Reasons leading to deviations in the motor sphere. Movement disorders - abstract. Differential diagnosis of movement disorders

Skeletal muscle contractions and tone are associated with the excitation of alpha motor neurons, which are located in the spinal cord. The force of muscle contraction, as well as its tone, depend on the number of excited mononeurons and the frequency of their discharges. Motor neurons are excited due to impulses coming directly from the afferent fibers of sensory neurons. The mechanism underlies all spinal reflexes. The Renshaw system is represented by cells that have an inhibitory effect on mononeurons and are activated by impulses coming from alpha motor neurons. Disturbances in motor functions occur when these parts of the central nervous system are damaged, as well as when the conduction of impulses along the motor nerves is disrupted.

Causes of motor dysfunction

A common form of movement disorders is paralysis And paresis. There is a loss and weakening of movements due to impaired motor function of the nervous system. Doctors call paralysis of the muscles of one half of the body hemiplegia, and paralysis of both limbs - paraplegia.

Depending on the pathogenesis of paralysis, the tone of the affected muscles may be lost or increased. In addition, experts distinguish peripheral and central pathogenesis. Impaired motor function in the body may be associated with pathology of the end plate and motor nerves.

Myasthenia gravis

Myasthenia gravis or asthenic bulbar palsy is characterized by severe weakness and increased muscle fatigue. Any muscle in the body can be involved in this process. Motor dysfunction associated with pathology of the end plate and motor nerves. . If a patient with myasthenia gravis is asked to forcefully clench his hand into a fist several times in a row, he will succeed only the first time. Then, with each subsequent movement, the strength in the muscles of his arms rapidly decreases. Muscle weakness is observed in many skeletal muscles, including facial, oculomotor and swallowing muscles.

The causes of myasthenia gravis have not been fully identified, but some hypotheses state that a curare-like substance accumulates in the blood of patients or excessive accumulation of cholinesterase in the area of ​​the end plates. Recent studies have shown that in patients with myasthenia gravis, antibodies to acetylcholine receptors are often found in the blood serum. Removal of the thymus gland in these cases leads to an improvement in the patient's condition.

Spinal shock

Spinal shock associated with dysfunction of the spinal cord. Caused by injury or spinal cord rupture. It is expressed in a sharp drop in excitability, inhibition of the activity of all reflex centers located below the site of injury. The consequence of spinal shock is:

    decreased blood pressure;

    absence of vascular reflexes;

    acts of defecation;

    acts of miction.

Shock occurs as a result of domestic and military injuries. The spinal cord is not damaged and there are no complications from the internal organs, then over time the reflexes are restored. Some time after the disappearance of the phenomena of spinal shock, reflex activity sharply increases. A patient with a spinal cord interruption has all spinal reflexes due to irradiation of excitation in the spinal cord they lose their normal localization.

Decerebrate rigidity

Impairment of motor functions due to damage to the brainstem is accompanied by decerebrate rigidity. The patient needs to make significant efforts to bend the joints. At a certain stage, resistance may weaken - this is a lengthening reaction. The mechanism of development of decerebrate rigidity is a sharp increase in impulses from motor neurons. Increased muscle tone has a reflex origin; today doctors know that both tonic and phasic reflexes are regulated by a reticular formation.

Rigidity develops as a result of strong compression of the brain stem by a one-sided process that limits the intracranial space in the hemispheres and posterior regions.

In addition, the disease can be caused by:

    swelling of the brain (stroke);

    brain contusion;

    meningitis;

    meningoencephalitis;

    toxic encephalopathy;

    renal coma.

Compression of the midbrain is often accompanied by herniation of the cerebellar tonsils into the foramen magnum, which leads to even greater separation of the cerebral hemispheres and its lower parts.

Compression of the midbrain or local pathological processes in it disrupt the inhibitory influence of cortical and subcortical structures on the underlying centers of movement and regulation of muscle tone, as a result, the midbrain’s own mechanism is released and, as it were, the ancient standing reflex comes to life in a pathological form. Decerebrate rigidity is accompanied by respiratory arrest. This is precisely the danger of this condition - the patient needs urgent hospitalization and medical care.

Cerebellar lesion

The cerebellum is a highly organized center that regulates muscle function. The cerebellum receives a flow of impulses from receptors in muscles, joints, tendons and skin. Also, impulses come from the organs of vision, hearing, and balance. This organ is able to correct the motor reactions of the body, ensuring the accuracy of the body’s structures. Its function is to coordinate phasic and tonic components motor act. That is why damage to the cerebellum causes a number of serious disorders. In the first days after removal of the cerebellum, muscle tone, especially extensor muscles, sharply increases. However, then, as a rule, muscle tone sharply weakens and atony develops. Atony After a long period of time, it may again be replaced by hypertension.

Cerebellar lesion characterized by the following general features:

    decreased muscle tone;

    deviation of voluntary movements from a harmonious ideal line;

    violation of automatic movements.

In some cases, there may be a lack of coordination in the movements of muscle groups, dissymmetry and ataxia (impairment of the coordinated functioning of the body muscles). It may also appear intention tremor(increasing deviation from the main line of movement as you approach the goal). Characteristic manifestation ataxia(fast fatiguability).

Dysfunction of the cerebral cortex

Disturbances in the motor functions of the body are also associated with dysfunction of the cerebral cortex. Another movement disorder is also associated with dysfunction of the cerebral cortex - convulsions which are observed in epilepsy. In the tonic phase epileptic seizure The patient's legs are sharply extended and his arms are bent. Scientists have found that the basis of an epileptic seizure is excessive synchronization of discharges in cortical neurons. Pathological synchronization involves neurons in increased activity, which, as a result, cease to perform their normal functions. The cause of the development of the disease may be the following effects on the cerebral cortex:

  • cicatricial changes in the cortex;

    electricity;

    action of pharmacological drugs.

Hypotension limbs is more pronounced in acute than in chronic lesions of the cerebellum. This disease can be detected by a light blow to the wrists of the arms extended forward. In this case, the arm on the affected side makes a greater range of movement than on the healthy side (this reflects weak fixation of the arm in the shoulder joint). The pendulum knee reflex reflects hypotonia of the quadriceps and hamstrings. Problems in the structure of the brain stem have a destructive effect on dopamine neurons in the structures of the organ. This may cause parkinsonism- a group of chronic neurodegenerative diseases. The disease is characterized by movement disorders such as slowness of movements, increased muscle tone, limb tremor at rest, inability to maintain balance when changing body position or when walking.

E.M. MASTYUKOVA

CHILD

DEVIATIONS

DEVELOPMENT

EARLY DIAGNOSIS AND CORRECTION

MOSCOW "ENLIGHTENMENT" 1992


BBK 74.3 M32

Reviewer methodologist, station No. 890, Khoroshevsky district of Moscow L. T. Vorobyova

Mastyukova E. M.

M32 Child with developmental disorders: Early diagnosis and correction. - M.: Education, 1992. - 95 p.: ill. - ISBN 5-09-004049-4.

The book summarizes data from domestic and foreign research on the diagnosis and correction of various forms of abnormal development of young children.

The author considers abnormal development as a consequence of organic damage to the central nervous system. Particular attention is paid to early diagnosis and correction of deviations in the cognitive sphere of children.

The book is intended for defectologists, psychologists, educators of abnormal children, and will be of interest to students of defectology departments and parents.


4310010000-339 103(03)-92


Order according to KB-34-1991)


BBK 74.3

ISBN 5-09-004049-4


Early diagnosis and correction of deviations in the psychomotor development of children are the main condition for their effective education and upbringing, preventing severe disability and social maladjustment.

The role of the family and the child’s emotional and positive communication with surrounding adults for his normal mental development is known. However, for children with developmental disabilities this is not enough: from a very early age they need special conditions that ensure the correction of impaired functions.

The data obtained by modern medicine indicate the effectiveness of early correctional and educational interventions. events. This is due to the fact that it is in the first years of life that a child’s brain develops most intensively.

In addition, at the early stages of development, children acquire motor, speech and behavioral stereotypes. If in a child with developmental disabilities they are initially formed and secured incorrectly, then it is extremely difficult to correct them later.

The upbringing of children with developmental disabilities is distinguished by its originality, which lies, firstly, in its correctional orientation, and secondly, in the inextricable connection of correctional measures with the formation of practical skills and abilities. Specific features of raising such children depend on the type of abnormal development, the degree and nature of violations of various functions, as well as the compensatory and age-related capabilities of the child.

Many children with developmental disabilities, in addition to proper upbringing, training and correction of impaired functions, also require special treatment. All this necessitates early diagnosis of various abnormalities in psychomotor development.

When diagnosing abnormal development, it is not enough to just state intellectual, speech, motor or sensory impairment; it is necessary to make a clinical diagnosis that would reflect the cause and mechanism of the developmental disorder, determine the school and social prognosis, and also outline the ways and methods of treatment and correctional work. Therefore, specialists


Medical-psychological-pedagogical consultations and employees of preschool institutions must be well versed in the issues of diagnosing various forms of abnormal development, have an understanding of modern methods of their treatment and psychological-pedagogical correction.

The book brought to the attention of readers is the result of a generalization of the author’s many years of experience working with children with developmental disabilities, as well as a critical analysis of domestic and foreign literature. This made it possible to describe not only forms of abnormal development, but also diseases of the central nervous system (CNS), in which complex defects and deviations in psychomotor development occur.

