GRODNO STATE MEDICAL INSTITUTE
DEPARTMENT OF NEUROLOGY
LECTURE
Theme: MOTOR DISORDERS SYNDROMES.
PERIPHERAL AND CENTRAL PARALYSIS΄.
Learning goal
... Consider the issues of the organization of movements in the process of evolution of the nervous system, anatomy, physiology and topical diagnosis of movement disorders.
1
Lecture content
(2).
1. Evolution of the nervous system, definition and types of movement disorders. 2. Peripheral movement disorders. 3. Syndromes of central movement disorders. 4. Differential diagnosis of paralysis.
Grodno, 1997
Traffic- one of the main manifestations of life, both in the most primitive creature and in a highly organized organism, which is a person. To understand the complex motor functions of a person, it is necessary to briefly recall those stages of development that the nervous system went through in the process of evolution from the simplest forms to the most differentiated form in humans.
In a primitive creature, there is no differentiation into a receptor - perceiving stimulus and an effector - responsive apparatus. With the appearance of the ganglion cell, it becomes possible to transfer information from the receptor organ to the muscle cell. At the initial stage of development of the central nervous system, the independence of the nervous apparatus continues to exist in its individual segments, each of which, in general, refers to a certain metamer of the body. The ventrally located motor cell, which subsequently develops into the anterior horn cell, is initially associated only with the peripheral centripetal, receptor, and effector end apparatus of the same segment.
The next stage of development is the emergence of intersegmental connections of the motor cell of the anterior horn with the receptor apparatus of not only adjacent, but also distant segments of the spinal cord, which in turn leads to a complication of the motor function. With the further development of the brain, pathways are added that serve to regulate the function of the motor cells of the anterior horn from the side of the higher parts of the nervous system. Thus, the organ of vision has a regulatory effect on the motor cell of the anterior horn through tractus tecto-spinalis, the organ of balance through tractus vestibulo-spinalis, the cerebellum through tractus rubro-spinalis, and subcortical formations through tractus reticulo-spinalis. Thus, the anterior horn cell is influenced by a number of systems important for movement and muscle tone, connected, on the one hand, with the entire musculature, and, on the other, through the optic tubercle and reticular substance with all receptor apparatus.
During further phylogenetic development, the most important pathway - tractus cortico-spinalis pyramidal arises, which originates mainly in the anterior central gyrus of the cerebral cortex and, in contrast to the pathways listed above, contributing to the implementation of large mass movements, conducts impulses to the cells of the anterior horns for the most differentiated, voluntary movements.
Consequently, the cell of the anterior horn is, as it were, a pool into which a lot of irritations are poured, but from which only one stream of impulses flows to the muscle - this is the final motor path. The cells of the anterior horns of the spinal cord in the brainstem correspond to the cells of the nuclei of the motor cranial nerves.
It becomes obvious that these movement disorders are fundamentally different depending on whether the final movement pathway is affected or any of the pathways that regulate it.
Movement disorders can be divided into the following types:
paralysis due to damage to bulbar or spinal motoneurons;
paralysis due to damage to cortico-spinal, cortico-bulbar or stem descending (subcortico-spinal) neurons;
coordination disorders (ataxia) as a result of lesions of the afferent and efferent fibers of the cerebellar system;
violations of movements and body position due to damage to the extrapyramidal system;
apraxia or non-paralytic disorders of purposeful movements due to damage to certain areas of the brain.
Definitions of movement disorders.
In everyday medical practice, the following terminology is used to characterize movement disorders:
paralysis (plegia) - complete absence of active movements, due to the interruption of one or more motor paths leading from the brain to the muscle fiber;
paresis - limitation of active movements due to a decrease in muscle strength.
Peripheral movement disorders.
Peripheral motor neuron paralysis is caused by physiological blockage or destruction of anterior horn cells or their axons in the anterior roots and nerves. The main clinical signs of peripheral motor neuron damage are:
hypo - areflexia - loss of tendon reflexes;
hypo - atony - lethargy and a drop in the tone of the affected muscles;
degenerative atrophy, muscle (qualitative and quantitative), 70-80% of the total muscle mass;
both muscle groups and individual muscles are affected;
plantar reflex, if triggered, then of the normal, flexion type;
fasciculations, with electromyography, a decrease in the number of motor units, fibrillation.
Syndromes of the defeat of the anterior horns. They are characterized by the presence of peripheral movement disorders without sensory disturbances. Paralysis of muscles innervated by different nerves is observed. The asymmetric distribution of paralysis is especially typical. With an incomplete pathological process, fibrillation is possible with corresponding changes on the EMG. The defeat of the anterior cells rarely covers the entire length of the spinal cord. Usually the process is limited to one or another area, often characteristic of certain forms of the disease.
The syndrome of damage to cells of the anterior horns of the spinal cord is the leading one in the clinic polio one of the most severe and already common childhood diseases. This is an acute viral infection, the causative agent of which has a significant affinity for the cells of the anterior horns of the spinal cord and the motor nuclei of the trunk. After a relatively short acute general infectious period, peripheral paralysis develops, which at first have a more widespread character, and then concentrate in limited segments, where destructive changes in the cells of the anterior horns are especially strong.
Scattered localization of the process at different levels is characteristic. Often it is limited to one side and touches some of the muscles belonging to the same spinal segment. The distal ends of the limbs are less commonly affected. Much more often, paralysis is localized in the proximal regions: on the arms - in the deltoid muscle, in the muscles of the shoulder, on the legs - in the quadriceps, in the muscles of the pelvic girdle. With poliomyelitis, not only muscles atrophy, but bone growth of the corresponding affected limb is impaired. Characterized by persistent areflexia, respectively, the affected segments.
The defeat of the cells of the anterior horns of the spinal cord with localization in the cervical spine is characteristic of another neuroviral infection - spring-summer tick-borne encephalitis. The disease occurs in the spring and summer months and develops sharply 10-15 days after the tick bite. Against the background of general infectious symptoms of the disease, already in the first days, one can note the appearance of paralysis, at first widespread, affecting the arms and shoulder girdle, later usually limited to the muscles of the neck, shoulder girdle and proximal arms. Atrophies develop early, often with fibrillar twitching. Paralysis of the muscles of the legs and trunk are rare.
Anterolateral syndrome is the main clinical sign spinal amyotrophy of Werdnig-Hoffmann ... The disease belongs to the hereditary group. The first symptoms appear in the second half of life. Flaccid paresis is initially localized in the legs, then quickly spreads to the muscles of the trunk and arms. Muscle tone and tendon reflexes fade away. Fasciculations, fibrillations of the tongue with the development of bulbar paralysis are typical. Lethal outcome by 14-15 years.
The syndrome of the lesion of the anterior horns is included in the picture of the disease, which is not limited to the peripheral neuron, but also extends to the central motor neuron - to the pyramidal pathway. A clinical picture appears amyotrophic lateral sclerosis characterized by amyotrophy and pyramidal symptoms with the subsequent development of bulbar paralysis.
In a number of cases, anterolateral syndrome is part of the clinical picture of diseases such as syringomyelia, intramedular tumor of the spinal cord.
Anterior root lesion syndromes. Diseases of the anterior roots are characterized by atrophic paralysis, which is difficult to distinguish from paralysis when cells of the anterior horns of the spinal cord are affected. It should be especially noted that this purely radicular atrophy is never accompanied by fibrillar twitching. In this case, coarser fascicular muscle twitching may be observed. Since the anterior roots are usually affected due to a disease of the membranes of the spinal cord or vertebrae, along with the anterior root syndrome, symptoms from the posterior roots, spine and spinal cord are almost always present.
Plexus lesion syndromes. The anterior and posterior roots of the spinal cord, joining in the intervertebral foramen, form the spinal nerve, which, upon exiting the spine, is divided into anterior and posterior branches. The posterior branches of the spinal nerves are directed to the skin and muscles of the occiput and back. The front branches, anastomosing with each other, form plexuses in the cervical and lumbosacral regions.
Cervical plexus syndrome (C1-C4) is characterized by paralysis of the deep cervical muscles in combination with paralysis or symptoms of phrenic nerve irritation. It occurs with tumors, enlarged lymph nodes, purulent and other processes in the upper cervical vertebrae, lung cancer, aneurysms of the aorta and subclavian artery. Brachial plexus syndromes are manifested in a combination of paralysis of individual muscles related to different nerves. With the defeat of the entire brachial plexus due to dislocation of the shoulder or fracture of the clavicle, gunshot wound or birth injury, all muscles, both the shoulder girdle and the upper limb, are affected.
According to the topographic division of the plexus into two parts, two main forms of paralysis of the brachial plexus are clinically distinguished upper (Erb-Duchenne) and lower (Dejerine-Klumpke ). The upper type of plexus paralysis develops when a certain area is damaged above the collarbone on the finger outward from the sternocleidomastoid muscle (Erb's point), where the 5th and 6th cervical nerves are connected to form a plexus. In this case, it is impossible to raise and abduct the arm, bend at the elbow. With lower paralysis, which is much less common than the upper one, small muscles of the hand, individual muscles of the palmar surface of the forearm, suffer.
Lumbosacral plexus syndrome is manifested by symptoms of damage from the femoral and sciatic nerves. Etiological factors are tumors and fractures of the pelvis, abscesses, an increase in retroperitoneal nodes.
Syndromes of central movement disorders.
