Infantile psychosis in children. Psychosis in children is atypical. Therapy and prevention of psychotic disorders at an early age

In psychiatry, atypical childhood psychosis refers to a range of psychotic disorders that affect young children. This is characterized by the presence of some manifestations that are typical of early childhood autism. Symptoms include movements that are repeated stereotypically, as well as lesions, echolalia, delayed speech development, and disturbed social relationships. Moreover, such disorders occur in children, regardless of their intellectual level, although more often atypical childhood psychosis occurs in children with mental retardation. If we talk about psychosis in general, then in children they are observed infrequently, and at the same time they are divided into two groups.

These are early childhood psychosis, which occurs in infants and preschoolers, and late childhood psychosis, which occurs in preadolescence and adolescence. Childhood autism, which belongs to the category of early psychoses, is characterized by the fact that the child does not seek to communicate with others, even with the closest parents. Usually such a child goes to the doctor about a serious deviation in speech development. Such a patient is distinguished by isolation, he can be alone for hours, and this does not bother him. All this time, the baby can enthusiastically engage in one toy, not paying attention to others. If someone tries to play with him together, the child does not react to it in any way. At the same time, if you try to interrupt his game, a very bright outburst of anger may follow.

The child falls to the floor, knocks with his feet, and so on. Actions are active, and often entail damage. The baby can follow the movement of his own fingers, or taste things. This indicates a high level of consciousness and the presence of sensitivity to certain stimuli. But there is a reduced reaction to pain sensations, there is no orienting reaction that occurs to loud sudden sounds, which is a confirmation of a decrease in sensitivity to other stimuli. As a rule, there is a decrease in the mental abilities of the baby. But if speech is developed, then the abilities are quite adequate.

Features of the disease

It often happens that an autistic child has a certain isolated talent, and it is not clear what mechanism in this case implies the presence of atypical childhood psychosis. Observations of psychiatrists show that among the causes of the disease can be called brain damage, constitutional insufficiency, neurophysiological disorders, various autointoxications, chronic and acute infections, adverse environmental conditions. If a child has autism, then treatment, of course, is carried out, but it is sometimes ineffective. Tranquilizers are used only if aggressive behavior occurs. Treatment of such children is carried out in a hospital.

In atypical childhood psychosis, there is no clear clinical definition. The pathology itself, characteristic of the disease, occurs from the second year of life to the age of five. The appearance of a younger child in the family can act as a provoking factor, and at the same time the older one experiences panic, expressed very sharply. There is its combination with the regression of the behavior and abilities of the child in the intellectual plane. Speech before the onset of the disease can be fully mastered, but in this situation it loses its communicative function and becomes jargon. Symptoms can reach secondary level autism. At the same time, the condition is quite stable, chronic, similar to early childhood autism.

If we are talking about late childhood psychoses, then in this case the reactions are similar to those that occur in adults. This also causes symptoms. In this case, it is disturbed thinking, delirium, disordered behavior, rejection of existing interpersonal relationships. In this case, the child loses a sense of reality. If we compare with early psychosis, then late psychoses occur in those families that are at risk for. Although experts note that in this case the prognosis is more favorable. When prescribing conventional therapeutic measures, family and individual therapy, reception, and behavior modification are included. In acute periods of the disease, hospitalization is recommended.

When does atypical childhood psychosis appear?

It has now been established that the disease in this form of autism sometimes does not manifest itself for quite a long time, for years. If autism has a mild form, the main symptoms that distinguish atypical childhood psychosis are not detected. Therefore, it is not surprising that a lot of time is required to clarify the diagnosis, and everything happens with a delay. Moreover, patients with this disease have other disorders. However, their development is higher than the level of those patients who suffer from classic autism. At the same time, there are signs that can be called common. First of all, these are violations in the field of social interaction.

The symptomatology has a different degree of severity, and has a peculiar character. For example, some children experience complete indifference to interaction with others. Others, as the complete opposite, strive for communication. But at the same time they do not know how to build it correctly. In atypical childhood psychosis, patients often have problems with language acquisition, and sometimes they do not understand others. It is very noticeable that the patient's vocabulary is limited, and clearly does not correspond to age. Each word is understood by patients only in its direct meaning.


Third stage– diagnostics of development: carried out by psychologists and teachers, aimed at identifying the individual characteristics of the child, characterizing his communication capabilities, cognitive activity, emotional and volitional sphere.

A complex of methods is of great research and scientific-practical interest all over the world. PEP(Psychoeducation Profile), proposed by American scientists E. Schopler and R. Reichler et al. in 1979. PEP-3 is currently in use. This technique was created and is intended to assess the developmental characteristics of children with autistic disorders. In this methodology, along with a quantitative scoring, a qualitative assessment of various areas of the mental activity of a child with autistic disorders or mental retardation is also provided. The psychoeducational test is used to dynamically assess the formation of mental functions, the presence of cognitive impairments and the severity of pathological sensory signs. The PEP scale, designed specifically to assess the mental age and development of children with autistic disorders, mental underdevelopment, allows you to determine the degree of maturity of 7 cognitive areas and parameters of a child’s mental activity: imitation, perception, fine motor skills, gross motor skills, hand-eye coordination, cognitive representations, verbal realm. Along with this assessment, PEP allows you to assess the severity of autistic disorders in 5 autistic areas: affect, relationships, use of material, sensory patterns, speech features. The total score obtained as a result of the implementation of 12 PEP subscales reflects the cognitive (cognitive, intellectual) development and the possibilities of social adaptation, communication in patients with autistic disorders (Schopler E., Reichler R., Bashford A., Lansing M., Marcus L. , 1988).

Experimental-psychological (pathopsychological) the study provides information about the individual psychological properties and mental state of a patient with ASD, which are necessary to clarify the diagnosis and select psychotherapeutic tactics. Intelligence measurement scales are used Veksler(the original version of WISC-IV, and its domestic modifications for children from 5 years to 15 years 11 months and for preschoolers from 4 to 6.5 years).

For the study of cognitive functions, the study of memory is used: 10 words (or 5, 7 depending on the age and characteristics of the child), paired associations, methods for tactile and stereognostic memory; to study attention, encryption, Schulte tables (at the appropriate age) are used; for the study of thinking, they include a small subject classification, geometric classification, the intersection of classes, the inclusion of a subclass in a class, the construction of objects, Koos cubes, etc.; for the study of perception (visual) - Leeper's figures, form identification, perceptual modeling, sectional object pictures.

To study emotions and personality, graphic samples are used (drawing of oneself, family, residence permit, and other options), plot pictures that simulate everyday situations, recognition of the facial expression of the main emotions of a person (grief, joy, pleasure, displeasure, fear, anger, seal), recognition of emotionally expressive movements, postures and gestures.

Neuropsychological diagnostic study

Aimed at identifying deviations of higher mental functions with an analysis of the formation of the so-called. regulatory functions (programming, regulation and control). This allows you to assess the child's cognitive activity and develop an individual correction program.

