Psychomotor disorders are manifested by sudden, rash actions without motivation, as well as complete or partial motor immobility. They can be the result of various mental illnesses, both endogenous (schizophrenia, epilepsy, bipolar affective disorder(BD), recurrent depression, etc.) and exogenous (intoxication (delirium), psychotrauma). Also, psychomotor disorders can be observed in some patients with pathologies of the neurosis-like and neurotic spectrum (dissociative (conversion), anxiety and depressive disorders, etc.).

Hyperkinesia – states with motor excitation

Conditions associated with inhibition of motor activity

Akinesia is a state of complete immobility – stupor.

• Depressed - oppression motor activity at the height of depression.
• Manic – at the height of manic excitement, periods of numbness.
• Catatonic – accompanied by parakinesia.
• Psychogenic – occurs as a result of mental trauma (“imaginary death reflex” according to Kretschmer).

Parakinesia

Parakinesias are paradoxical motor reactions. In most sources, the synonym is catatonic disorders. Occurs only in schizophrenia. This type of violation is characterized by pretentiousness and caricature of movements. Patients make unnatural grimaces, have a specific gait (for example, only on the heels or tangentially geometric shapes). They arise as a result of a perverted volitional action and have opposite variants of the development of symptoms: catatonic stupor, catatonic agitation.

Let's look at the symptoms characteristic of catatonic states:

Catatonic symptoms also include impulsive actions, characterized by unmotivation, short duration, suddenness of onset and end. In catatonic states, hallucinations and delusions may occur.

Among parakinesias, there are conditions in a patient when his behavior is characterized by opposite tendencies:

• Ambivalence – mutually exclusive relationships (the patient says: “How I love this cat,” but at the same time hates animals).
• Ambitiousness – mutually exclusive actions (for example, a patient puts on a raincoat and jumps into a river).

conclusions

The presence of one or another type of psychomotor disorder is important symptom in diagnosing a mental illness, when the medical history, complaints and mental condition patient over time.

Content

Introduction

1. Movement disorders

2. Speech pathology. Organic and functional speech disorders

Conclusion

Bibliography

Introduction

Speech as a specific mental process develops in close unity with motor skills and requires the implementation of a series of necessary conditions– such as: anatomical integrity and sufficient maturity of those brain systems that are involved in speech function; preservation of kinesthetic, auditory and visual perception; a sufficient level of intellectual development that would satisfy the need for verbal communication; normal structure of the peripheral speech apparatus; adequate emotional and speech environment.

The emergence of speech pathology (including cases of combination of such disorders with movement disorders) is due to the fact that, on the one hand, its formation is caused by the presence of varying degrees of severity of organic lesions of individual cortical and subcortical structures of the brain involved in providing speech functions, on the other hand, secondary underdevelopment or delayed “maturation” of premotor-frontal and parieto-temporal cortical structures, disturbances in the rate and nature of the formation of visual-auditory and auditory-visual-motor nerve connections. In movement disorders, the afferent effect on the brain is distorted, which in turn enhances existing cerebral dysfunctions or causes the appearance of new ones, leading to asynchronous activity of the cerebral hemispheres.

Based on research into the causes of these disorders, we can talk about the relevance of considering this problem. The topic of the abstract is devoted to consideration of the causes and types of speech pathologies and movement disorders.

1. Movement disorders

If we talk about the causes of movement disorders, it can be noted that most of them arise as a result of a violation of the functional activity of mediators in the basal ganglia; the pathogenesis can be different. The most common causes are degenerative diseases (congenital or idiopathic), possibly drug-induced, organ system failure, central nervous system infections, or basal ganglia ischemia. All movements are carried out through the pyramidal and parapyramidal tracts. As for the extrapyramidal system, the main structures of which are the basal ganglia, its function is to correct and refine movements. This is achieved mainly through influences on the motor areas of the hemispheres through the thalamus. The main manifestations of damage to the pyramidal and parapyramidal systems are paralysis and spasticity.

Paralysis can be complete (plegia) or partial (paresis), sometimes it is manifested only by awkwardness of the hand or foot. Spasticity is characterized by increased jackknife-like tone of the limb, increased tendon reflexes, clonus, and pathological extensor reflexes (for example, the Babinski reflex). It can also manifest itself only in clumsiness of movements. TO frequent symptoms also include spasms of the flexor muscles, which occur as a reflex to constant uninhibited impulses from skin receptors.

Correction of movements is also provided by the cerebellum (The lateral sections of the cerebellum are responsible for the coordination of movements of the limbs, the middle sections are responsible for postures, gait, and body movements. Damage to the cerebellum or its connections is manifested by intention tremor, dysmetria, adiadochokinesis and decreased muscle tone.), mainly through influences on vestibulospinal tract, as well as (with switching in the nuclei of the thalamus) to the same motor zones of the cortex as the basal ganglia (motor disorders that occur when the basal ganglia are damaged (extrapyramidal disorders) can be divided into hypokinesia (decreased volume and speed of movements; example - Parkinson's disease or parkinsonism of another origin) and hyperkinesis (excessive involuntary movements; for example, Huntington's disease). Hyperkinesis also includes tics.).

With certain mental illnesses (primarily with catatonic syndrome), one can observe conditions in which the motor sphere gains some autonomy, specific motor acts lose connection with internal mental processes, and are no longer controlled by the will. In this case, the disorders become similar to neurological symptoms. It should be recognized that the similarity is only external, since, unlike hyperkinesis, paresis, and impaired coordination of movements in neurological diseases, movement disorders in psychiatry lack an organic basis, are functional and reversible.

Those suffering from catatonic syndrome cannot somehow psychologically explain the movements they make and do not realize their painful nature until the moment of copying psychosis. All movement disorders can be divided into hyperkinesia (excitement), hypokinesia (stupor) and parakinesia (perversion of movements).

Excitement, or hyperkinesia, in mentally ill patients is a sign of exacerbation of the disease. In most cases, the patient's movements reflect the richness of his emotional experiences. He may be driven by fear of persecution, and then he flees. In manic syndrome, the basis of his motor skills is a tireless thirst for activity, and in hallucinatory states he may look surprised and strive to draw the attention of others to his visions. In all of these cases, hyperkinesia acts as a symptom secondary to painful emotional experiences. This type of arousal is called psychomotor.

In catatonic syndrome, movements do not reflect the internal needs and experiences of the subject, therefore excitation in this syndrome is called purely motor. The severity of hyperkinesia often indicates the severity of the disease and its severity. However, at times there are severe psychoses with agitation limited to the confines of the bed.

Stupor is a state of immobility, an extreme degree of motor retardation. Stupor may also reflect vivid emotional experiences (depression, asthenic affect of fear). With catatonic syndrome, on the contrary, the stupor is devoid of internal content and is meaningless. To designate conditions accompanied by only partial inhibition, the term “substupor” is used. Although stupor implies a lack of motor activity, in most cases it is considered as a productive psychopathological symptomatology, since it does not mean that the ability to move is irreversibly lost. Like other productive symptoms, stupor is a temporary condition and responds well to treatment with psychotropic drugs.

Catatonic syndrome was originally described by K.L. Kahlbaum (1863) as an independent nosological unit, and is currently considered as a symptom complex. One of the important features of the catatonic syndrome is the complex, contradictory nature of the symptoms. All motor phenomena are meaningless and are not associated with psychological experiences. Characteristic is tonic muscle tension. Catatonic syndrome includes 3 groups of symptoms: hypokinesia, hyperkinesia and parakinesia.

Hypokinesia is represented by the phenomena of stupor and substupor. The complex, unnatural, and sometimes uncomfortable postures of patients are noteworthy. A sharp tonic muscle contraction is observed. This tone sometimes allows patients to hold for some time any position that the doctor gives them. This phenomenon is called catalepsy, or waxy flexibility.