Central paralysis occurs due to damage to cortico-spinal, cortico-bulbar and subcortico-spinal neurons. The cortico-spinal pathway originates from the giant and small Betz cells of the anterior central gyrus, the premotor zone of the superior frontal and postcentral gyri and represents the only direct connection between the brain and the spinal cord. The fibers leading to the nuclei of the cranial nerves are separated at the level of the midbrain, where they cross the midline and are directed to the opposite side to the corresponding nuclei in the trunk. The intersection of the cortico-spinal pathway is carried out at the border of the medulla oblongata and the spinal cord. Two thirds of the pyramidal path intersect. Subsequently, the fibers are directed to the motor cells of the anterior horns of the spinal cord. Central paralysis occurs when the cerebral cortex, subcortical white matter, internal capsule, brainstem, or spinal cord is affected and is characterized by the following general clinical features:
increased muscle tone by the type of spasticity (the "folding knife" phenomenon);
hyperreflexia of deep and areflexia of surface reflexes;
moderate muscle atrophy of the quantitative type (from inaction);
pathological symptoms of the extensor (sm Babinsky) and flexion (sm Rossolimo) type;
strengthening of protective reflexes;
the presence of pathological synkinesis (friendly movements);
Bilateral prolapse of the cortico-bulbar function. pathways (from the cortex to the nuclei of the cranial nerves) gives a picture of _pseudobulbar paralysis with disorder of chewing, swallowing, with dysarthria (speech impairment due to paralysis of the muscles involved in articulation). At the same time, the face is ammimic, the mouth is half-open, saliva flows out of it. Unlike bulbar paralysis, the chewing muscles and muscles of the tongue are not atrophic, and there are no fibrillar twitchings. All tendon reflexes of the face are increased. Violent laughter and crying are characteristic. Pseudobulbar paralysis is caused by bilateral hemispheric foci, which often develop at different times. The combination of pseudobulbar paralysis with tetraplegia can occur when the base of the pons varoli is affected.
Damage to the central neuron of the motor tract occurs in many diseases of the brain and spinal cord, in particular, in various types of vascular pathology (strokes), multiple sclerosis, amyotrophic lateral sclerosis, trauma, tumors, abscesses, encephalitis.
Differential diagnosis of paralysis.
When diagnosing paralysis, the localization and spread of muscle weakness should be considered. The diagnostic sign may be the presence or absence of atrophy of the muscles of the paretic limb.
Monoplegia. It must be remembered that this prolonged immobility of the limb can lead to its atrophy. However, in this case, atrophy usually does not reach the same degree of severity as it happens in diseases leading to muscle denervation. Tendon reflexes are unchanged. Electroexcitability and EMG differ little from the norm.
The most common cause of monoplegia without a decrease in muscle mass is damage to the cerebral cortex. With lesions of the cortico-spinal tract at the level of the capsule, trunk and spinal cord, monoplegia syndrome occurs rarely, since the fibers directed to the upper and lower extremities in these sections are compactly located. The most common cause of monoplegia is vascular lesions in the cerebral cortex. In addition, some injuries, tumors, and abscesses can cause similar symptoms. Weakness in one limb, especially in the lower limb, can develop with multiple sclerosis and spinal tumors, especially in the early stages of the disease.
Paralysis, accompanied by muscle atrophy, is characteristic of a pathological process in the spinal cord, roots or peripheral nerves. The level of damage can be determined by the nature of the distribution of weakness in the muscles, as well as using additional paraclinical diagnostic methods (CT, NMR and others). Brachial atrophic monoplegia can occur with trauma to the brachial plexus, poliomyelitis, syringomyelia, amyotrophic lateral sclerosis. Femoral monoplegia is more common and can be caused by damage to the thoracic and lumbar spinal cord in trauma, tumor, myelitis, multiple sclerosis. Unilateral paralysis of the lower limb may result from compression of the lumbosacral plexus by a retroperitoneal tumor.
Hemiplegia. Most often, paralysis in humans is expressed in the appearance of one-sided weakness in the upper and lower extremities and half of the face. The localization of the lesion, as a rule, is established according to the corresponding neurological manifestations. Among the causes of hemiplegia, lesions of the cerebral vessels and the trunk (strokes) prevail. Less significant causes include trauma (brain contusion, epidural and subdural hematomas, brain tumor, abscess, encephalitis, demyelinating diseases, complications after meningitis).
Paraplegia. Paralysis of both lower extremities can develop due to lesions of the spinal cord, spinal roots and peripheral nerves. As a rule, with acute injuries of the spinal cord, paralysis of all muscles occurs below this level. In the case of extensive lesions of the white matter, sensory disorders often occur below the level of the lesion, the function of the sphincters of the bladder and intestines is impaired. An intermittent spinal block (dynamic block, increased protein, or cytosis) often occurs. With an acute onset of the disease, sometimes difficulties arise in the differential diagnosis from neural paralysis, since in any acute process, spinal shock can lead to complete areflexia.
The most common causes of acute paraplegia (or tetraplegia) are spontaneous hematomyelia in spinal cord vascular malformations, anterior spinal artery thrombosis with infarction, dissecting aortic aneurysm, occlusion of spinal arteries with subsequent infarction (myelomalacia), spinal cord injuries and tumor metastases.
Subacute (rarely acute) development of paraplegia is observed in post-vaccination and post-infectious myelitis, acute demyelinating myelitis (Devik's disease), necrotizing myelitis, and epidural abscess with spinal cord compression.
Chronic paraplegia can develop with multiple sclerosis, spinal cord tumors, herniated disc of the cervical spine, chronic epidural infectious processes, familial spastic paraplegia, syringomyelia. The source of chronic asymmetric paraplegia can be parasagital meningioma.
Tetraplegia... The possible causes of tetraplegia are similar to those of paraplegia, except that this spinal cord injury is most often located at the level of the cervical spinal cord.
Isolated paralysis... Paralysis of an isolated muscle group indicates damage to one or more peripheral nerves. Diagnosis of an individual peripheral nerve lesion is based on the presence of weakness or paralysis of a muscle or muscle group and deterioration or loss of sensation in the area of innervation of the nerve of interest. EMG study is of significant diagnostic value.
Content
Introduction
1. Disorders of the motor sphere
2. Pathology of speech. Organic and functional speech disorders
Conclusion
Bibliography
Introduction
Speech as a specific mental process develops in close unity with motor skills and requires for its formation the fulfillment of a number of necessary conditions, such as: anatomical preservation and sufficient maturity of those cerebral systems that are involved in speech function; preservation of kinesthetic, auditory and visual perception; a sufficient level of intellectual development, which would provide the need for verbal communication; normal structure of the peripheral speech apparatus; adequate emotional and speech environment.
The emergence of speech pathology (including cases of a combination of such disorders with movement disorders) is due to the fact that, on the one hand, its formation is caused by the presence of varying degrees of severity of organic lesions of individual cortical and subcortical brain structures involved in ensuring speech functions, on the other hand, by secondary underdevelopment. or delayed "maturation" of the premotor-frontal and parieto-temporal cortical structures, disturbances in the rate and nature of the formation of visual-auditory and auditory-visual-motor nerve connections. In movement disorders, the afferent effect on the brain is distorted, which in turn intensifies existing cerebral dysfunctions or causes the appearance of new ones, and leads to asynchronous activity of the cerebral hemispheres.
Based on research into the causes of these disorders, we can talk about the relevance of considering this problem. The topic of the essay is devoted to the consideration of the causes and types of speech pathologies and movement disorders.
1. Disorders of the motor sphere
If we talk about the causes of movement disorders, it can be noted that most of them arise as a result of a violation of the functional activity of mediators in the basal ganglia, the pathogenesis can be different. The most common causes are degenerative diseases (congenital or idiopathic), possibly triggered by medication, organ failure, CNS infections, or ischemia of the basal ganglia. All movements are carried out through the pyramidal and parapyramidal paths. As for the extrapyramidal system, the main structures of which are the basal nuclei, its function is to correct and refine the movements. This is achieved mainly through influences on the motor zones of the hemispheres through the thalamus. The main manifestations of damage to the pyramidal and parapyramidal systems are paralysis and spasticity.
Paralysis can be complete (plegia) or partial (paresis), sometimes it is manifested only by the awkwardness of the hand or foot. Spasticity is characterized by an increase in the tone of the limb like a "folding knife", increased tendon reflexes, clonus, and pathological extensor reflexes (for example, Babinsky's reflex). She, too, can manifest itself only by the awkwardness of movements. Frequent symptoms also include flexor muscle spasms, which occur as a reflex to constant, uninhibited impulses from skin receptors.
Correction of movements is also provided by the cerebellum (The lateral parts of the cerebellum are responsible for coordinating the movements of the limbs, the middle parts are responsible for posture, gait, and trunk movements. Damage to the cerebellum or its connections is manifested by intentional tremor, dysmetria, adiadochokinesis and decreased muscle tone.), Mainly through the influence on the vestibulospinal pathway, as well as (with switching in the nuclei of the thalamus) to the same motor zones of the cortex as the basal nuclei (movement disorders that occur when the basal nuclei are damaged (extrapyramidal disorders), can be divided into hypokinesia (a decrease in the volume and speed of movements; for example, Parkinson's disease or parkinsonism of another origin) and hyperkinesis (excessive involuntary movements; for example, Huntington's disease. Hyperkinesis also includes tics.).
In individual mental illnesses (primarily with catatonic syndrome), conditions can be observed in which the motor sphere gains some autonomy, specific motor acts lose their connection with internal mental processes, and are no longer controlled by the will. In this case, the disorders become similar to neurological symptoms. It should be recognized that the similarity is only external, since, unlike hyperkinesis, paresis, and impaired coordination of movements in neurological diseases, movement disorders in psychiatry are devoid of an organic basis, functional and reversible.
