Movement disorder syndromes. Movement disorders II. damage to the pyramidal and parapyramidal systems

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 the clinical symptoms of the disease 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 hypotonia is not clearly expressed and is not combined with other neurological disorders, it either does not affect 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." Most often, muscular dystonia is observed in children who have suffered 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 psychomotor development disorders 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 the thoracic 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 at 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 (syncinesia) play an important role in the pathogenesis of motor disorders in children with cerebral palsy.

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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Visual disorders

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

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

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

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

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

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

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

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

Normal vision is taken as one.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

C) in 2 cases anomalies of a different nature.

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

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

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

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

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

Disorders of motor functions that arise from various local brain lesions can be divided into relatively elementary ones, associated with damage to the executive, efferent mechanisms of movements, and more complex ones, extending to voluntary movements and actions and associated mainly with damage to the afferent mechanisms of motor acts.

Relatively elementary movement disorders occur when the subcortical parts of the pyramidal and extrapyramidal systems are damaged. When the cortical part of the pyramidal system (4th field), located in the precentral region, is damaged, movement disorders are observed in the form paresis or paralysis a specific muscle group: arms, legs or torso on the side opposite to the lesion. Lesion of the 4th field is characterized by flaccid paralysis (when the muscles do not resist passive movement), occurring against the background of decreased muscle tone. But with foci located anterior to the 4th field (in the 6th and 8th fields of the cortex), a picture of spastic paralysis appears, i.e., loss of corresponding movements against the background of increased muscle tone. The phenomena of paresis, together with sensory disorders, are also characteristic of damage to the post-central parts of the cortex. These motor dysfunctions are studied in detail by neurology. Along with these neurological symptoms, damage to the cortical part of the extrapyramidal system also causes disturbances in complex voluntary movements, which will be discussed below.

When the pyramidal tracts are damaged in the subcortical areas of the brain (for example, in the area of ​​the internal capsule), complete loss of movements (paralysis) occurs on the opposite side. Complete unilateral loss of movements of the arms and legs (hemiplegia) appears with rough lesions. More often, in the clinic of local brain lesions, phenomena of partial decrease in motor functions on one side (hemiparesis) are observed.

When crossing the pyramidal path in the pyramidal zone - the only zone where the pyramidal and extrapyramidal paths are anatomically separated - voluntary movements are realized only with the help of the extrapyramidal system.

The pyramidal system is involved in the organization of predominantly precise, discrete, spatially oriented movements and in the suppression of muscle tone. Damage to the cortical and subcortical parts of the extrapyramidal system leads to the appearance of various movement disorders. These disorders can be divided into dynamic (i.e., disturbances in actual movements) and static (i.e., disturbances in posture). With damage to the cortical level of the extrapyramidal system (6th and 8th fields of the premotor cortex), which is associated with the ventrolateral nucleus of the thalamus, globus pallidus and cerebellum, spastic motor disorders occur in the contralateral limbs. Stimulation of the 6th or 8th fields causes turns of the head, eyes and body in the opposite direction (adversia), as well as complex movements of the contralateral arm or leg. Damage to the subcortical striopallidal system, caused by various diseases (parkinsonism, Alzheimer's disease, Pick's disease, tumors, hemorrhages in the area of ​​the basal ganglia, etc.), is characterized by general immobility, adynamia, and difficulty moving. At the same time, violent movements of the contralateral arms, legs, and head appear - hyperkinesis. In such patients, there is a violation of tone (in the form of spasticity, rigidity or hypotonia), which forms the basis of the posture, and a violation of motor acts (in the form of increased tremor - hyperkinesis). Patients lose the ability to care for themselves and become disabled.

Selective damage to the pallidum zone (a more ancient part than the striatum) can lead to athetosis or choreoathetosis(pathological wave-like movements of the arms and legs, twitching of the limbs, etc.)

The defeat of striopallidal formations is accompanied by another type of motor symptoms - a violation facial expressions And pantomimes, i.e., involuntary motor components of emotions. These disorders can appear either in the form of amymia (mask-like face) and general immobility (lack of involuntary movements of the whole body during various emotions), or in the form of forced laughter, crying or forced walking, running (propulsion). Often these patients suffer from subjective experience of emotions.

Finally, in such patients the physiological synergies - normal combined movements of different motor organs (for example, swinging arms while walking), which leads to unnaturalness of their motor acts.