The purpose of this book is to show employees of special and general preschool institutions, as well as parents, the structure and nature of developmental deviations in children, age-related patterns in the formation of their psyche, techniques and methods for correcting impaired functions.


TYPES AND CAUSES OF DEVELOPMENTAL DEVIATIONS IN CHILDREN

TYPES OF DEVELOPMENTAL DISORDERS

Psychomotor development is a complex dialectical process, which is characterized by a certain sequence and uneven maturation of individual functions, and their qualitative transformation at a new age stage. Moreover, each subsequent stage of development is inextricably linked with the previous one.

Psychomotor development is based on a genetic program, which is implemented under the influence of various environmental factors. Therefore, if a child is developmentally delayed, it is first necessary to take into account the role of hereditary factors in this delay.

Various adverse effects in the prenatal period, during childbirth (birth trauma, asphyxia), and also after birth can lead to disturbances in the psychomotor development of the child.

For successful therapeutic, correctional and pedagogical work with children with developmental disabilities, knowledge of the causes and nature of developmental disorders is important.

It is well known that children suffering from the same disease have different developmental delays. This is due to the genotypic characteristics of their central nervous system, various environmental influences, as well as how timely the correct diagnosis was made and treatment, correctional and pedagogical work was started.

Under reason developmental deviations understand the impact on the body of an external or internal unfavorable factor, which determines the specifics defeats or developmental disorders psychomotor functions.

It is known that almost any more or less long-term adverse effect on the developing brain of a child can lead to deviations in psychomotor development. Their manifestations will vary depending on the time of the adverse impact, i.e. on what stage of brain development it took place, its duration, on the hereditary structure of the body and, above all, the central nervous system, as well as on the social conditions in which a child is being raised. All these factors together determine leading defect, which manifests itself in the form of insufficiency of intelligence, speech, vision, hearing, motor skills, disorders of the emotional-volitional sphere, and behavior. In some cases there may be several violations, then they talk about complicated or complex defect.


A complex defect is characterized by a combination of two or more disorders that equally determine the structure of abnormal development and difficulties in teaching and raising a child. For example, a complex defect occurs in a child with simultaneous damage to vision and hearing, or hearing and motor skills, etc.

With a complicated defect, it is possible to identify the leading, or main, disorder and the disorders complicating it. For example, a child with mental retardation may have mild defects in vision, hearing, musculoskeletal system, emotional and behavioral disorders.

Both the leading and the complicating defect can have the character of both damage, damage so and underdevelopment. A combination of these is often observed.

A peculiarity of the children's brain is that even its slight damage does not remain partial, local, as is the case in adult patients, but negatively affects the entire process of maturation of the central nervous system. Therefore, a child with speech, hearing, vision, or musculoskeletal disorders, in the absence of early corrective measures, will lag behind in mental development.

The developmental disorders described above are primary. However, along with the primary ones, there are often so-called secondary violations, the structure of which depends on the nature of the leading defect. Thus, mental retardation in children with general systemic underdevelopment of speech will primarily manifest itself in weakness of verbal memory and thinking, and in children with cerebral palsy - in insufficiency of spatial concepts and constructive activity.

In children with hearing impairments, the development of understanding of spoken speech is disrupted, and it is difficult to form an active vocabulary and coherent speech. With visual defects, the child experiences difficulty correlating a word with the designated object; he can repeat many words without sufficiently understanding their meaning, which delays the development of the semantic side of speech and thinking.

Secondary developmental disorders primarily affect those mental functions that develop most intensively in early and preschool age. These include speech, fine differentiated motor skills, spatial concepts, and voluntary regulation of activity.

A major role in the occurrence of secondary developmental deviations is played by the insufficiency or absence of early therapeutic, correctional and pedagogical measures, and especially mental deprivation." For example, an immobilized child with childhood

Mental deprivation- a mental state that arises in conditions when the subject does not have the opportunity to satisfy his basic mental needs in sufficient measure and for a sufficiently long time. (See: Langmeyer I., Matejcek 3. Mental deprivation in childhood - Prague, 1984.)


A person with cerebral palsy who has no experience communicating with peers is characterized by personal and emotional-volitional immaturity, immaturity, and increased dependence on others.

Undiagnosed developmental deviations, for example, mild visual and hearing defects, primarily delay the rate of mental development of the child, and can also contribute to the formation of secondary emotional and personality deviations in children. Being in mass preschool institutions, without a differentiated approach to themselves and without receiving therapeutic and correctional assistance, these children can remain in a situation of failure for a long time. Under such conditions, they often develop low self-esteem and a low level of aspirations; they begin to avoid communication with peers, and gradually secondary disorders increasingly aggravate their social maladjustment.

Thus, early diagnosis, medical and psychological-pedagogical correction make it possible to achieve significant success in shaping the personality of children with developmental disabilities.

CAUSES OF DEVELOPMENTAL DEVELOPMENT

The occurrence of developmental anomalies is associated with the action of both a variety of unfavorable environmental factors and various hereditary influences.

Recently, data have been obtained on new hereditary forms of mental retardation, deafness, blindness, complex defects, pathology of the emotional-volitional sphere and behavior, including early childhood autism (ECA).

Modern advances in clinical, molecular, biochemical genetics and cytogenetics have made it possible to clarify the mechanism hereditary pathology. Through special structures of the parents' germ cells - chromosomes - information about signs of developmental anomalies is transmitted. Chromosomes contain functional units of heredity, which are called genes.

In case of chromosomal diseases, special cytological studies are used to detect changes in the number or structure of chromosomes, which causes a gene imbalance. According to the latest data, per 1000 newborns there are 5-7 children with chromosomal abnormalities. Chromosomal diseases, as a rule, are characterized by a complex or complicated defect. Moreover, in half of the cases there is mental retardation, which is often combined with defects in vision, hearing, musculoskeletal system, and speech. One of these chromosomal diseases, primarily affecting the intellectual sphere and often combined with sensory defects, is Down syndrome.

Developmental anomalies can be observed not only with chromosomal, but also with so-called gene diseases, when the number


and chromosome structure remain unchanged. A gene is a microsection (locus) of a chromosome that controls the development of a specific hereditary trait. Genes are stable, but their stability is not absolute. Under the influence of various unfavorable environmental factors, their mutation occurs. In these cases, the mutant gene programs the development of the altered trait.

If mutations occur in a single microregion of a chromosome, then they speak of monogenic forms of abnormal development; if there are changes in several chromosomal loci - o polygenic forms of abnormal development. In the latter case, developmental pathology is usually the result of a complex interaction of both genetic and external environmental factors.

Due to the wide variety of hereditary diseases of the central nervous system that cause developmental abnormalities, their differential diagnosis is very difficult. At the same time, it should be noted that the correct early diagnosis of the disease is of paramount importance for carrying out timely therapeutic and corrective measures, assessing the development prognosis, as well as for preventing the rebirth of children with developmental disabilities in a given family.

Along with hereditary pathology, disorders of psychomotor development can arise as a result of exposure to various unfavorable environmental factors on the developing brain of a child. These are infections, intoxications, injuries, etc.

Depending on the time of exposure to these factors, there are intrauterine, or prenatal, pathology(exposure during fetal development); natal pathology(damage during childbirth) and postnatal(adverse effects after birth).

It has now been established that intrauterine pathology is often accompanied by damage to the child’s nervous system during childbirth. This combination in modern medical literature is referred to as perinatal encephalopathy. The cause of perinatal encephalopathy, as a rule, is intrauterine hypoxia 1 in combination with asphyxia 2 and birth trauma.

The occurrence of intracranial birth trauma and asphyxia is facilitated by various disorders of intrauterine development of the fetus, reducing its protective and adaptive mechanisms. Birth trauma leads to intracranial hemorrhages and the death of nerve cells at the sites of their origin. In premature babies, intracranial hemorrhages often occur due to the weakness of their vascular walls.

The most severe developmental disorders occur when clinical death newborns, which occurs when a combination

1 Hypoxia - oxygen deficiency of the body.

2 Asphyxia- oxygen starvation of the fetus during childbirth.


research of intrauterine pathology with severe asphyxia during childbirth. A certain relationship has been established between the duration of clinical death and the severity of damage to the central nervous system. With clinical death lasting more than 7-10 minutes, irreversible changes in the central nervous system often occur with further manifestations of cerebral palsy, speech disorders, and mental development disorders.

Let us recall that severe birth injuries, hypoxia and asphyxia during childbirth can be either the sole cause of abnormal development or a factor combined with intrauterine underdevelopment of the child’s brain.

Among the reasons causing deviations in the psychomotor development of a child, a certain role may play immunological incompatibility between mother and fetus based on Rh factor and blood antigens.

Rhesus or group antibodies, penetrating the placental barrier, cause the breakdown of fetal red blood cells. As a result of this breakdown, a special substance that is toxic to the central nervous system is released from red blood cells - indirect bilirubin. Under the influence of indirect bilirubin, the subcortical parts of the brain and auditory nuclei are primarily affected, which leads to hearing, speech, emotional and behavioral disorders. There is a so-called bilirubin encephalopathy.

With predominantly intrauterine brain lesions, the most severe developmental abnormalities occur, including mental retardation, speech underdevelopment, visual, hearing, and musculoskeletal defects. These complex defects can be combined with malformations of internal organs, which are often observed in various infectious, especially viral, diseases of a pregnant woman. The most severe damage to the fetus occurs when the mother becomes ill in the first trimester of pregnancy.

