Mental retardation (oligophrenia) - symptoms and treatment

General information

Mental retardation is a congenital or acquired condition in early childhood (up to 3 years) of general underdevelopment of the psyche with a pronounced lack of intellectual abilities.

Mental retardation can be caused by various etiological and pathogenetic factors acting during intrauterine development, childbirth or in the first years of life. In most cases, mental retardation is not a painful process, but a pathological condition, the result of harmfulness that once acted, and has no tendency to progress.

For a long time, the generally accepted term for denoting states of mental retardation was the term “oligophrenia” (Greek: oligos - small, phren - mind, i.e. dementia), which was proposed by E. Kraepelin (1915) to distinguish the congenital dementia he designated from acquired dementia (dementia).

How to make an appointment with a neurologist

Mental retardation requires an integrated approach, so you need to make an appointment with not just one specialist, but several. Initially, it is recommended to see a neurologist, who, after an examination, will determine which doctors the patient still needs. JSC "Medicine" (clinic of academician Roitberg) is located in the center of Moscow near the Mayakovskaya, Novoslobodskaya, Chekhovskaya, Belorusskaya metro stations. You can make an appointment with a neurologist, speech therapist, child psychiatrist and other doctors by phone. Also use the feedback form by sending a request, or request a call back.

Classification of mental retardation

There are different approaches to classifying mental retardation conditions. The most common clinical classification is the division of mental retardation according to the degree of intellectual defect. Traditionally, there were three degrees of mental retardation: debility, imbecility and idiocy. In the International Classification of Diseases, 10th revision (ICD-10), mental retardation is presented in a separate section (F7) and is divided according to severity into four degrees: mild (F70), moderate (F71), severe (F72) and profound (F73). Another clinical classification involves the division of mental retardation states (regardless of the depth of mental underdevelopment) into sthenic, dysphoric, asthenic and atonic forms (D.N. Isaev). In addition, there are “nuclear” forms of mental retardation (N.I. Ozeretsky), which are characterized by the totality of mental underdevelopment, affecting the entire psyche as a whole, and atypical forms, which are characterized by an uneven structure of mental defect with signs of partial mental underdevelopment.

According to etiopathogenesis, mental retardation conditions are divided into three main groups (G.E. Sukhareva):

1. conditions caused by hereditary (gene and chromosomal) diseases

. This group includes: Down syndrome, Klinefelter syndrome, Turner syndrome, Martin-Bell syndrome, true microcephaly, enzymopathic forms associated with hereditary metabolic disorders (phenylketonuria, galactosuria, etc.), hereditary neurological and neuromuscular diseases with mental retardation.

2. conditions caused by the action of various hazards during intrauterine development (embryopathy and fetopathy).

This includes conditions caused by intrauterine infections (rubella viruses, influenza, paratitis, cytomegalovirus, pathogens of syphilis, toxoplasmosis, etc.), intoxications (for example, alcohol), hemolytic disease of the fetus, etc.

3. conditions caused by the action of various hazards during childbirth or in the first months and years of life.

There are mental retardation associated with birth trauma and asphyxia during childbirth, with traumatic brain injuries and neuroinfections suffered in early childhood.

In many cases, it is not possible to reliably identify the etiological causes of mental retardation, therefore such conditions are designated as undifferentiated

forms.
In turn, differentiated
forms of mental retardation are nosologically independent diseases with an established etiopathogenesis and characteristic clinical picture. Often, in differentiated forms, mental retardation is only one of the symptoms among other severe manifestations of these diseases.

Clinical manifestations and dynamics of mental retardation

Mental disorders in mental retardation, as noted above, are polymorphic in nature and severity.

Severity of intellectual defect.

According to the severity of insufficiency of intellectual abilities in ICD-10, the following are distinguished:

1. Profound mental retardation (idiocy).

In idiocy, cognitive abilities are significantly limited: patients are practically unable to understand speech addressed to them, do not recognize the people caring for them (for example, mother), do not distinguish edible from inedible (they can eat inedible objects), have no idea of ​​spatial relationships (for example , about height: they can fall from a great height), rarely form ideas about hot, sharp, etc. (they can get damaged, burns). Most patients are not able to master even the simplest self-care skills (get dressed, wash, use cutlery, etc.). Speech is either not formed at all (such patients produce only inarticulate sounds) or consists of several simple words. The motor functions of patients are significantly underdeveloped, and therefore many of them cannot stand or walk independently and move by crawling. Behavior in some cases is characterized by lethargy, inactivity, in others - a tendency to monotonous motor excitation with stereotypical movements (swaying the body, waving arms, clapping hands), and in some patients with periodic manifestations of aggression and auto-aggression (they can suddenly hit, bite others, scratch themselves, hit themselves, etc.). In most cases, severe neurological disorders and severe somatic abnormalities occur. The life of such patients, who need constant care and supervision from others, is determined by the satisfaction of the simplest needs of life. The IQ (D. Wechsler’s standardized method for measuring intelligence) in persons with severe mental retardation is below 20.

2. Severe mental retardation (severe variants of imbecility)

Cognitive activity is limited by the ability to form only the simplest ideas; abstract thinking and generalizations are inaccessible to patients. Patients acquire only basic self-care skills; their training is impossible. The vocabulary is limited to one to two dozen words, sufficient to communicate one’s basic needs, and articulation defects are pronounced. Neurological disorders and gait disturbances are often present. Patients need constant monitoring and maintenance. The IQ of these patients ranges from 20-34.

3. Moderate mental retardation (variants of mild and moderate imbecility)

These patients are able to form a larger number and more complex ideas than patients with severe mental retardation. Patients master self-care skills and can be accustomed to simple work by training in imitative actions. Their vocabulary is richer, they are able to express themselves in simple phrases and maintain a simple conversation. Relative adaptation of patients with moderate mental retardation is possible only in conditions that are well known to them; any change in the situation can put them in a difficult position due to the impossibility of moving from specific ideas obtained through direct experience to generalizations that allow them to transfer existing experience to new situations. Patients cannot live independently and need constant guidance and control. Some of them can perform simple work in specially created conditions (for example, in occupational therapy workshops). The IQ of these patients is in the range of 35-49.

4. Mild degree of mental retardation (debility).

Cognitive disorders in these patients include difficulty in forming complex concepts and generalizations, the impossibility or difficulty of abstract thinking. Their thinking is predominantly concrete and descriptive, and everyday speech is quite developed. Patients with mild mental retardation are capable of mastering special programs based on concrete visual learning, which is carried out at a slower pace, as well as the ability to master simple labor and professional skills. Due to the relatively higher rate of mental development in patients with mental retardation than in other degrees of mental retardation, satisfactory adaptation to normal living conditions is possible in many cases. Often these patients show good practical awareness (“their skills are greater than their knowledge” - E. Kraepelin). Many patients with mild mental retardation graduate from specialized schools and vocational schools, work productively, start families, and run their own households. Compared to other degrees of oligophrenia, the personality and character traits of patients are more differentiated and individual. However, these patients have difficulty forming their own judgments, but easily adopt the views of others, sometimes falling under the unhealthy influence of others (for example, they can be involved in the delusional experiences of mentally ill patients with the formation of induced delusions, or become a tool in the hands of attackers who manipulate them for their own gain) . The IQ of these patients is in the range of 50-69.

Emotional-volitional disorders

Intellectual failure is the most striking manifestation of mental retardation, but it is only part of the general mental underdevelopment of the individual. With oligophrenia, emotional and volitional processes suffer significantly. D.N. Isaev, based on the characteristics of violations of the emotional-volitional sphere, regardless of the severity of mental underdevelopment, identifies the following forms of mental retardation:

1. Stenic.

The volitional processes in these patients have sufficient strength and stability. The patients are efficient and active. With mild degrees of intellectual disability, they have a good ability to adapt and are able to fully use the acquired skills and knowledge. Some patients experience affective instability, so there are two variants of the sthenic form: balanced and unbalanced.

2. Dysphoric.

It is characterized by a constant angry-sad affect, a tendency to dysphoria, impulsive actions, negativism, conflict, and disinhibition of drives. Even with minor intellectual impairment, such patients are incapable of learning and working. During dysphoria, they often show aggression (usually towards loved ones caring for them, and the aggression can be very cruel and sophisticated) and auto-aggression (inflicting deep cuts on themselves, burning their skin with a cigarette, pulling out hair, etc.).

3. Asthenic

. It is characterized by instability of volitional processes, rapid exhaustion, fatigue, slowness, disturbances of attention, difficulties in mastering and using practical skills.

