” of the individual before the illness, “the influence of acute psychotic conditions” and “lack of exercise.” On the latter occasion, he quotes the words of the great Renaissance figure Leonardo da Vinci, who argued that a razor becomes covered with rust through disuse:

Criticizing the idea of ​​the outcome of mental illness in dementia, N. N. Pukhovsky notes that the phenomena attributed to “schizophrenic dementia” are closely related to toxic-allergic complications with inadequate tactics of active treatment of psychoses (including neuroleptic, ECT, insulin comatose therapy, pyrotherapy), with remnants of the system of constraint in psychiatric hospitals and the phenomena of hospitalism, desocialization, coercion, separation and isolation, and everyday discomfort. He also associates "schizophrenic dementia" with the defense mechanism of regression and repression (parapraxis).

Nevertheless, the discrepancy between intellectual reactions and stimuli indicates the presence of dementia in patients with schizophrenia, albeit in a unique version.

Particular dementia in patients with schizophrenia, 4 years after E. Bleuler created the very concept of the disease, was described by the Russian psychiatrist A. N. Bernstein in 1912 in “Clinical Lectures on Mental Illnesses”.

According to A. O. Edelshtein’s classification, based on the degree of personality disintegration, the following are distinguished:

1. Syndrome of "apathetic" dementia ("dementia of impulses");
2. “Organic” type of dementia - according to the type of organic disease, for example, Alzheimer's disease;
3. Ruining syndrome with the onset of insanity;
4. “Personal disintegration” syndrome.

The pathogenesis of schizophrenic dementia, like schizophrenia itself, is not fully known. However, some aspects of it are described. The Austrian psychiatrist Joseph Berze in 1914 considered schizophrenic dementia to be a “hypotension of consciousness.” It is noteworthy that later many other scientists agreed with him: major researchers of schizophrenia K. Schneider, A. S. Kronfeld and O. K. E. Bumke (English) Russian. . The Soviet physiologist I.P. Pavlov also considered schizophrenia to be a chronic hypnoid state. However, this is not enough to understand the pathogenesis of schizophrenic dementia. In schizophrenia, while the elements of intelligence are preserved, its structure is disrupted. In this regard, the main clinical picture of the condition appears. According to V. A. Vnukov, expressed back in 1934, the basis of schizophrenic dementia is splitting of intellect and perceptions, paralogical thinking and flattened affect.

Perceptual disorders

Profound disturbances in perception in schizophrenia, primarily symbolism, derealization and depersonalization, have a negative impact on the intellect.

Thought disorders

Thinking in schizophrenic dementia is ataxic, with elements of pretentiousness, symbolism, formality, mannerism, mosaic. At one time, even E. Kraepelin, exploring “dementia praecox”, noted the “driving around”, “sliding”, “pulling apart” of thoughts. So-called ataxic thinking appears, externally manifested by speech disorders, often in the form of schizophasia, when sentences are grammatically correct, but their content is meaningless, slippage from the topic occurs, neologisms, contaminations arise, symbolic understanding occurs, perseveration, embolophrasia, paralogicality, combination of incongruous things and separation indivisible.

Memory disorders

Memory in schizophrenic dementia, as in schizophrenia in general, is preserved for a long time. Such patients are well oriented in their own personality, space and time. According to E. Bleuler, the phenomenon when patients with schizophrenia, along with psychotic ones, have preserved some aspects of intelligence, is figuratively called “double-entry bookkeeping.”

Since schizophrenia is a chronic and progressive disease, the prognosis for recovery from such dementia, if it has already occurred, is usually questionable. However, since this dementia is transient, if the course of the disease itself can be stopped, the prognosis can be relatively favorable. In other cases, an extremely unfavorable outcome is possible. Either an extreme increase in negative symptoms occurs in the form of complete apathy, abulia and autism, which manifests itself in absolute indifference, untidiness, disintegration of social connections and lack of speech, or with elements of the previous clinical form of schizophrenia: defect hebephrenia, residual catatonia, rudiments of delusions in the paranoid form. However, the prognosis for life is favorable, and for work ability it is relatively favorable with successful treatment.

Symptoms and treatment of dementia in schizophrenia

An irreversible change in the psyche is called dementia. A variety of comorbidities give dementia its unique characteristics. Schizophrenic dementia is marked by a lack of intelligence provoked by emotional breakdowns.

This type of dementia is temporary. A person who was considered sick for many years suddenly begins to communicate, showing the full presence of intelligence.

Schizophrenic dementia: what is this disease?

Dementia in schizophrenia is not characterized by deep organic changes. Acquired knowledge, professional skills and intelligence are retained by the subject. But he doesn't always know how to use them.

Intellectual disability, according to Grule, depends on the individual. Researchers Grule and Bertse discovered that the patient retains his memory, emotions, and acquired knowledge throughout his life. But he doesn’t use them because he loses interest in it.

In schizophrenia, qualities that lie outside the boundaries of intelligence are violated:

People with schizophrenia have an unusual way of thinking that makes doctors think about dementia. Bernstein wrote about incomprehensible mental constructs that are alien to normal people even before Grule, at the beginning of the twentieth century.

Stages of development and life expectancy

It is believed that schizophrenic dementia, once it appears, can become chronic. But, dementia in this case can also be temporary. Therefore, if it is possible to stop the course of chronic schizophrenia, the prognosis for recovery is quite favorable.

The patient can live for many years, remaining clean, well-mannered, not forgetting about hygiene and his professional achievements.

The distinct stages of transient dementia are difficult to determine.

In rare cases, an unfavorable outcome occurs gradually, with the presence of acute elements of delirium, paranoia, and hallucinations.

However, with successful treatment, the individual is able to maintain working capacity and the prognosis for life is quite favorable.

What should relatives do?

At moments when the patient exhibits an acute stage of the disease, in the form of delusions or hallucinations, an ambulance should be called. The person is hospitalized for 1-2 months. There he will receive intensive treatment and nutrition. The patient will be able to take care of himself independently.

When a family member returns home, he behaves absolutely normally, works, prepares food, maintains hygiene, and is polite to his family. You should not blame him for non-standard solutions to some issues. It is still unknown which people are sicker in this life and whose decisions are more correct.

The person is not dangerous either to himself or to others. Don't create for him stressful situations so that the condition does not worsen. Show more love and understanding.

Causes of dementia in schizophrenia

There is a debate among doctors about whether dementia in schizophrenia should be considered such at all. Since a person retains memory and general judgments, intelligence, only the manner of thinking changes.

A person suddenly begins to be afraid and hide. Emotions of fear arise from fantastic hallucinations. It can be assumed that the person was afraid of something. The cause of the exacerbation of the condition could be stress, some terrible event that occurred in a person’s life. Anxiety, depression, lack of understanding and love from others can lead to an exacerbation of the disease.

Symptoms of schizophrenic dementia

Symptoms of dementia appear during an exacerbation period, when a person is depressed and afraid. The following behavior changes are possible:

• a person hides in fear;
• orientation in space disappears;
• children's behavior in adults;
• touches the ear instead of the nose, at the request of the doctor;
• speech becomes meaningless, but remains literate;
• excitement gives way to apathy and lethargy.

Gradually, orientation in space and time returns. Anxiety disappears, the patient becomes adequate and communicates normally. The period of exacerbation of psychosis falls out of memory.

Diagnosis of the disease

Schizophrenic dementia is easily confused with various other mental illnesses. The psychiatrist must conduct tests and talk with relatives.

The general state of health is determined by blood and urine tests, and an ECG.

Treatment

Psychotherapy helps a person get rid of fears and feelings of loneliness and misunderstanding. Sessions of hypnotic, calm, shallow sleep, accompanied by relaxation music, very positively change a person’s thinking. When the patient understands that he is loved, he feels better.

Drugs

Modern psychiatrists prescribe new drugs that are easier to tolerate than in earlier generations.

Patients with schizophrenia are prescribed:

• neuroleptics;
• anti-anxiety tranquilizers;
• sedatives;
• antidepressants.

For hallucinations and delusions they take antipsychotics. In the future, these medications are taken to reduce the risk of exacerbations, as maintenance therapy.

In the absence of attacks of schizophrenia, dementia of this type does not appear.