The frequency of fetal damage in various viral diseases of the expectant mother is not the same. The most unfavorable in this regard are rubella, mumps, and measles. Damage to the fetus can also occur when a pregnant woman becomes ill with infectious hepatitis, chicken pox, influenza, etc.

Women who have had rubella during pregnancy, especially during the period of embryogenesis, i.e. from 4 weeks to 4 months, have a high incidence of giving birth to children with malformations of the brain, defects of the organs of hearing, vision, and also the cardiovascular system, in other words In the babies of these women, the so-called rubeolar embryopathy.

Intrauterine pathology occurs when a pregnant woman has hidden (latent) chronic infections, especially such as toxoplasmosis, cytomegaly, syphilis, etc. Damage to the fetal brain with these infections often leads to mental retardation, combined with visual impairment, musculoskeletal disorders, epileptic seizures, etc.


Intrauterine intoxication and metabolic disorders in a pregnant woman also have an adverse effect on the development of the fetal brain.

Intrauterine intoxication can occur when the mother uses medications during pregnancy. It has been proven that most drugs pass through the placental barrier and enter the fetal circulatory system. Such drugs include antipsychotics, hypnotics and sedatives, many antibiotics, salicylates and, in particular, aspirin, analgesics, including drugs used for headaches, and many others. Various hormonal drugs and even large doses of vitamins and calcium can have an adverse effect on the development of the fetal brain. The toxic effect of all these drugs is especially pronounced in the early stages of pregnancy.

A particularly adverse effect on the developing fetus is the use of alcohol, drugs, and smoking by the mother during pregnancy.

Special studies in recent years have shown a connection between the duration of pregnancy and the nature of the influence of alcohol on the offspring. Alcohol consumption by the expectant mother in the first trimester of pregnancy, especially in the first weeks after conception, usually causes the death of embryonic cells, which leads to gross malformations of the fetal nervous system. Alcoholization of the fetus in later stages of pregnancy causes structural changes in its nervous and skeletal systems, as well as in various internal organs. Such systemic manifestations of fetal alcohol damage in the prenatal period are called fetal alcohol syndrome. In fetal alcohol syndrome, severe disturbances in psychomotor development, including mental retardation, are usually combined with multiple developmental defects: defects in the structure of the skull, face, eyes, ears, skeletal abnormalities, congenital heart defects and severe dysfunction of the central nervous system.

It has been established that chronic alcoholism of the mother, as a rule, is combined with systematic smoking, more frequent use of drugs and medications with narcotic effects. In these cases, the child has pronounced developmental deviations, combined with behavioral disorders and often convulsive seizures. In addition, many of these children are characterized by severe physical weakness and low vitality.

Various metabolic disorders in a pregnant woman, most often occurring during late toxicosis of pregnancy, especially with nephropathy, have an adverse effect on the development of the fetal brain.

Diseases such as diabetes mellitus and hormonal imbalance also have a negative impact on fetal development.

sufficiency, various hereditary metabolic diseases, such as phenylketonuria.

The cause of disruption of fetal development can be various physical factors, primarily ionizing radiation, as well as the action of high-frequency currents, ultrasound, etc. In addition to the direct damaging effect on the fetal brain, these factors have a mutagenic effect, i.e. they damage the germ cells of the parents and lead to genetic diseases.

Psychomotor development disorders also occur under the influence of various unfavorable factors after birth. In these cases it is noted postnatal abnormalities in development, having an organic or functional nature.

Causes of an organic nature include primarily various neuroinfections - encephalitis, meningitis, meningoencephalitis, as well as secondary inflammatory diseases of the brain that arise as complications of various infectious childhood diseases (measles, scarlet fever, chicken pox, etc.). In inflammatory diseases of the brain, the death of nerve cells often occurs, followed by their replacement with scar tissue. In addition, under these conditions, hydrocephalus may develop with increased intracranial pressure (hydrocephalic-hypertensive syndrome). Both of these factors - the death of nerve cells and the development of hydrocephalus - contribute to the atrophy of parts of the brain, which leads to various deviations in psychomotor development, which manifest themselves in the form of motor and speech disorders, memory impairment, attention, mental performance, emotional sphere and behavior. In addition, headaches and seizures are sometimes observed.

Traumatic brain injuries can also cause organic damage to the central nervous system. The nature of the consequences of a traumatic brain injury depends on its type, extent and location of brain damage. However, it should be borne in mind that when the immature brain is damaged, there is no direct correlation between the localization and severity of the lesion, on the one hand, and long-term consequences in terms of disturbances in psychomotor development, on the other. Therefore, when assessing the role of exogenous-organic factors in the occurrence of deviations in psychomotor development, it is necessary to take into account the time, nature and location of damage, as well as the plasticity features of the child’s nervous system, its hereditary structure, and the degree of formation of neuropsychic functions at the time of brain damage.

Psychomotor development disorders are observed in children with severe and long-term somatic diseases. It is known that many somatic diseases in newborns and infants can cause damage to the nervous system as a result of metabolic disorders and the accumulation of toxic products that adversely affect developing nerve cells. Damage to the nervous system due to somatic diseases often occurs in premature and hypotrophic infants.

children, as well as in cases of intrauterine hypoxia and asphyxia during childbirth.

Thus, delayed psychomotor development of varying degrees of severity can be observed in children with impaired intestinal absorption (malabsorption). Neuropsychic abnormalities appear in them already from the first months of life: they are characterized by increased nervous excitability, sleep disturbances, and delayed formation of positive emotional reactions and communication with adults. Subsequently, these children lag behind in mental and speech development; all integrative functions, in particular hand-eye coordination, are formed with a delay.

Functional reasons causing deviations in psychomotor development include socio-pedagogical neglect, emotional deprivation (lack of emotionally positive contact with adults), mainly in the first years of life. It is known that unfavorable upbringing conditions, especially in infancy and early childhood, slow down the development of children's communicative and cognitive activity. The outstanding Russian psychologist L. S. Vygotsky repeatedly emphasized; that the process of formation of a child’s psyche is determined by the social situation of development.

Psychomotor development disorders have different dynamics. Along with persistent developmental deviations caused by organic brain damage, there are many so-called reversible variants that occur with mild brain dysfunction, somatic weakness, pedagogical neglect, and emotional deprivation. These deviations can be completely overcome provided that the necessary treatment and correction measures are carried out in a timely manner.

Among such reversible forms of disorders in the first years of life, delays in the development of motor skills and speech are most often observed.

The importance of medical diagnosis of such functional disorders should be noted. Only a comprehensive evolutionary analysis of the development of a child in general and his neurological disorders in particular is the basis for a correct diagnosis and prognosis.

Practice shows that many parents, if their children have speech and motor disorders, attach primary importance to drug treatment, clearly underestimating the importance of correctional work.

It has now been established that there are many variants of functional, partial (partial) deviations, manifested primarily in delayed development of speech or motor skills, which are caused by the characteristics of brain maturation. The approach to treating and overcoming these deviations is highly individual, and not all children are indicated for intensive stimulating treatment.

The vast majority of motor dysfunctions are associated with damage to the central nervous system, i.e. certain parts of the brain and spinal cord, as well as peripheral nerves. Movement disorders are often caused by organic damage to the nerve pathways and centers that carry out motor acts. There are also so-called functional motor disorders, for example, with neuroses (hysterical paralysis). Less commonly, movement disorders are caused by developmental anomalies of the musculoskeletal organs (deformities), as well as anatomical damage to bones and joints (fractures, dislocations). In some cases, motor failure is based on a disease of the muscular system, for example, in certain muscle diseases (myopathy, etc.). A number of parts of the nervous system take part in the reproduction of a motor act, sending impulses to the mechanisms that directly perform the movement, i.e. to the muscles.

The leading link of the motor system is the motor analyzer in the frontal lobe cortex. This analyzer is connected through special pathways to the underlying parts of the brain - subcortical formations, midbrain, cerebellum, the inclusion of which imparts the necessary smoothness, accuracy, plasticity to the movement, as well as to the spinal cord. The motor analyzer closely interacts with afferent systems, i.e. with systems that conduct sensitivity. Along these pathways, impulses from proprioceptors enter the cortex, i.e. sensitive mechanisms located in motor systems - joints, ligaments, muscles. The visual and auditory analyzers have a controlling influence on the reproduction of motor acts, especially during complex labor processes.

Movements are divided into voluntary, the formation of which in humans and animals is associated with the participation of the motor parts of the cortex, and involuntary, which are based on automatisms of the stem formations and the spinal cord.

The most common form of motor disorders in both adults and children are paralysis and paresis. Paralysis refers to the complete absence of movement in the corresponding organ, in particular in the arms or legs (Fig. 58). Paresis includes disorders in which motor function is only weakened, but not completely disabled.

The causes of paralysis are infectious, traumatic or metabolic (sclerosis) lesions that directly cause disruption of nerve pathways and centers or upset the vascular system, as a result of which the normal supply of blood to these areas ceases, for example, during strokes.

Paralysis varies depending on the location of the lesion - central and peripheral. There are also paralysis of individual nerves (radial, ulnar, sciatic, etc.).