Hyperkinesia in catatonic syndrome is expressed in attacks of excitement. Characterized by senseless, chaotic, unfocused movements. Motor and speech stereotypes (swinging, jumping, waving arms, howling, laughing) are often observed. An example of speech stereotypy is verbigeration, which is manifested by the rhythmic repetition of monotonous words and meaningless sound combinations.

Parakinesia is manifested by strange, unnatural movements, such as elaborate, mannered facial expressions and pantomime.

With catatonia, a number of echo symptoms have been described: echolalia (repetition of the words of the interlocutor), echopraxia (repetition of other people's movements), echomia (copying the facial expressions of others). The listed symptoms can occur in the most unexpected combinations.

It is customary to distinguish between lucid catatonia, which occurs against the background of clear consciousness, and oneiric catatonia, accompanied by confusion and partial amnesia. Despite the external similarity of the set of symptoms, these two conditions differ significantly in course. Oneiric catatonia is an acute psychosis with dynamic development and a favorable outcome. Lucid catatonia, on the contrary, serves as a sign of non-remission malignant variants of schizophrenia.

Hebephrenic syndrome has significant similarities with catatonia. The predominance of movement disorders with unmotivated, meaningless actions is also characteristic of hebephrenia. The very name of the syndrome indicates the infantile nature of the patients’ behavior.

Speaking about other syndromes accompanied by agitation, it can be noted that psychomotor agitation is one of the common components of many psychopathological syndromes.

Manic agitation differs from catatonic agitation in the purposefulness of its actions. Facial expressions express joy, patients strive to communicate, they talk a lot and actively. With pronounced excitement, the acceleration of thinking leads to the fact that not everything said by the patient is understandable, but his speech is never stereotypical.

Agitated depression manifests itself as a combination of severe melancholy and anxiety. Facial expressions reflect suffering. Characterized by lamentations and crying without tears. Often anxiety is accompanied by nihilistic megalomaniac delirium with ideas of the destruction of the world (Cotard's syndrome). Acute hallucinatory-delusional states are also often expressed by psychomotor agitation. Acute hallucinosis can also manifest itself as psychomotor agitation.

Quite often, the cause of psychomotor agitation is confusion. The most common among the syndromes of stupefaction - delirium - is manifested not only by disorientation and pig-like true hallucinations, but also by extremely pronounced agitation. Patients try to escape from the hallucinatory images that are pursuing them, attack them, try to defend themselves with a knife, throw heavy objects, fleeing, and can go out the window.

Amentia syndrome is characterized by an even greater severity of the condition. The patients are exhausted and cannot get out of bed. Their movements are chaotic, uncoordinated (yactation): they wave their arms, utter senseless screams, crumple in their hands and tear the sheet, and shake their heads.

Oneiric stupefaction is manifested by the catatonic symptoms described above. During twilight stupefaction, there are both automated actions that are safe for others, and attacks of absurd chaotic excitement, often accompanied by frantic anger and brutal aggression.

Another variant of epileptic excitation is historical attacks, although not accompanied by confusion and amnesia, but also often leading to dangerous, aggressive actions.

The danger of psychomotor agitation forced psychiatrists until the mid-twentieth century. frequently use various means of restraint (belts, straitjackets, isolation wards). The appearance of powerful barbiturates at the beginning of the century, and especially the introduction of new psychotropic drugs into practice at the end of the 50s, made it possible to almost completely abandon the use of restraint measures. Currently, various antipsychotics and, somewhat less frequently, benzodiazepine tranquilizers are used to relieve psychomotor agitation.

Stupor is less common in psychiatric practice than agitation. In addition to catatonic syndrome, it can be a manifestation of severe depression, apathetic-abulic syndrome and hysteria.

Among other syndromes accompanied by stupor, the presence of depressive stupor is noted, which is closely related in its manifestations to the affect of melancholy. The patients' faces express suffering. The entire state is characterized by integrity and the absence of paradoxes.

Apathetic stupor is observed relatively rarely. The face of such patients is amicable and expresses indifference. With apathetic-abulic syndrome, there is no suppression of desires, so patients never refuse food. From prolonged inactivity they become very fat. Unlike patients with catatonic stupor, they loudly express dissatisfaction if someone disturbs their comfort, forces them to get out of bed, wash themselves, or get a haircut. Causes of apathetic stupor - schizophrenia or defeat frontal lobes brain

Hysterical stupor, like hysterical excitement, appears immediately after the occurrence of a traumatic situation. The clinical picture can take the most unexpected forms.

In addition to hysterical ones, they describe psychogenically occurring stuporous states in life-threatening situations. Stupor in most cases is not social dangerous condition, since motor retardation is only one of the manifestations of any syndrome.

2. Speech pathology. Organic and functional speech disorders

The problem of the etiology of speech disorders went the same way historical development, as the general doctrine about the causes of painful conditions.

Since ancient times, two points of view have emerged - brain damage or disorders of the local speech apparatus as the causes of disorders.

Despite this, it was not until 1861, when the French physician Paul Broca showed the presence of a field in the brain specifically related to speech, and linked loss of speech to its damage. In 1874, a similar discovery was made by Wernicke: a connection was established between understanding and the preservation of a certain area of ​​the cerebral cortex. Since that time, the connection between speech disorders and morphological changes in certain parts of the cerebral cortex has become proven.

The issues of the etiology of speech disorders began to be developed most intensively in the 20s of this century. During these years, domestic researchers made the first attempts to classify speech disorders depending on the causes of their occurrence. Thus, S. M. Dobrogaev (1922) among the causes of speech disorders identified “diseases of higher nervous activity", pathological changes in the anatomical speech apparatus, lack of education in childhood, as well as "general neuropathic conditions of the body."

M.E. Khvattsev was the first to divide all the causes of speech disorders into external and internal, especially emphasizing their close interaction. He also identified organic (anatomical-physiological, morphological), functional (psychogenic), socio-psychological and neuropsychiatric causes.

Organic causes included underdevelopment and brain damage in the prenatal period. They identified organic central (brain lesions) and organic peripheral causes (damages to the organ of hearing, cleft palate and other morphological changes in the articulatory apparatus). Functional reasons M.E. Khvattsev explained the teachings of I.P. Pavlov about violations of the relationship between the processes of excitation and inhibition in the central nervous system. He emphasized the interaction of organic and functional, central and peripheral causes. He included mental retardation, memory impairment, attention disorders and other disorders of mental functions as psychoneurological causes.

The important role of M.E. Khvattsev also attributed socio-psychological reasons, understanding by them various unfavorable environmental influences. Thus, he was the first to substantiate the understanding of the etiology of speech disorders on the basis of a dialectical approach to assessing cause-and-effect relationships in speech pathology.

The cause of speech disorders is understood as the impact on the body of an external or internal harmful factor or their interaction, which determine the specifics of a speech disorder and without which the latter cannot occur.

The motor mechanism of speech is also provided by the following brain structures located more highly:

With damage to the subcortical-cerebellar nuclei and pathways that regulate muscle tone and the sequence of muscle contractions of the speech muscles, synchrony (coordination) in the work of the articulatory, respiratory and vocal apparatus, as well as the emotional expressiveness of speech, individual manifestations of central paralysis (paresis) are observed with violations of muscle tone, strengthening of individual unconditioned reflexes, as well as a pronounced violation of the prosodic characteristics of speech - its tempo, smoothness, volume, emotional expressiveness and individual timbre.

Damage to the conduction systems that ensure the conduction of impulses from the cerebral cortex to the structures of the underlying functional levels of the motor apparatus of speech (to the nuclei of the cranial nerves located in the brain stem) causes central paresis (paralysis) of the speech muscles with an increase in muscle tone in the muscles of the speech apparatus, strengthening of unconditioned reflexes and the appearance of reflexes of oral automatism with a more selective nature of articulatory disorders.