Instrumental Research

Among the paraclinical methods in a multidisciplinary approach to the study of ASD, it is widely used electroencephalography (EEG). Sick children with both syndromic and non-syndromic (including psychotic) forms of ASD have certain EEG patterns that naturally change as the disease progresses and correlate with the characteristics of clinical conditions. This made it possible to identify specific EEG markers of some forms of ASD, which are used for differential diagnostic clarifications. Despite the nosological non-specificity of the EEG, it can be used to detect the relationship of certain changes in the electrical activity of the brain with clinical symptoms, to establish the degree of their pathogenetic significance for resolving issues of diagnosis, prognosis, and selection of therapy.

An accessible and inexpensive EEG method, introduced into the standards of outpatient and inpatient care, allows not only to detect epileptic activity, but also to assess the level of maturity and functional activity of the brain. Sometimes, especially in children with mental developmental disorders, the functional characteristics of the EEG may be more informative than the results of MRI or PET studies, often not confirming brain development anomalies.

Neuroimaging methods: computed tomography, magnetic nuclear resonance imaging carried out according to indications.

Biological markers (test systems), along with clinical and pathopsychological data, make a significant contribution to solving issues of diagnosis, selection of individual therapy, and monitoring of patients' condition.

CLINIC AND TYPOLOGY OF RAS

Kanner syndrome (F84.0)

Classic childhood autism Kanner syndrome (KS) manifests itself from birth in the form of asynchronous disintegrative autistic dysontogenesis with incomplete and uneven maturation of higher mental functions, inability to form communication and is characterized by the presence of a “triad” of the main areas of impairment: lack of social interaction (detachment, rejection, scarcity of eye contact, lack of adequate reactions to the emotions of others people), the lack of mutual communication, as well as the presence of stereotypical regressive forms of behavior.

Receptive and expressive speech develop with a delay: there is no gesticulation, cooing and babbling are poor. In expressive speech, the first words (in the form of echolalia, repetitions of the last and first syllables of words) appear in the second - fourth year of life, and are preserved in subsequent years. Patients pronounce them singsongly, sometimes clearly, sometimes blurry. Vocabulary replenishes slowly, after three to five years short phrases-cliches are noted, egocentric speech prevails. Patients with SC are not capable of dialogue, retelling, do not use personal pronouns. The communicative side of speech is practically absent.

The lack of mutual communication is manifested in the absence of an imitation game, a creative game with peers.

Gross motor skills are angular with motor stereotypes, athetosis-like movements, walking relying on the toes, muscular dystonia. The emotional sphere does not develop or develops with a long delay, there is no reaction of revival to the parents' attempts to take them in their arms (with a pronounced symbiosis with the mother), the distinction between insiders and outsiders is not formed. The revival complex arises spontaneously, within the framework of autistic interests, and is manifested by general motor excitation.

Instinctive activity is disturbed in the form of eating behavior, inversion of the sleep-wake cycle. Mental activity is impoverished, stereotyped with symptoms of identity and lack of imitation. Patients do not develop abstract thinking. In patients with SC, with a pronounced lag in the development of higher mental functions, there is dissociation, disintegration within certain areas of mental activity.

The course of the disease, the outcome. Autism in a severe form persists throughout life, stops the mental development of the child. Relief of autistic symptoms is noted in the second (6-8 years) delayed critical age period (then a slight positive trend in the development of speech and fine motor skills is possible). Cognitive impairments are noted from the period of infancy, by puberty the intellect is reduced in 75% of cases (IQ).

The prevalence of Kanner syndrome 2: 10,000 child population.

Infantile psychosis (F84.02)

In childhood infantile psychosis (IP), manifest attacks with leading catatonic symptoms occur in the first 3 years of a child's life, against the background of dissociated dysontogenesis or normal development. Catatonic disorders (CD), comorbid with ASD (DSM-V, 2013), occupy a leading place in an attack, have a generalized hyperkinetic character in most patients (running in a circle, along a wall, from corner to corner, bouncing, swinging, climbing up , athetosis, shaking hands, walking with support on the toes, variable muscle tone). They have expressed vegetative reactions, sweating. Motor excitation is accompanied by negativism. Children do not need to communicate with others, relatives and friends, often "keep their own territory", with intervention - there is anxiety, aggression, crying, rejection of communication. Speech is slurred, egocentric, incoherent, with perseverations, echolalia. The severity of autism in a manifest attack on the average on the CARS scale is 37.2 points (the lower limit of severe autism). The combination of catatonic disorders with autism in IP suspends the physiological (ontogenetic) development of the child during the attack, contributes to the formation of mental retardation. The duration of manifest attacks is 2-3 years.

In remission, children cannot sit still, run, jump, spin in a chair during classes. Attention is drawn to motor clumsiness (violation of the proportionality of movements, rhythm and tempo disorders in complex movements, organization of movements in space). Excessive monotonous motor activity in patients is combined with attention disorders: slight distractibility or excessive concentration, "stuck" attention. At this stage of the course of the disease, patients in a third of cases are mistakenly diagnosed with Attention Deficit Hyperactivity Disorder (ADHD, DSM-5).

Patients are also characterized by stereotypical desires (holding stools, urination, eating behavior with fixation on certain types of food). In the course of the habilitation in patients by the age of 7-9, the hyperkinetic syndrome (with a predominance of hyperactivity and impulsivity) is stopped, mental retardation is overcome. Only with emotional stress does a fleeting “complex of revival” arise with repetitive stereotypical movements, which can be interrupted by a remark, switching the patient to other types of movements. Patients still have problems in independent organization and planning of pastime. In the absence of outside help, social interaction is disrupted. Patients experience communication difficulties in building a full-fledged dialogue. In some patients, a decrease in interest in social relationships persists, attempts to make friends look strange and usually end in failure. At puberty, patients are weighed down by the absence of comrades.

With the manifestation of infantile psychosis by polymorphic seizures, catatonic disorders are short-term and are noted only at the height of a manifest attack.

The course of the disease, the outcome. The dissociated mental retardation formed during the period of a manifest attack in most cases softens and is overcome against the background of habilitation. IQ in all patients> 70. Autism loses its positive component and decreased to an average of 33 points (mild / moderate on the CARS scale). In high-functioning autism, it was not determined using the CARS scale. In patients, the emotional sphere develops, developmental delay is overcome, mild cognitive dysontogenesis is preserved. The age and development factors (positive trends in ontogenesis), rehabilitation contribute to a favorable outcome in 84% of cases ("practical recovery" - in 6%; "high-functioning autism" - in 50%, regressive course - in 28%). Nosology - childhood autism, infantile psychosis.

The prevalence of PV reaches 30–40 per 10,000 children.

Atypical autism (F84.1)

The ICD-10 first formulated the concept of "atypical" autism, which has been given great importance in the last 10-15 years. Atypical autism in childhood includes most of the most severe forms of autism in various nosologies, in the structure of which autism often acts as a psychotic component (Bashina V.M., Simashkova N.V., Yakupova L.P., 2006; Simashkova N.V. ., 2006; 2013; Gillberg C., Hellgren L., 2004 and others).