It matters which motor neuron is affected - central or peripheral. Depending on this, the clinical picture of paralysis has a number of features, taking into account which a specialist doctor can determine the location of the lesion. Central paralysis is characterized by increased muscle tone (hypertension), increased tendon and periosteal reflexes (hyperreflexia), and often the presence of pathological reflexes of Babinsky (Fig. 59), Rossolimo, etc. There is no loss of muscle mass in the arms or legs, and even a paralyzed limb may be somewhat swollen due to circulatory disorders and inactivity. On the contrary, with peripheral paralysis there is a decrease or absence of tendon reflexes (hypo- or areflexia), a drop in muscle tone

(atony or hypotension), sudden muscle loss (atrophy). The most typical form of paralysis that affects the peripheral neuron is cases of infantile paralysis - polio. One should not think that all spinal lesions are characterized only by flaccid paralysis. If there is an isolated lesion of the central neuron, in particular the pyramidal tract, which, as is known, starting in the cortex, passes through the spinal cord, then the paralysis will have all the signs of a central one. These symptoms, expressed in a milder form, are designated as “paresis”. The word "paralysis" in medical terminology is defined as "plegia". In this regard, they distinguish: monoplegia (monoparesis) when one limb is affected (arms or legs); paraplegia (paraparesis) with damage to both limbs; hemiplegia (hemiparesis) when one half of the body is affected (the arm and leg on one side are affected); tetraplegia (tetraparesis), in which damage to both arms and legs is detected.

Paralysis resulting from organic damage to the central nervous system is not completely restored, but may be weakened under the influence of treatment. Traces of damage can be detected at different ages in varying degrees of severity.

The so-called functional paralysis or paresis is not based on structural disorders of the nervous tissue, but develops as a result of the formation of stagnant foci of inhibition in the area of ​​the motor zone. More often they are caused by acute reactive neuroses, especially hysteria. In most cases they have a good outcome.

In addition to paralysis, movement disorders can be expressed in other forms. So, for example, violent, inappropriate, unnecessary movements may occur, which are combined under the general name of hyperkinesis. To them

These include forms such as convulsions, i.e. involuntary muscle contractions. There are clonic convulsions, in which muscle contractions and relaxations that quickly follow each other are observed, acquiring a peculiar rhythm. Tonic spasms are characterized by prolonged contraction of muscle groups. Sometimes there are periodic twitchings of individual small muscles. This is the so-called myoclonus. Hyperkinesis can manifest itself in the form of peculiar violent movements, most often in the fingers and toes, reminiscent of the movements of a worm. Such peculiar manifestations of seizures are called athetosis. Tremors are violent rhythmic vibrations of muscles that acquire the character of trembling. Tremors may occur in the head, arms or legs, or even the entire body. In school practice, hand tremors are reflected in students’ writing, which takes on an irregular character in the form of rhythmic zigzags. Tics - they usually mean stereotypically repeated twitching in certain muscles. If a tic is observed in the facial muscles, then peculiar grimaces appear. There are tics of the head, eyelids, cheeks, etc. Some types of hyperkinesis are more often associated with damage to the subcortical nodes (striatum) and are observed with chorea or in the residual stage of encephalitis. Certain forms of violent movements (tics, tremors) may be functional in nature and accompany neuroses.

Movement disorders are expressed not only in a violation of their strength and volume, but also in a violation of their accuracy, proportionality, and harmony. All these qualities determine the coordination of movements. Correct coordination of movements depends on the interaction of a number of systems - the posterior columns of the spinal cord, brainstem, vestibular apparatus, and cerebellum. Loss of coordination is called ataxia. In the clinic, various forms of ataxia are distinguished. Ataxia is expressed in the disproportion of movements, their inaccuracy, as a result of which complex motor acts cannot be performed correctly. One of the functions that arises as a result of the coordinated actions of a number of systems is walking (gait pattern). Depending on which systems are particularly disturbed, the nature of the gait changes dramatically. When the pyramidal tract is damaged due to hemiplegia or hemiparesis, a hemiplegic gait develops: the patient pulls up the paralyzed leg, the entire paralyzed side

When moving, the body seems to lag behind the healthy one. Ataxic gait is more often observed with damage to the spinal cord (posterior columns), when the pathways carrying deep sensitivity are affected. Such a patient walks, spreading his legs wide to the sides, and hits the floor with his heel, as if placing his foot in a big way. This is observed with tabes dorsalis and polyneuritis. Cerebellar gait is characterized by particular instability: the patient walks, balancing from side to side, which creates a resemblance to the walking of a very intoxicated person (drunk gait). In some forms of neuromuscular atrophy, for example, in Charcot-Marie disease, the gait takes on a peculiar type: the patient seems to be performing, raising his legs high (“the gait of a circus horse”).

Features of motor disorders in abnormal children. Children who have lost hearing or vision (blind, deaf), as well as those suffering from underdevelopment of intelligence (oligophrenic), in most cases are characterized by the originality of the motor sphere. Thus, pedagogical practice has long noted that the majority of deaf children have a general lack of coordination of movements: when walking, they shuffle their soles, their movements are impetuous and abrupt, and there is uncertainty. A number of authors in the past (Kreidel, Bruck, Betzold) conducted various experiments aimed at studying both the dynamics and statics of deaf-mutes. They checked the gait of deaf-mutes on a plane and when climbing, the presence of dizziness when rotating, the ability to jump on one leg with eyes closed and open, etc. Their opinions were quite contradictory, but all authors noted the motor retardation of deaf children compared to hearing schoolchildren.

Prof. F.F. Zasedatelev conducted the following experiment. He forced normal schoolchildren and deaf-mutes to stand on one leg. It turned out that hearing schoolchildren could stand on one leg with their eyes open and closed for up to 30 seconds; deaf children of the same age could stand in this position for no more than 24 seconds, and with their eyes closed the time sharply decreased to 10 seconds.

Thus, it has been established that deaf people in the motor sphere lag behind hearing people both in dynamics and statics. Some attributed the unstable balance of deaf people to insufficiency of the vestibular apparatus of the inner ear, while others attributed it to disorders of the cortical centers and cerebellum. Some observations made by O.D. Kudryasheva, S.S. Lyapidevsky, showed that, with the exception of a small

The groups are deaf with obvious damage to the motor sphere; in most of them, motor impairment is transient. After systematically conducted physical education and rhythm classes, the movements of the deaf acquire quite satisfactory stability, speed and smoothness. Thus, the motor retardation of the deaf is often functional in nature and can be overcome with appropriate exercises. A powerful stimulus in the development of the motor sphere of the deaf is physical therapy, dosed occupational therapy, and sports.

Similar things can be said about blind children. It is quite natural that the lack of vision reduces the range of motor capabilities, especially in a wide space. Many are blind, writes Prof. F. Tsekh, indecisive and timid in their movements. They stretch their arms forward to avoid bumping into them, drag their feet, feeling the ground, and walk bent over. Their movements are angular and awkward, there is no flexibility in them when bending, during a conversation they do not know where to put their hands, they grab onto tables and chairs. However, the same author points out that as a result of proper education, a number of deficiencies in the motor sphere of the blind can be eliminated.

Studies of the motor sphere of the blind, which we conducted at the Moscow Institute of the Blind in 1933 - 1937, showed that severe motor failure occurs only in the first years of education, with the exception of a small group of children who suffered severe brain diseases (meningoencephalitis, consequences of a removed cerebellar tumor and etc.). Subsequently, special classes in physical education perfectly developed the motor skills of the blind. Blind children could play football, volleyball1, jump over obstacles, and perform complex gymnastic exercises. The sports Olympiads for blind children organized every year (Moscow school) once again confirm what success can be achieved with children deprived of vision using special pedagogy. However, this is not easy and involves a lot of work for both the blind child and the teacher. Development of compensatory adaptations based on the plasticity of the nervous system

1 With blind children, games of football and volleyball are played with a sounding ball.

This also applies to the motor sphere, which is noticeably improved under the influence of special corrective measures. The time of onset of blindness and the conditions in which the blind person was located are of great importance. It is known that people who lose their vision at a late age do not compensate well for their motor function. Those who are early blind, as a result of appropriate training from a young age, better control their movements, and some can freely navigate a wide space. However, here too the conditions of upbringing matter. If an early-blind child, while in a family, was under the constant supervision of his mother, grew up pampered, did not encounter difficulties, and did not practice orientation in a wide space, then his motor skills will also be limited. It is in this group of children that the above-mentioned fear of wide space is observed, sometimes acquiring the character of a special fear (phobia). A study of the anamnesis of such children shows that their early development took place in conditions of constant “holding their mother’s hand.”

We find more severe changes in the motor-motor sphere in children with intellectual disabilities (oligophrenics). This is determined primarily by the fact that dementia is always the result of underdevelopment of the brain in the prenatal period due to certain diseases or its damage during childbirth or after birth. Thus, the mental disability of a child arises on the basis of structural changes in the cerebral cortex caused by a previous neuroinfection (meningoencephalitis) or under the influence of traumatic brain injuries. Naturally, inflammatory, toxic or traumatic lesions of the cortex are often diffusely localized and also affect the motor areas of the brain to varying degrees. Profound forms of oligophrenia are often accompanied by severe motor dysfunction. In these cases, paralysis and paresis are observed, and more often spastic hemiparesis or various forms of hyperkinesis. In milder cases of oligophrenia, local motor disorders are rare, but there is a general insufficiency of the motor sphere, which is expressed in some retardation, clumsy, clumsy movements. The basis of such insufficiency, apparently, most likely lies in neurodynamic disorders - a kind of inertia of nervous processes. In these cases, it is possible to significantly correct motor retardation through special corrective measures (physical therapy, rhythm, manual labor).

