Syndromes of movement disorders
Movement disorders in newborns and infants are fundamentally different from those in older children and adults. Damage to the brain in the early stages of ontogenesis in most cases causes generalized changes, which makes topical diagnosis extremely difficult; more often it is possible to speak only about the primary lesion of those or other parts of the brain.
It is very difficult in this age period to differentiate pyramidal and extrapyramidal disorders. The main characteristics in the diagnosis of motor disorders in the first year of life are muscle tone and reflex activity. Symptoms of changes in muscle tone may look different 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 pronounced physiological hypertension.
Changes in muscle tone are manifested by muscle hypotension, dystonia and hypertension. The syndrome of muscular 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 may be normal, increased, reduced or absent depending on the level of damage to the nervous system. Muscular hypotension is one of the most frequently detected syndromes in newborns and infants. It can be expressed from birth, as is the case with congenital forms of neuromuscular diseases, asphyxia, intracranial and spinal birth trauma, damage to the peripheral nervous system, some hereditary metabolic disorders, chromosomal syndromes, in children with congenital or early acquired dementia. At the same time, hypotension may appear or become more pronounced at any age if the clinical symptoms of the disease begin several months after birth or are of a progressive nature.
Hypotension, expressed from birth, can transform into normotonia, dystonia, hypertension, or remain a leading symptom throughout the first year of life. The severity of clinical manifestations of muscular hypotension varies from a slight decrease in resistance to passive movements to complete atony and the absence of active movements.
If the syndrome of muscular hypotension is not pronounced and is not combined with other neurological disorders, it either does not affect the age 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 sits for 9 months, but cannot sit down on its own. Such children later begin to walk, and the period of walking with support is delayed for a long time.
Muscular hypotension may be limited to one limb (obstetric paresis of the arm, traumatic paresis of the leg). In these cases, the delay will be partial.
A pronounced syndrome of muscular hypotension has a significant impact 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 can correspond to the age of 2-3 months. The delay in motor development, in turn, causes the peculiarities of the formation of mental functions. For example, the lack of the possibility of arbitrary capture of an object leads to underdevelopment of visual-motor coordination, manipulative activity. Since muscular hypotension is often combined with other neurological disorders (convulsions, hydrocephalus, cranial nerve paresis, etc.), the latter can modify the nature of the developmental delay determined by hypotension as such. It should also be noted that the quality of the hypotension syndrome itself and its impact on developmental delay will vary depending on the disease. With convulsions, congenital or early acquired dementia, it is not so much hypotension as delayed mental development that is the cause of 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 in which muscular hypotension alternates with hypertension). At rest, in these children with passive movements, general muscle hypotonia is expressed. When you try to actively perform any movement, with positive or negative emotional reactions, muscle tone increases sharply, pathological tonic reflexes become pronounced. Such conditions are called "dystonic attacks". Most often, muscular dystonia is observed in children who have had hemolytic disease as a result of Rh or ABO incompatibility. The pronounced syndrome of muscular dystonia practically makes it impossible for the child to develop straightening reflexes of the body 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, limitation of spontaneous and voluntary motor activity, increased tendon reflexes, expansion of their zone, foot clonus. 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. Due to the incompleteness of the myelination processes, the symptoms of Babinsky, Oppenheim, Gordon, etc. cannot always be considered pathological. Normally, they are expressed unsharply, inconsistently, 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 muscular hypertension can vary from a slight increase in resistance to passive movements to complete stiffness (posture of decerebrate rigidity), when any movements are practically impossible. In these cases, even muscle relaxants are not able to cause muscle relaxation, and even more so passive movements. If the syndrome of muscular hypertension is not pronounced, is not combined 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 are more toned, 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 capture of a toy, the manipulation of objects, etc. is noted. The development of the grasping ability of the hands is especially disturbed. Along with the fact that the child later begins to take the toy, he retains the ulnar grip, or grip with the whole hand, for a long time. The finger grip (tweezer grip) develops slowly and sometimes requires additional stimulation. The development of the protective function of the hands may be delayed, then the balance reactions in the position on the stomach, sitting, standing and walking are 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 are reluctant to stand up, prefer to crawl, stand on their toes on a support.
Cerebellar disorders in children of the first year of life may be the result of underdevelopment of the cerebellum, damage to it 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 during hand movements, a disorder of balance reactions when trying to master the skills of sitting, standing, standing and walking. Actually cerebellar symptoms - intentional tremor, impaired coordination, ataxia can be detected only after the development of voluntary motor activity of the child. Disorders of co-ordination can be suspected by observing how the child reaches out to the toy, grabs it, brings it to the mouth, sits, stands, walks.
Infants with impaired coordination, when trying to grab a toy, make a lot of unnecessary movements, this becomes especially pronounced in the sitting position. Skills of independent sitting 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. Because of the fear of falling, the child does not manipulate objects with both hands for a long time; Walking begins after a year, often falls. Some children with balance disorders prefer to crawl when they should already be able to walk 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 craniocerebral innervation can give a certain specificity to developmental delay in the form of a more pronounced delay in the function of fixing the gaze and tracking, hand-eye coordination, and impaired spatial orientation. Dysarthria 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 cerebral palsy (ICP). The clinical manifestations of this syndrome depend on the severity of muscle tone, the increase of 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, and unconditioned reflexes are depressed. By the end of the second month of life, when the child in the position on the stomach and vertically makes attempts to hold the head, the dystonic stage appears. The child periodically becomes restless, his muscle tone increases, his arms are extended with internal rotation of the shoulders, the forearms and hands are pronated, the fingers are clenched into fists; legs are extended, adducted and often crossed. Dystonic attacks last a few seconds, recur throughout the day, and can be provoked by external stimuli (loud knocking, crying of another child).