Traditional methods

You should consult your doctor about the use of tinctures and decoctions.

Motherwort and valerian can be taken as sedatives.

If a person has asthenia or low blood pressure, tinctures of ginseng and Chinese lemongrass help.

Tea with lemon balm and peppermint helps to improve sleep.

As maintenance therapy, herbal soothing infusions reduce the risk of exacerbations of dementia.

Nutrition, diet

A varied and high-calorie diet is necessary to maintain good health and mood.

Freshly squeezed juices in moments of exacerbation are more likely to return a person to a normal state. In normal times, fruits and vegetables should be on the table every day.

Eggs, sour cream, milk and fermented baked milk, poultry, rabbit, and nuts must be included in the diet. Food must contain enough fats, proteins, fiber, vitamins, and carbohydrates to maintain normal human life.

Then the patient will not have thoughts of fear and oppression, abandonment.

Exercises

Leonardo da Vinci said that a razor begins to rust from disuse, and the mind, having stopped exercising, begins to weaken and indulges in idleness.

Therefore, a patient with schizophrenia should solve mathematical problems and study physics lessons with children. Chess, corner games, puzzles and rebuses preserve intelligence well.

Light physical activity is also helpful. Pleasant music and dancing heal spiritual wounds and give gymnastics to the mind. Memorizing complex movements is useful. At this time, the brain begins to work, new neural chains appear.

Prevention

In order not to subject a person’s psyche to unbearable tests, one should protect him from stress and surround him with love and care.

Kind words, sincere conversations, pleasant music soothe, relieve fears and phobias.

Proper nutrition, no alcohol, sports, travel, walks in the forest, all this keeps a person a healthy psyche. In summer it is useful to go to the pool, swim in the sea and river. Outdoor games and theater, ballet and pop music, all this is interesting and useful in order to never get dementia.

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Dementia in schizophrenia

Dementia means a persistent irreversible decline in mental activity. But with different concomitant diseases, dementia has specific symptoms. For example, dementia in schizophrenia is characterized by a lack of intelligence, caused largely by emotional and volitional deviations, but without deep organic changes. You can also find names like vesanic, ataxic or apathetic dementia. There is still a lot of uncertainty about the causes of the origin of this disease, as with schizophrenia itself.

Clinical picture

First of all, patients develop apathy, in which there is no interest in anything, the person is passive, and is characterized by a lack of hobbies or attachment. Such a patient either does not answer questions at all, or the answer will be inadequate - usually the first thing that comes to mind. It is easier for him to answer “I don’t know” to the question posed. The patient is unable to use his knowledge and skills to solve even a simple life situation, so planning becomes impossible for him. The patient's behavior can be described as helpless and strange. It is very difficult for such a person to concentrate. But when performing any task, the patient, ignoring serious issues, will pay all attention to minor details.

In schizophrenic dementia, memory remains unchanged for a long time, the ability for abstract thinking is preserved, but there is no focus. Most often, passivity and indifference make it impossible to achieve any result. It should also be added that patients retain the ability to navigate in time and space for a long time. Not feeling the need for work, these people do not strive to work. Outwardly, they look sloppy due to their unwillingness to wash or dress appropriately.

A characteristic feature of the disease is the occurrence of ataxic thinking - the presence in the patient’s speech of incompatible concepts. The patient’s speech contains unexpected turns of phrase (neologisms, symbolism). There are usually no errors in arithmetic operations

Gradually, as a result of inaction of the intellect, a loss of knowledge and skills occurs. There is a depletion of emotions and impaired thinking; this condition is called apathetic-abulsic syndrome. As dementia progresses, it increases, a sharper decline in intelligence is noticeable, apathy and absent-mindedness increase, and in some patients autism develops.

At a later stage, patients are completely indifferent to what is happening, sit or lie motionless, ignoring even their natural needs, they often need to be spoon-fed, and verbal communication with them is impossible. But for a long time, familiar gestures remain.

Schizophrenic dementia is characterized primarily by emotional disturbances, while intellectual disorders, as well as acquired knowledge and skills, are initially virtually unaffected. However, patients cannot use them. Therefore, psychiatrists often call this pathology a schizophrenic defect, and not dementia.

Forecast

The prognosis for this disease is questionable. If further deterioration of dementia can be stopped, the prognosis may be favorable. Otherwise, there is an increase in complete apathy. With proper treatment, the manifestations of the disease can be smoothed out, but it is impossible to get rid of the disease completely. However, today there are individual programs treatment, as well as social and rehabilitation measures.

Dementia and defect in schizophrenia

Dementia is a total change and devastation of personality, severe thinking disorders, apathetic or disorganized behavior in the absence of criticism of one’s condition.

Specificity of schizophrenic dementia.

Loss or sharp decline in spontaneity and initiative;

Profound impairment of intellectual activity (a sharp decrease in the ability to mock, judge, generalize, understand the situation - complete loss of all intellectual baggage, the entire stock of knowledge, destruction of any interests.

All this creates a “ruin syndrome” (described by A.O. Edelshtein in the 30s).

Ruining syndrome is observed in 15% - 22% of cases of schizophrenia. Its formation is difficult to associate with any form of schizophrenia, but more often with catatonic and hebephrenic forms.

Clinic: complete indifference and indifference, a frozen smile, lack of understanding of basic questions, answers like schizophasia, indifference when meeting with relatives, lack of the slightest concern for the family, gluttony, sloppiness (they often do not use a spoon when eating).

The defect, unlike dementia, is a relatively mild form of partial weakening of mental activity. Patients in the stage of stable remission tend to restore, to varying degrees, a critical attitude towards the manifestations of the defect.

A defect is a primary negative symptom, i.e. reflecting persistent deficit personality changes. They must be distinguished from secondary negative ones - associated with the current exacerbation of psychosis, depression, neurolepsy.

It is impossible to determine the depth and type of negative/deficit disorder at the active stage of the process. During an exacerbation or in the stage of incomplete remission, both primary and secondary negative disorders are present in the clinic.

Primary negative disorders (consequences of the disease itself) are extremely difficult to distinguish from the side effects of medications, hospitalization, loss of social status, lowering the level of expectations from relatives and doctors, getting used to the role of a “chronically ill person,” loss of motivation, and hope.

Typology of defect in schizophrenia.

When assessing the nature and severity of the defect and the prognosis of the condition, one should remember two provisions of D.E. Melekhov (1963).

1) signs of increasing severity of the defect or the appearance of new symptoms in its structure indicate the continued activity of the process;

2) even pronounced manifestations of the defect are available for compensation if the process has stopped in its development, enters the stage of stable remission, post-processual (residual) state and takes a long, slow, sluggish course without frequent exacerbations.

1) Asthenic - or nonspecific “pure” defect (Huber), “reduced energy potential” (Conrad K.), “dynamic devastation” (Janzarik W), “primary adynamia” (Weitbrecht) - this is a decrease in energy potential and spontaneous activity, and level of goal-directed thinking and emotional responsiveness (Huber).

“Decreased energy potential” according to Conrad K. (1958) is characterized by a decrease in the strength of mental tension, will, intensity of desires, interests, level of motivation, dynamic activity in achieving a goal;

“Dynamic devastation” according to Janzarik W (1954, 1974) - includes a decrease in emotional tension, concentration, intentional impulsiveness, readiness for action, which is manifested by emotional coldness, dishonesty, lack of interests, and lack of initiative.

The structure of an asthenic defect is intellectual and emotional impoverishment, mildly expressed thinking disorders, and a narrowing of the range of interests. The behavior of patients is outwardly ordered. Household and simple professional skills, selective attachment to one of the relatives or medical staff are preserved, and the feeling of one’s own change is preserved.

2) Fershroben (acquired deficit or expansive schizoidia according to Smulevich A.B., 1988).