The research diagnostic criteria attached to the ICD-10 state that “autism may be atypical in age of onset (F84.10) and in phenomenology (F84.11). Atypical autism (AA) includes psychotic (atypical childhood psychosis) and non-psychotic (mild mental retardation with autistic features) variants.

1. ADP at the onset of the disease at an "atypical age" - after 3 years. The clinical picture is close to the previously described childhood infantile autism.

2. ADP with atypical symptoms - with an onset in the first 5 years of life, the absence of a complete clinical picture of childhood autism, the similarity of the clinical picture of psychoses in different nosologies (schizophrenia, UMO, Rett syndrome, etc.).

3. Syndromic non-psychotic forms of AA, comorbid with UMO, chromosomal origin in Martin-Bell syndrome, Down syndrome, Williams, Angelman, Sotos and a number of others; metabolic origin (with phenylketonia, tuberous sclerosis and others).

In atypical childhood psychosis, endogenous (F84.11 ) manifest regressive-catatonic seizures occur against the background of autistic dysontogenesis or normal development at the 2-5th year of life. They begin with a deepening of autistic withdrawal up to "extremely severe" autism (52.8 points on the CARS scale). The leading one is the regression of higher mental functions: speech, motor skills (with partial loss of walking), neatness skills, eating behavior (up to eating inedible), game regression. Catatonic disorders occur after negative ones (autistic and regressive). Being in motion for most of the day, some patients lie down for a short time on the floor, chairs, “freeze”, then continue to move again. In the hands, monotonous movements of the ancient archaic rubro-spinal and striopalidary level are noted: “washing”, folding, rubbing type, beating on the chin, flapping the arms like wings. Their kaleidoscope is so large that behavioral phenotypes often change and are indistinguishable in different nosologies. Regression, catatonia, severe autism stop the mental development of the child . The duration of ADP attacks is 4.5-5 years.

The course of the disease and outcome. The course of the disease in 80% is progressive, malignant. Remissions in endogenous ADP of low quality, with the preservation of severe autism (42.2 points), cognitive deficit. Catatonic motor stereotypes pass as a through symptom during the course of the disease in the form of subcortical protopathic motor stereotypes. Habilitation is ineffective. Statistically significantly improved gross motor skills (walking skills). Own speech is not formed, a third of patients develop echo speech. Thinking remains concrete, abstract forms of cognition are not available, the emotional sphere does not develop. Delusions and hallucinations in patients do not appear in childhood, and it is difficult to distinguish an oligophrenic-like defect from a pseudo-organic one after 3-4 years from the onset of the disease. In 30% of cases, patients with ADP are trained according to the correctional program of the VIII type, the rest are adapted to stay in the family or placed in boarding schools for social protection. Atypical childhood psychosis according to the ICD-10 criteria is coded under the heading "general disorders of psychological development" with a decrease in intelligence (F84.11). Negative dynamics during the course of the disease, an increase in cognitive deficit allow us to make a diagnosis of malignant childhood schizophrenia (F20.8xx3) - the cultural aspect of the Russian Federation (ICD-10, 1999). In the USA, childhood schizophrenia is extremely rarely diagnosed before the age of 14, in Europe - earlier than 9 years. In ICD-10 (1994), the childhood form of schizophrenia is not singled out, the differential diagnosis of childhood schizophrenia with atypical childhood psychosis is still relevant throughout the world. The diagnosis of DS should be made already at the stage of manifest regressive-catatonic psychosis without fear of "stigma in psychiatry".

Psychotic syndrome forms of atypical autism with a decrease in intelligence (F84.11, F70) have a phenotypically universal clinical picture and in catatonic-regressive seizures do not differ from endogenous ADP (go through similar stages in development: autistic - regressive - catatonic). They differ phenotypically in a set of motor stereotypes: subcortical catatonic stereotypes in patients with Down syndrome, archaic catatonic stem stereotypes in patients with ADP with Rett and Martin-Bell syndrome. They are united by the increase in asthenia from the stage of "regression", the preservation of characteristic stereotypes throughout life.

Syndromic non-psychotic forms of AA, comorbid with ULV or “mental retardation with features of autism” can be traced in selected genetic syndromes (Martin-Bell, Down, Williams, Angelman, Sotos, etc.) and diseases of metabolic origin (phenylketonia, tuberous sclerosis, etc.), in which autism is comorbid with UMO ( F84.11, F70) .

Data on the prevalence of atypical autism in general are not available in the medical literature.

Rett syndrome (F84.2)

A verified degenerative monogenic disease caused by a mutation in the MeCP2 regulator gene, which is located on the long arm of the X chromosome (Xq28) and is responsible for 60-90% of cases of CP. Classical SR begins at 1-2 years of age with a peak of manifestation at 16-18 months and goes through a number of stages in its development:

In I "autistic" (lasting 3-10 months), detachment appears, cognitive activity is disturbed, mental development stops.

In stage II - "rapid regression" (from several weeks to several months), against the background of increased autistic detachment, movements of the ancient, archaic level appear in the hands - "washing" type, rubbing type; there is a regression in the activity of all functional systems; retarded head growth.

Stage III "pseudo-stationary" (up to 10 years or more). Autistic detachment weakens, communication, understanding of speech, pronunciation of individual words are partially restored. Regressive catatonic stereotypes persist. Any activity is short-term, patients are easily exhausted. In 1/3 of cases, epileptic seizures occur.

Stage IV - "total dementia" is characterized mainly by neurological disorders (spinal atrophy, spastic rigidity), complete loss of walking.

The course of the disease, the outcome: unfavorable in 100% of cases, cognitive deficit increases. Death occurs at different times (usually 12-25 years after the onset of the disease).

SR prevalence : 1 in 15,000 children aged 6 to 17 (orphan disease).

Other disintegrative disorders of childhood, Heller's syndrome (F84.3)

Heller's dementia is the loss or progressive deterioration of speech, intellectual, social and communication abilities during childhood. It appears at the age of 2-4 years. Children are characterized by increased irritability, self-care. Their speech becomes incomprehensible, there are disturbances in memory and perception, anxious moods or aggressiveness. Patients are not oriented in social situations, often lose their previously acquired neatness skills; they have stereotyped movements. As a result of a regression in behavior and a violation of the communicative function, an assumption arises about childhood autism. The full clinical picture of dementia gradually develops.

Despite severe dementia, facial features in patients do not become rough. In general, the disorder is progressive in nature. Prevalence of Heller's syndrome: 0.1:10,000 child population (orphan disease).

Hyperactive disorder associated with mental retardation and stereotyped movements (F84.4) in are also extremely rare (less than 1: 10,000 of the child population), refers to orphan diseases.

Asperger's syndrome (F84.5)

Evolutionary-constitutional Asperger's syndrome is formed from birth, but is usually diagnosed in patients in situations of integration into society (attending kindergarten, school).