4. Atonic.

It is characterized by an almost complete lack of ability for mental stress and purposeful activity. Patients are either completely inactive or in a state of chaotic motor disinhibition.

Dynamics of mental retardation

In most cases, mental retardation conditions are relatively stable (“non-progressive”). However, sometimes, under the influence of internal and external factors, their positive or negative dynamics are noted. With timely and active implementation of therapeutic, correctional and educational measures, the majority of patients suffering from mild and moderate mental impairment are able to work. In the process of age-related evolution and under the influence of therapeutic measures, there is a reduction in motor disinhibition, impulsivity, negativism, asthenic conditions, etc. Negative dynamics of mental retardation is possible with the addition of additional pathogenetic mechanisms of brain damage (for example, amyloid deposition in Down's disease), under the influence of additional external hazards (traumatic brain injuries, alcoholism, etc.), psychogenia, unfavorable social environment, during periods of age-related crises, etc. Decompensation in mental retardation can manifest itself as cerebroasthenic and psychopathic disorders, psychoses with stupefaction, hallucinatory-delusional, affective psychoses, etc. .

Differentiated forms of mental retardation

Conditions caused by hereditary (gene and chromosomal) diseases

Down syndrome

Caused by trisomy 21 chromosomes. It was first described by the English physician J. Down in 1866, but the connection between the violation of the number of chromosomes and the clinical manifestations of the disease was established only in 1959 (J. Lejeune). The birth rate of children with Down syndrome is approximately 1:700, but currently, due to the possibilities of prenatal diagnosis, there is a tendency to reduce it. The most important risk factor for this chromosomal aberration is the age of the mother (over 35 years).

Clinical manifestations:

Mental retardation in Down syndrome can be expressed in different ways, most often it is moderate and severe, less often mild. Patients have a late appearance and pronounced underdevelopment of speech (insufficient understanding of speech, poor vocabulary, dysarthria). Children with Down syndrome are usually unable to learn even in a special school program and require individual education. The emotional sphere remains quite intact: for the most part, patients are affectionate, obedient, attached to their parents, friendly, good-natured (“sunny children”), although they can be stubborn. Many of them are curious and have a good ability to imitate, which contributes to the development of self-service skills and simple work processes. Indifferent and angry patients are rare. As a rule, children with Down syndrome develop better in parental families, feeling the care of loved ones, but even in this case, they do not achieve a satisfactory level of social adaptation and need constant care.

A feature of the age-related dynamics of Down's disease is late puberty and early appearance of signs of involution (at 30-40 years). With Down syndrome, there is a high incidence of early development (after 35 years) of atrophic changes in the cerebral cortex and accumulation of amyloid in the form of senile plaques, i.e. morphological changes similar to Alzheimer's disease. At the same time, patients quickly lose everyday skills and vocabulary, become inactive, indifferent, and neurological disorders appear.

Patients with Down syndrome are characterized by a specific physical phenotype, determined by many stigmas of dysontogenesis, which makes it possible to diagnose this condition at birth. Children are usually small in stature; at birth they often have low body weight (up to 2500 g). Head circumference is reduced. The face is flat, Mongoloid eye shape (the first name for the syndrome is “Mongolism”), wide bridge of the nose, short nose, occasionally spotted coloring of the central part of the iris is observed; Cataracts are common. The tongue is large, striated, the mouth is half open. The ears are small and flat. The hands are wide, the fingers are short, there is a transverse groove on the palmar surface of the hand. Pathologies of the structure of the cardiovascular system, endocrine disorders (hypofunction of the thyroid gland, pituitary gland, adrenal glands, gonads), and muscle hypotension are often encountered. Characterized by increased susceptibility to infections. The life expectancy of patients is significantly reduced, no more than 10% live more than 40 years.

Turner syndrome (Shereshevsky-Turner)

Monosomy of the X chromosome (45, X0). Prevalence 1:3300 newborns.

Clinical manifestations:

Mental retardation is found only in some patients; usually mild. Patients are hardworking and complacent. Many patients have criticism of their condition and experience a defect; there is a tendency to neurotic reactions

Congenital anomalies of the structure give patients a peculiar appearance: short stature (usually does not exceed 150 cm), disproportionate physique (predominance of the upper body, broad shoulders, narrow pelvis, shortening of the lower extremities, constitution approaches that of a man). The neck is short with excess skin on the posterolateral surface, which in many patients appears as a cervical fold. Signs of sexual infantilism are revealed (the external genitalia are underdeveloped, the mammary glands are not developed, the nipples are retracted, pubic and axillary hair is absent or scant). Characteristic signs are primary amenorrhea, anomalies in the structure of the internal genital organs.