Structure – autism in the form of pretentiousness, absurdity of actions with a separation from reality and life experience. Reduced sensitivity and vulnerability, disappearance of the tendency to internal conflict, fading of related feelings. The sense of tact, humor, and distance disappears. In general, there is a decrease in criticality and emotional hardening. Former creative abilities are lost (decreased). Cognitive activity comes down to the use of insignificant, latent properties and relationships of objects, considering them in unusual aspects and connections, the use of rare words, neologisms, and a tendency to pretentious expressions. “Pathological autistic activity” comes down to pretentious actions, divorced from reality and past life experience. There are no clear plans or intentions for the future. The lack of criticism is manifested by a disorder in assessing one’s “I”, in the form of awareness of one’s own individuality through comparison with others. In everyday life, oddities - cluttered home, unkemptness, neglect of hygiene, contrast with the pretentiousness of the hairstyle and toilet details. Facial expressions are unnatural, artificial, motor skills are dysplastic, movements are angular. Emotional hardening is manifested by a reduction in sensitivity and vulnerability, the disappearance of the tendency to internal conflict, and the extinction of related feelings. The sense of distance and tact is grossly violated. Often - euphoria, out of place jokes, complacency, empty pathos, regressive syntony.

3) Psychopathic-like (pseudopsychopathy) – typologically comparable to constitutional personality anomalies (psychopathy).

This type of defect is predisposed by: a) the association of active (manifesting) periods of the disease with age-related crises, b) a poorly progressive course, c) the presence in the initial period of schizophrenia of an affinity for disorders of the psychopathic circle.

Pseudopsychopathies in the clinic of paroxysmal-progressive schizophrenia are described in the idea of ​​2 options for post-processual personality development (Smulevich A.B., 1999).

1. “idealists alien to the world” according to E. Kretschmer (1930) - with a new approach to reality, hermits, unsociable eccentrics, indifferent to the fate of relatives, with a worldview subordinate to the ideas of spiritual self-improvement, detached from vain affairs, with autistic hobbies. This also includes personality changes of the “second life” type (Vie J., 1939) with a radical break with the entire system of premorbid social, professional and family ties. Change of occupation, formation of a new family.

2. residual states according to the type of dependent individuals (psychasthenic remissions according to V.M. Morozov, R.A. Nadzharov). Doubts about any reason, loss of initiative, the need for constant encouragement, passive submission, the position of “adult children” in the family. In production conditions, they get lost with minor deviations from their usual activities, and in non-standard situations they take a passive position with avoidant behavior and refusal reactions.

4) Syndrome of monotonous activity and rigidity of affect (D.E. Melekhov, 1963).

Patients are distinguished good performance, passion, tirelessness, invention, innovation, professional erudition in stereotyping the working day and planning. The range of interests is preserved, but with the possibility of one hobby. Along with this, there is a lack of emotional resonance, a decrease in sympathy and empathy, dryness and restraint of emotional manifestations, external sociability and breadth of contacts in the absence of truly close people, inflexibility and avoidance of solving family problems. There is resistance to frustration, lack of reactive lability, inflated self-esteem, not always adequate optimism, lack of critical attitude and rationalization in explaining the causes of the attack.

5) Pseudoorganic - formed during the development of schizophrenia on organically altered soil.

It is characterized by a drop in mental activity and productivity, intellectual decline, rigidity of mental functions, leveling of personal characteristics, narrowing of contacts and range of interests (simple deficiency type defect (Ey H., 1985), autochthonous asthenia (Glatzel J., 1978)). It is formed more often against the background of a family predisposition to schizoid psychopathy.

5) Syndrome of infantilism and juvenileism - most often formed during atypical attacks suffered in adolescence and adolescence with heboid, pseudoneurotic, atypical depressive, dysmorphophobic disorders or overvalued formations such as metaphysical intoxication. “Juvenilism” is reflected in the manner of dressing, behaving in a group, in the choice of hobbies, friends, profession and worldview.

Neurocognitive deficits in schizophrenia.

In recent years, the paradigm of the biological basis of mental disorders has received intensive development in psychiatry, and within its framework is the concept of neurocognitive deficit in schizophrenia.

The neurobiological model of schizophrenia suggests a violation of the formation of the central nervous system, in the form of a decrease in the volume of gray matter, a decrease in the level of metabolism, membrane synthesis and regional blood flow of the prefrontal cortex, and a decrease in delta sleep on the EEG. But there is no evidence of damage to any specific area of ​​the brain. The disturbances occur at the synaptic level, although there is evidence in the literature of structural disturbances.

Neurocognitive deficit is a form of information processing disorder, deficiency of cognitive function: memory, attention, learning, executive function. It is observed in 97% of patients with schizophrenia and only 7% in the healthy population. Cognitive decline is also observed in relatives of patients with schizophrenia. The main intellectual decline occurs in the first 2 years of the disease.

Neurocognitive deficits are considered to be the "third core group of symptoms" in schizophrenia, along with negative and productive disorders.

Intellectual functioning in patients with schizophrenia is relatively unaffected (IQ is only 10% lower than in healthy people). But at the same time, a “deficit” of memory, attention, speed of information processing, and executive functions is revealed. This affects the social, professional viability and quality of life of patients with schizophrenia.

Memory disorders – relate to verbal and auditory modality, working memory deficit (working memory - the ability to record information for use in subsequent activities). A working memory deficit is manifested in a violation of retaining information for a short period during which it is processed and coordinated with other long-term mental operations, which ultimately leads to the development of a response. The ability to concentrate is an indicator of ability to solve problems and acquire skills.

Attention impairment - auditory and visual modality, difficulty maintaining attention for a long time, sensitivity to distractions.

Insufficiency of executive function in schizophrenia (drawing up and implementing plans, solving new problems that require the use of new knowledge. The state of executive function determines the ability to live in society) - weak ability to plan, regulate behavior and set goals.

“Cognitive profile” of patients with schizophrenia (based on the results of averaged neurocognitive tests).

A normal or near normal reading test result;

The lower limit of tests assessing simple sensory, speech and motor functions;

a decrease of 10 points in IQ according to the Wechsler test;

Reduction by 1.5 - 3 standard deviations in test scores for memory assessment and more complex motor, spatial, and linguistic tasks;

Extremely low results in tests for attention (especially stability of attention) and tests testing problem-solving behavior.

AFFECTIVE MOOD DISORDERS.

Affective disorders are a group of mental disorders with various course options, the main clinical manifestation of which is a pathological decrease or increase in mood, accompanied by disruption of various areas of mental activity (motivation of activity, drives, voluntary control of behavior, cognitive functions) and somatic changes (vegetative, endocrine regulation, trophism, etc.)..

Ancient period -Hippocrates “melancholy”, “black bile”

1686 Theophile Bonet: “manico-melancolicus”

1854 J. Falret and Baillarger: “circular madness”

1904 Emil Kraepelin“manic-depressive psychosis”.

Symptomatology – polar, phasic affective fluctuations

Emotions - melancholy, depression, sadness, hopelessness, worthlessness, a feeling of twina, the meaninglessness of existence; anxiety, fears, worry; pessimism; loss of interest in family, friends, work, sex; inability to have fun, have fun - anhedonia

Thinking - slowness of thinking, difficulty concentrating, making decisions; thoughts of failure, low self-esteem, inability to switch from negative thoughts; loss of a sense of reality, possible appearance of hallucinations and delusional ideas of depressive content; suicidal thoughts (about 15% of untreated patients with affective illnesses commit suicide).

Physical condition - changes in appetite and weight (70% lose weight, others gain); sometimes an excessive desire for sweets develops; sleep disorders: although insomnia is a common complaint, about 10% feel an increased need for sleep and they do not feel rested even after hours of sleep; loss of energy, weakness, drowsiness; various pain sensations (headaches, muscle pain; bitter taste in the mouth, blurred vision, digestive disorders, constipation; agitation and restlessness.

Behavior - slow speech, movements, general “lethargy”; excessive tearfulness or, conversely, the absence of tears even with the desire to cry; alcohol and/or drug abuse.

Typology of depressive syndromes: Melancholic depression; Depression with anxiety; Anesthetic depression; Adynamic depression; Depression with apathy; Dysphoric depression; Smiling (or ironic) depression; Tearful depression; Masked depression (“depression without depression”, somatization of depression) Somatization is a manifestation of a mental disorder in the form of physical suffering.