Movement disorders in cerebral palsy are due to the fact that the defeat of the immature brain disrupts the sequence of stages of its maturation. Higher integrative centers do not have an inhibitory effect on primitive stem reflex mechanisms. The reduction of unconditioned reflexes is delayed, and pathological tonic neck and labyrinth reflexes are released. Combined with an increase in muscle tone, they prevent the consistent formation of the reactions of straightening and balance, which are the basis for the development of static and locomotor functions in children of the first year of life (holding the head, grasping a toy, sitting, standing, walking).
To understand the features of psychomotor development disorders in children with cerebral palsy, it is necessary to consider the influence of tonic reflexes on the formation of voluntary motor activity, as well as speech and mental functions.
Tonic 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 mouth, 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 an object in all directions, an optical rectifying reflex to the head does not develop, head movements cannot freely follow the movement of the eyes. Violated the development of visual-motor coordination. In such children, it is difficult to turn from the back to the side, and then to the stomach. In severe cases, even by the end of the first year of life, the turn from back to stomach is carried out only in a "block", i.e., there is no torsion between the pelvis and upper body. If the child cannot tilt his head in the supine position, turn on his stomach with torsion, he has no prerequisites for the development of the sitting function. The severity of the tonic labyrinth reflex is directly dependent on the degree of increase in muscle tone.
With the severity of the tonic labyrinth reflex in the position on the stomach, as a result of an increase in flexor tone, the head and neck are bent, the shoulders are pushed forward and down, the arms bent in all joints are under the chest, the hands are clenched into fists, the pelvis is raised. In this position, the child cannot raise his head, turn it to the sides, release his arms from under the chest and lean on them to support the upper body, bend his legs and kneel. Difficulty turning from stomach to back for sitting down. Gradually bent back leads to the development of kyphosis in the thoracic spine. This posture prevents the development of chain rectifying reflexes in the prone position and the acquisition of a vertical position by the child, 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 also be expressed in the prone position. Therefore, children lying on their stomachs, instead of bending, unbend their heads, throw them back, and raise their upper torso. Despite the extensor position of the head, the muscle tone in the flexors of the arms remains elevated, the arms do not provide support for the body, and the child falls on his back.
Asymmetric cervical tonic reflex (ASTR) is one of the most pronounced reflexes in cerebral palsy. The severity of ASTR depends on the degree of increase in muscle tone in the arms. In severe damage to the hands, the reflex appears almost simultaneously with turning the head to the side. If the arms are only slightly affected, as is the case with mild spastic diplegia, ASTD occurs intermittently and requires a longer latent period to appear. ASTR is more pronounced in the supine position, although it can also be observed in the sitting position.
ASTR, combined with the tonic labyrinth reflex, prevents the capture of a toy and the development of hand-eye coordination. The child cannot bring his arms forward 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, because when trying to bend the hand, the head turns in the opposite direction. Due to the extension of the arm, many children cannot suck their fingers, as most healthy children do. ASTR is usually more pronounced on the right side, so many children with cerebral palsy prefer to use their left hand. With a pronounced ASTR, 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, spastic torticollis is formed. scoliosis of the spine.
Combined with the tonic labyrinth reflex, ASTR makes it difficult to turn on the side and on the stomach. When the child turns his head to the side, the resulting ASTR prevents the movement of the body following the head, and the child cannot release his arm from under the body. Difficulty turning on its side prevents the child from developing the ability to transfer the center of gravity from one hand to the other when moving the body forward, which is necessary for the development of reciprocal crawling.
ASTR disturbs the balance in the sitting position, since the distribution of muscle tone on one side (increasing it mainly in the extensors) is opposite to its distribution on the other (primary 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 impact of ASTR 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.
Symmetric neck tonic reflex. With a pronounced symmetrical neck tonic reflex, a child with increased flexor tone in the arms and torso, kneeling, 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 drawn in, the arms are brought forward, bent at the elbow joints, the hands are clenched into fists. As a result of the influence of a symmetrical cervical tonic reflex in the position on the stomach, the child has a sharp increase in muscle tone in the extensors of the legs, so that it is difficult to bend them at the hip and knee joints and put him on his knees. This position can be eliminated if you passively raise the child's head, taking him by the chin.
With the severity of a symmetrical cervical tonic reflex, it is difficult for a child to maintain head control, and, accordingly, to stay in a sitting position. Raising the head in a sitting position increases the extensor tone in the arms, and the child falls back; lowering the head increases the flexion tone in the arms and the child falls forward. The isolated effect of symmetrical neck tonic reflexes on muscle tone is rarely revealed, since in most cases they are combined with ASTR.