Patients have deviations in two-way social communications, in non-verbal behavior (gestures, facial expressions, mannerisms, eye contact), and are not capable of emotional empathy. They have early speech development, a rich speech reserve, good logical and abstract thinking. Patients with SA are characterized by original ideas. The communicative side of speech suffers, they speak when they want, they do not listen to the interlocutor, they often have a conversation with themselves, they are characterized by peculiar deviations in the intonation of speech, unusual turns of speech.

Patients with AS strive, but do not know how to establish contacts with peers and older people, do not keep distance, do not understand humor, react aggressively to ridicule, and are not capable of emotional empathy.

Severe attention disorders, motor clumsiness, disharmony in development, poor orientation in people, in society, arrogance in the realization of their desires lead to the fact that they easily become the object of ridicule, they are forced to change schools, despite their good intelligence. Monomanic stereotypical interest in specific areas of knowledge, one-sided narrowly specific interests in directed learning can form the basis of a future specialty, contribute to socialization.

The course of the disease, the outcome. By the age of 16-17, autism softens, in 60% a schizoid personality with sensitive character traits is formed. Patients are successful in the specialty chosen according to their interests; by the age of 30-40 they create a family.

In 40% of patients with SA, the condition may worsen during the crisis periods of development with the addition of phasic-affective, obsessional disorders, masked by psychopathic manifestations, which are stopped with timely and effective pharmacotherapy, rehabilitation without further deepening of personal identity.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis of autism spectrum disorders should be carried out primarily within the ASD group, and then differentiated from other nosologies, using the possibilities of a modern clinical and biological approach. The classic evolutionary-procedural childhood autism - Kanner's syndrome - should be differentiated from the evolutionary-constitutional Asperger's syndrome. Similar in type of dysontogenesis (bearing disintegrative, dissociated in both cases), they differ primarily in the time of verification of the onset of the disease, in the areas of speech and intellect development, and also in the features of the motor sphere (see Table 1).

Table number 1. Clinical differentiation of evolutionary autism


Asperger's Syndrome

Kanner syndrome

Autism

Light/medium; softens over the years, social awkwardness persists

Severe autism persists for

life, changes mental development

Speech

Early development of grammatically and stylistically correct speech

Patients begin to speak late, speech does not perform a communicative function (echolalia) and is poorly developed in 50%

Motor skills

Motor clumsiness

Gross motor skills are angular with motor stereotypes, athetosis-like movements, walking with support on the toes, muscular dystonia

Intelligence

High or above average. Patients are trained according to the general educational program, receive higher education.

After 35-40 years they create a family.
Cognitive impairment from birth. By puberty, intelligence is dissociated reduced (IQ. They are trained according to the correctional program of the VIII type.

From a paraclinical perspective, these two types of non-psychotic autism also differ. In patients with AS, the main neurophysiological marker is the dominance of the alpha rhythm of a higher frequency than normal. On the EEG in patients with MC, there is a delay in the formation of the alpha rhythm, which is clearly seen at a younger age. As patients with KS age, EEG parameters normalize.

Pathopsychological indicators in Asperger's syndrome are dissociative in nature within the framework of unexpressed cognitive dysontogenesis; with Kanner's syndrome, there is a distinct cognitive deficit.

A pervasive developmental disorder defined by the presence of abnormal and/or impaired development that begins before the age of 3 years and abnormal functioning in all three areas of social interaction, communication, and restricted, repetitive behaviour. In boys, the disorder develops 3-4 times more often than in girls.

Diagnostic instructions:

There is usually no preceding period of undoubtedly normal development, but if there is, then anomalies are detected before the age of 3 years. Qualitative violations of social interaction are always noted. They appear in the form of an inadequate assessment of socio-emotional signals, which is noticeable by the absence of reactions to the emotions of other people and / or the absence of modulation of behavior in accordance with the social situation; poor use of social cues and little integration of social, emotional, and communicative behaviour; the absence of socio-emotional reciprocity is especially characteristic. Qualitative disturbances in communication are equally obligatory. They act in the form of a lack of social use of existing speech skills; violations in role-playing and social simulation games; low synchronicity and lack of reciprocity in communication; insufficient flexibility of speech expression and the relative lack of creativity and fantasy in thinking; lack of emotional response to verbal and non-verbal attempts by other people to enter into a conversation; impaired use of tonalities and expressiveness of the voice to modulate communication; the same absence of accompanying gestures, which have an amplifying or auxiliary value in conversational communication. This condition is also characterized by limited, repetitive and stereotyped behavior, interests and activities. This is manifested by a tendency to establish a rigid and once and for all routine in many aspects of daily life, usually this applies to new activities, as well as old habits and play activities. There may be a special attachment to unusual, often hard objects, which is most characteristic of early childhood. Children may insist on a special order for non-functional rituals; there may be a stereotypical preoccupation with dates, routes, or schedules; motor stereotypes are frequent; characterized by a special interest in the non-functional elements of objects (such as smell or tactile surface qualities); the child may resist changes to routines or details of his environment (such as decorations or home furnishings).

In addition to these specific diagnostic features, children with autism often exhibit a number of other non-specific problems, such as fears (phobias), sleep and eating disorders, temper tantrums, and aggressiveness. Self-injury (for example, as a result of biting the wrists) is quite common, especially with concomitant severe mental retardation. Most children with autism lack spontaneity, initiative, and creativity in leisure activities and find it difficult to use general concepts when making decisions (even when tasks are well within their abilities). The specific manifestations of the defect characteristic of autism change as the child grows, but throughout adulthood this defect persists, manifesting itself in many respects by a similar type of problems of socialization, communication and interests. To make a diagnosis, developmental anomalies must be noted in the first 3 years of life, but the syndrome itself can be diagnosed in all age groups.

In autism, there can be any level of mental development, but in about three-quarters of cases there is a distinct mental retardation.

Differential Diagnosis:

In addition to other variants of general developmental disorder, it is important to consider: specific developmental disorder of receptive language (F80.2) with secondary socio-emotional problems; reactive attachment disorder in childhood (F94.1) or childhood attachment disorder of the disinhibited type (F94.2); mental retardation (F70 - F79) with some associated emotional or behavioral disorders; schizophrenia (F20.-) with unusually early onset; Rett syndrome (F84.2).

Included:

autistic disorder;

Infantile autism;

Infantile psychosis;

Kanner syndrome.

Excluded:

Autistic psychopathy (F84.5)

F84.01 Childhood autism due to organic brain disease

Included:

Autistic disorder caused by an organic brain disease.

F84.02 Childhood autism due to other causes

AUTISM CHILDREN

a property of a child or adolescent whose development is characterized by a sharp decrease in contacts with others, poorly developed speech and a peculiar reaction to changes in the environment.

F84.0 Childhood autism

A. Abnormal or impaired development manifests before the age of 3 years in at least one of the following areas:

1) receptive or expressive speech used in social communication;

2) development of selective social attachments or reciprocal social interaction;

3) functional or symbolic game.