Those suffering from catatonic syndrome cannot psychologically explain the movements they make, do not realize their painful nature until the moment of copying the psychosis. All disorders of the motor sphere can be divided into hyperkinesia (agitation), hypokinesia (stupor) and parakinesia (movement perversion).
Excitement, or hyperkinesia, in mentally ill people is a sign of an exacerbation of the disease. In most cases, the patient's movements reflect the richness of his emotional experiences. He can be controlled by fear of persecution, and then he flees. In manic syndrome, the basis of his motor skills is an indefatigable thirst for activity, and in hallucinatory states, he may look surprised, strive to draw the attention of others to his visions. In all these cases, hyperkinesia acts as a symptom secondary to painful emotional experiences. This type of excitement is called psychomotor.
In the case of catatonic syndrome, movements do not reflect the internal needs and experiences of the subject, therefore, arousal in this syndrome is called purely motor. The severity of hyperkinesia often speaks of the severity of the disease, its severity. However, at times there are severe psychoses with arousal confined to the bed.
Stupor is a state of immobility, an extreme degree of motor inhibition. Stupor can also reflect vivid emotional experiences (depression, asthenic affect of fear). In case of catatonic syndrome, on the contrary, stupor is devoid of internal content, meaningless. The term "substupor" is used to denote conditions accompanied by only partial lethargy. Although stupor implies a lack of motor activity, in most cases it is considered a productive psychopathological symptomatology, since it does not mean that the ability to move is irreversibly lost. Like other productive symptoms, stupor is a temporary condition and can be easily treated with psychotropic drugs.
The catatonic syndrome was originally described by K.L. Kalbaum (1863) as an independent nosological unit, and is currently considered as a symptom complex. One of the important features of the catatonic syndrome is the complex, contradictory nature of the symptoms. All motor phenomena are meaningless and not associated with psychological experiences. Tonic muscle tension is characteristic. Catatonic syndrome includes 3 groups of symptoms: hypokinesia, hyperkinesia and parakinesia.
Hypokinesias are represented by the phenomena of stupor and sub-stupor. Attention is drawn to the complex, unnatural, sometimes uncomfortable postures of patients. There is a sharp tonic muscle contraction. Taoky tone allows patients to sometimes hold any posture given by the doctor for some time. This phenomenon is called catalepsy, or waxy flexibility.
Hyperkinesia with catatonic syndrome is expressed in bouts of excitement. Characterized by the commission of senseless, chaotic, non-targeted movements. Motor and speech patterns are often observed (rocking, bouncing, waving hands, howling, laughing). An example of speech stereotypes is verbigeration, manifested by the rhythmic repetition of monotonous words and meaningless sound combinations.
Parakinesias are manifested by strange, unnatural movements, such as pretentious, campy facial expressions and pantomime.
In case of catatonia, a number of echo symptoms have been described: echolalia (repetition of the interlocutor's words), echopraxia (repetition of other people's movements), echomimia (copying the facial expressions of others). The listed symptoms can occur in the most unexpected combinations.
It is customary to distinguish lucid catatonia, proceeding against the background of clear consciousness, and oneiric catatonia, accompanied by clouding of consciousness and partial amnesia. With the outward similarity of the set of symptoms, these two conditions differ significantly along the course. Oneiric catatonia is an acute psychosis with dynamic development and a favorable outcome. Lucid catatonia, on the other hand, is a sign of remission-free malignant variants of schizophrenia.
Hebephrenic syndrome has significant similarities with catatonia. The predominance of movement disorders with lack of motivation, meaninglessness of actions is also characteristic of hebephrenia. The very name of the syndrome indicates the infantile nature of the behavior of patients.
Speaking about other syndromes accompanied by arousal, it can be noted that psychomotor agitation is one of the frequent components of many psychopathological syndromes.
Manic arousal differs from catatonic arousal in the purposefulness of actions. Mimicry expresses joy, patients strive to communicate, talk a lot and actively. With pronounced arousal, the acceleration of thinking leads to the fact that not everything said by the patient is clear, but his speech is never stereotyped.
Agitated depression is manifested by a combination of intense melancholy and anxiety. Mimicry reflects suffering. Wailing, crying without tears is characteristic. Often, anxiety is accompanied by a nihilistic megalomaniac delirium with the idea of the death of the world (Cotard syndrome). Acute hallucinatory - delusional states are also often expressed by psychomotor agitation. Acute hallucinosis can also manifest itself as psychomotor agitation.
Quite often, the cause of psychomotor agitation is clouding of consciousness. Delirium, the most common among the syndromes of confusion of consciousness, is manifested not only by disorientation disorders and pig-like true hallucinations, but also by extremely pronounced arousal. Patients seek to escape from the hallucinatory images pursuing them, attack them, try to defend themselves with a knife, throw heavy objects, fleeing, and can go out the window.
Amentive syndrome is characterized by an even greater severity of the condition. Patients are emaciated, unable to get out of bed. Their movements are chaotic, uncoordinated (yakation): they wave their arms, emit meaningless screams, crumple in their hands and tear the sheet, shake their head.
Oneyroid clouding of consciousness is manifested by the catatonic symptoms described above. With the twilight clouding of consciousness, there are both automated, safe actions for others, and attacks of ridiculous chaotic excitement, often accompanied by violent anger, brutal aggression.
Another variant of epileptic arousal is episodes of history, although not accompanied by clouding of consciousness and amnesia, but also often leading to dangerous, aggressive actions.
The danger of psychomotor agitation forced psychiatrists until the middle of the twentieth century. often use various means of restraint (belts, straitjackets, isolation wards). The emergence of powerful barbiturates at the beginning of the century, and especially the introduction of new psychotropic drugs into practice at the end of the 50s, made it possible to almost completely abandon the use of restraint measures. Currently, various antipsychotics are used to relieve psychomotor agitation, and, somewhat less often, benzodiazepine tranquilizers.
Stupor is less common in psychiatric practice than agitation. In addition to the catatonic syndrome, it can be a manifestation of severe depression, apathy-abulic syndrome and hysteria.
Among other syndromes accompanied by stupor, depressive stupor is noted, which is closely associated in its manifestations with the affect of melancholy. The face of the sick expresses suffering. The entire state is characterized by integrity, the absence of paradoxes.
Apathetic stupor is relatively rare. The face of such patients is amimic, expresses indifference. In apathic-abulic syndrome, there is no suppression of drives, so patients never refuse to eat. From prolonged inactivity, they become very fat. Unlike patients with catatonic stupor, they out loud show dissatisfaction if someone violates their comfort, makes them get out of bed, wash or cut their hair. The causes of apathetic stupor are schizophrenia or damage to the frontal lobes of the brain.
Hysterical stupor, like hysterical excitement, appears immediately after the emergence of a traumatic situation. The clinical picture can take the most unexpected forms.
In addition to hysterical, they describe psychogenically arising stupor states in life-threatening situations. Stupor in most cases is not a socially dangerous condition, since motor retardation is only one of the manifestations of any syndrome.
2. Pathology of speech. Organic and functional speech disorders
The problem of the etiology of speech disorders has followed the same path of historical development as the general doctrine of the causes of disease states.
Since ancient times, two points of view have been outlined - brain damage or disorders of the local speech apparatus, as the causes of disorders.
Despite this, only in 1861, when the French physician Paul Broca showed the presence in the brain of a field specifically related to speech, and associated the loss of speech with its defeat. In 1874, a similar discovery was made by Wernicke: a connection was established between understanding and the preservation of a certain area of the cerebral cortex. Since that time, the connection between speech disorders and morphological changes in certain parts of the cerebral cortex has been proven.
The most intensively questions of the etiology of speech disorders began to be developed from the 20s of this century. During these years, domestic researchers made the first attempts to classify speech disorders depending on the reasons for their occurrence. So, SM Dobrogaev (1922) singled out "diseases of higher nervous activity", pathological changes in the anatomical speech apparatus, inadequacy of education in childhood, as well as "general neuropathic states of the body" among the causes of speech disorders.
ME Khvatsev for the first time divided all the causes of speech disorders into external and internal, especially emphasizing their close interaction. He also identified organic (anatomical-physiological, morphological), functional (psychogenic), socio-psychological and neuropsychiatric causes.
Underdevelopment and brain damage in the prenatal period were attributed to organic reasons. He identified organic central (brain damage) and organic peripheral causes (damage to the organ of hearing, cleft palate and other morphological changes in the articulatory apparatus). Functional reasons M.E.Khvatsev explained by the teaching of I.P. Pavlov about disturbances in the ratio of the processes of excitation and inhibition in the central nervous system. He emphasized the interaction of organic and functional, central and peripheral causes. For neuropsychiatric reasons, he attributed mental retardation, memory impairment, attention and other disorders of mental functions.
The important role of M.E. Khvatsev also referred to socio-psychological reasons, understanding them as various adverse environmental influences. Thus, he was the first to substantiate the understanding of the etiology of speech disorders on the basis of a dialectical approach to the assessment of cause-and-effect relationships in speech pathology.
The cause of speech disorders is understood as the effect on the body of an external or internal harmful factor or their interaction, which determine the specifics of a speech disorder and without which the latter cannot arise.