The main symptom of mania is increased elation. As a rule, this mood grows in a certain dynamic sequence, which includes a sequential change of the following phases:

Elevation of mood within normal limits: happiness, joy, fun (hyperthymia);

Moderate rise: increased self-esteem, increased ability to work, activity, decreased need for sleep (hypomania);

Mania itself: manic symptoms increase and begin to disrupt the patient’s normal social activity;

- “delusional” or psychotic mania: excessive overactivity, irritability, hostility, possible aggression, delusions of grandeur and hallucinations

Emotions - elevated mood, feeling of elation, euphoria, ecstasy.

But the following are possible: irritability, anger, excessive reaction to ordinary things, lability, rapid mood swings: a feeling of happiness and a minute later anger for no apparent reason, hostility.

Thinking - increased self-esteem, ideas of greatness, personal power; incorrect interpretation of events, introducing your own meaning into comments of ordinary content; distractibility, lack of concentration; jumping ideas, flight of thoughts, jumping from one topic to another; lack of criticism of one’s condition; loss of sense of reality, possible appearance of hallucinations and delusions.

Physical state - increased energy, shorter sleep - sometimes only 2 hours of sleep is enough, heightened perception of all senses - especially colors and light.

Behavior – involvement in adventures and grandiose plans. involuntary uncontrollable desire to communicate: can call friends on the phone many times at any time of the night to discuss their plans, excessive spending of money, often just giving money away, meaningless numerous purchases, jumping from one activity to another, laughing, joking, singing, dancing. Possible: malice and demandingness. Talkativeness, speech is fast and loud. The emergence of a new interest in collecting something, increased sexual activity.

In the ICD-10 classification - combined under heading F3 “AFFECTIVE MOOD DISORDERS”

According to modern concepts, painful episodes of mood disorders are a combination of symptoms (manic or depressive) that make up a dominant affective state.

Etiology: predominantly hereditary, autochthonous course.

The first episodes of the disease are often preceded by mental trauma (mental and physical stress), physiological changes (pregnancy, childbirth), exogenous factors (TBI, intoxication, somatic diseases) and subsequently their significance weakens.

TYPES OF AFFECTIVE DISORDERS (according to ICD-10, DSM-1V classification).

Recurrent depression (Major depression)

Other depressive disorder

Other bipolar disorders

3.Other affective disorders:

Recurrent depression (DSM-1V major depression)

Epidemiology: Prevalence: men 2-4%, women 5-9% (men: women = 1:2), mean age of onset:

Genetic: 65-75% - monozygotic twins, 14-19% dizygotic twins

Biochemical: neurotransmitter dysfunction at the synaptic level (decreased activity of serotonin, norepinephrine, dopamine)

Psychodynamic (low self-esteem matters)

Cognitive (negative thinking matters).

Risk factors - gender: female, age: onset in the age range of years; presence in the family history (heredity) of depression, alcohol abuse, personality disorders.

History (especially early) - loss of one of the parents before the age of 11; negative conditions of upbringing (violence, lack of attention).

Personality type: suspicious, dependent, obsessive.

Psychogenics - recent stress/psychotraumatic situations (illness, trial, financial difficulties), postpartum trauma, lack of close, warm relationships (social isolation).

DYSTYMIA is a variant of depressive disorders with moderately severe symptoms and a chronic course (more than 2 years).

Features of low mood with dysthymia:

increased sensitivity to the environment, irritability, touchiness, and angry reactions predominate. Inconsistency of actions and thoughts. Emotional and sensory hyperesthesia. Unstable (usually inflated in a hidden form) self-esteem. Lethargy, relaxation. Getting stuck on grievances and failures, imagining the ill will of others. Preservation of motives when it is difficult to realize them. More often increased appetite

If syndromic complete depression develops against the background of dysthymia, “double depression” is diagnosed.

BIPOLAR DISORDER (BD).

Bipolar disorder type 1 is characterized by the presence of 1 or more manic or mixed episodes and at least 1 episode of syndromic-complete depression.

Bipolar disorder type 11 - 1 or more syndromic-complete depressive episodes and at least 1 hypomanic episode.

1) Genetic predisposition - concordance of monozygotic twins is 65-85%, dizygotic twins - 20%, 60-65% of patients with bipolar disorder have a family history of mood disorders

2) Environmental factors contributing to the manifestation of BD - stress, antidepressant therapy, sleep-wake rhythm disturbances, abuse of PA substances.

Prevalence - Lifetime prevalence: 1.3% (3.3 million people in U.S.) Age of onset: teenage years and around 20 years

The flow is periodic, in the form of double phases, and continuous.

80-90% of patients with bipolar disorder have multiple relapses. The average number of episodes of the disease during life is 9

The duration of remissions (periods without symptoms of the disease) decreases with age and the number of previous episodes.

Diagnostics. Patients visit an average of 3.3 doctors before a correct diagnosis is made

The average time to correct diagnosis is 8 years after the first visit to the doctor (60% of patients do not receive treatment within 6 months of the initial episode; 35% of patients do not even seek help for 10 years after the first symptoms of the disease; 34% patients are initially given a diagnosis other than bipolar disorder).

Suicide rate. 11-19% of patients with bipolar disorder commit suicide. At least 25% attempt suicide. 25-50% of patients have suicidal thoughts in a state of mixed mania

Differentiation between BD and unipolar depression is important.

Family history - Individuals with BD are more likely to have a family history of mood disorders, as well as substance abuse.

PD has a more pronounced hereditary predisposition.

Age of onset – PD often manifests itself in adolescence, and UD – after 25 years.

Course - PD occurs in more defined phases (with abrupt start and cliff) and has a more pronounced seasonality in its manifestations.

Response to therapy – in PD, antidepressants are less effective and often promote progression to mania.

CYCLOTHYMIA is a mild variant of bipolar affective disorder. Often seasonal. There are winter-spring and autumn depressions.

For many years, since 1911, criticism of Bleuler's concept of schizophrenia has not stopped. E. Bleuler meant by schizophrenia a whole group of mental illnesses: from severe psychoses to states that are close to normal - borderline states. That is, those states that are the subject of study of the so-called. minor psychiatry. You and I must understand and figure out why and for what E.Bleuler is criticized.

It must be said that he is scolded and criticized for something that is not his fault. If E. Bleuler spoke about a group of schizophrenias, then let us understand him the way he wanted to say. E. Bleuler is criticized for expanding the boundaries of schizophrenia. But when creating the concept of schizophrenia, he spoke about that boundless sea mental disorders who have one connecting disorder - mental splitting. And under this general definition, naturally, a whole group of mental disorders fell: from asthenic, neurotic and characteropathic to affective, delusional, hallucinatory and even purely neurological, up to stupefaction.

Therefore, E. Bleuler’s criticism regarding the exorbitant expansion of the boundaries of schizophrenia is not entirely justified. After all, he said what he wanted to say, doubting the unity of schizophrenia. But we must then understand where the origins of this criticism come from. The sources are objective and subjective.

Objective is that dementia praecox, created by the teachings of E. Kraepelin and first systematically and clearly symptomatologically described in 1896 in the 5th edition of his “Textbook of Psychiatry,” represented this disease as a single disease. E.Bleuler really expanded the boundaries of the so-called. dementia praecox, premature dementia.

As is known, E. Kraepelin used the principle of systematization of mental illnesses, which underlay somatic medicine in general. This is a clear description of the symptomatology and a constant comparison of it with the course, i.e. identification of the nosological unit of the disease according to the principle of somatosis, a principle that took into account the unity of etiology, pathogenesis and outcome. For more than 20 years, E. Kraepelin has constantly changed the classification of mental illnesses. He began working at a time when there was complete confusion in psychiatric nosography and nosology. There were a lot of different nosological units, distinguished according to a static syndromic principle: what is the syndrome, so is the disease. As a result, it turned out that if you trace the disease in the same subject over decades, throughout your entire life, it turns out that the same person suffers from dozens of mental illnesses, although the process should, naturally, be the same.

To understand the inconsistency in the views of various clinical psychiatrists and the confusion that reigns now, it is necessary to take into account objective and subjective factors. Objective, as I already said, is inherent in the very essence of the disease process, which is extremely diverse in symptomatology. The subjective factor is that psychiatrists have different schools, ideologies and training. That is why we should first look at a trivial case, which over many years has almost never caused any disagreement or doubt about the diagnosis of schizophrenia among any of the psychiatrists of various schools.