Along with tonic neck and labyrinth reflexes, a positive supporting reaction and friendly movements (synkinesias) play an important role in the pathogenesis of movement disorders in children with cerebral palsy.
Positive supportive response. The influence of a positive supportive reaction to movements is manifested in an increase in extensor tone in the legs when the legs come into contact with the support. Since children with cerebral palsy always touch the ball of their feet first when standing and walking, this reaction is constantly maintained and stimulated. There is a fixation of all joints of the legs. Rigid limbs can support the child's body weight, but they make it much more difficult to develop balance reactions, which require joint mobility and fine regulation of the constantly reciprocally changing static state of the muscles.
Concomitant reactions (synkinesias). The effect of synkinesis on the child's motor activity is to increase muscle tone in various parts of the body during an active attempt to overcome the resistance of spastic muscles in any limb (i.e., perform movements such as grabbing a toy, extending an arm, taking a step, etc. ). So, if a child with hemiparesis strongly squeezes the ball with his healthy hand, muscle tone may increase on the paretic side. Trying to straighten the spastic arm can cause increased extensor tone in the homolateral leg. Strong flexion of the affected leg in a child with hemplegia causes friendly reactions in the affected arm, which are expressed in increased flexion in the elbow and wrist joints and fingers. Strenuous movement of one leg in a patient with double hemiplegia may 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, combined with each other, therefore it is difficult to identify them in isolation, although in each individual case one can 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 predominates, tonic reflexes are pronounced. With double hemiplegia, when the arms and legs are equally affected, or the arms are more affected than the legs, the tonic reflexes are pronounced, are observed simultaneously and do not tend to slow down. They are less pronounced and constant in spastic diplegia and hemiparetic form of cerebral palsy. In spastic diplegia, when the hands are relatively intact, the development of movements is prevented mainly by a positive supporting 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. However, it should be noted that in children of the first year of life, hyperkinesis is slightly expressed. They become more noticeable in the second year of life. In the atonic-astatic form of cerebral palsy, balance reactions, coordination and static functions suffer more. Tonic reflexes can be observed only occasionally.
Tendon and periosteal reflexes in cerebral palsy are high, but due to muscle hypertension, they are often difficult to elicit.
Motor pathology in combination with sensory deficiency also leads to impaired speech and mental development [Mastyukova E. M., 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 arbitrary vocal reactions. With pronounced ASTR, the tone in the articulatory muscles increases asymmetrically, more on the side of the "occipital limbs". The position of the tongue in the oral cavity is also often asymmetrical, which 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 back of the tongue, the tip of the tongue is fixed, ill-defined and often boat-shaped.
Disorders of the articulatory apparatus make it difficult to form voice activity and the sound-producing side of speech. The cry of such children is quiet, slightly modulated, often with a nasal tone or in the form of separate sobs that the child produces at the moment of inspiration. The disorder of the reflex activity of the articulatory muscles is the cause of the late appearance of cooing, babbling, the first words. Cooing and babbling are characterized by fragmentation, low vocal activity, and poor sound complexes. In severe cases, a true drawn-out cooing 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 during hand movements. At the same time, the child opens his mouth very wide, a violent smile appears. Oral synkinesis and excessive expression of the unconditioned sucking reflex also prevent the development of voluntary activity of the 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 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 a generalizing function of the brain. Paresis and paralysis limit the manipulation of objects, make it difficult to perceive them by touch. In combination with the underdevelopment of visual-motor coordination, the absence of objective actions hinders the formation of objective perception and cognitive activity. In violation of cognitive activity, speech disorders also play an important role, which impede the development of contact with others.
Lack of practical experience may be one of the causes of disorders of higher cortical functions at an older age, especially the unformed spatial representations. Violation of communication ties with the environment, the impossibility of full-fledged gaming activity, pedagogical neglect also contribute to mental retardation. Muscular 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 light severity, neurological symptoms and a delay in the formation of age-related psychomotor skills are not so pronounced. The child gradually develops valuable symmetrical reflexes. Motor skills, despite their late development and inferiority, still enable the child to adapt to his defect, especially if the hands are easily affected. These children develop head control, object grasping, hand-eye coordination, and body rotation. It is somewhat more difficult and longer for children to master the skills to sit, stand and walk independently, maintaining their balance. The range of motor, speech and mental disorders in children of the first year of life with cerebral palsy can vary widely. It can concern both all functional systems that make up the core of cerebral palsy, and its individual elements. The syndrome of cerebral palsy is usually combined with other neurological syndromes: lesions of the cranial nerves, hypertensive-hydrocephalic, cerebrasthenic, convulsive, autonomic-visceral dysfunctions.
Introduction
1. Movement disorders
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 the fulfillment of a number of necessary conditions for its formation, such as: anatomical safety and sufficient maturity of those brain systems that are involved in the speech function; preservation of kinesthetic, auditory and visual perception; a sufficient level of intellectual development that would provide the need for verbal communication; normal structure of the peripheral speech apparatus; adequate emotional and speech environment.
The occurrence 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 structures of the brain involved in providing speech functions, on the other hand, secondary underdevelopment or delayed "maturation" of the premotor-frontal and parietal-temporal cortical structures, disturbances in the rate and nature of the formation of visual-auditory and auditory-visual-motor nerve connections. With motor disorders, the afferent effect on the brain is distorted, which in turn enhances existing cerebral dysfunctions or causes new ones to appear, leading to asynchronous activity of the cerebral hemispheres.