The motor mechanism of speech is also provided by the higher located following brain structures:
With the defeat of the subcortical-cerebellar nuclei and the pathways that regulate muscle tone and the sequence of muscle contractions of the speech muscles, synchrony (coordination) in the work of the articulatory, respiratory and vocal apparatus, as well as the emotional expressiveness of speech, there are separate manifestations of central paralysis (paresis) with disorders of muscle tone, strengthening of individual unconditioned reflexes, as well as with a pronounced violation of the prosodic characteristics of speech - its tempo, smoothness, loudness, emotional expressiveness and individual timbre.
The defeat of the conducting systems that provide the conduction of impulses from the cerebral cortex to the structures of the underlying functional levels of the motor apparatus of speech (to the nuclei of the cranial nerves located in the brain stem), causes central paresis (paralysis) of the speech muscles with an increase in muscle tone in the muscles of the speech apparatus, strengthening of unconditioned reflexes and the appearance of reflexes of oral automatism with a more selective nature of articulatory disorders.
When the cortical regions of the brain are damaged, which provide both a more differentiated innervation of the speech muscles and the formation of speech praxis, various central motor speech disorders occur.
Speech disorders often occur with various mental traumas (fear, feelings of separation from loved ones, long-term traumatic situation in the family, etc.). This delays the development of speech, and in some cases, especially with acute mental trauma, it causes psychogenic speech disorders in the child: mutism, neurotic stuttering. These speech disorders, according to the classification of M. Ye. Khvatsev, can be conditionally classified as functional.
Functional speech disorders also include disorders associated with adverse effects on the child's body: general physical weakness, immaturity due to prematurity or intrauterine pathology, diseases of internal organs, rickets, metabolic disorders.
Thus, any general or neuropsychiatric illness of a child in the first years of life is usually accompanied by a violation of speech development. Hence, it is legitimate to distinguish between defects of formation and defects of formed speech, considering the age of three as their conditional subdivision.
The leading place in the perinatal pathology of the nervous system is occupied by asphyxia and birth trauma.
The occurrence of intracranial birth trauma and asphyxia (oxygen starvation of the fetus at the time of delivery) is facilitated by the violation of intrauterine development of the fetus. Birth trauma and asphyxia aggravate fetal brain development disorders that have arisen in utero. Birth trauma leads to intracranial hemorrhage and death of nerve cells. Intracranial hemorrhages can also capture the speech zones of the cerebral cortex, which entails various speech disorders of cortical genesis (alalia). In premature babies, intracranial hemorrhages occur most easily as a result of the weakness of their vascular walls.
In the etiology of speech disorders in children, a certain role can be played by the immunological incompatibility of the blood of the mother and the fetus (according to the Rh factor, the ABO system and other erythrocyte antigens). Rhesus or group antibodies, penetrating the placenta, cause the breakdown of fetal red blood cells. Under the influence of a substance toxic to the central nervous system - indirect bilirubin - the subcortical parts of the brain, the auditory nuclei are affected, which leads to specific disturbances in the sound-articulating side of speech in combination with hearing impairments. With intrauterine brain lesions, the most severe speech disorders are noted, combined, as a rule, with other polymorphic developmental defects (hearing, vision, musculoskeletal system, intelligence). At the same time, the severity of speech disorders and other developmental defects largely depends on the time of brain damage in the prenatal period.
Infectious and somatic diseases of the mother during pregnancy can lead to disorders of the uteroplacental circulation, nutritional disorders and oxygen starvation of the fetus. Violations of intrauterine development of the fetus - embryopathies - can occur in connection with viral diseases, taking medications, ionizing radiation, vibration, alcoholism and smoking during pregnancy. The adverse effects of alcohol and nicotine on offspring have been noted for a long time.
Toxicosis of pregnancy, prematurity, short-term asphyxia in childbirth cause mild minimal organic brain damage (children with minimal cerebral dysfunction - MMD).
Currently, with mild cerebral insufficiency, a special type of mental dysontogenesis is distinguished, which is based on the superior age-related immaturity of individual higher cortical functions. With minimal cerebral dysfunction, there is a delay in the rate of development of the functional systems of the brain, which require integrative activity for their implementation: speech, behavior, attention, memory, spatio-temporal representations and other higher mental functions.
Children with minimal cerebral dysfunction are at risk for speech disorders.
Speech disorders can also occur as a result of the impact of various adverse factors on the child's brain and at subsequent stages of its development. The structure of these speech disorders is different depending on the time of exposure to harm and the localization of brain damage. Hereditary factors are also of some importance in the etiology of speech disorders in children. Often they are predisposing conditions that are realized in speech pathology under the influence of even minor adverse influences.
Thus, the etiological factors causing speech disorders are complex and polymorphic. The most common combination of hereditary predisposition, unfavorable environment and damage or impairment of brain maturation under the influence of various unfavorable factors.
Dwelling on the types of speech disorders, one should focus directly on the existing deviations and pathologies of speech associated with congenital or acquired causes of their occurrence.
Violation of sound pronunciation with normal hearing and intact innervation of the vocal apparatus, or dyslalia, is one of the most common pronunciation defects. There are two main forms of dyslalia, depending on the localization of the disorder and the reasons for the defect in sound pronunciation; functional and mechanical (organic).
In cases where organic disorders (peripherally or centrally caused) are not observed, they speak of functional dyslalia. With deviations in the structure of the peripheral speech apparatus (teeth, jaws, tongue, palate), one speaks of mechanical (organic) dyslalia. Functional dyslalia includes defects in the reproduction of speech sounds (phonemes) in the absence of organic disorders in the structure of the articulatory apparatus. The causes are biological and social: general physical weakness of the child due to somatic diseases; mental retardation (minimal brain dysfunction), delayed speech development, selective violation of phonemic perception; an unfavorable social environment that hinders the development of a child's communication.
Rhinolalia (violation of the timbre of the voice and sound pronunciation, due to anatomical and physiological defects of the speech apparatus) in its manifestations differs from dyslalia in the presence of an altered nasalized timbre of the voice. Depending on the nature of the dysfunction of the palatine-pharyngeal closure, various forms of rhinolalia are distinguished. With the open form of rhinolalia, oral sounds acquire nasality. Functional open rhinolalia is due to various reasons. It is explained by insufficient rise of the soft palate during phonation in children with sluggish articulation.
One of the functional forms is the "habitual" open rhinolalia. It is often observed after removal of adenoid enlargements or, less often, as a result of post-diphtheria paresis, due to prolonged limitation of the mobile soft palate. Organic open rhinolalia can be acquired or congenital. Acquired open rhinolalia is formed with perforation of the hard and soft palate, with cicatricial changes, paresis and paralysis of the soft palate. The cause may be damage to the glossopharyngeal and vagus nerves, injuries, tumor pressure, etc. The most common cause of congenital open rhinolalia is congenital cleavage of the soft or hard palate, shortening of the soft palate.
Dysarthria is a violation of the pronunciation side of speech due to insufficient innervation of the speech apparatus.
The leading defect in dysarthria is a violation of the sound-articulating and prosodic aspects of speech, associated with organic damage to the central and peripheral nervous systems.
Disturbances of sound pronunciation in dysarthria manifest themselves to varying degrees and depend on the nature and severity of the damage to the nervous system. In mild cases, there are individual distortions of sounds, "blurred speech", in more severe cases, distortions, replacements and omissions of sounds are observed, tempo, expressiveness, modulation suffer, in general, the pronunciation becomes indistinct.
With severe lesions of the central nervous system, speech becomes impossible due to complete paralysis of the speech motor muscles. Such disorders are called anarthria (a - the absence of a given sign or function, arthron - a joint).
Dysarthric speech disorders are observed with various organic brain lesions, which in adults have a more pronounced focal character. Less pronounced forms of dysarthria can be observed in children without obvious movement disorders, who have undergone mild asphyxia or birth trauma, or have a history of the influence of other mild adverse effects during intrauterine development or during childbirth.
In 1911 N. Gutzmann defined dysarthria as a violation of articulation and identified two of its forms: central and peripheral.
The initial study of this problem was carried out mainly by neuropathologists in the framework of focal brain lesions in adult patients. The work of M.S.Margulis (1926), who for the first time clearly distinguished dysarthria from motor aphasia and divided it into bulbar and cerebral forms, greatly influenced the modern understanding of dysarthria. The author proposed a classification of cerebral forms of dysarthria based on the localization of the brain lesion focus.
The pathogenesis of dysarthria is determined by organic damage to the central and peripheral nervous system under the influence of various unfavorable external (exogenous) factors affecting the prenatal period of development, at the time of childbirth and after birth. Among the reasons, asphyxia and birth trauma, damage to the nervous system in hemolytic disease, infectious diseases of the nervous system, craniocerebral trauma, less often cerebral circulation disorders, brain tumors, malformations of the nervous system, for example, congenital aplasia of the nuclei of the cranial nerves are of great importance. (Moebius syndrome), as well as hereditary diseases of the nervous and neuromuscular systems.
Clinical and physiological aspects of dysarthria are determined by the localization and severity of brain damage. The anatomical and functional relationship in the location and development of motor and speech zones and pathways determines the frequent combination of dysarthria with motor disorders of various nature and severity.
Violations of sound pronunciation in dysarthria result from damage to various brain structures necessary to control the motor mechanism of speech (peripheral motor nerves to the muscles of the speech apparatus; nuclei of these peripheral motor nerves located in the brain stem; nuclei located in the stem and in the subcortical parts of the brain) ... The defeat of the above structures gives a picture of peripheral paralysis (paresis): nerve impulses do not enter the speech muscles, metabolic processes in them are disrupted, the muscles become flaccid, flabby, their atrophy and atony are observed, as a result of an interruption of the spinal reflex arc, reflexes from these muscles will disappear, begins areflexia.