B. A total of at least 6 symptoms from 1), 2) and 3) must be present, with at least two from list 1) and at least one from lists 2) and 3):

1) Qualitative violations of reciprocal social interaction are manifested in at least one of the following areas:

a) inability to adequately use eye contact, facial expressions, gestures and body postures to regulate social interaction;

b) inability to establish (in accordance with mental age and contrary to available opportunities) relationships with peers, which would include common interests, activities and emotions;

c) the absence of socio-emotional reciprocity, which is manifested by a disturbed or deviant reaction to the emotions of other people and (or) the absence of modulation of behavior in accordance with the social situation, as well as (or) the weakness of the integration of social, emotional and communicative behavior.

d) the absence of a spurious search for shared joy, common interests or achievements with other people (for example, the child does not show other people the objects of interest to him and does not draw their attention to them).

2) Qualitative anomalies in communication appear in at least one of the following areas:

a) delay or complete absence of colloquial speech, which is not accompanied by an attempt to compensate for this lack of gestures and facial expressions (often preceded by the absence of communicative cooing);

b) relative inability to start or maintain a conversation (at any level of speech development) that requires communicative reciprocity with another person;

c) repetitive and stereotyped speech and/or idiosyncratic use of words and expressions;

d) the absence of spontaneous diverse spontaneous role-playing games or (at an earlier age) imitative games.

3) Restricted, repetitive, and stereotyped behaviors, interests, and activities that manifest themselves in at least one of the following areas:

a) preoccupation with stereotypical and limited interests that are anomalous in content or direction; or interests that are anomalous in their intensity and limited nature, though not in content or direction;

b) externally obsessive attachment to specific, non-functional acts or rituals;

c) stereotypical and repetitive motor mannerisms that include slapping or twisting fingers or hands, or more complex whole body movements;

d) increased attention to parts of objects or non-functional elements of toys (to their smell, touch of the surface, noise or vibration emitted by them).

B. The clinical picture cannot be explained by other types of general developmental disorder: specific developmental disorder of receptive speech (F80.2) with secondary socio-emotional problems; reactive attachment disorder of childhood (F94.1) or disinhibited attachment disorder of childhood (F94.2), mental retardation (F70-F72) associated with certain emotional and behavioral disorders, schizophrenia (F20) with unusually early onset and Rett syndrome (F84.2)

Childhood autism

see also Autism) - early childhood autism (English infantile autism), first identified as a separate clinical syndrome by L. Kanner (1943). Currently, it is considered as a pervasive (general, multilateral) disorder, a distortion of mental development, due to the biological deficiency of the central nervous system. child; revealed its polyetiology, polynosology. R.d.a is noted in 4-6 cases per 10 thousand children; more common in boys (4-5 times more common than in girls.). The main features of R.d.a. are the child's congenital inability to establish affective contact, stereotyped behavior, unusual reactions to sensory stimuli, impaired speech development, early onset (before the 30th month of life).

Autism in children (infantile)

a relatively rare disorder, the signs of which are already detected in infancy, but usually established in children in the first 2 to 3 years of life. Childhood autism was first described by L. Kanner in 1943 in a work under a poor translation of its title “Autistic Disorders of Affective Communication”. L. Kanner himself observed 11 children with this disorder. He insisted that it is not related to schizophrenia and is an independent form of mental disorder. This opinion is shared at the present time, although it is not argued in any way. Meanwhile, in some patients, affective mood disorders are detected, some symptoms of the disorder are actually identical to the manifestations of catatonia and parathymia, which may indicate an attack of schizophrenia suffered in infancy (E. Bleiler, as you know, believed that 1% of all cases of onset of schizophrenia belong to the first year of life after birth). The prevalence of childhood autism, according to various sources, ranges from 4-5 to 13.6-20 cases per 10,000 children under the age of 12, there is a tendency to increase. The causes of childhood autism have not been established. It is reported that it is more common in mothers who have had measles rubella during pregnancy. Indicate that in 80-90% of cases, the disorder is caused by genetic factors, in particular, the fragility of the X chromosome (see Fragile X Syndrome). There is also evidence that children with autism develop or experience cerebellar abnormalities in early childhood. In boys, the disorder occurs 3-5 times more often than in girls. In most cases, the signs of the disorder are detected at the age of children under 36 months, its most striking manifestations are between the ages of 2 and 5 years. By the age of 6-7 years, some manifestations of the disorder are smoothed out, but its main symptoms persist in the future. The symptom complex of the disorder is represented by the following main features:

1. the infant’s lack of a readiness posture when picking him up, as well as the absence of a revival complex when the mother’s face appears in his field of vision;

2. sleep disturbances, digestion, thermoregulation and other, usually numerous somatic dysfunctions, difficulties in the formation of neatness skills, in other words, severe neuropathic manifestations observed already in the first year of life;

3. ignoring the child of external stimuli, if they do not hurt him;

4. lack of need for contacts, attachment, isolation from what is happening with an extremely selective perception of reality, detachment from others, lack of desire for peers;

5. lack of a social smile, that is, an expression of joy when the face of the mother or another close person appears in the field of view;

6. long-term lack of ability in a number of patients to distinguish between living and inanimate objects (up to 4-5 years). For example, a 5-year-old girl is talking to a working vacuum cleaner or refrigerator;

7. egocentric speech (echolalia, monologue, phonographisms), incorrect use of personal pronouns. Some patients show mutism for a long time, so that parents consider them to be suffering from muteness. Half of the children have significant speech development disorders, especially those related to the communicative aspects of speech. So, children cannot learn such social speech skills as the ability to ask questions, formulate requests, express their needs, etc. Up to 60-70% of patients are unable to master satisfactory speech. Some of the patients do not speak at all and do not respond to the speech of others until the age of 6-7 years;

8. neophobia, or more precisely, the phenomenon of identity (the term of L. Kanner), that is, fear of the new or irritation, dissatisfaction with changes in the external environment, the appearance of new clothes or unfamiliar food, as well as the perception of loud or, on the contrary, quiet sounds, moving objects. For example, a child prefers the same, almost utterly worn out clothes or eats only two types of food, protesting when parents offer him something new. Such children do not like new words and phrases either; they should be addressed only with those to which they are accustomed. Cases of a pronounced reaction of children's indignation even to omissions or substitutions of words in the lullabies of their parents are described;

9. monotonous behavior with a tendency to self-stimulation in the form of stereotypical actions (multiple repetition of meaningless sounds, movements, actions). For example, a patient runs up dozens of times from the first to the second floor of his house and just as rapidly descends, without pursuing any goal that is understandable to others. The monotony of behavior will most likely continue, and in the future, the life of such patients will be built according to some rigid algorithm, from which they prefer not to make any exceptions that cause them anxiety;

10. strange and monotonous games, devoid of social content, most often with non-game items. Most often, patients prefer to play alone and whenever someone interferes with their game or is even present, they are indignant. If they use toys at the same time, then the games are somewhat abstract from social reality. For example, a boy, playing with cars, lines them up in a row, along one line, makes squares, triangles out of them;