Let me introduce you to the patient. Please, Igor Petrovich.

Patient Ts. Zinaida Ivanovna, born in 1919, 55 years old, disabled person of the 1st group. She was admitted to our hospital many times. Last received on January 21 this year. From the anamnesis it is known that the paternal grandfather suffered from some kind of seizures. The patient's early development was without any features. She grew up lively, active and sociable. She studied well, smoothly, and was fond of sports. At the age of 16, she received a prize for running - a gold watch. Before finishing 10th grade (17 years old), I studied a lot and slept little. After the exams, she became irritable and often cried for no reason. She couldn't decide what to do next. She was bothered by headaches and sometimes complained of pain in the heart area. I did nothing for about a year, rested at the insistence of my parents and was treated by a neurologist. At this time, she was not interested in anything, was withdrawn, and strived for solitude.

In April 1938 (age 18), a psychotic state with confusion, grandiosity and psychomotor agitation developed acutely. In this condition, she was admitted to the hospital for the first time. P.B. Gannushkina. She was treated for about 3 months and received insulin therapy. She was discharged in satisfactory condition and in the fall of 1939 she entered the 1st Medical Institute. She studied well, was very diligent, diligent, and studied a lot. At the same time, increased fatigue was noted, and sensitive ideas of attitude arose occasionally. It seemed that those around her were showing increased interest in her, because... she was treated at psychiatric hospital. Because of this, I left lectures and sometimes took exams later than others. At the same time, she had her own circle of friends, in which she was sociable and lively.

In 1942 (22 years old), a bomb hit the clinic where the patient was working. I came home depressed, anxious, and my sleep was disturbed. After 2 days, speech motor agitation developed with vivid, dream-like fantastic experiences. In this condition, she was admitted to the hospital for the second time. She was treated for more than 2 months, received insulin therapy, and was discharged in good condition. Soon she started studying and studied with excellent marks. She also passed the state exams with “excellent” marks in 1945.

Upon graduation, she was assigned to the periphery. When I found out about this, I was very upset and tried to get her to stay in Moscow, but to no avail. During this period of about 2 months, the state ranged from depression with irritability and suicidal thoughts to fussy hyperactivity with causeless gaiety.

In September 1945 (25 years old), sleep was disturbed, she became anxious, experienced fears and auditory deceptions. In this condition she was admitted to the hospital for the 3rd time. Soon after admission, she was consulted by A.V. Snezhnevsky. Conclusion: a state of confusion with oneiroid elements, changes in the affective sphere similar to the basic schizophrenic mood. Shape from a catatonic circle. Insulin therapy is recommended. Upon discharge, the patient was re-examined by A.V. Snezhnevsky. Final diagnosis: schizophrenia, catatonic-oneiric form.

After discharge, I was on disability for 6 months, did not work, and helped with housework at home. I read a lot, met with friends, willingly went to the cinema, theater, and concerts. After the end of the period of disability, i.e. Six months after discharge, she actively tried to find a job. She became a laboratory doctor, but left her job after a week because... I experienced headaches while working with the microscope. Then she got a job several more times, but after a short time she left her job due to occasional sensitive ideas about the relationship.

In the summer of 1947 (28 years old), psychomotor agitation developed acutely, and the patient was admitted to the hospital for the 4th time. Upon admission, she was consulted by A.V. Snezhnevsky. Conclusion: the patient’s condition is characterized by psychomotor agitation, fragmented thinking, reaching the level of verbal hash, mannerisms, inappropriate laughter and crying, as well as a syndrome of mental automatism and psychosensory disorders in the form of a violation of the body diagram. Diagnosis: schizophrenia. Insulin therapy in combination with electroconvulsive therapy is recommended.

During this treatment, the patient experienced a short-term improvement in her condition, during which she told the doctors that every time she was admitted to the hospital she experienced the same experiences. She imagines that she is in an institute where experiments are being conducted to extend the lives of government members, and she is directly related to this. At the same time, she constantly experiences fear for her life, because... believes that they are going to kill her. Then the condition worsened again and ranged from anxious-delusional timidity to foolishness with agitation and impulsiveness.

In December 1947, she was consulted by Professor M.Ya. Sereisky. Diagnosis: schizophrenia, hebephrenic form. Due to the severity of the disease and the failure of active therapy, a lobotomy is indicated. In December 1947 and January 1948 (28 years old), a lobotomy operation was performed twice on the right and left, because After the first operation, there were no changes in the mental state. After the 2nd operation, apatoabulic signs became most pronounced in the condition. She was gluttonous and gained a lot of weight.

After discharge at home, she was inactive, foolish, and after 4 months she was hospitalized again. This time the patient was advised by G.A. Rotshtein. Diagnosis: schizophrenia, defective state. It is recommended to stay in a home for mentally disabled people. Contrary to the advice of doctors, the parents took the patient home with a signature. Gradually, after six months, her health improved, and at the end of 1948 the patient got a job as a laboratory assistant in one of the clinics of the 1st Medical Institute. I coped with the job for more than 1.5 years.

In April 1950 (age 31) there was deterioration again: ideas of relationship and persecution appeared. The patient became anxious and in June 1950 was admitted to the hospital for the 6th time. Upon admission, she was consulted by A.V. Snezhnevsky. Conclusion: exacerbation of schizophrenia, accompanied by fear, ideas of relationship, persecution and senestopathies. Insulin therapy is recommended. After 29 comatose states, the patient, against a background of wariness and suspicion, began to show foolishness and puerility in her behavior. She was discharged home with slight improvement.

The patient was at home for about 3 years, but it was not possible to adapt her to any systematic work. There were elements of foolishness in her behavior, she often expressed ridiculous fantastic thoughts, talked to herself, and had no contact with others.

In 1953 (33 years old) he was admitted to the hospital for the 7th time. Consulted by G.A. Rotshtein. Diagnosis: schizophrenia, exacerbation with hebephrenic manic affect and figurative delusions. Insulin therapy is indicated. During insulin therapy, it turned out that the patient became resistant to insulin and coma could not be achieved. However, upon discharge, the behavior was much more orderly and she was passively submissive.

She was at home for about a year, involved in household chores, and helped her mother. Then she began to accuse her mother of allegedly trying to poison her. In 1954 (34 years old) she was hospitalized twice and was discharged with slight improvement. At home she was inactive, then lay in bed all day, then became agitated, angry, and aggressive.

From the age of 35, with each hospitalization, paraphrenic features were clearly identified in the structure of the patient’s psychotic manifestations. She called herself a special person, a saint; she said that she had made an outstanding discovery in medicine, for which she received 5 Stalin Prizes; called famous people her relatives; claimed that her husband was the son of the leader of the peoples, etc. Along with this, there were auditory pseudohallucinations and gross disturbances of thinking, up to schizophasia.

Until 1959, the patient was hospitalized annually; no improvements in her condition were noted. On the contrary, since 1956 (37 years old), the patient began to experience convulsive seizures with loss of consciousness, tonic and clonic phases. Seizures were rare and stopped in 1959 (40 years).

From 1959 to 1965 the patient was not hospitalized. She helped with housework and did handicrafts. She led a secluded lifestyle, carefully visited the dispensary and received outpatient treatment.

Since 1965 (46 years old), headaches began to bother her, auditory deceptions intensified, and she became irritable and angry. For this reason, she was stationary. After discharge, from 1966 to 1971, she visited the day hospital and performed cardboard work, which she coped with quite well. With outwardly ordered behavior, she expressed thoughts of a paraphrenic nature. There were significant disturbances in thinking, fragmentation, and schizophasia.

Since 1971 (52 years old), the patient has been hospitalized 2-3 times a year. At the same time, between admissions, in 1973 (54 years old), she began to attend occupational therapy workshops. As a rule, she herself asks for hospitalization.

Mental status from the age of 35 generally remains the same and fluctuates in intensity in terms of paraphrenia, thinking disorders up to schizophasia and chronic pseudohallucinosis.

(A sick woman enters the audience.)