Voice disorders are also referred to as speech disorders. Voice impairment is the absence or disorder of phonation due to pathological changes in the vocal apparatus. There are two main terms for the pathology of the voice: aphonia - a complete absence of voice and dysphonia - partial disturbances in pitch, strength and timbre.
Voice disorders associated with various diseases of the vocal apparatus are common in both adults and children. The pathology of the larynx in children has increased over the past two decades, which is associated with the expansion of resuscitation measures.
Voice disorders are divided into central and peripheral, each of them can be organic and functional. Most of the disorders are manifested as independent, the causes of their occurrence are diseases and various changes only in the vocal apparatus. But they can accompany other more severe speech disorders, entering the structure of the defect in aphasia, dysarthria, rhinolalia, stuttering.
Voice pathology resulting from anatomical changes or chronic inflammatory processes of the vocal apparatus is considered organic. Peripheral organic disorders include dysphonia and aphonia in chronic laryngitis, paresis and paralysis of the larynx, conditions after tumor removal.
Central paresis and paralysis of the larynx depend on damage to the cerebral cortex, bridge, medulla oblongata, and pathways. In children, they are found in infantile cerebral palsy.
The most common and varied are functional disorders of the voice. They are not accompanied by inflammatory or any anatomical changes in the larynx. Peripheral functional disorders include phonasthenia, hypo- and hypertonic aphonia and dysphonia.
Phonasthenia is a violation of the voice in a number of cases, especially in the initial stages, is not accompanied by visible objective changes in the vocal apparatus. Phonasthenia is manifested in a violation of the coordination of breathing and phonation, the impossibility of mastering the voice - to strengthen and weaken the sound, the appearance of detonation and a number of subjective sensations.
Hypotonic dysphonia (aphonia) is caused, as a rule, by bilateral myopathic paresis, i.e., paresis of the internal muscles of the larynx. They occur with some infections (ARVI, influenza, diphtheria), as well as with severe overexertion of the voice. The pathology of the voice can manifest itself from mild hoarseness to aphonia with symptoms of vocal fatigue, tension and pain in the muscles of the neck, neck and chest.
Hypertonic (spastic) voice disorders are associated with an increase in the tone of the laryngeal muscles with a predominance of tonic spasm at the time of phonation. The causes of their occurrence are not fully understood, but spastic dysphonia and aphonia develop in people who force their voice.
Rhinophonia and rhinolalia stand somewhat apart from other vocal disorders, since their pathophysiological mechanism consists in the improper function of the soft palate of an organic or functional nature. With a closed rhinophony, nasal consonants acquire oral resonance, vowels lose sonority, and the timbre becomes unnatural.
Open rhinophonia manifests itself in the pathological nasalization of all oral sounds, while the voice is weak, stifled. Voice defects, in addition to impaired resonance, are due to the fact that the soft palate is functionally connected with the internal muscles of the larynx and affects the symmetry and tone of the vocal folds.
Functional disorders of the voice of central origin include functional, or psychogenic aphonia. It arises suddenly as a reaction to a traumatic situation in persons prone to hysterical reactions, more often in girls and women.
Violations of the tempo of speech include bradilalia and tachilalia. With these disorders, the development of both external and internal speech is impaired. The speech is hard to understand for others.
Bradilalia is a pathologically slow speech rate. With bradilalia, the voice is monotonous, loses modulation, constantly maintains the same pitch, sometimes a nasal tint appears. The musical accent also changes with the pronunciation of individual syllables, the pitch of the voice fluctuates upward or downward. Non-speech symptoms in bradilalia are expressed in disorders of general motor skills, fine motor skills of hands, fingers, facial muscles. The movements are slow, sluggish, insufficiently coordinated, incomplete in volume, motor awkwardness is observed. The face is amimic. The features of mental activity are also noted: slowness and disorders of perception, attention, memory, thinking.
Tachilalia is a pathologically accelerated speech rate. ME Khvatsev (1959) considered the main cause of tachyllalia to be congenital speech motor deficiency of the speech apparatus, as well as sloppy, uneven speech of others, lack of attention and timely correction of the child's rapid speech. A. Liebmann distinguished between the deficiencies of motor and acoustic perception that underlie tachyllia. G. Gutzman argued that this disorder is a consequence of impaired perception. According to E. Frechels, accelerated speech arises due to the fact that thoughts rush extremely quickly and one concept is displaced by the next one before the first can be uttered. M. Nedolechny believed that the reason for the accelerated speech was insufficient articulation, since patients experience difficulties in pronouncing unusual and long words.
Stuttering is a violation of the tempo-rhythmic organization of speech, caused by the convulsive state of the muscles of the speech apparatus.
Alalia - the absence or underdevelopment of speech due to organic damage to the speech areas of the cerebral cortex in the prenatal or early period of the child's development. Intrauterine pathology leads to diffuse damage to the brain substance, birth craniocerebral trauma and asphyxia of newborns cause more local disorders. Somatic diseases only exacerbate the impact of pathological causes of a neurological nature, which are the leading ones.
Some authors (R. Cohen, 1888; M. Zeeman, 1961; R. Luchzinger, A. Salei, 1977, and others) emphasize the role of heredity, family predisposition in the etiology of alalia. However, there are no convincing scientific data on the role of heredity in the origin of alalia in the literature. In recent years, the significant role of minimal brain damage (minimal cerebral dysfunction) has been emphasized in the development of alalia.
Aphasia is a complete or partial loss of speech due to local brain lesions.
The causes of aphasia are disorders of cerebral circulation (ischemia, hemorrhage), trauma, tumors, infectious diseases of the brain. Aphasias of vascular origin most often occur in adults. As a result of rupture of cerebral aneurysms, thromboembolism caused by rheumatic heart disease, and traumatic brain injury. Aphasias are often observed in adolescents and young people.
Aphasia occurs in about a third of cases of cerebrovascular accident, most often motor aphasia is observed.
Aphasia is one of the most severe consequences of brain damage, in which all types of speech activity are systemically impaired. The complexity of speech disorder in aphasia depends on the location of the lesion. With aphasia, the implementation of different levels, sides, and types of speech activity (oral speech, speech memory, phonemic hearing, understanding of speech, writing, reading, counting, etc.) is specifically systematically impaired.
Acoustic-Gnostic sensory aphasia was first described by the German psychiatrist Wernicke. He showed that aphasia, which he called sensory, occurs when the posterior third of the superior temporal gyrus of the left hemisphere is affected. A distinctive feature of this form of aphasia is a violation of understanding of speech when it is perceived by ear.
Acoustic-mnestic aphasia occurs when the middle and posterior parts of the temporal region are affected (A.R. Luria, 1969, 1975; L. S. Tsvetkova, 1975). A.R. Luria believes that it is based on a decrease in auditory-speech memory, which is caused by an increased inhibition of auditory traces. With the perception of each new word and its awareness, the patient loses the previous word. This violation also manifests itself when repeating a series of syllables and words.
Amnestic-semantic aphasia occurs when the parieto-occipital region of the dominant hemisphere is affected. With the defeat of the parieto-occipital (or posterior inferior parietal) parts of the cerebral hemisphere, a smooth syntagmatic organization of speech is preserved, no searches for the sound composition of the word are noted, there are no phenomena of a decrease in auditory-speech memory or a violation of phonemic perception.
Afferent kinesthetic motor aphasia occurs when the secondary zones of the postcentral and inferior parietal parts of the cerebral cortex are affected, located behind the central, or Roland's, sulcus.
Effective motor aphasia occurs when the anterior branches of the left middle cerebral artery are affected. It is accompanied, as a rule, by kinetic apraxia, which is expressed in the difficulties of assimilating and reproducing the motor program.
The defeat of the premotor parts of the brain causes pathological inertia of speech stereotypes, leading to sound, syllabic and lexical permutations and perseveration, repetitions. Perseverations, involuntary repetitions of words, syllables, resulting from the impossibility of timely switching from one articulatory act to another.
Dynamic aphasia occurs when the posterior frontal parts of the left hemisphere dominant in speech are affected, that is, the parts of the third functional block - the block of activation, regulation and planning of speech activity.
The main speech defect in this form of aphasia is the difficulty, and sometimes the complete impossibility of active development of the utterance. With a severe severity of the disorder, not only speech is noted, but also general spontaneity, lack of initiative, pronounced echolalia occurs, and sometimes echopraxia.
In the aspect of speech pathologies, a violation of written speech is also considered. These include: alexia, dyslexia, agraphia, dysgraphia.
Dyslexia is a partial specific violation of the reading process, caused by the lack of formation (violation) of higher mental functions and manifested in repeated errors of a persistent nature.
The etiology of dyslexia is associated with the impact of biological and social factors. Dyslexia is caused by organic damage to the areas of the brain involved in the reading process. Functional causes can be associated with exposure to internal and external factors. Thus, in the etiology of dyslexia, both genetic and exogenous factors (pathology of pregnancy, childbirth, asphyxia "chain" of childhood infections, head trauma) are involved.
Dysgraphia is a partial specific violation of the writing process. This violation is due to the underdevelopment (disintegration) of the higher mental functions that carry out the process of writing in the norm.