The consequences of damage to other structures of the extrapyramidal system have been studied to a lesser extent, with the exception, of course, of the cerebellum. Cerebellum It is the most important center for coordinating various motor acts, the “organ of balance”, providing a number of unconditional motor acts associated with visual, auditory, skin-kinesthetic, vestibular afferentation. Damage to the cerebellum is accompanied by a variety of movement disorders (primarily disorders of coordination of motor acts). Their description constitutes one of the well-developed sections of modern neurology.

Damage to pyramidal and extrapyramidal structures spinal cord comes down to dysfunction of motor neurons, as a result of which the movements controlled by them are lost (or disrupted). Depending on the level of damage to the spinal cord, the motor functions of the upper or lower extremities are impaired (on one or both sides), and all local motor reflexes are carried out, as a rule, normally or are even enhanced due to the elimination of cortical control. All these movement disorders are also discussed in detail in the neurology course.

Clinical observations of patients who have damage to one or another level of the pyramidal or extrapyramidal system have made it possible to clarify the functions of these systems. The pyramidal system is responsible for the regulation of discrete, precise movements, completely subordinate to voluntary control and well afferented by “external” afferentation (visual, auditory). It controls complex spatially organized movements in which the whole body is involved. The pyramidal system regulates predominantly the phasic type of movements, i.e. movements that are precisely dosed in time and space.

The extrapyramidal system controls mainly the involuntary components of voluntary movements; In addition to the regulation of tone (the background of motor activity against which phasic short-term motor acts are played out), these include: maintaining posture; regulation of physiological tremor; physiological synergies; coordination of movements; general coordination of motor acts; their integration; body plasticity; pantomime; facial expressions, etc.

The extrapyramidal system also controls a variety of motor skills and automatisms. In general, the extrapyramidal system is less corticolized than the pyramidal system, and the motor acts regulated by it are less voluntary than the movements regulated by the pyramidal system. It should, however, be remembered that the pyramidal and extrapyramidal systems represent a single efferent mechanism, the different levels of which reflect different stages of evolution. The pyramidal system, as an evolutionarily younger system, is to a certain extent a “superstructure” over the more ancient extrapyramidal structures, and its emergence in humans is primarily due to the development of voluntary movements and actions.

4. Violations of voluntary movements and actions. The problem of apraxia.

Disturbances of voluntary movements and actions are complex movement disorders, which are primarily associated with damage to the cortical level of motor functional systems.

This type of motor dysfunction is called apraxia in neurology and neuropsychology. Apraxia refers to such disorders of voluntary movements and actions that are not accompanied by clear elementary movement disorders - paralysis and paresis, obvious disorders of muscle tone and tremor, although combinations of complex and elementary movement disorders are possible. Apraxia primarily refers to disorders of voluntary movements and actions performed with objects.

The history of the study of apraxia goes back many decades, but until now this problem cannot be considered completely solved. The difficulties of understanding the nature of apraxia are reflected in their classifications. The most well-known classification, proposed at one time by G. Lipmann and recognized by many modern researchers, distinguishes three forms of apraxia: ideational, suggesting the disintegration of the “idea” of movement, its concept; kinetic, associated with a violation of the kinetic “images” of movement; ideomotor, which is based on the difficulties of transmitting “ideas” about movement to “movement execution centers.” G. Lipmann associated the first type of apraxia with diffuse brain damage, the second with damage to the cortex in the lower premotor region, and the third with damage to the cortex in the lower parietal region. Other researchers identified forms of apraxia in accordance with the affected motor organ (oral apraxia, apraxia of the trunk, apraxia of the fingers, etc.) or with the nature of the disturbed movements and actions (apraxia of expressive facial movements, object apraxia, apraxia of imitative movements, gait apraxia, agraphia etc.). To date, there is no unified classification of apraxia. A. R. Luria developed a classification of apraxia based on a general understanding of the psychological structure and brain organization of a voluntary motor act. Summarizing his observations of disorders of voluntary movements and actions, using the method of syndromic analysis, which isolates the main leading factor in the origin of disorders of higher mental functions (including voluntary movements and actions), he identified four forms of apraxia. First he designated it as kinesthetic apraxia. This form of apraxia, first described by O. F. Foerster in 1936, and later studied by G. Head, D. Denny-Brown and other authors, occurs when the lower parts of the postcentral region of the cerebral cortex are affected (i.e., the posterior parts of the cortical nucleus motor analyzer: 1, 2, partially 40th fields, predominantly of the left hemisphere). In these cases, there are no clear motor defects, muscle strength is sufficient, there are no paresis, but the kinesthetic basis of movements suffers. They become undifferentiated and poorly controlled (the “shovel hand” symptom). Patients have impaired movements when writing, the ability to correctly reproduce various hand postures (postural apraxia); They cannot show without an object how this or that action is performed (for example, how tea is poured into a glass, how a cigarette is lit, etc.). While the external spatial organization of movements is preserved, the internal proprioceptive kinesthetic afferentation of the motor act is disrupted.