(The patient leaves)

For us now, a thorough analysis of her condition and the course of the disease is not of particular importance. Why? Because if you carefully analyze her current state and go over the entire course in a scientific sense, then you can read the whole schizophrenia in this patient. Therefore, our task is to highlight and separate some periods of the disease that led her to delirium of grandeur, reminiscent of manic delirium during progressive paralysis: absurd, fantastic, uncontrollable, grandiose.

What are the objective difficulties inherent in the very concept of “schizophrenia” or “dementia praecox”? If we start a discussion about dementia now, we are unlikely to come to a consensus. A variety of points of view will be expressed and mutually exclusive evidence will be presented.

The classical concept of feeblemindedness, dementia or feeble-mindedness is very far from the concept of schizophrenic dementia. Classical clinicians, more E. Kraepelin, less E. Bleuler, wrote about dementia. E. Bleuler said that schizophrenic dementia is a special kind of dementia. Zinaida Ivanovna has a special kind of dementia.

Then the question arises: what is its speciality? Negative side. There is no basic and characteristic decline in intelligence, synthetic and analytical activity of thinking from higher to lower, from abstract to concrete, to emasculation. What's here? In a conversation with the patient, we see that she suddenly transfers abstract concepts to concrete ones, and begins to extend and abstract concrete ones, to which we are accustomed quite unambiguously. This is some kind of special, incomprehensible symbolization for us. And when the patient does not understand our concepts in an abstract sense, higher and abstract concepts, relationships between people, then it seems to us that this is idiocy. And when we suddenly see that she begins to subtly notice something, even in her condition, knows how to behave, grasps the meaning and intonation of words addressed to her, returns to her childhood, gives an assessment of it, then we think that she is not weak-minded . That is, the patient before us simultaneously appears both feeble-minded and not feeble-minded.

This is the peculiarity of schizophrenic dementia, which everyone puts in quotation marks, which is absolutely correct. It may even be better not to use this term in order to, in a working and cognitive sense, differentiate dementia in schizophrenia from dementia, which primarily affects the intellect and thinking.

The mental state of our patient is determined primarily by paraphrenia. What kind of paraphrenia is this? By the way she speaks, when she expresses some absurd ideas of greatness, now others, when they are scattered, and we do not find a single, unifying, logically developed line, we conclude that there is no systematized paraphrenia here.

When we further talk with the patient and see that there is an insignificant proportion of pseudohallucinations that do not determine her real mental state and behavior, we say that there is no Alberstadt’s hallucinatory paraphrenia here.

The background mood is upbeat, there are some elements of bliss, contentment, even complacency. But there is no special elation, exaltation, and we say that this is not expansive paraphrenia.

We are left with fantastic and confabulatory paraphrenia (or “confabulosis” in the old terminology). In this case, we have a fantastic paraphrenia. You can object to me that there are some fabrications here. Certainly. In any paraphrenia there are always certain elements from another paraphrenia. After all, the very name of paraphrenia already speaks of the fantastic. In systematized paraphrenia there is also a fantastic quality, some fictions that can be grasped. Here, in fantastic paraphrenia, they are always larger, but this is not what defines it. What other feature of this paraphrenia? Its fragmentation, polymorphism, extreme absurdity. But you can object to me again that when it comes to paraphrenia, the delirium is fantastic and, therefore, absurd, it is stupidity. Yes, paraphrenia is always stupidity, be it acute or chronic stupidity.

When there is paranoid delusion, i.e. logical development, a system of evidence (and when we have endlessly made mistakes, are making mistakes and will continue to make mistakes, not seeing nonsense that is difficult to identify because it is close to reality), then we do not say that this is paraphrenia.

So, here is a fantastic paraphrenia with a change in personality, which I now called schizophrenic dementia or severe personality degradation with parathymia and thought disorder. There is one more sign in favor of dementia. In the presence of such dementia and split personality, there is a dual, ambivalent feeling, elements of the consciousness of the disease, more directed towards the past. It is surprising to me that the patient, currently in a state that is approaching the initial, final state, can analyze and remember what happened at the beginning of the disease. The medical history states that the disease began at the age of 17. Yesterday I asked Igor Petrovich to write a short statement, and he tells me that the patient fell ill at the age of 17. I thought that this couldn’t happen, because... the disease almost never manifests itself acutely; there is always a prodrome, an initial period. Here we found out in the patient that at the age of 15 the first breakdown occurred (in the terminology of A. Kronfeld, who described the so-called mild schizophrenia). What happened from 15 to 17 years old? We are opening the International Classification of Diseases, 8th revision (we will adhere to this classification, since in practical activities you are required to enter codes), the “mental illnesses” section, the “schizophrenia” section and we are looking. Where does this fit?

Latent schizophrenia. If we had talked with the patient at that time and observed her behavior, then, in all likelihood, we would not have identified any illness. For us, the disease became obvious when asthenoadynamic depression developed at the age of 17. This condition was longer, prolonged. What to call it and where to take it? I will list the main forms of schizophrenia: simple, hebephrenic, catatonic, paranoid, latent, acute schizophrenic episode and, finally, schizoaffective psychosis.

And here is this asthenoadynamic depression. If we had noticed in her elements of personality change and splitting, then perhaps we would have raised the question - is there a schizophrenic process here. Or maybe they would differentiate it with cyclothymic psychosis, cyclothymia. If we had identified some kind of psychotrauma and corresponding experiences during that period, we might have diagnosed reactive depression. But now, when we already know what is in front of us, we will classify it as “others”, because the state does not fit into any other forms.

At the age of 18, this condition was followed by a manic-delusional attack. True, then the ideas of greatness were not yet so absurd, but it was acute attack. If we analyze the disease from the age of 18, then we can immediately revise the diagnosis: the period of asthenia, astheno-apathetic depression before the age of 18, we would regard as a negative phase, a manic-delusional attack - as a positive phase, and would call the disease circular schizophrenia or schizoaffective psychosis.

Then came remission or intermission. Here the information in the medical history is not particularly clear, but we must clarify what was there in remission. It is now difficult to assess in retrospect whether it was complete or not. Until the age of 22, everything seemed to be fine. If we had qualified this period as deep remission (3 years is sufficient duration), we would have settled on the diagnosis of “schizoaffective psychosis” or “recurrent schizophrenia”. I don’t like the term “periodic” because there are almost no periodic psychoses. It is more correct to say recurrent or recurrent schizophrenia. But if in remission we noticed some affective fluctuations, a great change in personality (maybe this was the case here), then we would raise the question of whether there is a schizophrenic process here, which occurs in shifts, attacks, fur coats, because it already gives changes. Affective fluctuations themselves, their episodes, do not mean anything; they also happen in intermission. But if there is already a decline in personality, change, and a different pathocharacterological structure is being formed, then we say that the disease is undergoing shifts.

At the age of 22, the attack developed after a serious psychogenic provocation - a bomb exploded. Then slowly, gradually, but steadily, oneiric catatonia develops (when A.V. Snezhnevsky looked at the patient). But at the beginning, upon admission, all this was hidden. If there had been psychomotor catatonic agitation, the patient would have been diagnosed with a catatonic form of schizophrenia. Later it was already oneiric catatonia, and at the time when the patient was diagnosed, there were different ideas than now. At that time, oneiric catatonia was considered a favorable form. Do you see what a favorable form this is? As with a recurrent, recurrent form, the attack ended with resitutio ad integrum - complete recovery, i.e. with access to intermission. Our patient, after such a severe attack, again experienced a 3-year remission, after which an affective-delusional attack developed again.

But we see only psychopathology, the clinic, the disease, and during this period the patient enters a medical institute, successfully studies and graduates with honors.

Let's skip ahead a bit. After she had already become a doctor, and the illness continued (by the way, at the institute one could envy the patient’s sense of purpose; she was active, collected, somewhat dry), at the age of 28 an affective-delusional attack again developed, reaching the level of acute manic paraphrenia. But this attack was special - manic paraphrenia with a great hebephrenic flavor began to pass, the excitement became more foolish, flat, superficial, flattened, with twists. During this period, the patient was consulted by several specialists, and Mark Yakovlevich Sereysky was forced to put her on a hebephrenic form. This means that the patient was given the catatonic form, now - hebephrenic. What does it mean to diagnose the hebephrenic form of schizophrenia? Hopeless, with rapid (4-5 years) decay. There was a doctrine of hebephrenia by E. Hecker and the patient’s condition, her status suggested this diagnosis. True, apparently, it is necessary to take into account that this hebephrenia grew out of mania, that there was not that mixture that is characteristic of hebephrenia. In any case, the patient’s stupidity, her regression, the inability to cope with her, the prospect that this would be some kind of animal existence, forced her to undergo a lobotomy.