Based on studies of 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. Movement disorders
If we talk about the causes of movement disorders, it can be noted that most of them arise as a result of a violation of the functional activity of mediators in the basal ganglia, the pathogenesis can be different. The most common causes are degenerative diseases (congenital or idiopathic), possibly triggered by medication, organ system failure, CNS infections, or basal ganglia ischemia. All movements are carried out through the pyramidal and parapyramidal pathways. As for the extrapyramidal system, the main structures of which are the basal nuclei, its function is to correct and refine movements. This is achieved mainly through influences on the motor areas of the hemispheres through the thalamus. The main manifestations of damage to the pyramidal and parapyramidal systems are paralysis and spasticity.
Paralysis can be complete (plegia) or partial (paresis), sometimes it is manifested only by the awkwardness of the hand or foot. Spasticity is characterized by an increase in the tone of the limb according to the "jackknife" type, increased tendon reflexes, clonus and pathological extensor reflexes (for example, the Babinski reflex). It can also be manifested only by the awkwardness of movements. Frequent symptoms also include spasms of the flexor muscles, which occur as a reflex to constant uninhibited impulses from skin receptors.
Correction of movements is also provided by the cerebellum (The lateral sections of the cerebellum are responsible for the coordination of limb movements, the middle sections are responsible for postures, gait, body movements. Damage to the cerebellum or its connections is manifested by intentional tremor, dysmetria, adiadochokinesis and a decrease in muscle tone.), mainly through influences on the vestibulospinal path, as well as (with switching in the nuclei of the thalamus) to the same motor areas of the cortex as the basal nuclei (motor disorders that occur when the basal nuclei are damaged (extrapyramidal disorders), can be divided into hypokinesia (decrease in the volume and speed of movements; an example is Parkinson's disease or parkinsonism of another origin) and hyperkinesis (excessive involuntary movements; an example is Huntington's disease). Tics also belong to hyperkinesis.).
With certain mental illnesses (primarily with catatonic syndrome), one can observe conditions in which the motor sphere receives some autonomy, specific motor acts lose their connection with internal mental processes, cease to be controlled by the will. In this case, the disorders become similar to neurological symptoms. It should be recognized that this similarity is only external, since, unlike hyperkinesis, paresis, and motor coordination disorders in neurological diseases, movement disorders in psychiatry have no organic basis, are functional and reversible.
Those suffering from a catatonic syndrome cannot somehow psychologically explain the movements they make, they are not aware of their painful nature until the moment of copying psychosis. All disorders of the motor sphere can be divided into hyperkinesia (excitation), hypokinesia (stupor) and parakinesia (distortion of movements).
Excitation, or hyperkinesia, in mentally ill patients is a sign of an exacerbation of the disease. In most cases, the patient's movements reflect the richness of his emotional experiences. He may be controlled by the fear of persecution, and then he flees. In a 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 mental experiences. This type of arousal is called psychomotor.
In catatonic syndrome, movements do not reflect the internal needs and experiences of the subject, therefore, excitation in this syndrome is called purely motor. The severity of hyperkinesia often indicates the severity of the disease, its severity. However, at times there are severe psychoses with arousal limited to the bed.
Stupor - a state of immobility, an extreme degree of motor inhibition. Stupor can also reflect vivid emotional experiences (depression, asthenic affect of fear). In catatonic syndrome, on the contrary, stupor is devoid of internal content, meaningless. The term "substupor" is used to refer to states accompanied by only partial inhibition. Although stupor implies a lack of motor activity, in most cases it is considered a productive psychopathological symptom, since it does not mean that the ability to move is irreversibly lost. Like other productive symptoms, stupor is a temporary condition and responds well to treatment with psychotropic drugs.
The catatonic syndrome was originally described by KL 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 devoid of meaning and are not associated with psychological experiences. Characterized by tonic muscle tension. Catatonic syndrome includes 3 groups of symptoms: hypokinesia, hyperkinesia and parakinesia.
Hypokinesias are represented by the phenomena of stupor and substupor. Complex, unnatural, sometimes uncomfortable postures of patients attract attention. There is a sharp tonic contraction of the muscles. This tone allows patients sometimes for some time to hold any position that the doctor gives them. This phenomenon is called catalepsy, or waxy flexibility.
Hyperkinesia in catatonic syndrome is expressed in bouts of excitement. Characterized by the commission of meaningless, chaotic, non-purposeful movements. Motor and speech stereotypes (rocking, bouncing, waving arms, howling, laughing) are often observed. An example of speech stereotypes are verbigerations, which are manifested by the rhythmic repetition of monotonous words and meaningless sound combinations.
Parakinesias are manifested by strange, unnatural movements, such as frilly, mannered facial expressions and pantomime.
With catatonia, a number of echo symptoms are described: echolalia (repeating the words of the interlocutor), echopraxia (repetition of other people's movements), echomimicry (copying the facial expressions of others). These symptoms can occur in the most unexpected combinations.