In case of defeat cortical sections brain, providing both more differentiated innervation of speech muscles and the formation of speech praxis, various central motor speech disorders arise.

Speech disorders often occur due to various mental traumas (fear, feelings of separation from loved ones, long-term traumatic situation in the family, etc.). This delays the development of speech, and in some cases, especially with acute mental trauma, causes psychogenic speech disorders in the child: mutism, neurotic stuttering. These speech disorders, according to the classification of M. E. Khvattsev, can conditionally be classified as functional.

Functional speech disorders also include disorders associated with adverse effects on the child’s body: general physical weakness, immaturity due to prematurity or intrauterine pathology, diseases of internal organs, rickets, metabolic disorders.

Thus, any general or neuropsychic disease of a child in the first years of life is usually accompanied by a violation of speech development. Hence, it is legitimate to distinguish between defects of formation and defects of formed speech, considering the age of three as their conditional division.

Asphyxia and birth trauma occupy a leading place in the perinatal pathology of the nervous system.

The occurrence of intracranial birth trauma and asphyxia (oxygen starvation of the fetus at the time of birth) is facilitated by disruption of intrauterine development of the fetus. Birth trauma and asphyxia aggravate developmental disorders of the fetal brain that occur in utero. Birth trauma leads to intracranial hemorrhage and death of nerve cells. Intracranial hemorrhages can also involve the speech zones of the cerebral cortex, which entails various speech disorders of cortical origin (alalia). In premature babies, intracranial hemorrhages occur most easily as a result of the weakness of their vascular walls.

In the etiology of speech disorders in children, immunological incompatibility of the blood of mother and fetus (for Rh factor, ABO system and other erythrocyte antigens) may play a certain role. Rhesus or group antibodies, penetrating the placenta, cause the breakdown of fetal red blood cells. Under the influence of a substance toxic to the central nervous system - indirect bilirubin - the subcortical parts of the brain and auditory nuclei are affected, which leads to specific disturbances in the sound-pronunciation aspect of speech in combination with hearing impairment. With intrauterine brain lesions, the most severe speech disorders are observed, usually combined with other polymorphic developmental defects (hearing, vision, musculoskeletal system, intelligence). Moreover, the severity of speech disorders and other developmental defects largely depends on the time of brain damage in the prenatal period.

Infectious and somatic diseases of the mother during pregnancy can lead to disorders of the uteroplacental circulation, nutritional disorders and oxygen starvation fetus Disorders of intrauterine development of the fetus - embryopathies - can occur in connection with viral diseases, taking medications, ionizing radiation, vibration, alcoholism and smoking during pregnancy. The adverse effects of alcohol and nicotine on offspring have been noted for a long time.

Toxicoses of pregnancy, prematurity, short-term asphyxia during childbirth cause mildly expressed minimal organic damage to the brain (children with minimal brain dysfunction - MMD).

Currently, in cases of mild brain failure, a special type of mental dysontogenesis is distinguished, which is based on superior age-related immaturity of individual higher cortical functions. With minimal brain dysfunction, there is a delay in the rate of development of functional brain systems that require integrative activity for their implementation: speech, behavior, attention, memory, spatio-temporal representations and other higher mental functions.

Children with minimal brain dysfunction are at risk for developing speech disorders.

Speech disorders can also arise as a result of the influence of various unfavorable factors on the child’s brain and at subsequent stages of its development. The structure of these speech disorders varies depending on the time of exposure to harmfulness and the location of brain damage. Hereditary factors also play a certain role in the etiology of speech disorders in children. Often they are predisposing conditions that develop into speech pathology under the influence of even minor adverse influences.

Thus, the etiological factors causing speech disorders are complex and polymorphic. The most common combination of hereditary predisposition, unfavorable environment and damage or disruption of brain maturation under the influence of various unfavorable factors.

When dwelling on the types of speech disorders, emphasis should be placed directly on existing speech abnormalities and pathologies associated with congenital or acquired causes of their occurrence.

Violation of sound pronunciation with normal hearing and intact innervation of the speech apparatus, or dyslalia, is one of the most common pronunciation defects. There are two main forms of dyslalia, depending on the location of the disorder and the reasons causing the defect in sound pronunciation; functional and mechanical (organic).

In cases where there are no organic disorders (peripherally or centrally caused), they speak of functional dyslalia. When there are deviations in the structure of the peripheral speech apparatus (teeth, jaws, tongue, palate), they speak of mechanical (organic) dyslalia. Functional dyslalia includes defects in the reproduction of speech sounds (phonemes) in the absence of organic disorders in the structure of the articulatory apparatus. The causes are biological and social: general physical weakness of the child due to somatic diseases; mental retardation (minimal brain dysfunction), delayed speech development, selective impairment of phonemic perception; unfavorable social environment that impedes the child’s communication development.

Rhinolalia (violation of voice timbre and sound pronunciation, caused by anatomical and physiological defects of the speech apparatus) differs in its manifestations from dyslalia by the presence of an altered nasal timbre of the voice. Depending on the nature of the dysfunction of the velopharyngeal closure, various forms of rhinolalia are distinguished. At open form rhinolalia, oral sounds become nasal. Functional open rhinolalia is caused by for various reasons. It is explained by insufficient elevation of the soft palate during phonation in children with sluggish articulation.

One of the functional forms is “habitual” open rhinolalia. It is often observed after removal of adenoid growths or, less commonly, as a result of post-diphtheria paresis, due to prolonged restriction of the mobile soft palate. Organic open rhinolalia can be acquired or congenital. Acquired open rhinolalia is formed with perforation of the hard and soft palate, with cicatricial changes, paresis and paralysis of the soft palate. The cause may be damage to the glossopharyngeal and vagus nerve, injuries, tumor pressure, etc. The most common cause of congenital open rhinolalia is congenital cleft of the soft or hard palate, shortening of the soft palate.

Dysarthria is a violation of the pronunciation side of speech, caused by insufficient innervation of the speech apparatus.

The leading defect in dysarthria is a violation of the sound pronunciation and prosodic aspects of speech associated with organic damage to the central and peripheral nervous systems.

Sound pronunciation disturbances in dysarthria manifest themselves to varying degrees and depend on the nature and severity of damage to the nervous system. In mild cases, there are individual distortions of sounds, “blurred speech”; in more severe cases, distortions, substitutions and omissions of sounds are observed, tempo, expressiveness, modulation suffer, and in general the pronunciation becomes slurred.

With severe damage to the central nervous system, speech becomes impossible due to complete paralysis of the speech motor muscles. Such disorders are called anarthria (a - absence of a given sign or function, artron - articulation).

Dysarthric speech disorders are observed with various organic brain lesions, which in adults have a more pronounced focal nature. Less severe forms of dysarthria may be observed in children without obvious movement disorders, who have suffered mild asphyxia or birth trauma, or who have a history of other mild adverse effects during fetal development or childbirth.

In 1911, N. Gutzmann defined dysarthria as a disorder of articulation and identified its two forms: central and peripheral.

The initial study of this problem was carried out mainly by neuropathologists in the context of focal brain lesions in adult patients. The work of M. S. Margulis (1926), who was the first to clearly distinguish dysarthria from motor aphasia and divide it into bulbar and cerebral forms, had a great influence on the modern understanding of dysarthria. The author proposed a classification of cerebral forms of dysarthria based on the location of the brain lesion.

The pathogenesis of dysarthria is determined by organic damage to the central and peripheral nervous system under the influence of various unfavorable external (exogenous) factors acting in the prenatal period of development, at the time of childbirth and after birth. Among the causes, asphyxia and birth trauma, damage to the nervous system due to hemolytic disease, infectious diseases of the nervous system, traumatic brain injuries, and, less commonly, disorders cerebral circulation, brain tumors, malformations of the nervous system, such as congenital aplasia of the cranial nerve nuclei (Moebius syndrome), as well as hereditary diseases of the nervous and neuromuscular systems.