Conclusion
Based on the research experience of such scientists as P. Broca, Wernicke, K.L. Kalbaum, S.M. Dobrogaev, M.E. Khvatsev, L.S. Volkova, A.R. Luria, M. S. Margulis, A. Liebmann, G. Gutzman, E. Frechels, M. Nedolechny and others - who made a significant contribution to the study of the problems of speech and motor pathologies, modern trends (both theoretical and practical) in the field of studying the mechanisms of impairment of motor and speech disorders makes it possible not only to more thoroughly and thoroughly delve into the essence of this problem, but also creates promising conditions for direct corrective and adaptive assistance to people suffering from these disorders. In order for help to be as effective as possible, it is necessary not only to know the essence of the mechanisms of mental processes and the action of motor skills, the mechanism of their violation. Specialists engaged in the study of these problems need to constantly and continuously orient their activities towards preventing the occurrence of pathologies, as well as systematically monitor the state of impaired functions, prevent violations, and provide specific assistance to patients in this area.
List of used literature
1. Zharikov MN, Tyulpin YG Psychiatry. - M .: Medicine, 2002.
2. Zeigarnik B.V. Pathopsychology. - M .: Publishing house of Moscow University, 1986.
3. Liebmann A. Pathology and therapy of stuttering and tongue-tied. (St. Petersburg - 1901) // Speech therapy reader (extracts and texts). Textbook for students of higher and secondary educational institutions: In 2 vols. T.I / Ed. L.S.Volkova and V.I.Seliverstov. - M .: Humanit. ed. center VLADOS, 1997.
4. Speech therapy: Textbook for students defectol. fac. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskoy. - M .: Humanit. ed. center VLADOS, 1998.
5. Luria.A.R. Stages of the traversed path // Scientific autobiography. - M .: Publishing house of Moscow. un-that, 1982.
6. Neiman L.V., Bogomilsky M.R. Anatomy, physiology and pathology of the organs of hearing and speech // Textbook. for stud. higher. ped. educational Head - M.: Gumanit. ed. center VLADOS, 2003.
7. Jaspers K. General psychopathology // Per. with him. L.O. Akopyan, ed. doct. honey. VF Voitsekh and Ph.D. Philos. Sciences O. Yu. Boytsova. - M .: Practice, 1997.
Speech therapy: A textbook for students defectol. fac. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskoy. - M .: Humanit. ed. center VLADOS, 1998, p. 230.
Speech therapy: A textbook for students defectol. fac. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskoy. - M .: Humanit. ed. center VLADOS, 1998, p. 243
Speech therapy: A textbook for students defectol. fac. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskoy. - M .: Humanit. ed. center VLADOS, 1998, p. 248
Speech therapy: A textbook for students defectol. fac. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskoy. - M .: Humanit. ed. center VLADOS, 1998, p. 86.
Zeigarnik B.V. Pathopsychology. - M .: Publishing house of Moscow University, 1986, S. 180.
Speech therapy: A textbook for students defectol. fac. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskoy. - M .: Humanit. ed. center VLADOS, 1998, p. 93.
Neiman L.V., Bogomilsky M.R. Anatomy, physiology and pathology of the organs of hearing and speech // Textbook. for stud. higher. ped. educational Head - M.: Gumanit. ed. center VLADOS, 2003, p. 177.
Speech therapy: A textbook for students defectol. fac. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskoy. - M .: Humanit. ed. center VLADOS, 1998, p. 93
Zeigarnik B.V. Pathopsychology. - M .: Publishing house of Moscow University, 1986, p. 184.
Speech therapy: A textbook for students defectol. fac. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskoy. - M .: Humanit. ed. center VLADOS, 1998, p. 95.
Zeigarnik B.V. Pathopsychology. - M .: Publishing house of Moscow University, 1986, p. 187.
Speech therapy: A textbook for students defectol. fac. ped. universities / Ed. L.S. Volkova, S.N. Shakhovskoy. - M .: Humanit. ed. center VLADOS, 1998, p. 176.
Catatoic syndrome psychopathological syndrome (a group of syndromes), the main clinical manifestation of which is movement disorders. In the structure of the catatonic syndrome, there are catatonic agitation and catatonic stupor.
Catatonic stupor is characterized by motor retardation, silence, muscle hypertension. Patients can be in a constrained state for several weeks or even months. All kinds of activity, including instinctive, are violated.
There are three types of catatonic stupor:
Wax flexible stupor(cataleptic stupor) is characterized by the patient freezing for a long time in the position he has adopted or given to him, even very uncomfortable. Not responding to loud speech, they can respond to a quiet whispering speech, spontaneously disinhibit in conditions of night silence, becoming available to contact.
Negativistic stupor characterized, along with motor retardation, constant resistance of the patient to any attempts to change his posture.
Stupor with torpor characterized by the greatest severity of motor inhibition and muscle hypertension. Patients accept and maintain embryoposis for a long time, a symptom of an air cushion may be observed. Mutual transitions of one type of stupor to another, pathetic to impulsive excitement are possible, although this is rarely observed. Mutual transitions of catatonic excitement to stupor and vice versa are possible: pathetic excitement can be replaced by cataleptic stupor, impulsive - negativistic or stupor with stupor, just as stupor can be suddenly interrupted by the corresponding type of excitement. With a cataleptic stupor, hallucinations, delusional disorders, and sometimes signs of impaired consciousness of the type of oneyroid can be observed - the so-called. oneiroid catatonia, upon exit from which most of the productive symptoms amnesia. Negativistic stupor and stupor with stupor are represented by the so-called. lucid (transparent, pure) catatonia, in which there are no productive symptoms, no clouding of consciousness, patients are oriented, aware and remember their surroundings. Catatonic syndromes are observed in schizophrenia, infectious, organic and other psychoses. According to two studies, 12-17% of young people with autism have catatonic symptoms.
Movement disorders: types of arousal.
Catatonic syndrome- psychopathological syndrome (a group of syndromes), the main clinical manifestation of which is movement disorders. In the structure of the catatonic syndrome, catatonic excitement and catatonic stupor are distinguished.
There are two forms of catatonic excitement:
Pathetic catatonic arousal characterized by gradual development, moderate motor and speech excitement. There is a lot of pathos in the speech, echolalia can be noted. The mood is elevated, but it has the character not of hyperthymia, but of exaltation, occasionally there is unreasonable laughter. With an increase in symptoms, features of hebephrenia appear - hebephrenic-catatonic excitement. Impulsive actions are possible. Disorders of consciousness do not arise.
Impulsive catatonic excitement develops sharply, actions are impetuous, often cruel and destructive, are socially dangerous. Speech consists of individual phrases or words, characterized by echolalia, echopraxia, perseveration. With the extreme severity of this type of catatonic excitement, the movements are chaotic, can acquire a choreiform character, patients are prone to self-harm, are silent
Disinhibition syndrome.
Hyperdynamic syndrome, or motor disinhibition syndrome, manifests itself, first of all, in the form of excessive motor mobility, restlessness, fussiness.
At the same time, the so-called fine motor skills suffer, the child's movements are inaccurate, sweeping, somewhat angular. The coordination of movements and their purposefulness are very often violated. Such children are usually clumsy. Along with this, self-service skills suffer, it is difficult for them to independently make a toilet, brush their teeth, and wash themselves. A simple morning washing and brushing procedure can easily turn into a morning bath.
Hyperdynamic syndrome. The hyperactive child has sloppy blotted writing and gnarled drawings. Hyperdynamic syndrome in children is always combined with unstable attention, lack of focus. They are characterized by increased distraction during any activity. All this is often combined with increased fatigue and early exhaustion. The syndrome of motor disinhibition is typical for children of preschool and early school age.
In kindergartens, hyperactive children are called fidgets. They are constantly in motion, like clockwork running on the court, changing toys in the game with great speed, trying to participate in several games at the same time. It is very difficult to attract the attention of such a “keen” child. It is very difficult to put an overactive child to rest during the day, and if it succeeds, then the sleep is not long and the child wakes up drenched with sweat. It is characterized by increased sweating. Often, blood vessels appear on the forehead and temples, and some blue can be seen under the eyes.
Hyperactive children do not sit still, even in elementary school. Their attention is constantly shifting from one activity to another. Such children often get up in class, walk around the classroom. It is extremely difficult for them to stay in one place, and even more so to sit through the entire lesson at a desk. A hyperactive child is characterized by a situation in which he falls into the category of hooligans with pedagogical neglect precisely because of increased fatigue and exhaustion. By the end of the lesson, such a child can literally jump at the desk, often changing posture and attracting the attention of other children.
The described behavior of hyperactive children is often joined by other "extra" movements, when the movements are repeated several times, like tics.
If you notice a behavior similar to that described in your child, then do not postpone a visit to a child psychiatrist. In most cases, hyperactivity in children can be removed.
Violations and their causes in alphabetical order:
motor disorder -
Movement disorders can occur with both central and peripheral damage to the nervous system. Movement disorders can occur with both central and peripheral damage to the nervous system.
Terminology
- Paralysis is a violation of motor function that occurs as a result of the pathology of the innervation of the corresponding muscles and is characterized by a complete absence of voluntary movements.
- Paresis is a violation of motor function that occurs as a result of the pathology of the innervation of the corresponding muscles and is characterized by a decrease in the strength and / or amplitude of voluntary movements.
- Monoplegia and monoparesis - paralysis or paresis of the muscles of one limb.
- Hemiplegia or hemiparesis - paralysis and paresis of both limbs, sometimes the face on one side of the body.
- Paraplegia (paraparesis) - paralysis (paresis) of both limbs (either upper or lower).
- Quadriplegia or quadriparesis (also tetraplegia, tetraparesis) - paralysis or paresis of all four limbs.