It is customary to distinguish lucid catatonia, which occurs against the background of a clear consciousness, and oneiroid catatonia, accompanied by clouding of consciousness and partial amnesia. With the outward similarity of the set of symptoms, these two conditions differ significantly in course. Oneiroid 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 a significant similarity with catatonia. The predominance of movement disorders with unmotivated, meaningless actions is also characteristic of hebephrenia. The very name of the syndrome indicates the infantile nature of the behavior of patients.
Speaking of other syndromes accompanied by arousal, it can be noted that psychomotor agitation is one of the frequent components of many psychopathological syndromes.
Manic excitation differs from catatonic in the purposefulness of actions. Facial expressions express joy, patients seek 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 understandable, but his speech is never stereotyped.
Movement disorders make it most difficult to carry out active rehabilitation treatment. It is persons with motor disorders that make up a significant part of all patients of the rehabilitation neurological department, are the least adapted to vigorous activity, including self-care, and most often need outside care. Therefore, the restoration of motor functions in people with diseases of the nervous system is an important part of their rehabilitation.
Higher motor centers are located in the so-called motor zone of the cerebral cortex: in the anterior central gyrus and adjacent areas. The fibers of the motor cells from the indicated region of the cortex pass through the inner capsule, the subcortical regions and at the border of the brain and spinal cord make an incomplete decussation with the transition of most of them to the opposite side. That is why, in diseases of the brain, motor disorders are observed on the opposite side: with damage to the right hemisphere of the brain, paralysis occurs in the left half of the body, and vice versa. Further, the fibers descend as part of the bundles of the spinal cord, approaching the motor cells (motoneurons) of the anterior horns of the latter. The motor neurons that regulate the movements of the upper limbs lie in the cervical thickening of the spinal cord (level V-VIII of the cervical and I-II thoracic segments), and the lower ones in the lumbar (level I-V lumbar and I-II sacral segments). To the same spinal motor neurons, fibers are also sent, starting from the nerve cells of the nuclei of the base nodes - the subcortical motor centers of the brain, from the reticular formation of the brain stem and cerebellum. Thanks to this, the regulation of coordination of movements is ensured, involuntary (automated) movements are carried out and voluntary movements are prepared. The fibers of the motor cells of the anterior horns, which are part of the nerve plexuses and peripheral nerves, end at the executive organs - the muscles.
Any motor act occurs when an impulse is transmitted along the nerve fibers from the cerebral cortex to the anterior horns of the spinal cord and then to the muscles. In diseases of the nervous system, the conduction of nerve impulses is difficult, and there is a violation of the motor function of the muscles. Complete loss of muscle function is called paralysis (plegia), and partial - paresis. According to the prevalence of paralysis, there are: monoplegia (lack of movement in one limb - arm or leg), hemiplegia (damage to the upper and lower limbs of one side: right-sided or left-sided hemiplegia), paraplegia (impaired movement in both lower limbs is called lower paraplegia, in the upper - upper paraplegia) and tetraplegia (damage to all four limbs). When peripheral nerves are damaged, paresis occurs in the zone of their innervation, which is called the corresponding nerve (for example, paresis of the facial nerve, paresis of the radial nerve, etc.).
To correctly determine the severity of paresis, and in cases of mild paresis, sometimes to identify it, it is important to quantify the state of individual motor functions: muscle tone and strength, and the volume of active movements. There are many scale systems for assessing motor functions described by various authors. However, some of them suffer from inaccurate formulations characterizing individual scores, others take into account only one function (muscle strength or tone), and some are overly complex and inconvenient to use. We propose to use a unified 6-point scale for assessing all three motor functions (muscle tone and strength, range of voluntary movements), which we have developed and convenient in practical terms, which makes it possible to compare them with each other and effectively control the results of rehabilitation treatment both in outpatient clinics and in hospitals. stationary conditions.
To study muscle tone, a passive antagonistic movement is performed (for example, when the forearm is extended, the tone of the forearm flexors is assessed), while the patient himself tries to completely relax the limb. When determining muscle strength, the patient provides maximum resistance to movement, which makes it possible to assess the strength of tensed muscles (for example, when extending the hand, the patient tries to bend the hand - this allows us to assess the strength of the flexor muscles of the hand).
The state of muscle tone is graduated from 0 to 5 points:
- 0 - dynamic contracture: the resistance of the antagonist muscles is so great that the examiner cannot change the position of the limb segment;
- 1 - a sharp increase in tone: applying maximum effort, the researcher achieves only a small amount of passive movement (no more than 10% of the normal volume of this movement);
- 2 - a significant increase in muscle tone: with great effort, the examiner manages to achieve no more than half of the volume of normal passive movement in this joint;
- 3 - moderate muscle hypertension: the resistance of the antagonist muscles allows only about 75% of the total volume of this passive movement to be carried out in the norm;
- 4 - a slight increase in resistance to passive movement compared with the norm and with a similar resistance on the opposite (symmetrical) limb of the same patient. A full range of passive movement is possible;
- 5 - normal resistance of muscle tissue during passive movement, no "looseness" in the joint.
With a decrease in muscle tone (muscle hypotension), the researcher experiences less resistance than on a symmetrical healthy limb. Sometimes such "looseness" in the joint even creates the impression of a complete lack of resistance during passive movement.