Clinical and physiological aspects of dysarthria are determined by the location and severity of brain damage. The anatomical and functional relationship in the location and development of motor and speech zones and pathways determines frequent combination dysarthria with motor disorders of varying nature and severity.

Sound pronunciation disorders in dysarthria occur as a result of damage to various brain structures necessary to control the motor mechanism of speech (peripheral motor nerves to the muscles of the speech apparatus; nuclei of these peripheral motor nerves located in the brain stem; nuclei located in the brain stem and in the subcortical regions of the brain) . Damage to the listed structures gives a picture of peripheral paralysis (paresis): nerve impulses do not reach the speech muscles, metabolic processes they are disturbed, the muscles become sluggish, flabby, their atrophy and atony are observed, as a result of a break in the spinal reflex arc, the reflexes from these muscles disappear, areflexia occurs.

Voice disorders are also classified as speech disorders. Voice disorder is the absence or disorder of phonation due to pathological changes in the vocal apparatus. There are two main terms for voice pathology: aphonia - complete absence of voice and dysphonia - partial disturbances in pitch, strength and timbre.

Voice disorders associated with various diseases of the vocal apparatus are common in both adults and children. Pathology of the larynx in children has increased over the past two decades, which is associated with the expansion of resuscitation measures.

Voice disorders are divided into central and peripheral, each of them can be organic and functional. Most disorders manifest themselves as independent, the causes of their occurrence are diseases and various changes in the vocal apparatus only. But they can also accompany other more severe speech disorders, being part of the structure of the defect in aphasia, dysarthria, rhinolalia, and stuttering.

Voice pathology that occurs as a result of anatomical changes or chronic inflammatory processes of the vocal apparatus is considered organic. Peripheral organic disorders include dysphonia and aphonia with chronic laryngitis, paresis and paralysis of the larynx, conditions after removal of tumors.

Central paresis and paralysis of the larynx depend on damage to the cerebral cortex, pons, medulla oblongata, conducting paths. In children they occur with cerebral palsy.

The most common and diverse are functional voice disorders. They are not accompanied by inflammatory or any anatomical changes in the larynx. Peripheral functional disorders include phonasthenia, hypo- and hypertonic aphonia and dysphonia.

Phonasthenia - a voice disorder in some cases, especially in the initial stages, is not accompanied by visible objective changes in the vocal apparatus. Phonasthenia manifests itself in a violation of the coordination of breathing and phonation, the inability to control the voice - to strengthen and weaken the sound, the appearance of detonation and a number of subjective sensations.

Hypotonic dysphonia (aphonia) is usually caused by bilateral myopathic paresis, i.e. paresis of the internal muscles of the larynx. They occur with certain infections (ARVI, influenza, diphtheria), as well as with severe voice strain. Voice pathology can manifest itself from mild hoarseness to aphonia with symptoms of vocal fatigue, tension and pain in the muscles of the neck, back of the head and chest.

Hypertonic (spastic) voice disorders are associated with increased tone of the laryngeal muscles with a predominance of tonic spasm at the time of phonation. The reasons for their occurrence are not fully understood, but spasmodic dysphonia and aphonia develop in people who force their voice.

Rhinophonia and rhinolalia stand somewhat apart from other voice disorders, since their pathophysiological mechanism lies in the abnormal function of the soft palate of an organic or functional nature. With closed rhinophony, nasal consonants acquire oral resonance, vowels lose sonority, and timbre becomes unnatural.

Open rhinophony manifests itself in pathological nasalization of all oral sounds, while the voice is weak and compressed. Voice defects, in addition to impaired resonance, are due to the fact that the soft palate is functionally connected to the internal muscles of the larynx and affects the symmetry and tone of the vocal folds.

Functional voice disorders of central origin include functional or psychogenic aphonia. It occurs suddenly as a reaction to a traumatic situation in people prone to hysterical reactions, more often in girls and women.

Speech rate disorders include bradyllalia and tachylalia. With these disorders, the development of both external and internal speech is disrupted. The speech is incomprehensible to others.

Bradylalia is a pathologically slow rate of speech. With bradylalia, the voice is monotonous, loses modulation, constantly maintains the same pitch, and sometimes a nasal tint appears. The musical accent also changes when pronouncing individual syllables, the pitch of the voice fluctuates up or down. Non-speech symptoms in bradyllalia are expressed in disorders of general motor skills, fine motor skills of the hands, fingers, and facial muscles. Movements are slow, sluggish, insufficiently coordinated, incomplete in volume, motor awkwardness is observed. The face is amicable. Features of mental activity are also noted: slowness and disturbances in perception, attention, memory, and thinking.

Tahilalia is a pathologically accelerated rate of speech. M.E. Khvattsev (1959) considered the main cause of tachylalia to be congenital speech-motor insufficiency of the speech apparatus, as well as sloppy, uneven speech of others, lack of attention and timely correction of the child’s rapid speech. A. Liebmann distinguished between deficiencies in motor and acoustic perception that underlie tachylalia. G. Gutzman argued that this disorder is a consequence of a perception disorder. According to E. Frechels, accelerated speech occurs due to the fact that thoughts rush extremely quickly and one concept is supplanted by the next one before the first can be pronounced. M. Nedolechny considered the cause of accelerated speech to be insufficiency of articulation, since patients experience difficulty pronouncing unusual and long words.

Stuttering is a violation of the tempo-rhythmic organization of speech, caused by the convulsive state of the muscles of the speech apparatus.

Alalia is the absence or underdevelopment of speech due to organic damage to the speech areas of the cerebral cortex in prenatal or early period child development. Intrauterine pathology leads to diffuse damage to the brain substance; birth traumatic brain injuries and asphyxia of newborns cause more local disorders. Somatic diseases only aggravate the impact of pathological causes of a neurological nature, which are leading.

Some authors (R. Cohen, 1888; M. Zeeman, 1961; R. Luchsinger, A. Salei, 1977, etc.) emphasize the role of heredity and family predisposition in the etiology of alalia. However, convincing scientific data on the role of heredity in the origin of alalia is not provided in the literature. IN last years in the occurrence of alalia, the significant role of minimal brain damage (minimal brain dysfunction) is emphasized.

Aphasia is a complete or partial loss of speech caused by local lesions of the brain.

The causes of aphasia are cerebral circulation disorders (ischemia, hemorrhoids), trauma, tumors, and infectious diseases of the brain. Aphasia of vascular origin most often occurs in adults. As a result of rupture of cerebral aneurysms, thromboembolism caused by rheumatic heart disease, and traumatic brain injuries. Aphasia is often observed in adolescents and young adults.

Aphasia occurs in about a third of cases of cerebrovascular accidents, with motor aphasia being the most common.

Aphasia is one of the most severe consequences of brain lesions, in which all types of speech activity. The complexity of the speech disorder in aphasia depends on the location of the lesion. With aphasia, the implementation of different levels, aspects, types of speech activity (oral speech, speech memory, phonemic hearing, speech understanding, written speech, reading, counting, etc.) is specifically systematically impaired.

Acoustic-gnostic sensory aphasia was first described by the German psychiatrist Wernicke. He showed that aphasia, which he called sensory, occurs when the posterior third of the superior temporal gyrus of the left hemisphere is damaged. A distinctive feature of this form of aphasia is a violation of the understanding of speech when perceiving it by ear.

Acoustic-mnestic aphasia occurs when the middle and posterior parts of the temporal region are damaged (A. R. Luria, 1969, 1975; L. S. Tsvetkova, 1975). A. R. Luria believes that it is based on a decrease in auditory-verbal memory, which is caused by increased inhibition of auditory traces. With the perception of each new word and its awareness, the patient loses the previous word. This disorder also manifests itself when repeating a series of syllables and words.