A unique form of movement disorder is apraxia. In this case, there is no paralysis, but the patient cannot perform a complex motor act. The essence of such disorders is that such a patient loses the sequence of movements necessary to perform a complex motor act. So, for example, a child loses the ability to make the usual movements, adjust, fasten clothes, lace shoes, tie a knot, thread a needle, sew a button, etc. Such patients also fail to perform imaginary actions when ordered, for example, to show how they eat soup with a spoon, how they fix a pencil, how they drink water from a glass, etc. The pathophysiological mechanism of apraxia is very complex. Here there is a breakdown, due to the action of certain harmful agents, of motor stereotypes, i.e. harmonious systems of conditioned reflex connections. Apraxia most often occurs with damage to the supra-marginal or angular gyrus of the parietal lobe. Writing disorders in children (dysgraphia) are one of the types of apraxic disorders.

The role of the motor analyzer is extremely important in our nervous activity. It is not limited only to the regulation of voluntary or involuntary movements that are part of normal motor acts. The motor analyzer also takes part in such complex functions as hearing, vision, and touch. For example, full vision is impossible without movement of the eyeball. Speech and thinking are fundamentally based on movement, since the motor analyzer moves all speech reflexes formed in other analyzers* “The beginning of our thought,” wrote I.M. Sechenov, “is muscle movement.”

Treatment of movement disorders such as paralysis, paresis, and hyperkinesis was considered ineffective for a long time. Scientists relied on previously created ideas about the nature of the pathogenesis of these disorders, which are based on irreversible phenomena, such as the death of nerve cells in cortical centers, atrophy of nerve conductors, etc.

However, a more in-depth study of pathological mechanisms in violations of motor acts shows that previous ideas about the nature of motor defects were far from complete. Analysis of these mechanisms in the light of modern neurophysiology and clinical practice shows that a movement disorder is a complex complex, the components of which are not only local (usually irreversible defects), but also a number of functional changes caused by neurodynamic disorders, which enhance the clinical picture of the motor defect. These violations, as shown by studies by M.B. Eidinova and E.N. Pravdina-Vinarskaya (1959), with the systematic implementation of therapeutic and pedagogical measures (the use of special biochemical stimulants that activate the activity of synapses, as well as special exercises in physical therapy, in combination with a number of educational and pedagogical measures aimed at nurturing the child’s will, purposeful activity to overcome the defect) in a significant number of cases remove these pathological layers. This in turn leads to restoration or improvement of impaired motor function.

Visual disorders

Causes and forms of visual impairment. Severe visual impairments are not necessarily the result of primary damage to the nervous devices of vision - the retina, optic nerves and cortical visual centers. Visual disturbances can also occur as a result of diseases of the peripheral parts of the eye - the cornea, lens, light-refracting media, etc. In these cases, the transmission of light stimuli to the receptor nerve devices may stop completely (total blindness) or be limited (poor vision).

The causes of severe visual impairment are various infections - local and general, including neuroinfections, metabolic disorders, traumatic eye injuries, and abnormal development of the eyeball.

Among visual disorders, first of all, there are forms in which visual acuity suffers, up to complete blindness. Visual acuity can be impaired if the eye apparatus itself is damaged: the cornea, lens, retina.

The retina is the inner layer of the eyeball, lining the fundus of the eye. In the central part of the fundus

There is an optic disc from which the optic nerve originates. A special feature of the optic nerve is its structure. It consists of two parts that carry irritation from the outer and inner parts of the retina. First, the optic nerve departs from the eyeball as a single unit, enters the cranial cavity and runs along the base of the brain, then the fibers carrying irritation from the outer parts of the retina (central vision) go posteriorly along their side, and the fibers carrying irritation from the inner parts of the retina (lateral vision), completely crossed. After the decussation, the right and left visual tracts are formed, which contain fibers from both their side and the opposite side. Both visual tracts are directed to the geniculate bodies (subcortical visual centers), from which the Graziole bundle begins, carrying irritation to the cortical fields of the occipital lobe of the brain.

When the optic nerve is damaged, blindness in one eye occurs - amaurosis. Damage to the optic chiasm is manifested by a narrowing of the visual fields. When the function of the optic tract is impaired, half of the vision occurs (hemianopia). Visual disorders with damage to the cerebral cortex in the occipital region are manifested by partial loss of vision (scotoma) or visual agnosia (the patient does not recognize familiar objects). A common case of this disorder is alexia (reading disorder), when a child loses the signal meaning of letter images in memory. Visual disorders also include loss of color perception: the patient cannot distinguish some colors or sees everything in gray.

In special pedagogical practice, there are two groups of children who require education in special schools - the blind and the visually impaired.

Blind children. Typically, people with vision loss such that there is no light perception are considered blind, which is rare. More often, these people have poor light perception, distinguish between light and dark, and, finally, some of them have insignificant remnants of vision. Usually the upper limit of such minimal vision is considered to be 0.03-0.04!. These remnants of vision can somewhat make it easier for a blind person to navigate in the external environment, but have no practical significance in training.

Normal vision is taken as one.

Study and work, which therefore have to be carried out on the basis of tactile and auditory analyzers.

From the neuropsychological perspective, blind children have all the qualities that are characteristic of a sighted child of the same age. However, the lack of vision causes a blind person to have a number of special properties in his nervous activity, aimed at adapting to the external environment, which will be discussed below.

Blind children are educated in special schools; training is carried out mainly on the basis of skin and auditory analyzers by specialist typhlopedagogues.

Visually impaired children. This group includes children who have retained some vestiges of vision. Typically, children are considered visually impaired if their visual acuity after correction with glasses ranges from 0.04 to 0.2 (according to the accepted scale). Such residual vision, in the presence of special conditions (special lighting, use of a magnifying glass, etc.), allows them to be taught on a visual basis in classes and schools for the visually impaired.

Features of nervous activity. Severe visual disturbances always cause changes in general nervous activity. What matters is the age at which vision loss occurred (congenital or acquired blindness), and the location of the lesion in the area of ​​the visual analyzer (peripheral or central blindness). Finally, the nature of the disease processes that caused severe visual impairment should be taken into account. In this case, it is especially important to distinguish those forms that are caused by previous brain lesions (meningitis, encephalitis, brain tumors, etc.). Based on the above, changes in nervous activity will differ in some originality. Thus, in cases of blindness caused by causes not related to brain lesions, nervous activity in the process of growth and development will be accompanied by the formation of compensatory adaptations that make it easier for such a person to participate in socially useful work. In cases of blindness resulting from a previous brain disease, the described path of development of compensatory adaptations may be complicated by the influence of other consequences that could occur after brain damage. We are talking about possible disorders in the area of ​​other analyzers (except for vision), as well as intelligence and the emotional-volitional sphere.

In these cases, there may be difficulties in learning, and subsequently limited ability to work. Finally, one should also keep in mind the influence of the temporary factor on the nature of nervous activity. Observations show that in people born blind or who have lost their vision at an early age, its absence most often does not cause severe mental changes. Such people have never used vision, and it is easier for them to tolerate its absence. For those who have lost their vision at a later age (school age, adolescence, etc.), the loss of this important function is often accompanied by certain neuropsychic disorders in the form of acute asthenic conditions, severe depression, and severe hysterical reactions. Some blind children have special phobias - fear of large spaces. They can only walk by holding their mother's hand. If such a child is left alone, he experiences a painful state of uncertainty and is afraid to take a step forward.

Some uniqueness of nervous activity, in contrast to the blind, is observed in persons classified as visually impaired. As mentioned above, such children have remnants of vision, which allow them, under special conditions in a special class, to learn on a visual basis. However, their volume of visual afferentation is insufficient; some tend to experience progressive loss of vision. This circumstance makes it necessary to acquaint them with the method of teaching the blind. All this can cause a certain overload, especially in people belonging to a weak type of nervous system, which can result in overstrain and disruption of nervous activity. However, observations show that reactive changes in nervous activity in the blind and visually impaired are more often observed at the beginning of training. This is due to the significant difficulties that children generally experience at the beginning of education and adaptation to work. Gradually, as compensatory adaptations are developed and stereotypes are created, their behavior noticeably levels out and becomes balanced. All this is the result of the remarkable properties of our nervous system: plasticity, the ability to compensate to one degree or another for lost or weakened functions.

Let us briefly describe the main stages in the development of scientific thought on the issue of the development of compensatory adaptations in persons with severe visual impairments.