A more accurate measurement of muscle tone is made by using special devices. To assess the elasticity (density) of the muscles under study, myotonometers designed by Uflyand, Sirmai and other authors are used. More important is the quantitative characteristic of contractile (i.e., associated with muscle stretching) tone, since in all cases, in the absence of devices, it is precisely by the resistance of the studied muscle group to passive stretching that doctors assess the degree of increase in its tone (as described in detail above). Contractile muscle tone is measured using a special attachment (tenzotonograph) to any ink-writing device (for example, to an ELCAR type electrocardiograph). Thanks to preliminary calibration, the results of measuring the tone when using a tensotonograph are expressed in units that are familiar and convenient for processing - in kilograms.
Muscle strength is also expressed in points from 0 to 5:
- 0 - no visible movement and no muscle tension is felt during palpation;
- 1 there is no visible movement, but tension in the muscle fibers is felt on palpation;
- 2 active visible movement is possible in a lightened initial position (the movement is performed under the condition that gravity or friction is removed), but the patient cannot overcome the resistance of the examiner;
- 3 implementation of a full or close to it volume of arbitrary movement against the direction of gravity when it is impossible to overcome the resistance of the researcher;
- 4 - a decrease in muscle strength with a pronounced asymmetry on healthy and affected limbs with the possibility of a full range of voluntary movement with overcoming both gravity and the resistance of the researcher;
- 5 - normal muscle strength without significant asymmetry in a bilateral study.
In addition, the strength of the muscles of the hand can be measured using a hand-held dynamometer.
The volume of active movements is measured using an goniometer in degrees, and then compared with the total volume of the corresponding movements in a healthy person and expressed as a percentage of the latter. The interest received is converted into points, with 0% equating to 0 points, 10% to 1, 25% to 2, 50% to 3, 75% to 4 and 100% to 5 points.
Depending on the localization of the lesion of the nervous system, peripheral or central paralysis (paresis) occurs. With the defeat of the motor cells of the anterior horns of the spinal cord, as well as the fibers of these cells, which are part of the nerve plexuses and peripheral nerves, a picture of peripheral (flaccid) paralysis develops, which is characterized by a predominance of symptoms of neuromuscular prolapse: limitation or absence of voluntary movements, a decrease in strength muscles, decreased muscle tone (hypotension), tendon, periosteal and skin reflexes - hyporeflexia (or their complete absence), often there is also a decrease in sensitivity and trophic disorders, especially muscle atrophy.
In some cases, when motor cells are damaged in the motor zone of the cerebral cortex (anterior central gyrus) or their axons, a syndrome of "flaccid" (atonic) paralysis is also observed, which is very reminiscent of the picture of peripheral paralysis: in both cases there is muscle hypotension, hyporeflexia, movement disorders and trophic. However, with central "flaccid" paralysis, there is no reaction of muscle degeneration (see below), and also pyramidal foot pathological symptoms of Babinsky, Oppenheim, Rossolimo, etc. appear, which never happens with damage to the peripheral nervous system.
Of great importance for the selection of composition and prediction of the results of restorative treatment of patients with peripheral paralysis is the study of the electrical excitability of muscles and nerves using the method of classical electrodiagnostics. To do this, various types of universal electric pulsers (UEI) are used, influencing galvanic and tetanizing currents on the motor points of peripheral nerves and muscles. A push-button active electrode connected to the negative pole (cathode) of the apparatus is placed on the motor point, and a larger flat indifferent electrode connected to the positive pole (anode) is placed on the interscapular region (when examining the upper limb) or lumbosacral (for the lower limb). limbs).
Normally, when exposed to the motor point of the nerve, galvanic and tetanizing currents cause a rapid contraction of the muscles innervated by the nerve under study. Under the influence of both types of current directly on the muscle, even with a small force (1-4 mA), a rapid contraction occurs. For the appearance of muscle contraction under the influence of galvanic current, its smaller force is required when shorting on the cathode than on the anode (GLC > ACS).
In persons with peripheral paralysis, destruction and death of the motor fibers of the nerves occur and characteristic changes in their electrical excitability occur, called the reaction of nerve degeneration. Prognostically, the most favorable for restoring the conduction of nerve impulses is a partial reaction of degeneration, when the excitability of the nerve to both types of current decreases, as well as the excitability of the muscle to the tetanizing current. Galvanic current causes a sluggish worm-like contraction of the muscle, and when the polarity of the current changes, the contraction from the anode occurs at a lower strength than from the cathode (AZS > KZS).
The prognosis is worse with a complete reaction of degeneration, when there is no contraction of the muscle, both when both types of current act on the nerve innervating it, and when the muscle itself is irritated by a tetanizing current; the muscle responds to the galvanic current with a worm-like contraction with a predominance of the anode-switching reaction (AZS > KZS). However, even in this case, under the influence of treatment, restoration of nerve conduction with normal muscle electrical excitability can occur.
In the case of a long-term absence of signs of recovery of movements in peripheral paralysis (for 1 year or more), a prognostically very poor complete loss of electrical excitability and nerves and muscles that do not respond to contraction to any type of current develops.