Amnestic-semantic aphasia occurs when the parieto-occipital region of the speech-dominant hemisphere is damaged. When the parietal-occipital (or posterior inferior-parietal) parts of the cerebral hemisphere are damaged, the smooth syntagmatic organization of speech is preserved, no searches for the sound composition of a word are noted, and there are no phenomena of decreased auditory-verbal memory or impaired phonemic perception.

Afferent kinesthetic motor aphasia occurs with damage to the secondary zones of the postcentral and inferior parietal parts of the cerebral cortex, located posterior to the central, or Rolandic, sulcus.

Effective motor aphasia occurs when the anterior branches of the left middle cerebral artery are damaged. It is usually accompanied by kinetic apraxia, which is expressed in difficulties in assimilating and reproducing a motor program.

Damage to the premotor parts of the brain causes pathological inertia of speech stereotypes, leading to sound, syllable and lexical rearrangements and perseveration, repetitions. Perseverations, involuntary repetitions of words and syllables, resulting from the impossibility of timely switching from one articulatory act to another.

Dynamic aphasia occurs when the posterior frontal parts of the left speech-dominant hemisphere are damaged, i.e., the parts of the third functional block - the block of activation, regulation and planning of speech activity.

The main speech defect in this form of aphasia is the difficulty, and sometimes complete impossibility, of actively developing a statement. With severe severity of the disorder, not only speech, but also general spontaneity, lack of initiative are noted, pronounced echolalia, and sometimes echopraxia, occurs.

In terms of speech pathologies, written speech disorders are also considered. These include: alexia, dyslexia, agraphia, dysgraphia.

Dyslexia is a partial specific disorder of the reading process, caused by the immaturity (impairment) of higher mental functions and manifested in repeated persistent errors.

The etiology of dyslexia is associated with exposure to biological and social factors. Dyslexia is caused by organic damage to areas of the brain involved in the reading process. Functional reasons may be associated with the influence of internal and external factors. Thus, the etiology of dyslexia involves both genetic and exogenous factors (pathology of pregnancy, childbirth, asphyxia “chain” of childhood infections, head injuries).

Dysgraphia is a partial specific disorder of the writing process. This disorder is caused by the underdevelopment (decay) of higher mental functions that carry out the normal writing process.

Conclusion

Based on the research experience of such scientists as P. Broca, Wernicke, K.L. Kalbaum, S.M. Dobrogaev, M.E. Khvattsev, L.S. Volkova, A.R. Luria, M. S. Margulis, A. Liebmann, G. Gutzman, E. Freshelsa, M. Nedolechny and others, who made a significant contribution to the study of problems of speech and motor pathologies, modern directions (both theoretical and practical) in the field of studying the mechanisms of motor and speech disorders makes it possible not only to delve into the essence of this problem in more detail and thoroughly, but also creates promising conditions for direct correctional and adaptive assistance to people suffering from these disorders. In order for help to be as effective as possible, you need not only to know the essence of the mechanisms of mental processes and the action of motor skills, the mechanism of their violation. Specialists involved in research on these problems need to constantly and continuously orient their activities towards preventing the occurrence of pathologies, as well as systematically monitor the state of impaired functions, preventive activities of disorders, and provide assistance to patients specific in this area.

List of used literature

1. Zharikov M.N., Tyulpin Yu.G. Psychiatry. – M.: Medicine, 2002.

2. Zeigarnik B.V. Pathopsychology. - M.: Moscow University Publishing House, 1986.

3. Liebmann A. Pathology and therapy of stuttering and tongue-tiedness. (St. Petersburg - 1901) // Reader on speech therapy (extracts and texts). Textbook for students of higher and secondary educational institutions: In 2 vols. T.I / Ed. L.S.Volkova and V.I.Seliverstova. - M.: Humanite. ed. VLADOS center, 1997.

4. Speech therapy: Textbook for students of defectology. fak. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskaya. - M.: Humanite. ed. VLADOS center, 1998.

5. Luria.A.R. Stages of the path traveled // Scientific autobiography. - M.: Publishing house Mosk. University, 1982.

6. Neiman L.V., Bogomilsky M.R. Anatomy, physiology and pathology of the organs of hearing and speech // Textbook. for students higher pedagogical textbook Head - M.: Humanit. ed. VLADOS center, 2003.

7. Jaspers K. General psychopathology // Trans. with him. L. O. Akopyan, ed. doc. honey. Sciences V.F. Voitsekha and Ph.D. Philosopher Sciences O. Yu. Boytsova. - M.: Praktika, 1997.

Speech therapy: Textbook for students of defectology. fak. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskaya. - M.: Humanite. ed. VLADOS center, 1998, p. 230.

Speech therapy: Textbook for students of defectology. fak. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskaya. - M.: Humanite. ed. VLADOS center, 1998, p. 243

Speech therapy: Textbook for students of defectology. fak. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskaya. - M.: Humanite. ed. VLADOS center, 1998, p. 248

Speech therapy: Textbook for students of defectology. fak. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskaya. - M.: Humanite. ed. VLADOS center, 1998, p.86.

Zeigarnik B.V. Pathopsychology. - M.: Moscow University Publishing House, 1986, P.180.

Speech therapy: Textbook for students of defectology. fak. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskaya. - M.: Humanite. ed. VLADOS center, 1998, p.93.

Neiman L.V., Bogomilsky M.R. Anatomy, physiology and pathology of the organs of hearing and speech // Textbook. for students higher pedagogical textbook Head - M.: Humanit. ed. VLADOS center, 2003, p.177.

Speech therapy: Textbook for students of defectology. fak. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskaya. - M.: Humanite. ed. VLADOS center, 1998, p.93

Zeigarnik B.V. Pathopsychology. - M.: Moscow University Publishing House, 1986, P.184.

Speech therapy: Textbook for students of defectology. fak. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskaya. - M.: Humanite. ed. VLADOS center, 1998, p. 95.

Zeigarnik B.V. Pathopsychology. - M.: Moscow University Publishing House, 1986, P.187.

Speech therapy: Textbook for students of defectology. fak. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskaya. - M.: Humanite. ed. VLADOS center, 1998, p. 176.

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, the basis of motor impairment is a disease muscular system, for example, with 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. Individual forms violent movements (tics, tremors) can 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 deeper study pathological mechanisms with 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 (hemianopsia). 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 training in special schools ah, - the blind and 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 upper limit This minimum 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 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 that allow them to special conditions in a special class, learn visually. 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 weak type 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 question 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 assigned 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 external environment and is that special property that allows a blind person to overcome a number of difficulties along 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 from the sphere of perception of such a powerful receptor as vision, which is part of the first signaling system, 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. Swiping the soft surface of the tip of both index fingers along the lines of raised dotted font in a specially printed book, a 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. Usage contact lenses turned out 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. 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.

Psychomotor is a set of human motor acts that is directly related to mental activity and reflects the constitutional features inherent in a given person. The term “psychomotor”, in contrast to simple motor reactions that are associated with the reflex activity of the central nervous system, denotes more complex movements that are associated with mental activity.

The influence of mental disorders.

With various types of mental illnesses, disorders of complex motor behavior may occur - so-called psychomotor movement disorders. Severe focal brain damage (for example, cerebral atherosclerosis) usually leads to paresis or paralysis. Generalized organic processes, such as brain atrophy (decrease in brain volume) are accompanied in most cases by lethargy of gestures and facial expressions, slowness and poverty of movements; speech becomes monotonous, gait changes, and general stiffness of movements is observed.

Mental disorders also affect psychomotor function. Thus, manic-depressive psychosis in the manic phase is characterized by general motor agitation.

Some psychogenic disorders in mental illness lead to sharply painful changes in psychomotor function. For example, hysteria is often accompanied by complete or partial paralysis of the limbs, reduced strength of movement, and impaired coordination. A hysterical attack usually makes it possible to observe various expressive and defensive facial movements.