11. sometimes excellent mechanical memory and the state of associative thinking, unique counting abilities with delayed development of the social aspects of thinking and memory;

12. refusal of patients from sparing conditions during illness or the search for pathological forms of comfort during malaise, fatigue, suffering. For example, a child with a high temperature cannot be put to bed, he finds for himself the place where he sees the most;

13. underdevelopment of expressive skills (a mask-like face, an expressionless look, etc.), an inability to non-verbal communication, a lack of understanding of the meaning of acts of expression of others;

14. affective blockade (in this case, the poverty of emotional manifestations is meant), underdevelopment of empathy, compassion, sympathy, that is, the disorder mainly concerns prosocial emotional manifestations, especially positive social emotions. Most often, patients are fearful, aggressive, sometimes show sadistic tendencies, especially in relation to the closest people and / or prone to self-harm;

15. the presence of significant, clinically significant motor restlessness in many patients, including various hyperkinesis, epileptic seizures are observed in a third of patients, serious signs of organic pathology of the brain are revealed;

16. lack of eye contact, patients do not look into the eyes of the person who comes into contact with them, but, as it were, somewhere in the distance, bypassing him.

There is no specific treatment for the disorder; mainly special methods of education and upbringing are used. It is difficult to judge the results of work with patients, but there are very few publications reporting significant successes, if any. Some of the children subsequently fall ill with schizophrenia, in other, the most frequent cases, the diagnosis is limited to ascertaining mental retardation or autistic personality disorder. There are known cases of a combination of early autism with Lennox-Gastaut syndrome (Boyer, Deschartrette, 1980). See Lennox-Gastaut syndrome. See: Children's autistic pichopathy.

Various psychotic disorders in young children, characterized by some of the manifestations of early childhood autism. Symptoms may include stereotypically repetitive movements, hyperkinesis, self-injury, speech delay, echolalia, and impaired social relationships. Such disorders can occur in children with any level of intelligence, but are especially common in mentally retarded children.

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psychotic forms of autism (infantile psychosis and endogenous atypical childhood psychosis) must also be differentiated. The possibility of separating these two types of psychosis finds clear confirmation in significant differences in clinical parameters. Similar in disintegrative dissociated dysontogenesis and the presence of catatonic disorders in seizures, they differ not so much in the time of manifestation of the disease [Bashina V.M., 1999; 2009], how much according to the presence or absence of regression in seizures, stereotypes in remission, duration of manifest seizures, outcomes [Simashkova N.V., 2011; Garralda M.E., Raynaud J.P., 2012]. The catatonic syndrome in PV occupies the main place in the structure of the attack, it is replaced by the acquired hyperkinetic syndrome - in remission. Catatonic disorders in ADP pass through the syndrome in an attack, remission, throughout life in the form of protopathic motor stereotypes. PI is characterized by a positive dynamics of the course of the disease, a favorable outcome - in 84% ["practical recovery" - in 6%; "high-functioning autism" (not to be confused with Asperger's syndrome) - in 50%; regressive course - in 28%]. Endogenous ADP is characterized by a progressive course of the disease with early formation of cognitive deficit in 80% of cases (Table 2).

Significantly differ in these diseases and the functional characteristics of the CNS, assessed by neurophysiological parameters. There is a correlation between the severity of the clinical picture and the degree of EEG impairment. In clinical EEG, a decrease in the power of the alpha rhythm and an increase in the power of slow rhythms in theta-delta ranges are considered to be a negative effect on the bioelectrical activity of the brain. Theta rhythm is a "visiting card" for severe illnesses with the collapse of higher mental functions and for sick children with significant developmental delay. In endogenous ADP, there is a correlation between the quantitative measure of the theta rhythm and the clinical manifestation of regression - as the condition improves, its severity decreases. In patients of this group, the theta rhythm, as a rule, persists for a long time (coinciding with the presence of motor stereotypes in the clinical picture of the disease), which confirms an unfavorable prognosis.

Table 2. Clinical differentiation of psychotic forms of ASD


Infantile psychosis

atypical childhood psychosis

Dysontogenesis

Dissociated dysontogenesis

ay tistic disintegrative dysontogenesis

catatonic syndrome

catatonic syndrome with changes to acquired hyperkinetic in remission and subsequently stops

Catatonic disorders in ADP in manifest seizures are combined with regressive ones and persist throughout life in the form of motor stereotypes.

Flow

Positive dynamics during the course of the disease

Progressive course with early formation

cognitive deficit, schism, anhedonia, alexithymia in 80%

Exodus

Favorable: in 6% - "practical recovery", in 50% - "high-functioning autism", in 44% - regressive course with mitigation of autism

Unfavorable in 80%: severe autism persists, oligophrenic defect

For a milder psychotic form of ASD - PV with catatonic disorders, the absence of theta rhythm and the presence of a regular alpha rhythm during an attack are characteristic, which is prognostically favorable. As an additional marker of this disease, a pronounced sensorimotor rhythm may appear, which appears during the period of remission, when catatonic disorders are replaced by an acquired hyperkinetic syndrome.

According to pathopsychological studies, ADP and PV have different outcomes of cognitive impairment: the persistence of a stable cognitive deficit in ADP and the partial leveling of cognitive dysontogenesis against the background of habilitation in PV.

Atypical childhood psychosis of endogenous origin should be differentiated from syndromic ADP. According to the behavioral phenotype at the height of a regressive-catatonic attack, patients with endogenous ADP are difficult to distinguish from patients with syndromic psychotic forms of ADP (with Martin-Bell syndrome, Down syndrome, Rett syndrome, etc.). These psychoses have a phenotypically similar clinical picture in different nosologies: a common sequence of changing stages in attacks (autistic - regressive - catatonic), unfavorable outcome. To clarify syndromic pathology, patients with regressive catatonic psychosis need molecular genetic studies. In patients with syndromic forms of ASD, certain EEG patterns were identified with the dominance of rhythmic theta activity at certain stages of the disease (Gorbachevskaya N.L., 1999, 2011; Yakupova L.P., 2005). As mentioned above, the same pattern was recorded in EEG studies of endogenous ADP in the stage of regression (Yakupova L.P., Simashkova N.V., Bashina V.M., 2006). Reduction of regressive manifestations on the background of therapy was accompanied by a partial reduction of the theta rhythm and restoration of the alpha rhythm. This distinguishes endogenous ADP from severe syndromic forms of ADP, in which the alpha rhythm was practically not recorded.

Atypical autism (AA) or "mental retardation with features of autism" in selected genetic syndromes (Martin-Bell, Down, Williams, Angelman, Sotos, etc.), diseases of metabolic origin (phenylketonuria, tuberous sclerosis, etc.) should be differentiated from the syndrome Kanner, in which severe autism persists throughout life, cognitive deficits increase. Motor stereotypes in syndromic forms of AA are phenotypically different. In non-psychotic forms of UMO with autistic features in sick children and adolescents, the emotional attitude to the outside world is less or not disturbed at all. In patients with syndromic forms of AA, epiactivity is noted in 20-30% of cases.