With paralysis of the central type, there is no destruction of the fibers of the peripheral nerves, and therefore there is no reaction of degeneration, only an increase in the threshold of the strength of both types of current, which causes muscle contraction, is noted.
A preliminary study of muscle electrical excitability is also necessary for performing some restorative procedures in the treatment of paralysis, especially for alcohol-novocaine blockades of spastic muscles, the methodology of which will be described below.
Biocurrents arise in any functioning muscle. The assessment of the functional state of the neuromuscular apparatus (including the determination of the magnitude of muscle tone) is also carried out using electromyography - a method of graphic registration of fluctuations in the bioelectrical activity of muscles.
Electromyography helps to determine the nature and location of damage to the nervous system or muscles, and also serves as a method of monitoring the process of restoring impaired motor functions.
In case of violation of the cortical-subcortical connections with the reticular formation of the brain stem or damage to the descending motor pathways in the spinal cord and, as a result, the function of the spinal motor neurons is activated as a result of a disease or brain injury, a syndrome of central spastic paralysis occurs. For him, in contrast to peripheral and central "flaccid" paralysis, it is characterized by an increase in tendon and periosteal reflexes (hyperreflexia), the appearance of pathological reflexes that are absent in healthy adults (reflexes of Babinsky, Oppenheim, Rossolimo, Zhukovsky, etc.), occurrence when trying voluntary action of a healthy or paralyzed limb of friendly movements (for example, abduction of the shoulder outward when the forearm of the paretic arm is bent or clenching the paralyzed hand into a fist with a similar voluntary movement of a healthy hand). One of the most important symptoms of central paralysis is a pronounced increase in muscle tone (muscle hypertension), which is why such paralysis is often called spastic. At the same time, two features are characteristic of muscular hypertension:
- it has an elastic character: muscle tone is maximum at the beginning of passive movement (the “penknife” phenomenon), and after the external influence is stopped, the limb tends to return to its original position;
- the increase in tone in different muscle groups is uneven.
Therefore, for most patients with central paralysis in case of a brain disease or injury, the Wernicke-Mann posture is characteristic: the shoulder is brought (pressed) to the body, the hand and forearm are bent, the hand is turned palm down, and the leg is extended at the hip and knee joints and bent at the foot. This reflects a predominant increase in muscle tone - flexors and pro-nators of the upper limb and extensors - in the lower.
The occurrence of symptoms characteristic of central paralysis is associated with a decrease in regulatory influences from higher cortical motor centers in diseases of the brain and spinal cord and the predominance of facilitating (activating) influences of the reticular formation of the brain stem on the activity of spinal motor neurons. The increased activity of the latter explains the symptoms of central paralysis described above.
In some cases, the same patient may experience both peripheral and central paralysis at the same time. This occurs in the case of damage to the spinal cord at the level of the cervical enlargement, when the function of the nerve fibers going to the lower extremities is simultaneously impaired (this leads to the formation of a lower central mono- or, more often, paraparesis), and the motor cells of the anterior horns of the spinal cord, which provide innervation of the upper limbs, resulting in the formation of peripheral mono- or paraparesis of the upper limbs.
When the focus of the disease is localized in the region of subcortical motor centers, specific motor disorders appear that are not accompanied by paresis. Most often, there is a syndrome of parkinsonism (or trembling paralysis, as it is sometimes called), which occurs when one of the subcortical motor centers, the substantia nigra, is damaged, with subsequent involvement of other subcortical structures in the process. The clinical picture of parkinsonism consists of a combination of three main symptoms: a specific increase in muscle tone according to the extrapyramidal type (muscle rigidity), a sharp decrease in the motor activity of patients (physical inactivity) and the appearance of involuntary movements (tremor).
A typical change in muscle tone in diseases of the subcortical motor centers differs from that in central pyramidal paralysis. Extrapyramidal rigidity is characterized by the preservation of increased tone throughout the entire passive movement, due to which it occurs in the form of uneven shocks (a symptom of "gear wheel"). As a rule, the tone of antagonistic muscles (for example, flexors and extensors) is increased evenly. An increase in tone leads to the constant maintenance of a typical patient posture: with the head tilted forward, the spine slightly bent forward ("hunchbacked" back), arms bent at the elbows and unbent at the wrist joints, legs bent at the knee and hip joints. Patients with parkinsonism usually appear smaller than they actually are.
At the same time, pronounced general physical inactivity is also observed: patients are inactive, prone to long-term preservation of the previously adopted posture ("freezing" in it). The face is inexpressive, motionless (amimic) even when talking on the most exciting topics for the patient. Interestingly, such disorders of voluntary movements are not associated with the presence of paralysis: on examination, it turns out that all active movements are preserved, and muscle strength is not reduced. It is difficult for the patient to start a new movement: change position, move from one place, start walking, but having started the movement, in the future he can walk quite quickly, especially following another person, or holding an object (chair) in front of him. Walking is not accompanied by synkinesis common in healthy people: there are no accompanying hand movements. The ability to maintain a normal body position is also impaired, due to which a healthy person does not fall forward or backward when walking: the patient, especially if necessary to stop, is drawn forward (this is called propulsion), and sometimes at the beginning of the movement - back (retropulsion).