- Hypertonicity - increased muscle tone. There are 2 types:
- Muscle spasticity, or classic pyramidal paralysis, - increased muscle tone (mainly flexors of the arm and extensors of the leg), characterized by uneven resistance in different phases of passive movement; occurs when the pyramidal system is damaged
- Extrapyramidal rigidity - a diffuse uniform wax-like increase in muscle tone, equally pronounced in all phases of active and passive movements (muscle agonists and antagonists are affected), due to damage to the extrapyramidal system.
- Hypotension (muscle flaccidity) - a decrease in muscle tone, characterized by their excessive compliance with passive movements; usually associated with damage to a peripheral motor neuron.
- Paratonia is the inability of some patients to completely relax their muscles, despite the doctor's instructions. In milder cases, rigidity is observed with rapid passive movement of the limb and normal tone with slow movement.
- Areflexia - the absence of one or more reflexes, caused by a violation of the integrity of the reflex arc or by the inhibitory effect of higher divisions of the nervous system.
- Hyperreflexia - increased segmental reflexes due to weakening of the inhibitory effects of the cerebral cortex on the segmental reflex apparatus; occurs, for example, when the pyramidal pathways are affected.
- Pathological reflexes - the general name for reflexes found in an adult when the pyramidal pathways are affected (in young children, such reflexes are considered normal).
- Clonus is an extreme degree of increase in tendon reflexes, manifested by a series of rapid rhythmic contractions of a muscle or muscle group, for example, in response to their single stretching.
The most common forms of movement disorders are paralysis and paresis - loss or weakening of movement due to impaired motor function of the nervous system. Paralysis of the muscles of one half of the body is called hemiplegia, both upper or lower limbs - paraplegia, all limbs - tetraplegia. Depending on the pathogenesis of the paralysis, the tone of the affected muscles can be either lost (flaccid paralysis) or increased (spastic paralysis). In addition, a distinction is made between peripheral paralysis (if it is associated with damage to the peripheral motor neuron) and central (as a result of damage to the central motor neurons).
For what diseases there is a motor impairment:
Causes of movement disorders
- Spasticity - damage to the central motor neuron along its entire length (cerebral cortex, subcortical formations, brain stem, spinal cord), for example, in stroke involving the motor zone of the cerebral cortex or cortico-spinal tract
- Rigidity - indicates dysfunction of the extrapyramidal system and is caused by damage to the basal nuclei: the medial part of the globus pallidus and the substantia nigra (for example, with parkinsonism)
- Hypotension occurs in primary muscular diseases, lesions of the cerebellum and some extrapyramidal disorders (Huntington's disease), as well as in the acute stage of pyramidal syndrome
- The phenomenon of paratonia is characteristic of lesions of the frontal lobe or diffuse cortical lesions
- Coordination of motor activity can be impaired due to muscle weakness, sensory disorders or damage to the cerebellum
- Reflexes decrease with damage to the lower motor neuron (cells of the anterior horns, spinal roots, motor nerves) and increase with damage to the upper motor neuron (at any level above the anterior horns, with the exception of the basal ganglia).
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Movement Disorders Syndromes
Movement disorders in newborns and infants are fundamentally different from those in older children and adults. Brain damage in the early stages of ontogenesis in most cases causes generalized changes, which extremely complicates topical diagnosis; more often we can only talk about the predominant lesion of certain parts of the brain.
Differentiation of pyramidal and extrapyramidal disorders in this age period 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 differ depending on the age of the child. This is especially true for the first and second age periods (up to 3 months), when the child has physiological hypertension.
Changes in muscle tone are manifested by muscle hypotension, dystonia, and hypertension. The syndrome of muscle hypotension 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. Muscle hypotension is one of the most commonly found 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, in children with congenital or early acquired dementia. At the same time, hypotension may appear or become more pronounced at any age period if the clinical symptoms of the disease begin several months after birth or are progredient in nature.
Hypotension, expressed from birth, can transform into normotonia, dystonia, hypertension, or remain the leading symptom throughout the first year of life. The severity of the clinical manifestations of muscle hypotension varies from a slight decrease in resistance to passive movements to complete atony and lack of active movements.
If the syndrome of muscle hypotension is mild and not combined with other neurological disorders, it either does not affect the age-related development of the child, 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 the coordinated activity of many muscle groups for their implementation. So, a planted child is 9 months old, but cannot sit on his own. These children begin to walk later, and the period of walking with support is delayed for a long time.
Muscle hypotension can be limited to one limb (obstetric paresis of the arm, traumatic paresis of the leg). In these cases, the delay will be partial.
The pronounced muscle hypotension syndrome has a significant effect on the delay in motor development. Thus, motor skills in the congenital form of Werdnig-Hoffmann spinal amyotrophy in a child of 9-10 months may correspond to the age of 2-3 months. The delay in motor development, in turn, becomes the cause of the peculiarities of the formation of mental functions. For example, the lack of the possibility of voluntary gripping of an object leads to underdevelopment of visual-motor coordination and manipulative activity. Since muscle hypotension is often combined with other neurological disorders (convulsions, hydrocephalus, cranial nerve paresis, etc.), the latter can modify the nature of developmental delay, determined by hypotension as such. It should also be noted that the quality of the muscle hypotension syndrome itself and its effect on developmental delay will vary depending on the disease. With convulsions, congenital or early acquired dementia, not so much hypotension as delayed mental development is the reason for the lag in motor development.
The syndrome of movement disorders in children of the first year of life may be accompanied by muscular dystonia (a condition when muscular hypotension alternates with hypertension). At rest in these children with passive movements, general muscular hypotonia is expressed. When you try to actively perform any movement, with positive or negative emotional reactions, muscle tone sharply increases, pathological tonic reflexes become pronounced. These conditions are called "dystonic attacks". Most often, muscular dystonia is observed in children who have undergone hemolytic disease as a result of Rh or ABO incompatibility. The pronounced syndrome of muscular dystonia makes it practically impossible for the child to develop straightening reflexes of the trunk and balance reactions due to the constantly changing muscle tone. The syndrome of mild transient muscular dystonia does not significantly affect the age-related motor development of the child.
The syndrome of muscular hypertension is characterized by an increase in resistance to passive movements, a limitation of spontaneous and voluntary motor activity, an increase in tendon reflexes, an expansion of their zone, and clonuses of the feet. An increase in muscle tone can 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. In connection with the incompleteness of the processes of myelination, the symptoms of Babinsky, Oppenheim, Gordon, and others cannot be considered always pathological. Normally, they are not sharply expressed, unstable and weaken as the child develops, but with an increase in muscle tone they become bright and do not tend to fade.
The severity of the syndrome of muscle hypertension can vary from a slight increase in resistance to passive movements to complete stiffness (posture of decerebral rigidity), when any movement is practically impossible. In these cases, even muscle relaxants are unable to induce muscle relaxation, much less passive movements. If the syndrome of muscular hypertension is not clearly expressed, does not combine with pathological tonic reflexes and other neurological disorders, its effect 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 the tone is more increased, differentiation and final consolidation of certain motor skills will be delayed. So, with an increase in muscle tone in the hands, a delay in the development of the direction of the hands to the object, the seizure of the toy, the manipulation of 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 take the toy later, he retains an ulnar grip for a long time, or the grip with the entire hand. Finger grip (forceps grip) is slow to form and sometimes requires additional stimulation. The development of the protective function of the hands may be delayed, then the balance reactions in the prone position, sitting, standing and walking are also delayed, respectively.
With an increase in muscle tone in the legs, the formation of the support reaction of the legs and independent standing is delayed. Children reluctantly get to their feet, prefer to crawl, stand on their toes on the support.
Cerebellar disorders in children of the first year of life can be the result of underdevelopment of the cerebellum, its defeat as a result of asphyxia and birth trauma, in rare cases - as a result of hereditary degeneration. They are characterized by a decrease in muscle tone, impaired coordination with hand movements, a disorder of balance reactions when trying to master the skills of sitting, getting up, standing and walking. Cerebellar symptoms proper - intentional tremor, impaired coordination, ataxia - can be detected only after the development of voluntary motor activity in the child. One can suspect disorders of the ordination by observing how the child reaches for the toy, grabs it, brings it to the mouth, sits, stands, walks.
Infants with impaired coordination make a lot of unnecessary movements when trying to grab a toy, this is especially pronounced in a sitting position. Self-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, take an object. For fear of falling, the child does not manipulate objects with both hands for a long time; begins to walk after a year, 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 disorders 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 can impart a certain specificity to developmental delay in the form of a more pronounced delay in the function of gaze fixation and tracking, hand-eye coordination, and impaired spatial orientation. Dysarthric disorders especially affect the development of expressive speech skills.
The most common form of movement disorders in children of the first year of life is the syndrome of infantile cerebral palsy (cerebral palsy). The clinical manifestations of this syndrome depend on the severity of muscle tone, an increase in which to one degree or another is observed in any form of cerebral palsy. In some cases, a 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, unconditioned relaxation is depressed. By the end of the second month of life, when the child is in a prone position and upright makes attempts to hold his head, the dystonic stage appears. The child periodically becomes restless, his muscle tone rises, his arms are straightened with internal rotation of the shoulders, the forearms and hands are pronated, the fingers are clenched into fists; legs are extended, given and often crossed. Dystonic attacks last a few seconds, are repeated throughout the day, and can be triggered by external stimuli (loud knocking, crying of another child).