Catatonia (a neuropsychic disorder that manifests itself in impaired voluntary movements and muscle spasms) is characterized by both minor changes in motor skills (weak facial expressions, deliberate pretentiousness of posture, gestures, gait, mannerisms) and vivid manifestations of catatonic stupor and catalepsy. The latter term denotes numbness or freezing, accompanied by loss of the ability to voluntarily move. Catalepsy can be observed, for example, during hysteria.

All movement disorders in mental illness can be divided into three types.

Types of movement disorders.

1. hypokinesia(disorders that are accompanied by a decrease in motor volume);
2. hyperkinesia(disorders that are accompanied by an increase in motor volume);
3. dyskinesia(disorders in which involuntary movements are observed as part of normally smooth and well-controlled movements of the limbs and face).

The category of hypokinesia includes various forms of stupor. Stupor is a mental disorder characterized by inhibition of all mental activity (movements, speech, thinking).

Types of stupor with hypokinesia.

1. Depressive stupor (also called melancholic numbness) manifests itself in immobility, a depressed state of mind, but the ability to respond to external stimuli (appeals) is preserved;

2. Hallucinatory stupor occurs during hallucinations provoked by poisoning, organic psychosis, schizophrenia; with such stupor, general immobility is combined with facial movements - reactions to the content of hallucinations;

3. Asthenic stupor manifests itself in indifference to everything and lethargy, in reluctance to answer simple and understandable questions;

4. Hysterical stupor is typical for people with a hysterical character (it is important for them to be the center of attention, they are overly emotional and demonstrative in expressing feelings); in a state of hysterical stupor, the patient lies motionless for a very long time and does not respond to calls;

5. Psychogenic stupor occurs as a reaction of the body to severe mental trauma; such stupor is usually accompanied by increased heart rate, increased sweating, and fluctuations blood pressure and other disorders of the autonomic nervous system;

6. Cataleptic stupor (also called waxy flexibility) is characterized by the ability of patients to remain in a given position for a long time.

Mutism (absolute silence) is also classified as hypokinesia.

Hyperkinesia.

Types of excitations in hyperkinesia.

1. Manic agitation caused by abnormally elevated mood. In patients with mild forms of the disease, behavior remains focused, although it is accompanied by exaggeratedly loud and fast speech, and movements remain well coordinated. In severe forms, the patient’s movement and speech are in no way connected with each other, and motor behavior becomes illogical.

2. Hysterical excitement, which is most often a reaction to the surrounding reality, this excitement is extremely demonstrative and intensifies if the patient notices attention to himself.

3. Hebephrenic arousal, which is absurd, cheerful, meaningless behavior, accompanied by pretentious facial expressions, is characteristic of schizophrenia.

4. Hallucinatory arousal is a vivid reaction of the patient to the content of his own hallucinations.

The study of psychomotor skills is extremely important for psychiatry and neurology. The patient's movements, his postures, gestures, and manners are regarded as very significant signs for a correct diagnosis.

Movement disorder syndromes

Motor disorders in newborns and infants are fundamentally different from those in older children and adults. Brain damage in the early stages of ontogenesis causes in most cases generalized changes, which makes topical diagnosis extremely difficult; more often we can only talk about the predominant damage to certain parts of the brain.

During this age period, the differentiation of pyramidal and extrapyramidal disorders is very difficult. The main characteristics in the diagnosis of movement disorders in the first year of life are muscle tone and reflex activity. The symptomatology of changes in muscle tone may look different depending on the age of the child. This especially applies to the first and second age periods (up to 3 months), when the child has physiological hypertension.

Changes in muscle tone are manifested by muscle hypotonia, dystonia and hypertension. Muscle hypotonia syndrome is characterized by a decrease in resistance to passive movements and an increase in their volume. Spontaneous and voluntary motor activity is limited, tendon reflexes can be normal, increased, decreased or absent depending on the level of damage to the nervous system. Muscular hypotonia is one of the most commonly detected syndromes in newborns and infants. It can be expressed from birth, as is the case with congenital forms of neuromuscular diseases, asphyxia, intracranial and spinal birth trauma, damage to the peripheral nervous system, some hereditary metabolic disorders, chromosomal syndromes, and in children with congenital or early acquired dementia. At the same time, hypotension can appear or become more pronounced at any age if clinical symptoms diseases begin several months after birth or are progressive in nature.

Hypotension, expressed from birth, can transform into normotension, dystonia, hypertension, or remain a leading symptom throughout the first year of life. The severity of clinical manifestations of muscle hypotonia varies from a slight decrease in resistance to passive movements to complete atony and absence of active movements.

If the syndrome of muscle hypotension is not clearly expressed and is not combined with other neurological disorders, it either has no effect on the child’s age-related development, or causes a delay in motor development, more often in the second half of life. The lag is uneven; more complex motor functions are delayed, requiring coordinated activity of many muscle groups for their implementation. So, a seated child sits for 9 months, but cannot sit up on his own. Such children begin to walk later, and the period of walking with support is delayed for a long time.

Muscular hypotonia may be limited to one limb (obstetric paresis of the arm, traumatic paresis of the leg). In these cases the delay will be partial.

A pronounced syndrome of muscle hypotonia has a significant impact on delayed motor development. Thus, motor skills in the congenital form of spinal amyotrophy Werdnig-Hoffmann in a child of 9-10 months can correspond to the age of 2-3 months. Delayed motor development, in turn, causes peculiarities in the formation of mental functions. For example, the inability to voluntarily grasp an object leads to underdevelopment of visual-motor coordination and manipulative activity. Since muscle hypotonia is often combined with other neurological disorders (convulsions, hydrocephalus, cranial nerve paresis, etc.), the latter can modify the nature of the developmental delay determined by hypotonia as such. It should also be noted that the quality of the hypotonia syndrome itself and its impact on developmental delay will vary depending on the disease. In cases of convulsions, congenital or early acquired dementia, it is not so much hypotension as delayed mental development that is the cause of delayed motor development.

The syndrome of movement disorders in children of the first year of life may be accompanied by muscular dystonia (a condition when muscle hypotension alternates with hypertension). At rest, these children show general muscle hypotonia during passive movements. When trying to actively perform any movement, with positive or negative emotional reactions, muscle tone increases sharply, and pathological tonic reflexes become pronounced. Such conditions are called "dystonic attacks." Muscular dystonia is most often observed in children who have had hemolytic disease as a result of Rh or ABO incompatibility. Severe muscular dystonia syndrome makes it almost impossible for a child to develop straightening trunk reflexes and balance reactions due to constantly changing muscle tone. Mild transient muscular dystonia syndrome does not have a significant effect on the age-related motor development of the child.

Muscular hypertension syndrome is characterized by an increase in resistance to passive movements, limitation of spontaneous and voluntary motor activity, increased tendon reflexes, expansion of their zone, and foot clonus. An increase in muscle tone may prevail in the flexor or extensor muscle groups, in the adductor muscles of the thighs, which is expressed in a certain specificity of the clinical picture, but is only a relative criterion for topical diagnosis in young children. Due to the incompleteness of the myelination processes, the symptoms of Babinsky, Oppenheim, Gordon, etc. cannot always be considered pathological. Normally, they are not sharply expressed, are not constant and weaken as the child develops, but with an increase in muscle tone they become bright and have no tendency to fade.