Loss of vision deprives a person of many advantages in the process of adapting to the external environment. However, vision loss is not a disorder that makes work completely impossible. Experience shows that blind people overcome primary helplessness and gradually develop in themselves a number of qualities that allow them to study, work and actively participate in socially useful work. What is the driving force that helps a blind person overcome his severe defect? This issue has been the subject of controversy for a long time. Various theories arose that tried in different ways to define the way for a blind person to adapt to the conditions of reality and master various forms of labor activity. Hence the view of the blind man has undergone changes. Some believed that the blind, with the exception of some restrictions in freedom of movement, possess all the qualities of a full-fledged psyche. Others attached great importance to the lack of visual function, which, in their opinion, has a negative impact on the psyche of the blind, even to the point of impaired intellectual activity. The mechanisms of adaptation of a blind person to the external environment were also explained in different ways. There was an opinion that the loss of one of the senses causes increased work of others, which, as it were, make up for the missing function. In this sense, the role of hearing and touch was emphasized, believing that in the blind, the activity of hearing and touch, with the help of which the blind person navigates the external environment and masters work skills, is compensatedly enhanced. Experimental studies were carried out in an attempt to prove that the blind have heightened (compared to sighted) skin sensitivity, especially in the fingers, and also have exceptionally developed hearing. Using these features, a blind person can compensate for the loss of vision. However, this position was disputed by the research of other scientists who did not find that hearing and skin sensitivity in the blind are better developed than in the sighted. In this sense, they completely rejected the accepted position that the blind have a highly developed ear for music. Some have come to the conclusion that the musical talent of the blind is no less or greater than that of the sighted. The problem of the psychology of the blind itself turned out to be controversial. Is there a special psychology for the blind? A number of scientists, including some typhlopedagogues, denied the existence of such a thing. Others, in particular Geller, believed that the psychology of the blind should be considered as one of the branches of general psychology. It was believed that the upbringing and education of a blind child, as well as his adaptation to socially useful activities, should be based on taking into account those features of his psychology that arise as a result of vision loss. Attempts to reveal the mechanisms of compensation ran into conflicting results from studies of hearing and touch in the blind. Some scientists found a special hyperesthesia (increased skin sensitivity) in the blind, others denied it. Similar conflicting results have been observed in the field of research into auditory nerve function in the blind. As a result of these contradictions, attempts arose to explain the compensatory capabilities of a blind person by mental processes. In these explanations, the issue of the enhanced work of the peripheral parts of the auditory and skin receptors, supposedly replacing the lost function of vision, the so-called vicariate of the senses, was no longer put forward in the first place, but the main role was given to the mental sphere. It was assumed that a blind person develops a special mental superstructure, which arises as a result of his contact with various influences of the external environment and is that special property that allows the blind person to overcome a number of difficulties on the path of life, i.e. first of all, to navigate the external environment, move without assistance, avoid obstacles, study the outside world, and acquire work skills. However, the very concept of the psychic superstructure, undoubtedly considered from an idealistic aspect, was quite vague. The material essence of the processes that took place in such cases was in no way explained by the hypothesis put forward about the role of the mental superstructure. Only much later, with the works of domestic scientists (E.A. Asratyan, P.K. Anokhin, A.R. Luria, M.I. Zemtsova, S.I. Zimkina, V.S. Sverlov, I.A. Sokolyansky), who based their research on teachings of I.P. Pavlov about higher nervous activity, significant progress has been made in solving this complex problem.

Neurophysiological mechanisms of compensatory processes in the blind. Psyche is the special property of our brain to reflect the external world, which exists outside of our consciousness. This reflection is carried out in the brain of people through their sense organs, with the help of which the energy of external stimulation is converted into a fact of consciousness. The physiological mechanisms of the function of reflecting the external world in our brain are conditioned reflexes, which ensure the highest balance of the body with constantly changing environmental conditions. In the cortex of a sighted person, conditioned reflex activity is caused by the receipt of stimuli from all analyzers. However, a sighted person does not use to a sufficient extent, and sometimes not at all, those analyzers that are not leading for him in this act. For example, when walking, a sighted person primarily focuses on vision; He uses hearing and especially touch to an insignificant extent. And only in special conditions, when a sighted person is blindfolded or when moving in the dark (at night), does he use hearing and touch - he begins to feel the soil with his soles and listen to surrounding sounds. But such positions are atypical for a sighted person. Hence, the enhanced formation of conditioned reflex connections from hearing and touch during certain motor acts, for example when walking, is not caused by a vital necessity in a sighted person. A powerful visual analyzer sufficiently controls the execution of the specified motor act. We note something completely different in the sensory experience of the blind. Being deprived of a visual analyzer, the blind, in the process of orientation in the external environment, rely on other analyzers, in particular hearing and touch. However, the use of hearing and touch, particularly when walking, is not auxiliary in nature, as in a sighted person. A peculiar system of nervous connections is actively formed here. This system in the blind is created as a result of long-term exercises of auditory and cutaneous afferentation caused by vital necessity. On this basis, a number of other specialized systems of conditional connections are formed, functioning under certain forms of adaptation to the external environment, in particular when mastering labor skills. This is the compensatory mechanism that allows a blind person to emerge from a state of helplessness and engage in socially useful work. It is controversial whether any specific changes occur in the auditory nerve or the sensory devices of the skin. As is known, studies of peri-

The pheric receptors - hearing and touch - have given conflicting results in the blind. Most researchers do not find local changes in the sense of increased auditory or cutaneous peripheral afferentation. Yes, this is no coincidence. The essence of the complex compensatory process in the blind is different. It is known that peripheral receptors produce only a very elementary analysis of incoming stimuli. Subtle analysis of stimulation occurs at the cortical ends of the analyzer, where higher analytical-synthetic processes are carried out and sensation turns into a fact of consciousness. Thus, by accumulating and training in the process of daily life experience numerous specialized conditioned connections from these analyzers, the blind person forms in his sensory experience those features of conditioned reflex activity that are not fully needed by a sighted person. Hence, the leading mechanism of adaptation is not the special sensitivity of the finger track or the cochlea of ​​the inner ear, but the higher department of the nervous system, i.e. the cortex and the conditioned reflex activity occurring on its basis.

These are the results of many years of debate about ways to compensate for blindness, which could find a correct resolution only in the aspect of modern brain physiology, created by I.P. Pavlov and his school.

Features of the pedagogical process when teaching blind and visually impaired children. The education and upbringing of blind and visually impaired children is a complex process that requires the teacher not only to have special knowledge of typhlopedagogy and typhlotechnics, but also to understand the psychophysiological characteristics that occur in persons who are completely or partially blind.

It was already said above that with the exclusion of such a powerful receptor as vision, which is part of the first signal system, from the sphere of perception, the cognitive activity of a blind person is carried out on the basis of the remaining analyzers. The leading ones in this case are tactile and auditory reception, supported by the increasing activity of some other analyzers. Thus, conditioned reflex activity acquires some unique features.

In pedagogical terms, the teacher faces a number of difficult tasks. In addition to purely educational (educational work,

Learning to read and write, etc.) problems of a very specific order arise, for example, the development of spatial concepts (orientation in the environment) in a blind child, without which the student turns out to be helpless. This also includes the development of motor skills, self-care skills, etc. All these points related to education are at the same time closely related to the educational process. For example, poor orientation in the environment, a kind of motor clumsiness and helplessness will dramatically affect the development of literacy skills, the development of which in the blind is sometimes associated with a number of specific difficulties. As for the features of teaching methods, in particular teaching literacy, the latter is carried out on the basis of touch and hearing.

The key point here is the use of skin reception. Technically, training is carried out using a special dotted font of the teacher L. Braille system, accepted throughout the world. The essence of the system is that each letter of the alphabet is represented by a different combination of the arrangement of six convex dots. A number of studies conducted in the past have shown that a dot is physiologically better perceived by the skin surface of the finger than a linear raised font. By running the soft surface of the tip of both index fingers along the lines of raised dotted type in a specially printed book, the blind person reads the text. In the physiological aspect, what happens here is roughly the same as when a sighted person reads, only instead of the eyes, the skin receptor acts.

Blind people write using special techniques that involve using a metal rod to press dotted letters onto paper placed in a special device. On the reverse side of the sheet, these indentations form a convex surface, which makes it possible for another blind person to read the written text. Tactile (skin) perception is also involved in other sections of the educational process, when it is necessary to acquaint a blind child with the shape of various objects, mechanisms, the body structure of animals, birds, etc. By feeling these objects with his hand, the blind person gets some impression of their external features. However, these ideas are far from accurate. Therefore, to help cutaneous reception in the educational process, an equally powerful receptor is involved - hearing, which makes it possible for the teacher to accompany tactile demonstration (feeling objects) with verbal explanations. The ability of the blind for abstract thinking and speech (which indicates good development of the second signaling system) helps, based on the teacher’s verbal signals, to make a number of adjustments when learning various objects and clarify their ideas about them. At subsequent stages of development in the cognitive activity of a blind person, the hearing and speech of others acquire special importance.

Further development of typhlopedagogy is impossible without taking into account the achievements that are taking place in technology. We are talking about the use, for example, of devices with which the blind are oriented in space, the creation of devices that allow the blind to use a book with a regular font, etc. Consequently, the current level of development of special pedagogy (especially when teaching the blind and deaf-mutes) requires a search for ways to use advances that are taking place in the field of radio engineering (radar), cybernetics, television, requires the use of semiconductors (transistor hearing aids), etc. In recent years, work has been underway to create devices that facilitate learning for people with visual and hearing impairments.

As for teaching visually impaired children, in these cases the pedagogical process is mainly based on the use of the remnants of vision available to the child. The specific task is to enhance visual gnosis. This is achieved by selecting appropriate glasses, using magnifying glasses, paying special attention to good classroom lighting, improving desks, etc.

To help visually impaired children, contact lenses, contact orthostatic magnifiers, and special machines for reading the usual type of graphic font have been created. The use of contact lenses has proven to be quite effective; they increase the performance of visually impaired schoolchildren and reduce fatigue. Taking into account that in some forms of low vision the progression of the disease process occurs, accompanied by a further decrease in vision, children receive the appropriate skills in mastering the dotted alphabet using the Braille system.