Movement disorders in cerebral palsy are due to the fact that damage to the immature brain disrupts the sequence of stages of its maturation. Higher integrative centers have no inhibitory effect on primitive stem reflex mechanisms. The reduction of unconditioned reflexes is delayed, the pathological tonic cervical and labyrinth reflexes are released. Combined with an increase in muscle tone, they prevent the sequential 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, gripping a toy, sitting, standing, walking).
To understand the peculiarities of impaired psychomotor development in children with cerebral palsy, it is necessary to consider the influence of tonic reflexes on the formation of voluntary motor activity, as well as speech and mental functions.
Tonic labyrinth reflex. Children with a pronounced tonic labyrinth reflex in the supine position cannot tilt their heads, stretch their arms forward to bring them to their mouths, grab an object, and later grab, pull themselves up and sit down. They lack the prerequisites for the development of fixation and free tracking of the object in all directions, the optical rectifying reflex on the head does not develop, and head movements cannot freely follow the movement of the eyes. The development of hand-eye coordination is impaired. In such children, it is difficult to turn from the back to one side, and then onto the stomach. In severe cases, even by the end of the first year of life, the turn from the back to the abdomen is carried out only in a "block", that is, 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, turn on his stomach with a torsion, he has no prerequisites for the development of the sitting function. The severity of the tonic labyrinth reflex is in direct proportion to the degree of increase in muscle tone.
With the severity of the tonic labyrinth reflex in the prone position as a result of increased flexor tone, the head and neck are bent, the shoulders are pushed forward and downward, the arms bent at 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, free his arms from under the chest and rest on them to support the upper body, bend his legs and kneel. Difficulty turning from the abdomen ^ to the back for sitting down. A gradually bent back leads to the development of kyphosis in the thoracic spine. This posture prevents the development of chain straightening reflexes in the prone position and the child's acquisition of an upright position, and also excludes the possibility of sensory-motor development and vocal reactions.
The influence of the tonic labyrinth reflex to a certain extent depends 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, unbend their heads, throw them back, and raise the upper part of the body. Despite the extension position of the head, muscle tone in the flexors of the arms remains elevated, the arms do not provide support for the torso, and the child falls on his back.
Asymmetric tonic cervical reflex (ASTR) is one of the most pronounced reflexes in infantile cerebral palsy. The severity of ASHTR depends on the degree of increase in muscle tone in the hands. With severe damage to the hands, the reflex appears almost simultaneously with the turn of the head to the side. If the hands are slightly affected, which occurs with mild spastic diplegia, ASHTR occurs inconsistently and requires a longer latency period for its appearance. ASHTR is more pronounced in the supine position, although it can also be observed in the sitting position.
ASHTR, combined with the tonic labyrinth reflex, prevents the seizure of the toy, the development of hand-eye coordination. The child cannot bring his hands forward in order to bring his hands closer to the midline, and accordingly hold the object he is looking at with both hands. The child cannot bring the toy put into the hand to the mouth, eyes, since when trying to bend the hand, the head turns in the opposite direction. Because of the extension of the arm, many children are unable to suck on their fingers, as most healthy children do. ASHTR is in most cases more pronounced on the right side, so many children with cerebral palsy prefer to use the left hand. With a pronounced ASHTR, the child's head and eyes are often fixed to one side, so it is difficult for him to follow the object on the opposite side; as a result, a syndrome of unilateral spatial agnosia develops, and spastic torticollis is formed. spinal scoliosis.
Combined with the tonic labyrinth reflex, ASHTR makes it difficult to turn to the side and to the stomach. When the child turns his head to the side, the arising ASHTR prevents the movement of the torso after the head, and the child cannot free his arm from under the torso. Difficulty turning to the side prevents the child from forming the possibility of transferring the center of gravity from one hand to the other when moving the body forward, which is necessary for the development of reciprocal crawling.
ASHTR disturbs the balance in the sitting position, since the spread of muscle tone on one side (its increase mainly in the extensors) is opposite to its spread to the other (predominant increase in the flexors). The child loses balance and falls to the side and back. In order not to fall forward, the child must tilt his head and torso. The effect of ARTH 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 tonic cervical reflex. With the severity of the symmetrical cervical tonic reflex, a child with increased flexor tone in the arms and body, put on his knees, will not be able to straighten his arms and lean on them to support his body weight. In this position, the head tilts, the shoulders are pulled in, the arms are brought, bend at the elbow joints, the hands are clenched into fists. As a result of the influence of the symmetrical cervical tonic reflex in the prone position in the child, the muscle tone in the extensors of the legs increases sharply, so that it is difficult to bend them in the hip and knee joints and put him on his knees. This position can be eliminated by passively raising the child's head, taking him by the chin.
With the severity of the symmetric cervical tonic reflex, it is difficult for a child to maintain control of the head, and, accordingly, to stay in a sitting position. Raising the head while sitting increases the extensor tone in the arms, and the child falls backwards; lowering the head increases the flexion tone in the arms and the child falls forward. The isolated effect of symmetrical cervical tonic reflexes on muscle tone is rarely revealed, since in most cases they are combined with ASRT.
Along with tonic cervical and labyrinth reflexes in the pathogenesis of motor disorders in children with cerebral palsy, a positive supportive reaction and friendly movements (synkinesia) play an important role.
Positive supportive response. The influence of a positive supportive reaction on movement is manifested in an increase in the extensor tone in the legs when the legs touch the support. Since children with cerebral palsy always touch the support first with the ball of their feet when standing and walking, this response is constantly supported and stimulated. All leg joints are fixed. Rigid limbs can support a child's body weight, but they significantly complicate the development of balance reactions, which require joint mobility and fine regulation of the constantly reciprocal static state of the muscles.
Friendly reactions (synkinesis). The effect of synkinesis on the child's motor activity is to increase muscle tone in various parts of the body while actively trying to overcome the resistance of spastic muscles in any limb (i.e., perform movements such as gripping a toy, extending the arm, taking a step, etc.). ). So, if a child with hemiparesis strongly squeezes the ball with a healthy hand, muscle tone can build up on the paretic side. Trying to straighten the spastic arm can cause an increase in extensor tone in the homolateral leg. Strong flexion of the affected leg in a child with hemcplegia 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 emergence of friendly reactions prevents the development of purposeful movements and is one of the reasons for the formation of contractures. With cerebral palsy, synkinesis most often manifests itself in the oral muscles (when trying to grab a toy, the child opens his mouth wide). With voluntary motor activity, all tonic reflex reactions act simultaneously, combining with each other, therefore it is difficult to identify them in isolation, although in each individual case it is possible to note the predominance of one or another tonic reflex. The degree of their severity depends on the state of muscle tone. If muscle tone is sharply increased and extensor spasticity prevails, tonic reflexes are pronounced. With double hemiplegia, when the arms and legs or arms are equally affected more than the legs, tonic reflexes are pronounced, observed simultaneously and do not have a tendency to inhibition. They are less pronounced and constant in spastic diplegia and hemiparetic cerebral palsy. In spastic diplegia, when the hands are relatively safe, 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. With 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 insignificant. They become more noticeable in the second year of life. In the atonic-astatic form of cerebral palsy, the reactions of balance, coordination and static functions suffer more. Tonic reflexes can be observed only sporadically.
Tendon and periosteal reflexes in cerebral palsy are high, however, due to muscle hypertension, they are often caused with difficulty.
Motor pathology in combination with sensory insufficiency also leads to impaired speech and mental development [Mastyukova EM, 1973, 1975]. Tonic reflexes affect the muscle tone of the articulatory apparatus. The labyrinth tonic reflex increases muscle tone at the root of the tongue, which makes it difficult to form voluntary vocal reactions. With pronounced ASHTR, 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 disrupts 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 dorsum of the tongue, the tip of the tongue is fixed, poorly expressed and often has the shape of a boat.
Violations of the articulatory apparatus complicate the formation of vocal activity and the sound-articulating side of speech. The cry in such children is quiet, little modulated, often with a nasal tinge or in the form of separate sobbing, which the child produces at the moment of inhalation. Disorder of the reflex activity of the articulatory muscles is the reason for 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 drawn-out humming and babbling may be absent.
In the second half of the year, when there is an active development of combined hand-mouth reactions, oral synkinesis may appear - involuntary opening of the mouth with hand movements. At the same time, the child opens his mouth very wide, a violent smile appears. Oral synkinesis and excessive severity of the unconditioned sucking reflex also prevent the development of voluntary activity of mimic 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 in the process of 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, a delay in the formation of static and locomotor functions contribute to the limitation of the 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 the child is facilitated by activities that result in the accumulation of knowledge about the environment and the formation of the 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 the underdevelopment of visual-motor coordination, the absence of object-related actions prevents the formation of object-oriented perception and cognitive activity. Speech disorders also play an important role in impaired cognitive activity, which impede the development of contact with the environment.
Lack of practical experience can be one of the causes of disorders of higher cortical functions at an older age, especially the lack of formation of spatial representations. Violation of communicative connections with the environment, the impossibility of full-fledged game activity, pedagogical neglect also contribute to mental retardation. 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 cases of moderate and mild neurological symptoms and a delay in the development of age-related psychomotor skills are not so pronounced. The child gradually develops valuable symmetrical reflexes. Motor skills, despite their late formation 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 longer for children to master the skills to sit, stand and walk independently, 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 infantile cerebral palsy, and its individual elements. Cerebral palsy syndrome is usually combined with other neurological syndromes: lesions of cranial nerves, hypertensive-hydrocephalic, cerebrasthenic, convulsive, vegetative-visceral dysfunctions.
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