Differential diagnosis of ASD with other nosologies requires a thorough study of the anamnesis, identification of the leading syndrome, follow-up observation in order to clarify the nature of the course of the disease. ASD should be differentiated primarily from early onset childhood schizophrenia (DS), in which there is also a dissociated disintegrative mental development, socialization disorders, stereotypes. The childhood form of schizophrenia (DS) is not mentioned in ICD-10 (1994). In the United States, childhood schizophrenia is extremely rarely diagnosed before the age of 14, in European countries - earlier than 9 years. In the process of adapting the ICD-10 in the Russian Federation (1999), a special section was introduced - "schizophrenia (children's type)" - F20.8xx3. It included severe forms of schizophrenia (catatonic, hebephrenic, paranoid) with a progressive, malignant course of the disease.

The typical symptomatology of ASD differs from, but overlaps with, DS. Genetic studies have shown an increased incidence of schizophrenia and other psychotic disorders in parents whose children have ASD. It remains controversial whether Leonhard's "early infantile catatonia" is the first manifestation of schizophrenia or a form of atypical autism. DSM-V (2013) identifies catatonia comorbid with mental disorders: schizophrenia, ASD, bipolar, depressive disorders, etc.

In addition, recently in Russia and a number of European countries, endogenous atypical childhood psychosis has been identified among autism spectrum disorders (Bashina V.M., 2009; Simashkova N.V. et al., 2006.2013; Garralda M.E., Raynaud J.P., 2012 ; Meyer-Lindenberg A., 2011), occupying 8-12% in the spectrum of autism disorders. It includes regressive forms of autism with comorbid catatonic symptoms and with early formation of an oligophrenic defect. It is difficult to distinguish between these forms of atypical autism and childhood schizophrenia. The biological markers identified in recent years, along with clinical and pathopsychological markers, can make a significant contribution to solving the problems of diagnosis, differentiation in the selection of individual therapy, and monitoring the condition of patients.

RAS should be differentiated from defects of the sense organs (vision and hearing) and mental retardation (UMR). In the latter, uniform total underdevelopment should be noted in the first place. Children and adolescents with UMO with autistic features have a lesser degree of impaired or not completely impaired emotional attitude to animate or inanimate objects of the surrounding world. Motor disorders in the form of stereotypes have their own characteristics and differ from motor stereotypes in childhood autism.

RAS must be distinguished from deprivation syndrome, attachment disorders as a result of severe pedagogical neglect. In these children, the ability to contact may also be impaired, but more often in the form of depressive symptoms. Sometimes there is no distance in behavior, but there is no typical ASD triad.

Discussing the presence of comorbidity of ASD with organic brain diseases (epilepsy, residual manifestations of early organic lesions of the central nervous system of perinatal origin, encephalopathy, brain injuries, etc.), we should dwell on the concept of the pathogenesis of autism, which has become popular among neurologists in recent years. due to non-convulsive epileptic encephalopathy. With this form of epilepsy, cognitive, autistic and other disorders of mental development are noted (Zenkov et al., 2004; Zenkov, 2007; 2008; Mukhin et al., 2011; Tuchman & Rapin, 1997; Chez & Buchanon, 1997; Kim et al. , 2006; Berney, 2000). In the EEG of such patients, a pronounced epileptiform activity (electric epileptiform status) is detected, mainly during the slow-wave stage of sleep, but there is no clinical picture of seizures. It is believed that the epileptiform activity detected in these cases is associated with congenital disorders of brain maturation processes (Doose, 1989, 2003; Mukhin et al., 2011). It is argued that it is after the appearance of epi-activity in a certain period of ontogeny that a significant regression occurs in the cognitive and mental spheres, which is called autistic epileptiform regression (Canitano, 2006; Characteristics of developmental regression in autistic children, 2010). This theory is supported by facts confirming that the treatment of nonconvulsive encephalopathies with anticonvulsants leads to a noticeable improvement in the condition of patients, and this solves the issue of causal treatment of ASD (Zenkov et al., 2004; Zenkov, 2007; Mukhin et al., 2011; Lewine et al. al., 1999). However, the causal relationship of events proposed in the above concept cannot be considered convincingly proven for all forms of ASD. For example, in Rett syndrome, autistic disorders appear much earlier than epileptic activity.

Discussing whether there is a link between epilepsy and autism, A.Berg and Plioplys (2012) emphasize that such a link is observed in cognitive impairment, when they are significantly pronounced in children with epilepsy or autism. In cases where there is no intellectual disability, there is little evidence of a risk of developing autism in children with epilepsy. To this we can add that in severe forms of UMO (for example, with Rett syndrome), the severity of autism is greater in those patients who have fewer neurological disorders (including epi-activity). Whether epilepsy is comorbid with autism, whether it is caused by autism, or whether epilepsy itself leads to the development of ASD, it is difficult to answer these questions unequivocally at the present stage of the development of science, and therefore the question of the relationship between different forms of autism spectrum disorders and epilepsy cannot be considered resolved to date.

HABILITATION

A unified preventive-therapeutic approach should be followed in the treatment of patients with ASD, the purpose of which is the overall development of children, adolescents and adults with autism. The complex use of drug and non-drug methods of treatment (defectological, psychological, pedagogical, neuropsychological correction, psychotherapeutic social work with the patient and his family) is one of the fundamental principles of curation of autistic disorders in children. Habilitation efforts are aimed at stopping the positive symptoms of the disease, reducing cognitive impairment, mitigating the severity of autism, social interaction, stimulating the development of functional systems, and creating prerequisites for learning opportunities. Depending on the leading cause of the increase in behavioral disorders, the structure of therapeutic measures is shifting towards either predominantly drug therapy or strengthening the correctional-pedagogical and psychotherapeutic components of complex treatment.

The main directions of treatment:

Impact on the pathogenetic mechanisms of the development of the disease;

Activation of the biological and psychological capabilities of the patient;

Impact on comorbid mental and somato-neurological disorders.

Principles of therapy:

Personalized approach, taking into account the established or alleged etiology, all links of pathogenesis, clinical components of the disease, the presence of comorbid disorders additional to autism;

Comprehensive use of drug and non-drug methods of treatment;

“multimodality” with participation in a team of specialists: psychiatrists, pediatricians, neurologists, psychologists, speech pathologists, speech pathologists, teachers, social workers.

PSYCHOPHARMACOTHERAPY

Early initiation of drug therapy is important as a prognostic factor. This is due to the patterns of brain development, positive trends in ontogenesis when the active course of the disease stops.

Treatment for different types of ASD varies dramatically. In addition, drug therapy is indispensable under the influence of external and internal adverse factors (changes in the environment, microsocial environment, critical periods of development). Medical correction is necessarily combined with developmental education, the principles of which will be outlined below. There is a correlation between the age of onset of therapeutic interventions and clinical and social prognosis for patients with autism. To prevent the formation of severe personality and oligophrenic defects, early and adequate preventive actions.