The severity of muscle hypertension syndrome can vary from a slight increase in resistance to passive movements to complete stiffness (decerebrate rigidity posture), when any movements are practically impossible. In these cases, even muscle relaxants are not able to cause muscle relaxation, much less passive movements. If the syndrome of muscular hypertension is mildly expressed and is not combined with pathological tonic reflexes and other neurological disorders, its influence on the development of static and locomotor functions may manifest itself in their slight delay at various stages of the first year of life. Depending on which muscle groups have more increased tone, differentiation and final consolidation of certain motor skills will be delayed. Thus, with an increase in muscle tone in the hands, a delay in the development of directing the hands to an object, grasping a toy, manipulating objects, etc. is noted. The development of the grasping ability of the hands is especially impaired. Along with the fact that the child begins to pick up the toy later, he retains an ulnar grip, or grip with the entire hand, for a long time. The finger grip (pincer grip) develops slowly and sometimes requires additional stimulation. The development of the protective function of the hands may be delayed, and then the balance reactions in the prone position, sitting, standing and when walking are delayed.

With an increase in muscle tone in the legs, the formation of the support reaction of the legs and independent standing is delayed. Children are reluctant to stand on their feet, prefer to crawl, and stand on their toes when supported.

Cerebellar disorders in children of the first year of life can be a consequence of underdevelopment of the cerebellum, damage to it as a result of asphyxia and birth trauma, and in rare cases - as a result of hereditary degeneration. They are characterized by a decrease in muscle tone, impaired coordination during arm movements, and a disorder of balance reactions when trying to master the skills of sitting, standing, standing and walking. The cerebellar symptoms themselves - intention tremor, loss of coordination, ataxia - can be identified only after the development of the child’s voluntary motor activity. You can suspect coordination disorders by observing how a child reaches for a toy, grabs it, brings it to his mouth, sits, stands, walks.

Infants with poor coordination make a lot of unnecessary movements when trying to grab a toy; this becomes especially pronounced in a sitting position. Independent sitting skills develop late, by 10-11 months. Sometimes even at this age it is difficult for children to maintain balance; they lose it when they try to turn to the side or pick up an object. Because of the fear of falling, the child does not manipulate objects with both hands for a long time; He begins to walk after a year and often falls. Some children with impaired balance reactions prefer to crawl when they should already be walking on their own. Less commonly, with cerebellar syndrome in children of the first year of life, horizontal nystagmus and speech disturbances can be observed as an early sign of cerebellar dysarthria. The presence of nystagmus and the frequent combination of cerebellar syndrome with other disorders of cranial innervation may impart certain specificity to developmental delay in the form of a more pronounced delay in the function of gaze fixation and tracking, visual-motor coordination, and disturbances in spatial orientation. Dysarthric disorders particularly affect the development of expressive language skills.

The most common form of motor disorders in children of the first year of life is cerebral palsy syndrome (CP). The clinical manifestations of this syndrome depend on the severity of muscle tone, an increase in which to varying degrees is observed in any form of cerebral palsy. In some cases, high muscle tone prevails in a child from birth. However, more often muscle hypertension develops after the stages of hypotension and dystonia. In such children, after birth, muscle tone is low, spontaneous movements are poor, and unconditioned reflexes are suppressed. By the end of the second month of life, when the child is in a prone position and tries to hold his head upright, the dystonic stage appears. The child periodically becomes restless, his muscle tone increases, his arms are extended with internal rotation of the shoulders, his forearms and hands are pronated, his fingers are clenched into fists; the legs are extended, adducted and often crossed. Dystonic attacks last a few seconds, are repeated throughout the day and can be triggered by external stimuli (loud knocking, another child crying).

Movement disorders in cerebral palsy are caused by the fact that damage to the immature brain disrupts the sequence of stages of its maturation. Higher integrative centers do not have an inhibitory effect on primitive brainstem reflex mechanisms. The reduction of unconditioned reflexes is delayed, and pathological tonic cervical and labyrinthine reflexes are released. Combined with an increase in muscle tone, they prevent the consistent development of straightening and balance reactions, which are the basis for the development of static and locomotor functions in children of the first year of life (holding the head, grasping a toy, sitting, standing, walking).

To understand the features of the violation psychomotor development in children with cerebral palsy, it is necessary to consider the influence of tonic reflexes on the formation of voluntary motor activity, as well as speech and mental functions.

Tonic labyrinthine reflex. Children with a pronounced tonic labyrinthine reflex in the supine position cannot tilt their head, stretch their arms forward to bring them to their mouth, grasp an object, and later grasp, pull themselves up and sit up. They do not have the prerequisites for the development of fixation and free tracking of an object in all directions, the optical righting reflex to the head does not develop, and head movements cannot freely follow eye movements. The development of hand-eye coordination is impaired. Such children have difficulty turning from their back to the side and then onto their stomach. In severe cases, even by the end of the first year of life, turning from the back to the stomach is carried out only with a “block”, i.e. there is no torsion between the pelvis and the upper part of the body. If a child cannot tilt his head in a supine position or turn onto his stomach with torsion, he does not have the prerequisites for the development of sitting function. The severity of the tonic labyrinthine reflex is directly dependent on the degree of increase in muscle tone.

When the tonic labyrinthine reflex is expressed in the prone position as a result of increased flexor tone, the head and neck are bent, the shoulders are pushed forward and down, the arms bent in all joints are under the chest, the hands are clenched into fists, the pelvis is raised. In this position, the child cannot raise his head, turn it to the sides, release his arms from under the chest and lean on them to support the upper body, bend his legs and kneel. It is difficult to turn from the stomach to the back to sit down. A gradually bent back leads to the development of kyphosis in thoracic region spine. This position prevents the development of chain righting reflexes in the prone position and the child’s acquisition of a vertical position, and also excludes the possibility of sensory-motor development and vocal reactions.

The influence of the tonic labyrinthine reflex depends to a certain extent on the initial type of spasticity. In some cases, extensor spasticity is so strong that it can be expressed in the prone position. Therefore, children lying on their stomachs, instead of bending, straighten their heads, throw them back, and raise their upper torsos. Despite the extension position of the head, muscle tone in the arm flexors remains elevated, the arms do not provide support for the body, and the child falls on his back.

The asymmetric cervical tonic reflex (ASTR) is one of the most pronounced reflexes in cerebral palsy. The severity of ASTR depends on the degree of increase in muscle tone in the arms. With severe damage to the hands, the reflex appears almost simultaneously with turning the head to the side. If the arms are only slightly affected, as is the case with mild spastic diplegia, ASTD occurs intermittently and requires a longer latency period for its onset. ASTR is more pronounced in the supine position, although it can also be observed in the sitting position.

ASTR, combined with the tonic labyrinthine reflex, prevents the grasping of a toy and the development of hand-eye coordination. The child cannot move his arms forward to bring his hands closer to the midline and, accordingly, hold the object he is looking at with both hands. A child cannot bring a toy placed in his hand to his mouth or eyes, because when he tries to bend his hand, his head turns in the opposite direction. Due to arm extension, many children are unable to suck their fingers as most healthy children do. ASTR is in most cases more pronounced on the right side, which is why many children with cerebral palsy prefer to use their left hand. With pronounced ASTD, the child’s head and eyes are often fixed in one direction, so it is difficult for him to follow an object on the opposite side; as a result, the syndrome of unilateral spatial agnosia develops, and spastic torticollis is formed. scoliosis of the spine.

Combined with the tonic labyrinthine reflex, ASTR makes it difficult to turn on the side and on the stomach. When a child turns his head to the side, the resulting ASTR prevents the body from moving along with the head, and the child cannot free his arm from under the body. The difficulty of turning on one side prevents the child from developing the ability to transfer the center of gravity from one hand to the other when moving the body forward, which is necessary for the development of reciprocal crawling.

ASTR disrupts balance in a sitting position, since the spread of muscle tone on one side (increased predominantly in the extensors) is opposite to its spread on the other (predominantly increased in the flexors). The child loses his balance and falls to the side and backwards. To avoid falling forward, the child must tilt his head and torso. The effect of ASTP on the "occipital" leg can eventually lead to subluxation of the hip joint due to a combination of flexion, internal rotation, and adduction of the hip.