I'm not going to criticize the person who introduced the lobotomy now. And now in the West, in some places, filigree lobotomy is being performed, and there are many opponents. At that time it was carried out here too. I would like to draw your attention to the fact that after the lobotomy, during the period when the reparation process was underway, the patient developed frontal apathetic-abulsic syndrome. But this frontal syndrome was most pronounced during the recovery (repair) period, when the organic process actually took place in the frontal lobe. It's over, the scars remain.

Further. The process that existed before the lobotomy continues. And we see that after the operation, a few months later the patient began to work. For a year and a half I worked as a doctor, albeit as a laboratory assistant, in a biochemical laboratory. In the period after the lobotomy, and even after hebephrenia, it was possible to state the apathetic dementia, which W. Griesinger once wrote about, or the apathetic dementia of E. Kraepelin as the initial state.

But it is no coincidence that the refined clinician and subtle psychopathologist Grigory Abramovich Rothstein, after examining the patient, makes a diagnosis: schizophrenia, a defect. Look, what are they putting on? A.V.Snezhnevsky - oneiric catatonia, M.Ya.Sereysky - hebephrenia, G.A.Rotshtein - defective condition. Diagnoses, or rather forms of the same disease, change.

Then the patient again experiences an exacerbation and, finally, a period comes when the course becomes essentially continuous, the remissions end. The undulation that was set at the beginning continues almost to the present day. But if earlier this undulation was on a deep scale, now it becomes barely noticeable. The patient gradually acquires a chronic, stationary (of course, relatively) paraphrenic state, in which she appears before us today. What form of schizophrenia can we attribute this paraphrenic state to? To paranoid, delusional.

So, we can diagnose one patient with several forms of schizophrenia. And then we can understand why at present we do not have a generally accepted doctrine of the classification and forms of schizophrenia. Is it possible to create one? After all, classification, systematics is the highest achievement of scientific thought; science strives for this in order to reveal the order that exists in nature, whether pathological or normal. With schizophrenia it doesn’t work. And from this point of view, one can understand E. Kraepelin, who, starting from the 5th and ending with the 9th and last edition of his “Textbook of Psychiatry,” continuously changed the forms of schizophrenia. In past years I have listed all of these E.Kraepelin cancellations. I believe that there is no need for this now. Let me just remind you of the words of K. Conrad that after the death of E. Kraepelin in 1926, frozen forms remained, and “there is no more E. Kraepelin in order to correct E. Kraepelin himself.”

But they are trying to fix it. Various schools of psychiatry create their own forms. You know that there is a “trend psychiatry”, which was proclaimed by E. Kraepelin himself. True, even before him, French clinical nosographists said that it was necessary to study the disease throughout the patient’s entire life. W. Mayer-Gross wrote that this is pointless, because... The life of a psychiatrist is not enough to observe the disease. Indeed, the life of one psychiatrist is not enough and therefore we have to be guided by some segments. However, we must strive to cover the disease as a whole, the entire clinical picture throughout the course of the disease, and then create forms along the way. But here, unfortunately, we do not have such great achievements.

We know the taxonomy of K. Conrad, you are well acquainted with our new ideas about the so-called. a single psychosis and the fact that in the group of schizophrenia there are 3 forms: recurrent schizophrenia (in the generally accepted sense - schizoaffective psychosis) with a phasic course and delusions; intermittent-progressive (in German terminology “fur-coat-like”) course of shifts, when after an attack regression and personal breakdown occur; continuous course (in the sense of V. Magnan and E. Kraepelin) - classic dementia praecox.

What is dementia praecox? Let's start with the form that was not heard at all in this patient. There was a whole classification: hebephrenia, catatonia, delusional, latent, acute schizophrenic episode, schizo-affective psychosis. But there was no simple form. Then we will begin with the form that was identified first and became the beginning of the doctrine of schizophrenic psychoses.

SIMPLE FORM OF SCHIZOPHRENIA

You are well aware that dementia praecox - premature, early dementia - was isolated by B.Morel, i.e. The founders of the doctrine of schizophrenia, of dementia praecox, are the French. This is no coincidence. Why? Because for the first time psychiatric nosology (the French called it nosography) was created in France, and not in Germany. French psychiatry at that time was advanced, German psychiatry was somewhat behind, although later they caught up.

Dementia praecox was isolated in 1857 based on the observation of many adolescent patients who unexpectedly experienced a particular decline in mental activity. Not just dementia as such, which was known, but that particularity that I have already spoken about. Simple schizophrenia fundamentally different from many others. This is a total coarsening, a change in the entire personality and, first of all, affectivity, syntony, and sociability. The feeling of affection and sympathy for people, empathy disappears and melts. It starts gradually, but progresses at a very fast pace (over 4-5 years) and leads to personality regression. What B. Morel described has remained unchanged to this day

What were the characteristic features? The predominance of negative disorders: the extinction of emotionality, volitional processes, a decrease in the range of interests and intelligence, which is not organic dementia in the narrow sense, but occurs more from a drop in energy potential. The patient does not think, does not reflect, does not decide, does not synthesize, does not analyze - and the impression of dementia is created. It is not without reason that these phenomena are called primary dementia.

You can object to me: is it correct to say this? Every symptom has a negative and a positive side. Of course, if you follow the teachings of H. Jackson, you can find a positive side here too. What's positive here? And the fact that characteropathy arises, a completely new personality with different habits: one-sided, one-sided, more approaching an empty, vegetative existence. This time. Unmotivated anger, affectivity, aggressiveness, reminiscent of some dysphoric states - these are two. Inadequacy, parathymia - these are three. Schizophrenic thinking disorders, reflection, introspection, and depth that we are used to seeing in schizophrenia are absent here. There are also no positive symptoms, which we often incorrectly call “productive” (extinction is production). There are episodic hallucinatory experiences - fleeting - which can sometimes even be, as it were, reactively caused. Rapidly passing rudimentary delusional ideas flare up. The personality falls apart, everything becomes rougher. This is dementia praecox.

It was introduced by B. Morel, but apathetic dementia was already described by W. Griesinger, A. Pick, R. Wenner, in our country - P. A. Butkovsky and many other psychiatrists. These conditions were described in the so-called section. secondary dementia. But this is early, primary dementia. That is why B. Morel’s concept of primary dementia met with harsh criticism in France and attacks from the most prominent clinicians of that time. It was not recognized in France, nor was it recognized in Germany, because there was an idea of ​​secondary dementia.

What is secondary dementia? I am talking about this in order to understand how the doctrine of schizophrenia developed. I would not like to talk about the period when E.A. Zeller-H. Neumann had already created the concept of a single psychosis. Long before this, there was a concept about the luck of the English scientist W. Cullen. What is luck? These are destructive, progressive processes that lead to dementia, but do not begin with dementia. And if they do not begin with dementia, then the dementia that then develops is called secondary.

And then suddenly B.Morel comes up with the concept of primary dementia, and even early dementia. None of the clinical psychiatrists agree. What is the concept of luck? According to it, any mental disorders, diseases as such (destructive-progressive) begin with affective (according to W. Griesinger - affectogenic) disorders: with mania or melancholy. Next comes excitement (in France they called it “alternating insanity”), delusions and hallucinations arise. In Germany, more attention was paid to catatonic phenomena. Finally, secondary dementia occurs - dementia secundaria.

This idea was so strong that it prevented all psychiatrists from seeing and recognizing primary, early dementia. The second reason that dementia praecox was not recognized during the time of B. Morel in France and Germany is the ideological background of B. Morel's concept of degeneration. The concept of degeneration was based on the doctrine of degeneration and had a political overtone, taken by B. Morel, apparently from Rousseau. B. Morel said that the norm is a man, a peasant, a white race that lives in the countryside and is not spoiled by civilization (even then we were talking about urbanization), but those who in cities are exposed to various harmful things (alcoholism, smoking, diseases and etc.) - they gradually accumulate these harmful things and degenerate, degenerate.