Features of the visual analyzer in deaf children. With the exception of rare cases when deafness is combined with blindness (deafblindness), the vision of most deaf people does not present any deviations from the norm. On the contrary, the observations of previous researchers, who based their decision on this issue on the idealistic theory of the vicariate of the senses, showed that the deaf have increased visual acuity due to lost hearing, and there were even attempts to explain this by a special hypertrophy of the optic nerve. At present, there is no reason to talk about the special anatomical qualities of the optic nerve of a deaf person. Visual adaptation of the deaf and mute is based on the same patterns that were mentioned above - this is the development of compensatory processes in the cerebral cortex, i.e. enhanced formation of specialized conditioned reflex connections, the existence of which in such a volume is not needed by a person with normal hearing and vision.

Features of the visual analyzer in mentally retarded children. Special pedagogical practice has noted for a relatively long time that mentally retarded children do not clearly enough perceive the features of those objects and phenomena that appear before their eyes. The poor handwriting of some of these children and the letters slipping off the lines of the notebook also created the impression of reduced visual function. Similar observations were made regarding auditory functions, which in most cases were considered weakened. In this regard, the opinion was created that the basis of mental retardation lies in the defective function of the sensory organs, which weakly perceive irritations from the outside world. It was believed that a mentally retarded child sees poorly, hears poorly, has poor touch, and this leads to decreased excitability and sluggish brain function. On this basis, special teaching methods were created, which were based on the tasks of selective development of the senses in special lessons (the so-called sensorimotor culture). However, this view of the nature of mental retardation is already a passed stage. Based on scientific observations, both psychological, pedagogical and medical, it is known that the basis of mental retardation is not selective defects of individual sensory organs, but underdevelopment of the central nervous system, in particular the cerebral cortex. Thus, against the background of an inferior structure, insufficient physiological activity develops, characterized by a decrease in higher processes - cortical analysis and synthesis, which is characteristic of the weak-minded. However, taking into account that oligophrenia occurs as a result of previous brain diseases (neuroinfections, traumatic brain injuries), isolated cases of damage to both the visual organ itself and the nerve pathways are possible. A special study of the visual organ in oligophrenic children conducted by L.I. Bryantseva, gave the following results:

A) in 54 out of 75 cases no deviations from the norm were found;

B) in 25 cases various refractive errors were found (the ability of the eye to refract light rays);

C) in 2 cases anomalies of a different nature.

Based on these studies, Bryantseva comes to the conclusion that the organ of vision of some students in auxiliary schools differs to some extent from the organ of vision of a normal schoolchild. A distinctive feature is a lower percentage of myopia compared to normal schoolchildren and a high percentage of astigmatism - one of the forms of refractive error1.

It should be added that in some mentally retarded children, as a result of meningoencephalitis, there are cases of progressive weakening of vision due to atrophy of the optic nerve. More often than in normal children, cases of congenital or acquired strabismus (strabismus) occur.

Sometimes, with deep forms of oligophrenia, underdevelopment of the eyeball, abnormal pupil structure, and running nystagmus (rhythmic twitching of the eyeball) are observed.

It should be noted that teachers of special schools are not attentive enough to the visual characteristics of their students and rarely refer them to ophthalmologists. Often, timely selection of glasses and special treatment dramatically improve a child’s vision and increase his performance at school.

1 Astigmatism is a lack of vision caused by improper refraction of rays due to the unequal curvature of the cornea of ​​the lens in different directions.

These include tremor, dystonia, athetotic tics and ballism, dyskinesia and myoclonus.

Classification of causes, symptoms, signs of movement disorders

Movement disorder Classification, causes, symptoms, signs
Tremor = rhythmic oscillating movements of a body part

Classification: resting tremor, intention tremor, essential tremor (usually postural and actional), orthostatic tremor Parkinsonism is characterized by resting tremor. Essential tremor often exists for many years before seeking medical attention and is usually bilateral; in addition, a positive family history is often noted. Intention and action tremor is often combined with damage to the cerebellum or efferent cerebellar pathways. Orthostatic tremor is expressed primarily by instability in a standing position and high-frequency trembling of the leg muscles.

Causes of increased physiological tremor (according to the standard of the German Society of Neurology): hyperthyroidism, hyperparathyroidism, renal failure, vitamin B2 deficiency, emotions, stress, exhaustion, cold, drug/alcohol withdrawal syndrome

Drug-induced tremor: neuroleptics, tetrabenazine, metoclopramide, antidepressants (mainly tricyclics), lithium drugs, sympathomimetics, theophylline, steroids, drugs against arrhythmia, valproic acid, thyroid hormones, cytostatics, immunosuppressive drugs, alcohol

Dystonia = long-lasting (or slow), stereotyped and involuntary muscle contraction, often with repeated twisting movements, unnatural postures and abnormal positions Classification: idiopathic dystonia in adults is usually focal dystonia (for example, blepharospasm, torticollis, dystonic writer's cramp, laryngeal dystonia), segmental, multifocal, generalized dystonia and hemidystonia are also distinguished. Rarely, primary dystonias (autosomal dominant dystonias, e.g. dopa-sensitive dystonia) or dystonias as part of an underlying degenerative disease (e.g. Hallerforden-Spatz syndrome) occur. Secondary dystonias have also been described, for example, in Wilson's disease and syphilitic encephalitis. Rarely: dystonic status with respiratory failure, muscle weakness, hyperthermia and myoglobinuria.

Tics = involuntary, sudden, brief and often repetitive or stereotyped movements. Tics can often be suppressed for a period of time. Often there is an obsessive desire to perform a movement followed by relief.
Classification: motor tics (clonic, dystonic, tonic, e.g., blinking, grimacing, head nodding, complex movements, e.g., grasping, adjusting clothing, copropraxia) and phonic (vocal) tics (e.g., coughing, coughing, or complex tics → coprolalia, echolalia). Juvenile (primary) tics often develop in association with Tourette's syndrome. Causes of secondary tics: encephalitis, trauma, Wilson's disease, Huntington's disease, drugs (SSRIs, lamotrigine, carbamazepine)

Choreiform movement disorders = involuntary, undirected, sudden and brief, sometimes complex movements Athetosis = slow choreiform movement, accentuated in the distal areas, sometimes worm-shaped, writhing)

Ballism/hemiballism=severe form with throwing motion, usually unilateral, affecting proximal limbs

Huntington's chorea is an autosomal dominant neurodegenerative disease that is typically accompanied by hyperkinetic and often choreiform movements (the lesion is in the striatum). Non-genetic causes of chorea: lupus erythematosus, chorea minor (Sydenham), chorea of ​​pregnancy, hyperthyroidism, vasculitis, drugs (eg, levodopa overdose), metabolic disorders (eg, Wilson's disease). The causes of hemiballismus/ballismus are typical lesions of the contralateral subthalamic nucleus, but other subcortical lesions should also be considered. Most often we are talking about ischemic foci. Rarer causes are metastases, arteriovenous malformations, abscesses, lupus erythematosus and drugs.
Dyskinesia = involuntary, continuous, repetitive, purposeless, often ritualized movements

Classification: simple dyskinesias (eg, tongue thrusting, chewing) and complex dyskinesias (eg, stroking movements, repetitive leg crossing, marching movements).

The term akathisia describes motor restlessness with complex stereotyped movements (“inability to sit still”), usually caused by antipsychotic therapy. Tardive dyskinesia (usually in the form of dyskinesia of the mouth, cheeks and tongue) occurs due to the use of antidopaminergic drugs (neuroleptics, antiemetics, for example, metoclopramide).

Myoclonus = sudden, involuntary, brief muscle jerks with a visible motor effect of varying degrees (from subtle muscle twitches to severe myoclonus affecting the muscles of the body and limbs)

Classification: Myoclonus can occur at the cortical, subcortical, reticular and spinal levels.

They can be focal segmental, multifocal or generalized.

  • Association with epilepsy (juvenile epilepsy with West syndrome, Lennox-Gastaut syndrome; progressive myoclonic epilepsy with Unferricht-Lundborg syndrome, Lafora body disease, MERRF syndrome)
  • Essential causes (sporadic, hereditary myoclonus usually with early onset) Metabolic disorders: hepatic encephalopathy, renal failure (dialysis encephalopathy due to chronic aluminum intoxication), diabetic ketoacidosis, hypoglycemia, electrolyte imbalance, pH crises
  • Intoxications: cocaine, LSD, marijuana, bismuth, organophosphates, heavy metals, drug overdose
  • Drugs: penicillin, cephalosporin, levodopa, MAO-B inhibitors, opiates, lithium, tricyclic antidepressants, etomidate
  • Storage diseases: lipofuscinosis, salidosis
  • Trauma/hypoxia: Lance-Adams syndrome (post-hypoxic myoclonus syndrome) after cardiac arrest, respiratory failure, traumatic brain injury
  • Paraneoplasia
  • Infections: encephalitis (typical of subacute sclerosing panencephalitis after measles infection), meningitis, myelitis, Creutzfeldt-Jakob disease
  • Neurodegenerative diseases: Huntington's chorea, Alzheimer's dementia, hereditary ataxias, parkinsonism

Diagnosis of movement disorders

Hyperkinetic movement disorder is initially diagnosed based on the clinical picture:

  • Rhythmic, such as tremor
  • Stereotypic (same repetitive movement), eg dystonia, tic
  • Irrhythmic and non-stereotypical, for example chorea, myoclonus.

Attention: drugs that were taken several months ago may also be responsible for the movement disorder!