Symmetrical cervical tonic reflex. If the symmetrical cervical tonic reflex is severe, a child with increased flexor tone in the arms and body, placed on his knees, will not be able to straighten his arms and lean on them to support the weight of his body. In this position, the head tilts, the shoulders retract, the arms are abducted, bent at the elbow joints, and the hands are clenched into fists. As a result of the influence of the symmetrical cervical tonic reflex in the prone position, the child’s muscle tone in the leg extensors sharply increases, so that it is difficult to bend them in the hip and knee joints and bring him to his knees. This position can be eliminated by passively raising the child's head by grasping his chin.

If the symmetrical cervical tonic reflex is severe, it is difficult for the child to maintain head control and, accordingly, to remain in a sitting position. Raising the head in a sitting position increases the extensor tone in the arms, and the child falls back; lowering the head increases the flexion tone in the arms and the child falls forward. The isolated influence of symmetrical cervical tonic reflexes on muscle tone can rarely be identified, since in most cases they are combined with ASTR.

Along with tonic cervical and labyrinthine reflexes, a positive supportive reaction and friendly movements(syncinesis).

Positive supportive reaction. The influence of a positive supportive reaction on movements is manifested in an increase in extensor tone in the legs when the legs come into contact with the support. Because children with cerebral palsy always touch the balls of their feet first when standing and walking, this response is constantly supported and stimulated. All leg joints are fixed. Rigid limbs can support the child’s body weight, but they significantly complicate the development of balance reactions, which require joint mobility and fine regulation of the constantly reciprocally changing static state of the muscles.

Friendly reactions (syncinesis). The effect of synkinesis on a child’s motor activity is to increase muscle tone in various parts of the body with an active attempt to overcome the resistance of spastic muscles in any limb (i.e., perform movements such as grasping a toy, extending an arm, taking a step, etc. ). Thus, if a child with hemiparesis squeezes a ball tightly with his healthy hand, muscle tone may increase on the paretic side. Trying to straighten a spastic arm can cause increased extensor tone in the homolateral leg. Strong flexion of the affected leg in a child with hemplegia causes friendly reactions in the affected arm, which are expressed in increased flexion in the elbow and wrist joints and fingers. Strenuous movement of one leg in a patient with double hemiplegia can increase spasticity throughout the body. The occurrence of friendly reactions prevents the development of purposeful movements and is one of the reasons for the formation of contractures. In cerebral palsy, synkinesis most often manifests itself in the oral muscles (when trying to grab a toy, the child opens his mouth wide). During voluntary motor activity, all tonic reflex reactions act simultaneously, combining with each other, so it is difficult to identify them in isolation, although in each individual case the predominance of one or another tonic reflex can be noted. The degree of their severity depends on the state of muscle tone. If muscle tone is sharply increased and extensor spasticity predominates, tonic reflexes are pronounced. With double hemiplegia, when the arms and legs are equally affected, or the arms are more affected than the legs, tonic reflexes are pronounced, observed simultaneously and have no tendency to inhibit. They are less pronounced and constant in spastic diplegia and hemiparetic form of cerebral palsy. In spastic diplegia, when the arms are relatively intact, the development of movements is hampered mainly by a positive supportive reaction.

In children who have had hemolytic disease of the newborn, tonic reflexes appear suddenly, leading to an increase in muscle tone - a dystonic attack. In the hyperkinetic form of cerebral palsy, the development of voluntary motor skills along with the indicated mechanisms is difficult due to the presence of involuntary, violent movements - hyperkinesis. It should be noted, however, that in children of the first year of life, hyperkinesis is slightly expressed. They become more noticeable in the second year of life. In the atonic-astatic form of cerebral palsy, balance reactions, coordination and static functions suffer more. Tonic reflexes can be observed only occasionally.

Tendon and periosteal reflexes in cerebral palsy are high, but due to muscle hypertension they are often difficult to evoke.

Motor pathology in combination with sensory deficiency also leads to disturbances in speech and mental development [Mastyukova E. M., 1973, 1975]. Tonic reflexes influence the muscle tone of the articulatory apparatus. The labyrinthine tonic reflex helps to increase muscle tone at the root of the tongue, which makes it difficult to form voluntary vocal reactions. With pronounced ASTR, the tone in the articulatory muscles increases asymmetrically, more on the side of the “occipital limbs”. The position of the tongue in the oral cavity is also often asymmetrical, which interferes with the pronunciation of sounds. The severity of the symmetrical cervical tonic reflex creates unfavorable conditions for breathing, voluntary opening of the mouth, and forward movement of the tongue. This reflex causes an increase in tone in the back of the tongue; the tip of the tongue is fixed, poorly defined and often boat-shaped.

Disorders of the articulatory apparatus complicate the formation of vocal activity and the sound-pronunciation aspect of speech. The cry in such children is quiet, slightly modulated, often with a nasal tint or in the form of separate sobs that the child produces at the moment of inspiration. A disorder in the reflex activity of the articulatory muscles is the cause of the late appearance of humming, babbling, and the first words. Humming and babbling are characterized by fragmentation, low vocal activity, and poor sound complexes. In severe cases, true prolonged humming and babbling may be absent.

In the second half of the year, when combined hand-mouth reactions actively develop, oral synkinesis may appear - involuntary opening of the mouth when moving the hands. At the same time, the child opens his mouth very wide and a forced smile appears. Oral synkinesis and excessive expression of the unconditioned sucking reflex also prevent the development of voluntary activity of facial and articulatory muscles.

Thus, speech disorders in young children suffering from cerebral palsy are manifested by a delay in the formation of motor speech in combination with various forms of dysarthria (pseudobulbar, cerebellar, extrapyramidal). The severity of speech disorders depends on the time of brain damage during ontogenesis and the predominant localization of the pathological process. Mental disorders in cerebral palsy are caused by both primary brain damage and secondary delay in its development as a result of underdevelopment of motor speech and sensory functions. Paresis of the oculomotor nerves, delay in the formation of static and locomotor functions contribute to the limitation of visual fields, which impoverishes the process of perception of the surrounding world and leads to a lack of voluntary attention, spatial perception and cognitive processes. The normal mental development of a child is facilitated by activities that result in the accumulation of knowledge about the environment and the formation of a generalizing function of the brain. Paresis and paralysis limit the manipulation of objects and make it difficult to perceive them by touch. In combination with underdevelopment of visual-motor coordination, the lack of objective actions impedes the formation of objective perception and cognitive activity. Speech disorders also play an important role in the disruption of cognitive activity, which complicates the development of contact with others.

Lack of practical experience may be one of the reasons for disorders of higher cortical functions at an older age, especially the immaturity of spatial concepts. Violation of communication connections with others, the impossibility of full-fledged play activities, and pedagogical neglect also contribute to delayed mental development. Muscle hypertension, tonic reflexes, speech and mental disorders in cerebral palsy can be expressed to varying degrees. In severe cases, muscle hypertension develops in the first months of life and, combined with tonic reflexes, contributes to the formation of various pathological postures. As the child develops, the delay in age-related psychomotor development becomes more pronounced.

In moderate and mild cases, neurological symptoms and delayed development of age-related psychomotor skills are not so pronounced. The child gradually develops valuable symmetrical reflexes. Motor skills, despite their late development and inferiority, still enable the child to adapt to his defect, especially if the hands are easily affected. These children develop head control, the function of grasping an object, hand-eye coordination, and torso rotation. It is somewhat more difficult and takes longer for children to master the skills of sitting, standing and walking independently while maintaining balance. The range of motor, speech and mental disorders in children of the first year of life with cerebral palsy can vary widely. It can concern both all functional systems that make up the core of cerebral palsy, as well as its individual elements. Cerebral palsy syndrome is usually combined with other neurological syndromes: damage to the cranial nerves, hypertensive-hydrocephalic, cerebrasthenic, convulsive, autonomic-visceral dysfunctions.