With increased visual control, movements can be compensated to a certain extent. When the left hemisphere is damaged, kinesthetic apraxia is usually bilateral in nature; when the right hemisphere is damaged, it often manifests itself only in one left hand.

Second form apraxia, identified by A. R. Luria, - spatial apraxia, or apraktoagnosia, - occurs with damage to the parieto-occipital cortex at the border of the 19th and 39th fields, especially with damage to the left hemisphere (in right-handed people) or with bilateral lesions. The basis of this form of apraxia is a disorder of visual-spatial synthesis, a violation of spatial representations (“top-bottom”, “right-left”, etc.). Thus, in these cases, visuospatial afferentation of movements is affected. Spatial apraxia can also occur against the background of intact visual gnostic functions, but more often it is observed in combination with visual optical-spatial agnosia. Then a complex picture of apraktoagnosia arises. In all cases, patients experience apraxia of posture and difficulties in performing spatially oriented movements (for example, patients cannot make the bed, get dressed, etc.). Strengthening visual control of movements does not help them. There is no clear difference when performing movements with open and closed eyes. This type of disorder also includes constructive apraxia- difficulties in constructing a whole from individual elements. With left-sided lesions of the parieto-occipital cortex, optical-spatial agraphia due to the difficulties of correctly writing letters that are differently oriented in space.

Third form apraxial - kinetic apraxia- associated with damage to the lower sections of the premotor area of ​​the cerebral cortex (6th, 8th fields - the anterior sections of the “cortical” nucleus of the motor analyzer). Kinetic apraxia is part of the premotor syndrome, i.e., it occurs against the background of impaired automation (temporal organization) of various mental functions. Manifests itself in the form of the disintegration of “kinetic melodies”, i.e. a violation of the sequence of movements, the temporary organization of motor acts. This form of apraxia is characterized by motor perseverations, manifested in the uncontrolled continuation of a movement that has once begun (especially one performed serially).

This form of apraxia was studied by a number of authors - K. Kleist, O. Förster, etc. It was studied in particular detail by A. R. Luria, who established in this form of apraxia the commonality of violations of the motor functions of the hand and speech apparatus in the form of primary difficulties in automating movements and developing motor skills . Kinetic apraxia manifests itself in a violation of a wide variety of motor acts: object actions, drawing, writing, and in the difficulty of performing graphic tests, especially with the serial organization of movements ( dynamic apraxia). With damage to the lower premotor cortex of the left hemisphere (in right-handed people), kinetic apraxia is observed, as a rule, in both hands.

Fourth form apraxia - regulatory or prefrontal apraxia- occurs when the convexital prefrontal cortex is damaged anterior to the premotor areas; occurs against the background of almost complete preservation of tone and muscle strength. It manifests itself in the form of violations of the programming of movements, the disabling of conscious control over their execution, and the replacement of necessary movements with motor patterns and stereotypes. With a gross breakdown of voluntary regulation of movements, patients experience symptoms echopraxia in the form of uncontrolled imitative repetitions of the experimenter’s movements. With massive lesions of the left frontal lobe (in right-handed people), along with echopraxia, echolalia - imitative repetitions of heard words or phrases.

Regulatory apraxia is characterized by systemic perseverations, i.e., perseveration of the entire motor program as a whole, and not of its individual elements. Such patients, after writing under dictation in response to a proposal to draw a triangle, trace the outline of the triangle with movements characteristic of writing, etc. The greatest difficulties in these patients are caused by changing programs of movements and actions. The basis of this defect is a violation of voluntary control over the implementation of movement, a violation of speech regulation of motor acts. This form of apraxia most clearly manifests itself when the left prefrontal region of the brain is damaged in right-handed people.

The classification of apraxia created by A. R. Luria is based mainly on the analysis of motor dysfunction in patients with damage to the left hemisphere of the brain. The forms of disturbance of voluntary movements and actions with damage to various cortical zones of the right hemisphere have been studied to a lesser extent; This is one of the urgent tasks of modern neuropsychology.

Literature:

1. II International Conference in Memory of A. R. Luria: Collection of reports “A. R. Luria and psychology of the XXI century.” / Ed. T. V. Akhutina, Zh. M. Glozman. - M., 2003.