Additionally, an MRI of the brain should be performed to differentiate between primary (eg, Huntington's disease, Wilson's disease) and secondary (eg, drug-induced) causes.

Routine laboratory tests should primarily include determination of electrolyte levels, liver and kidney function, and thyroid hormones.

In addition, it seems advisable to study the cerebrospinal fluid to exclude a (chronic) inflammatory process in the central nervous system.

In case of myoclonus, EEG, EMG and somatosensory evoked potentials are used to determine the topographic and etiological characteristics of the lesion.

Differential diagnosis of movement disorders

  • Psychogenic hyperkinesia: in principle, psychogenic movement disorders can imitate the entire spectrum of organic movement disorders listed in the table. Clinically, they appear as abnormal, involuntary and undirected movements, which are combined with disturbances in walking and speaking. Movement disorders usually begin acutely and progress rapidly. Movements, however, are most often heterogeneous and variable in severity or intensity (unlike organic movement disorders). It is not uncommon for multiple movement disorders to also appear. Patients can often be distracted and thus interrupted in their movements. Psychogenic movement disorders may increase if they are observed (“spectators”). Often, movement disorders are accompanied by “inorganic” paralysis, diffuse or anatomically difficult to classify sensitization disorders, as well as speech and walking disorders.
  • Myoclonus can also occur “physiologically” (=without an underlying disease causing it), such as sleep myoclonus, postsyncopal myoclonus, hiccups, or myoclonus after exercise.

Treatment of movement disorders

The basis of therapy is the elimination of provoking factors, such as stress for essential tremor or medications (dyskinesia). The following options are considered as options for specific treatment of various movement disorders:

  • For tremor (essential): beta-receptor blockers (propranolol), primidone, topiramate, gabapentin, benzodiazepine, botulinum toxin in case of insufficient effect of oral medications; in treatment-resistant cases with severe disability, deep brain stimulation is indicated.

Tremor in parkinsonism: initially, treatment of stupor and akinesis with dopaminergics, for persistent tremor, anticholinergics (caution: side effects, especially in elderly patients), propranolol, clozapine; for treatment-resistant tremor - deep brain stimulation if indicated

  • For dystonia, physiotherapy is generally also carried out, and orthoses are sometimes used
    • for focal dystonias: trial therapy with botulinum toxin (serotype A), anticholinergics
    • for generalized or segmental dystonia, first of all, drug therapy: anticholinergic drugs (trihexphenidyl, piperidene; attention: visual impairment, dry mouth, constipation, urinary retention, cognitive impairment, psychosyndrome), muscle relaxants: benzodiazepine, tizanidine, baclofen (in severe cases, sometimes intrathecal), tetrabenazine; in severe cases resistant to therapy, according to indications - deep brain stimulation (globus pallidus internus) or stereotactic surgery (thalamotomy, pallidotomy)
    • children often have dopa-sensitive dystonia (often also reacts to dopamine agonists and anticholinergics)
    • dystonic status: observation and treatment in the intensive care unit (sedation, anesthesia and mechanical ventilation if indicated, sometimes intrathecal baclofen)
  • For tics: explanation to the patient and relatives; drug therapy with risperidone, sulpiride, tiapiride, haloperidol (second choice due to unwanted side effects), aripiprazole, tetrabenazine or botulinum toxin for dystonic tics
  • For chorea: tetrabenazine, tiapride, clonazepam, atypical antipsychotics (olanzapine, clozapine) fluphenazine
  • For dyskinesias: cancel provoking drugs, trial therapy with tetramenazine, for dystonias - botulinum toxin
  • For myoclonus (usually difficult to treat): clonazepam (4-10 mg/day), levetiracetam (up to 3000 mg/day), piracetam (8-24 mg/day), valproic acid (up to 2400 mg/day)

Features of a child with musculoskeletal disorders.

With all the variety of congenital and early acquired diseases and injuries musculoskeletal system Most of these children have similar problems. The leading one in the clinical picture is a motor defect (delayed formation, underdevelopment, impairment or loss of motor functions).

Some children with this pathology do not have deviations in the development of cognitive activity and do not require special training and education. But all children with musculoskeletal disorders need special conditions for living, learning and subsequent work.

The majority of children with musculoskeletal disorders are children with cerebral palsy. CEREBRAL PALSY (CP) is a serious disease of the nervous system, which often leads to disability of the child.

Cerebral palsy occurs as a result of underdevelopment or damage to the brain in the early stages of development (during the prenatal period, at the time of birth and in the first year of life). Movement disorders in children with cerebral palsy are often combined with mental and speech disorders, and with dysfunction of other analyzers (vision, hearing). Therefore, these children need therapeutic, psychological, pedagogical and social assistance.

Causes of musculoskeletal disorders

1. Intrauterine pathology(at present, many researchers have proven that more than 400 factors can affect the central nervous system of the developing fetus, especially during the period up to 4 months of intrauterine development):

· infectious diseases of the mother: microbial, viral (in recent years, the prevalence of neuroinfections has increased, especially viral ones - such as influenza, herpes, chlamydia, etc.);

· consequences of acute and chronic somatic diseases of the mother (cardiovascular, endocrine disorders);

· severe toxicosis of pregnancy;

· incompatibility by Rh factor or blood groups;

· injuries, bruises of the fetus;

· intoxication;

· environmental hazards.

2. Birth trauma, asphyxia.

3. Pathological factors affecting the child’s body in the first year of life:

· neuroinfections (meningitis, encephalitis, etc.);

· injuries, bruises to the child’s head;

· complications after vaccinations.

The combination of intrauterine pathology with birth trauma is currently considered one of the most common causes of cerebral palsy.

Classification of musculoskeletal disorders.

Various types of pathology of the musculoskeletal system are noted.

1. Diseases of the nervous system:

· cerebral palsy

· poliomyelitis.

2. Congenital pathology of the musculoskeletal system:

· congenital dislocation of the hip,

· torticollis,

· clubfoot and other foot deformities,

abnormal development of the spine (scoliosis),

· underdevelopment and defects of the limbs,

· developmental anomalies of the fingers,

· arthrogryposis (congenital deformity).

3. Acquired diseases and injuries of the musculoskeletal system:

Traumatic injuries to the spinal cord, brain and limbs,

· polyarthritis,

skeletal diseases (tuberculosis, bone tumors, osteomyelitis),

Systemic skeletal diseases (chondrodystrophy, rickets).

FEATURES OF VIOLATIONS
IN CHILDREN WITH CEREBRAL PALSY.

In children with cerebral palsy, the formation of all motor functions is delayed and impaired: holding the head, sitting, standing, walking, and manipulating skills.

At the early stage of cerebral palsy, motor development may be uneven. The child may not yet be able to hold his head up at 8-10 months, but he is already beginning to turn and sit up. He does not have a support reaction, but he is already reaching for the toy and grasping it. At 7-9 months. the child can sit only with support, but stands and walks in the playpen, although the alignment of his body is defective.

The variety of movement disorders is caused by a number of factors:

1. pathology of muscle tone (type of spasticity, rigidity, hypotension, dystonia);

2. limitation or impossibility of voluntary movements (paresis and paralysis);

3. the presence of violent movements (hyperkinesis, tremor);

4. impaired balance, coordination and sensation of movement.

Motor disorders in children with cerebral palsy have varying degrees of severity: from severe, when the child cannot walk and manipulate objects, to mild, in which the child walks and cares for himself independently.

Deviations in mental development in cerebral palsy are also specific. They are determined by the time of brain damage, its degree and location. Lesions at an early stage of intrauterine development are accompanied by gross underdevelopment of the child's intelligence. A feature of mental development with lesions that developed in the second half of pregnancy and during childbirth is not only its slow pace, but also its uneven nature (accelerated development of some higher mental functions and the immaturity and lag of others).

Children with cerebral palsy are characterized by:

· various disorders of cognitive and speech activity;

· a variety of disorders of the emotional-volitional sphere (in some - in the form of increased excitability, irritability, motor disinhibition, in others - in the form of lethargy, lethargy), a tendency to mood swings;

· originality of personality formation (lack of self-confidence, independence; immaturity, naivety of judgment; shyness, timidity, hypersensitivity, touchiness).

Task 4. Definitions of speech disorders

  1. Dysphonia(aphonia) – absence or disorder of phonation due to pathological changes in the vocal apparatus. Synonyms: voice disorder, phonation disorder, phonotor disorder, vocal disorder.
  2. Bradylalia– pathologically slow rate of speech.
  3. Tahilalia– pathologically accelerated rate of speech.
  4. Stuttering– a violation of the tempo-rhythmic organization of speech, caused by a convulsive state of the muscles of the speech apparatus (logoneurosis).
  5. Dislalia– violation of sound pronunciation with normal hearing and intact innervation of the speech apparatus (sound pronunciation defects, phonetic defects, deficiencies in the pronunciation of phonemes).
  6. Rhinolalia– disturbances in voice timbre and sound pronunciation caused by anatomical and physiological defects of the speech apparatus.
  7. Dysarthria– a violation of the pronunciation side of speech, caused by insufficient innervation of the speech apparatus.
  8. Alalia– absence or underdevelopment of speech due to organic damage to the speech areas of the cerebral cortex in the prenatal or early period of a child’s development.
  9. Aphasia– complete or partial loss of speech caused by local brain lesions.
  10. Dyslexia– partial specific disorder of the reading process.
  11. Dysgraphia– partial specific violation of the writing process.