So dementia praecox is the 4th stage of degeneration. But since none of the progressive psychiatrists, of course, could accept such an ideological background, they did not recognize dementia praecox, which was a fact and reality. Here is an example of how ideology influences scientific positions and concepts. Well, was the concept of degeneration also erroneous and completely vicious? No, there was a rational grain in it. What is rational in this concept?

The concept of degeneration is, on the one hand, the origins and beginning of the doctrine of heredity (which, thank God, is now recognized), and on the other hand, the doctrine of endogenesis. It was in this direction that the doctrine of degeneration was later developed by Legrand du Saulle, V. Magnan and his student Legrain, who freed themselves from Morel’s ideological husk.

That is why for 40 years dementia praecox was not recognized anywhere: neither in France nor in Germany. And it took the genius of E. Kraepelin to see something in common in the dementia praecox of B. Morel and G. Schule (who described the same disease after B. Morel), in the hebephrenia of E. Hecker and in the catatonia of K. Kahlbaum, to unite them into one nosological unit.

But we are accustomed to consider schizophrenia a simple form, which was described only in 1903 by O. Diem. This is dementia praecox, but simple. And it’s simple because it doesn’t have positive symptoms. I emphasize - positive, not productive. I'll digress again.

Productive symptoms are present in any mental illness; there is no disease without productive symptoms. It is incorrectly stated in all our textbooks and manuals that with a simple form there are no productive symptoms. How is it not? What about dementia?..

...The French, the most subtle psychopathologists, to this day logically and ardently defend their point of view that the simple form, dementia praecox B. Morel, is a special disease, it exists as such. Whether I agree with this or not, it cannot be refuted. It differs from other schizophrenias and may have its own pathogenesis and clinical picture. And when such basic signs of nosology appear, then claims for a special nosological unit can be justified.

I am saying something that is currently unknown to clinical psychiatry. All those follow-up studies that were carried out according to the simple form (or rather, according to the diagnosis “simple form”) showed that after a few years literally only a few remained of it, and the rest turned out to be: delusional schizophrenia, paranoid, intermittent-progressive, catatonic , less often - hebephrenic, etc. Therefore, the simple form seems to evaporate and disappear. But she is in 1st place in the international classification.

But it still exists. Cases of primary insanity, more precisely, primary dementia, the simple form of O.Diem or primary dementia E.Kraepelin, B.Morel, G.Schule are sometimes encountered in our practice. Does it matter (besides academic interest) to make the correct diagnosis here? I would say that there is no need to rush it, given practice, empiricism and the fact that we are most often wrong. Because if we are confident in the diagnosis of “simple form,” then we know that it cannot be treated. The asyndromic nature of these conditions (which are now called simplex syndrome), their uncertainty, and amorphous nature are not amenable to any therapeutic measures. Very often in the literature one can find indications that with a simple form, patients subsequently adapt and even end up with higher education. educational establishments. This is not a simple form at all. These are the cases that occurred with asthenic, asthenic-depressive, etc. exacerbations or attacks. But the simple form, and there is very little of it, is a rapid collapse, a malignant form, it is also called juvenile.

Let me again dwell on some of the ambiguity that occurs here. Why is the simple form called youthful? Because manifestation occurs in adolescence. Manifestation is what is understood in psychiatry as an application. Psychosis is obvious to everyone, but what lasts until manifestation is not latency (I don’t like this word), but a small psychopath-like manifestation. The simple form, from my point of view, begins in childhood and at the beginning even proceeds according to the type of episodes. And in adolescence, this is, indeed, a manifestation not of psychosis, not of positive symptoms, but of a pronounced breakdown of personality. And here we almost don’t know what to do (the same in literature). Old experienced psychiatrists tried everything they could, giving insulin therapy - even worse. If I diagnose a simple form, then I will never prescribe insulin - we will ruin the patient even more.

It belongs to transient dementia. On this occasion he wrote:

There was a debate whether dementia in schizophrenia could be considered dementia itself. Thus, Kurt Schneider believed that in these cases, strictly speaking, dementia is not observed, since “general judgments and memory and other things that can be classified as intelligence do not undergo direct changes,” but only some disturbances in thinking are observed. A.K. Anufriev noted that a patient suffering from schizophrenia may simultaneously seem during a conversation with him to be both feeble-minded and not feeble-minded, and that the term “schizophrenic dementia” is quite justifiably put in quotation marks. According to G.V. Grule (German) Russian, intellectual disorder in schizophrenia depends on the characteristics of mental activity that do not directly affect intelligence and are volitional disorders such as apato-abulia and thinking disorders. Therefore, we cannot talk about changes in intelligence in schizophrenia as classic dementia. With schizophrenic dementia, it is not the intellect that suffers, but the ability to use it. As the same G.V. Grule said:

Other authors compare intelligence in schizophrenia to a bookcase full of interesting, smart and useful books, to which the key has been lost. According to M.I. Weisfeld (), schizophrenic dementia is caused by “distraction” (delusions and hallucinations), “insufficient activity” of the individual before the illness, “the influence of acute psychotic conditions” and “lack of exercise.” On the latter occasion, he quotes the words of the great Renaissance figure Leonardo da Vinci, who argued that a razor becomes rusty through disuse:

Criticizing the idea of ​​the outcome of mental illness in dementia, N. N. Pukhovsky notes that the phenomena attributed to “schizophrenic dementia” are closely related to toxic-allergic complications with inadequate tactics of active treatment of psychoses (including neuroleptic, ECT, insulin comatose therapy, pyrotherapy), with remnants of the system of constraint in psychiatric hospitals and the phenomena of hospitalism, desocialization, coercion, separation and isolation, and everyday discomfort. He also associates "schizophrenic dementia" with the defense mechanism of regression and repression (parapraxis).

Nevertheless, the discrepancy between intellectual reactions and stimuli indicates the presence of dementia in patients with schizophrenia, albeit in a unique version.

Story

Particular dementia in patients with schizophrenia, 4 years after E. Bleuler created the very concept of the disease, was described by the Russian psychiatrist A. N. Bernstein in “Clinical Lectures on Mental Illnesses”. Prior to this, in V. Kh. Kandinsky’s work “On Pseudohallucinations” (1890), the author pointed out the possibility of the disease ideophrenia (the modern analogue of which is schizophrenia) leading to dementia.

Classification

By classification A. O. Edelshteina based on the degree of personality disintegration, they are distinguished:

Pathogenesis

The pathogenesis of schizophrenic dementia, like schizophrenia itself, is not fully known. However, some aspects of it are described. The Austrian psychiatrist Joseph Berze considered schizophrenic dementia to be a “hypotension of consciousness.” It is noteworthy that later many other scientists agreed with him: major researchers of schizophrenia K. Schneider, A. S. Kronfeld and O. K. E. Bumke. The Soviet physiologist I.P. Pavlov also considered schizophrenia to be a chronic hypnoid state. However, this is not enough to understand the pathogenesis of schizophrenic dementia. In schizophrenia, while the elements of intelligence are preserved, its structure is disrupted. In this regard, the main clinical picture of the condition appears. According to V. A. Vnukov, expressed back in, the basis of schizophrenic dementia is splitting of intellect and perceptions, paralogical thinking and flattened affect.

Clinical picture

Perceptual disorders

Memory disorders

Memory in schizophrenic dementia, as in schizophrenia in general, is preserved for a long time. Such patients are well oriented in their own personality, space and time. According to E. Bleuler, the phenomenon when patients with schizophrenia, along with psychotic ones, have preserved some aspects of intelligence, is figuratively called “double-entry bookkeeping.”

Forecast

Since schizophrenia is a chronic and progressive disease, the prognosis for recovery from such dementia, if it has already occurred, is usually questionable. However, since this dementia is transient, if the course of the disease itself can be stopped, the prognosis can be relatively favorable. In other cases, an extremely unfavorable outcome is possible. Either an extreme increase in negative symptoms occurs in the form of complete