Klinefelter's syndrome

Disomy on the X chromosome in men (47, XXY). Prevalence 1:1400 newborns (boys).

Clinical manifestations:

Mental retardation occurs in about a quarter of patients, mostly in a mild degree. There is marked immaturity of the emotional-volitional sphere. Many patients often have a consciousness of their inferiority, which becomes a source of internal conflict; neurotic and pathocharacterological reactions are characteristic. Cases with depressive, hypochondriacal, obsessive, and schizophrenia-like disorders have been described

Appearance of patients: characterized by tall stature, asthenic build, narrow shoulders, elongated limbs, poorly developed muscles. Constant signs of Klinefelter syndrome are underdevelopment of the genital organs and infertility. Approximately half of the patients have gynecomastia and eunuchoid signs. In the neurological status, in some cases there is muscle hypotonia and diencephalic-vegetative disorders such as panic attacks.

Mental retardation caused by hereditary metabolic defects

Phenylpyruvic mental retardation (phenylketonuria, PKU, Felling's disease)

- a hereditary metabolic disorder (characterized by an autosomal recessive type of inheritance), caused by a deficiency of one of the metabolic enzymes of the amino acid phenylalanine, which leads to impaired oxidation of phenylalanine into tyrosine, insufficient synthesis of catecholamines (adrenaline and norepinephrine), thyroid hormones, melanin, serotonin. As a result, a gradual accumulation of phenylalanine and its metabolites occurs in the body, which have a toxic effect on the central nervous system, and a deficiency of hormones and mediators of the nervous system is formed with further delay in mental development. Phenylalanine and its metabolites (phenylketone substances) are excreted in the urine. There are significant ethnic differences in the prevalence of phenylketonuria. In Russia, the frequency among newborns is 1:6-10 thousand.

Clinical picture:

Children with phenylketonuria are born with a normally formed and functionally complete brain (since the biochemical processes of the fetus are ensured by the mother's metabolism). Biochemical disorders begin to develop immediately after birth. Already at 4-6 months. a lag in psychomotor development is revealed, which progresses noticeably. The comprehensive clinical picture of the disease includes severe or profound mental retardation, behavioral disorders and catatonic disorders (states of psychomotor agitation, impulsive actions, stereotypic movements, echopraxia, echolalia, substuporous states), asthenic states. An increase in muscle tone, convulsions (in 30% of patients), hyperkinesis, tremor of the fingers, ataxia, impaired coordination, and enuresis are often detected. Pigmentation defects are characteristic (most patients are blond, with light, pigmentless skin and blue eyes). Urine has a peculiar smell (“smell of wolf”, “mouse”, “musty”). Biochemical diagnosis of phenylketonuria is based on a positive reaction of urine with FeCl3 to phenylpyruvic acid (Felling test) and the detection of an increased concentration of phenylalanine in the blood plasma.

Phenylketonuria is an example of a hereditary disease with the possibility of a good effect with timely preventive therapy: to prevent the development of mental and neurological disorders from the first months of life until 10-12 years of age, diets with a sharp restriction of phenylalanine are used (animal protein is completely excluded, vegetable protein is significantly excluded, protein deficiency is compensated for by special mixtures of amino acids without phenylalanine). The sensitivity of nervous tissue to the toxic effects of phenylalanine metabolic products, as well as to other metabolic disorders, is highest at an early age (during brain maturation). After the completion of the myelination process, the increase in phenylalanine in the blood no longer has a pathogenic effect on the brain.

Mental retardation caused by exposure to harmful substances during intrauterine development (embryopathy and fetopathy)

Mental retardation caused by rubella virus (rubeolar embryopathy).

When a pregnant woman contracts rubella in the first trimester of pregnancy, embryopathy develops with gross structural disturbances of the nervous system (microcephaly, porencephaly), hearing and vision organs, and congenital defects of internal organs. Mental retardation in such patients is usually severe, and convulsive seizures are frequent.