Treatment is carried out taking into account the psychopathological structure of the exacerbation of the disease, which determines the choice of psychotropic drugs, as well as taking into account the characteristics of the therapeutic or spontaneous transformation of the syndrome in the course of treatment, which may be associated with the replacement or addition of other methods of treatment. The choice of a specific drug is carried out taking into account the spectrum of psychotropic activity of the antipsychotic and the nature of the resulting side effects, as well as contraindications for use and possible drug interactions. The dosage regimen, the average and maximum allowable daily doses and the possible route of administration of a particular neuroleptic is determined by the nature and severity of the existing psychopathological symptoms, the somatic condition and age of the patient. Polypharmacy should be avoided. The effectiveness of the therapy is evaluated based on the positive dynamics of clinical manifestations. The main indicators are the speed of development and persistence of the effect, as well as the safety of therapy.

In the case of the development of acute psychosis with a predominance of non-specific autistic manifestations (phobias, anxiety, psychomotor agitation, aggressiveness, one should resort to prescribing antipsychotics with a sedative component of action (chlorpromazine, levomepromazine, chlorprothixen, alimemazine, periciazine, etc.), including parenterally (convincing evidence AT).

Disinhibiting antipsychotics (sulpiride) are prescribed taking into account the disinhibitory, activating action (strength of evidence B).

The polymorphism of psychopathological disorders, the presence of symptoms of deeper registers requires the appointment of neuroleptics with a powerful general antipsychotic (incisive) effect (haloperidol, clozapine, risperidone).

Pharmacokinetics

There are precise data on the mechanisms of action of drugs. An important task of medical professionals dealing with autistic disorders (mainly child and adolescent psychiatrists) is to disseminate this knowledge both among doctors and other related professionals, as well as among parents. Persistent prejudice against drug treatment does not improve the condition of patients with autism.

The antipsychotic effect of neuroleptics is associated mainly with the blockade of D2-dopamine receptors and changes in dopaminergic neurotransmission, which in turn can cause extrapyramidal disorders and hyperprolactinemia. The development of certain clinical effects of D2 receptor blockade depends on the impact on various dopaminergic pathways in the CNS. Inhibition of neurotransmission in the mesolimbic system is responsible for the development of the antipsychotic effect itself, in the nigrostriatal region for extrapyramidal side effects (neuroleptic pseudoparkinsonism), and in the tuberoinfundibular zone for neuroendocrine disorders, including hyperprolactinemia. In mesocortical structures in patients with autism, a decrease in dopaminergic activity is observed. Antipsychotic drugs do not bind to D2 receptors in the same way in different brain structures. Some substances have a strong affinity and block receptors for a long time, while others, on the contrary, are quickly released from their binding sites. If this occurs at the level of the nigrostrial region and the blockade of D2 receptors does not exceed 70%, then extrapyramidal side effects (parkinsonism, dystonia, akathisia) either do not develop or are slightly expressed. Antipsychotics with anticholinergic activity rarely cause extrapyramidal symptoms, since the cholinergic and dopaminergic systems are in a reciprocal relationship, and blockade of type I muscarinic receptors leads to activation of dopaminergic transmission. The ability of central anticholinergic drugs (trihexyphenidyl, biperiden) to correct neuroleptic extrapyramidal disorders is based on the same mechanism of action. Some drugs, depending on the dose used, can block presynaptic D2 / 3 receptors and paradoxically facilitate dopaminergic neurotransmission, including at the cortical level (sulpiride). In the clinic, this can manifest itself as a disinhibitory or activating effect.

Atypical antipsychotics (type 2 neuroleptics) can also block 5-HT2 serotonin receptors, which is associated with their ability to reduce the severity of negative symptoms and cognitive impairment in patients with autistic disorders, since type 2 serotonin receptors are located mainly in the cerebral cortex (especially in the frontal regions). ) and their blockade leads to indirect stimulation of dopaminergic transmission. The appointment of atypical antipsychotics in the treatment of ASD in childhood requires the simultaneous administration of central anticholinergic drugs (trihexyphenidyl, biperiden).

Currently, there are significant age restrictions in the appointment of neuroleptics. Taking into account the constant work of various structures on the introduction of modern drugs into child psychiatric practice, age restrictions on successfully used drugs in adults are gradually being removed. When choosing a drug, one should also be guided by the current state of psychiatry and the recommendations of manufacturers in accordance with the laws of the Russian Federation.

Antipsychotics of the following groups are used to treat psychotic forms of ASD:

1. Phenothiazines and other tricyclic derivatives:


  • Aliphatic (alimemazine, promazine, chlorpromazine)

  • Piperidine (periciazine, pipothiazine, thioridazine)

  • Piperazines (perphenazine, thioproperazine, trifluoperazine)
2. Thioxanthenes (flupentixol, chlorprothixene)

3. Butyrophenones (haloperidol)

4. Substituted benzamides (sulpiride, tiapride)

5. Dibenzodiazepine derivatives (clozapine)

6. Benzisoxazole derivatives (risperidone)

Aliphatic phenothiazines have a strong adrenolytic and anticholinergic activity, which is clinically manifested by a pronounced sedative effect and a mild effect on the extrapyramidal system. Piperazine phenothiazines and butyrophenones have weak adrenolytic and anticholinergic, but strong dopamine-blocking properties, i.e. the most pronounced global antipsychotic effect and significant extrapyramidal and neuroendocrine side effects. Piperidine phenothiazines, thioxanthenes and benzamides occupy an intermediate position and have a predominantly average antipsychotic effect and moderate or mild extrapyramidal and neuroendocrine side effects. A separate group consists of atypical antipsychotics (risperidone, clozapine), which have a fairly pronounced general antipsychotic effect and dose-dependent extrapyramidal and neuroendocrine side effects, which requires the simultaneous administration of central anticholinergic drugs.

Most commonly used antipsychotics and other drugs in patients with ASD

When choosing a drug, one should be guided by the list of registered drugs approved for use in children, and the recommendations of manufacturing companies in accordance with the laws of the Russian Federation (see Tables No. 3-8).

Table 3 The most commonly used antipsychotics in patients with ASD


International non-proprietary name

Age of permitted use

Alimemazine, tab.

From 6 years old

Haloperidol, drop.

from 3 years old

Haloperidol, tab.

from 3 years old

Clopixol

children's age, no exact data

Clozapine, tab.

from 5 years old

Levomepromazine, tab.

from 12 years old

Periciazine, caps.

from 10 years old, with caution

Periciazine, drop.

from 3 years old

Perphenazine

over 12 years old

Risperidone, oral solution

from 5 years old

Risperidone, tab.

from 15 years old

Sulpiride

from 6 years old

Trifluoperazine

older than 3 years, with caution

Chlorpromazine, tablets, dragee
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