2. Current issues of functional interhemispheric asymmetry. – 2nd All-Russian Conference. M., 2003.

3. Luria, A. R. Lectures on general psychology - St. Petersburg: Peter, 2006. - 320 p.

4. Functional interhemispheric asymmetry. Reader / Ed. N.N. Bogolepova, V.F. Fokina. – Chapter 1. – M., 2004.

5. Khomskaya E.D. Neuropsychology. – St. Petersburg: Peter, 2006. – 496 p.

6. Reader on neuropsychology / Rep. ed. E. D. Chomskaya. - M.: “Institute of General Humanitarian Research”, 2004.

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

Classification of causes, symptoms, signs of movement disorders

Diagnosis of movement disorders

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

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

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

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

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

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

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

Differential diagnosis of movement disorders

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

Treatment of movement disorders

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

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

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

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

Relevance. Psychogenic movement disorders (PDD) are a fairly common problem in neurology; they occur in 2 to 25% of patients seeking neurological help. As a rule, patients visit many doctors before they are given the correct diagnosis, and most often the correct conclusion is reached by a specialist in the field of movement disorders. It is advisable to identify a psychogenic disorder as early as possible to avoid unnecessary examinations and prescriptions and to get the best chance of cure.

Pathophysiology. The use of functional neuroimaging methods has shown that in patients with PDD, the amygdala (Amygdala) is in a state of increased functional activity and is more activated to external stimuli. In addition, these patients showed more active limbic-motor functional connectivity, especially between the right Amg and supplementary motor cortex in response to emotional stimuli. Hyperactivated Amg appears to involve motor structures in the process of emotional arousal, generating subconscious motor phenomena. By analogy with conversion palsy, potentially key brain regions functionally involved in the pathological process are the limbic-motor connections and the ventromedial prefrontal cortex. It is no coincidence that the literature describes cases of effective treatment of PDD using transcranial magnetic stimulation ().

Diagnostic criteria for PDR. To date, the Fahn and Williams (1988) criteria for psychogenic movement disorder have been used. They included sudden onset, inconsistency in manifestations, increased emphasis on painful manifestations, reduction or disappearance of these manifestations when attention is distracted, false weakness or sensory disturbances, pain, exhaustion, excessive fearfulness, flinching from unexpected actions, unnatural, bizarre movements, and accompanying somatization. The diagnostic criteria of Fahn and Williams initially included identifying points for the diagnosis of psychogenic dystonias; later these criteria were extended to other PDDs. These criteria are set out below: [ A] Documented PDD: sustained improvement after psychotherapy, suggestion or placebo, no evidence of movement disorder when spectators are not present. [ IN] Clinically established PDD: inconsistency with the classic manifestations of known movement disorders, false neurological symptoms, multiple somatizations, obvious psychiatric disorders, excessive attention to painful manifestations, feigned slowness. [ WITH] Probable PDD: inconsistency in manifestations or inconsistency with the criteria for organic DD, decrease in motor manifestations when attention is distracted, multiple somatizations. [ D] Possible PDD: obvious emotional disturbances.

H. Shill, P. Gerber (2006), based on the original criteria of Fahn and Williams, developed and proposed a new version of the criteria for diagnosing PDD. [ 1 ] Clinically convincing PDD is if: it is curable with the help of psychotherapy; does not appear when there are no observers; premotor potential is detected on the electroencephalogram (only for myoclonus). [ 2 ] If these features are not typical, the following diagnostic criteria are used: [ 2.1 ] primary criteria – inconsistency in manifestations with organic DR * , excessive pain or fatigue susceptibility to a “pattern” of disease disorder; [ 2.2 ] secondary criteria – multiple somatizations ** (other than pain and fatigue) and/or obvious mental disorder.

* Multiple somatizations are considered as a spectrum of patient complaints, covering three different systems. Severe pain and fatigue were taken into account as diagnostic criteria if they were the dominant complaints, but did not correspond to objective data.

** Manifestations that conflict with an organic disease: false weakness and sensory disturbances, inconsistent development in a temporal aspect, a clear dependence of manifestations in response to distracting maneuvers of a specialist, sudden onset, the presence of spontaneous remissions, astasia-abasia, selective incapacity, involvement of tremor in repetitive movements, muscle tension accompanying tremors, atypical response to medication, overreaction to external stimuli.

To establish levels of diagnostic certainty, it is suggested to use the following: [ 1 ] clinically defined PDR: if at least three primary criteria and one secondary criterion are identified; [ 2 ] clinically probable: two primary criteria and two secondary; [ 3 ] clinically possible: one primary and two secondary or two primary and one secondary.

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