Mental retardation caused by hemolytic disease of the fetus and newborn

. Hemolytic disease of the fetus (erythroblastosis fetalis) is caused by a Rh conflict between mother and child, which leads to hemolysis of fetal red blood cells, anemia, high bilirubin levels, circulatory disorders, edema, and increased intracranial pressure. One of the consequences of this condition may be the formation of mental retardation, the severity of which varies.

Mental retardation caused by maternal alcoholism (alcoholic fetopathy).

Develops when mothers drink alcohol during pregnancy. According to a number of authors, it ranks first among the causes of mild mental retardation. The clinical picture consists of mental retardation (mostly mild), delayed physical development (especially pronounced at birth and in the first years of life), disturbances in the structure of the skull (microcephaly, shortening of the palpebral fissures, underdevelopment of the bones of the middle part - a convex forehead, a short nose with a wide flat nose bridge, hypoplasia of the upper jaw).

Conditions caused by exposure to harmful substances during childbirth or in the first months and years of life

Mental retardation caused by birth trauma or asphyxia during childbirth

. Mechanical damage to the baby's skull during childbirth can lead to intracranial hemorrhages or even direct damage to the brain and its membranes. Oxygen starvation causes metabolic disorders in nervous tissue. These factors can lead to the formation of organic pathology of the brain and, subsequently, mental retardation (the severity of which may vary). Birth injuries are characterized by focal neurological disorders, seizures, and sometimes hydrocephalus.

Mental retardation caused by neuroinfections suffered in early childhood

. After meningitis and meningoencephalitis, mental retardation of varying severity, focal neurological disorders, seizures, and hydrocephalus can develop.

Causes of the disease

There are many factors that can become provocateurs in the development of mental retardation. Among the most common primary sources of pathology are:

1. Exposure of a pregnant woman's body to poisons and chemicals. Hazardous substances cause intoxication of the body, are integrated into metabolic processes and lead to their disruption. This condition can develop under the influence of certain medications. If a pregnant woman takes them in doses that violate acceptable limits, the fetus’s body suffers first.
2. Infectious diseases in the expectant mother. These include influenza, scarlet fever, rubella and others.
3. A metabolic disorder that led to the development of a severe form of female dystrophy. Weight is rapidly decreasing, and the weight of the fetus is also becoming smaller. Organs and tissues can no longer perform their functions at the same level.
4. Injury to the fetus that occurs as a result of a bruise, fall, or blow to the stomach of the expectant mother. Mental retardation often results from damage to the newborn during labor and the application of forceps.
5. Retardation develops if the body of the mother, as well as the fetus, has been infected with parasites. The most dangerous disease is toxoplasmosis, transmitted from domestic animals (cows, pigeons, cats, dogs), as well as from mice and other small wild fauna.
6. Hereditary predisposition. Mental retardation is transmitted at the genetic level. This disease develops if there is a chromosomal disease or incompatibility of the Rh factor of the blood of the mother and child.
7. Inflammation of the meninges that occurs in a newborn often provokes mild or moderate retardation.
8. Disturbance of protein metabolic processes, phenylketonuria.
9. Poor ecology or exposure to radiation.
10. Bad habits of one of the parents - alcoholism and drug addiction. It is especially dangerous if the mother is diagnosed with addiction. Typically, such patients do not stop taking alcohol or drugs even after learning about pregnancy.
11. Poor nutrition, which leads to retardation in mental and physical development.

Therapy for this disease is possible when patients are admitted to an inpatient psychiatric hospital. Often they themselves cannot express their desire to undergo treatment, not realizing that they are really sick. Permission from relatives or guardians is required. Husband, wife, children, parents sign an agreement with the clinic, which describes the rights and obligations of each party.

Differential diagnosis

The diagnosis of mental retardation is based on the establishment of a mental defect, the central place in which is occupied by underdevelopment of intellectual abilities, on the detection of signs of mental retardation in childhood and adolescence, as well as the absence of progression, i.e. signs of deepening mental defect. In order to determine the degree of intellectual defect, special psychological methods for assessing intelligence are used (see Chapter 7). To clarify the etiology of some forms of mental retardation, additional laboratory and instrumental studies are required. It is necessary to differentiate mental retardation from conditions caused by pedagogical neglect (cases when a healthy child is deprived of the conditions for proper mental development) and progressive mental illnesses (primarily schizophrenia and epilepsy, manifesting in early childhood).

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