Often, violations of voluntary movements are accompanied by the appearance of involuntary ones in the form of trembling (tremor), which, with the course of the disease, intensifies and spreads to other parts of the limbs and head. Trembling increases with excitement, weakens with voluntary movements and disappears in sleep. Due to pronounced rigidity and trembling, patients sometimes become completely helpless: they cannot change their position in bed, get up, dress, toilet and eat on their own. In such cases, they need constant outside care, including during their stay in the rehabilitation department.
With extrapyramidal lesions, muscle rigidity, physical inactivity and involuntary movements occur with unequal frequency and are combined with each other in different proportions. In accordance with the predominance of certain symptoms, trembling, rigid, amyostatic (with a predominance of immobility) and mixed forms of the disease are distinguished, the latter being the most common.
Demidenko T. D., Goldblat Yu. V.
"Motor disorders in neurological disorders" and others
99. Movement disorders
With pathology of the nervous system
There are two types of motor functions: maintaining position
(poses) and the actual movement. To systems that regulate
movements, pyramidal system, extrapyramidal system,
structures responsible for the regulation of movement coordination : basal
ganglia and cerebellum.
Movement disorders depend on the level of localization of the pathological process and the degree of damage to certain regulatory systems.
Types of movement disorders: hypokinesia(reduction in volume and speed
voluntary movements) hyperkinesia(presence of involuntary
violent movements), g hypodynamia(decrease in motor activity
and the strength of muscle contractions during movement), ataxia (impaired coordination
movements).
Motor disorders in violation of the pyramidal system.
The defeat of the pyramidal tract is accompanied by the development of hypokinesia in the form
paralysis or paresis.
Paralysis (paralysis; Greek relax) - a disorder of the motor
functions in the form of a complete absence of voluntary movements due to
violations of the innervation of the corresponding muscles.
Paresis (paresis; Greek weakening, relaxation) - a decrease in strength and
(or) the amplitude of voluntary movements, due to a violation
innervation of the corresponding muscles.
Depending on the location of the lesion, there are central and
peripheral paralysis.
Peripheral (sluggish) paralysis occurs after injury or
complete disruption of the integrity of the peripheral motor neuron
(motor neuron). Interruption in impulse conduction along the motor nerves
can occur with mechanical trauma, with botulism, myasthenia gravis,
the action of poisons, toxins, poliomyelitis, encephalitis, amyotrophic
sclerosis.
Peripheral paralysis is characterized by the following symptoms:
1. Atony. pronounced decrease in muscle tone. muscles
become flabby, lethargic, doughy, redundancy is also noted
passive movements in the paralyzed limb.
2. Areflexia. lack of reflex motor reactions, including
number of defensive movements.
3. Atrophy. a decrease in muscle mass due to a deterioration in trophism
(during the first 4 months, denervated muscles lose up to 20-30% of their original
masses, and in the future. up to 70-80%).
4. Rebirth (degeneration) of muscles and nerves. reaction perversion
to electrical stimulation of a paralyzed muscle and
dysfunctional nerve.
Central (spastic) paralysis occurs when the
the first (central) neuron of the motor pathway from the cerebral cortex
to the motor neuron of the spinal cord.
Etiological factors are trauma, edema, brain tumors,
thrombosis of cerebral vessels, etc., under the action of which
damage to the first neurons or their processes (axons).
The following symptoms are characteristic of central paralysis:
1. Hypertonicity. increased muscle tone at rest and during passive
movements (due to the removal of the inhibitory effect of the central neuron of the cortex
on the motor neurons of the spinal cord)
2. Pathological reflexes. congenital reflexes that appear
again due to disinhibition of peripheral neurons.
3. Absence of degeneration (degeneration) of muscles and nerves.
4. Synkinesis - movements in a paralyzed limb synchronously
voluntary movements of a healthy limb.
Depending on the level of damage to the departments of the main motor
ways distinguish the following types of central paralysis:
Monoplegia - paralysis of one limb (arm or leg),
Hemiplegia - paralysis of the muscles of one (right or left) half of the body,
Paraplegia - paralysis of both arms or legs,
Tetraplegia - paralysis of the upper and lower extremities.
Motor disorders in case of damage to the extrapyramidal
Due to damage to the complex extrapyramidal (striate,
red nucleus, substantia nigra, body of Louis, nuclei of thalamus and
bridge) of the motor system, changes in muscle tone occur,
called hyperkinesis.
Hyperkinesis. involuntary violent movements. Hyperkinesis
may be fast and slow.
Rapid hyperkinesias include convulsions, chorea, tremors, and tics.
Seizures. sharp sudden involuntary muscle contractions.
Seizures are divided into clonic, tonic and mixed.
Clonic convulsions are characterized by a sharp change in the contraction period
and muscle relaxation (eg, seizures in epilepsy, chorea).
Stuttering. clonic convulsions of speech muscles. Teak. clonic
spasms of a group of muscles of the face. With tonic convulsions, there are
prolonged muscle contractions without periods of relaxation (opisthotonus
with tetanus).
Tremor(from lat. tremor - trembling). weak involuntary
contraction of skeletal muscles due to alternating changes
muscle tone. antagonists (flexors and extensors).
Chorea(from Latin "dance"). irregular, fast, uncoordinated,
involuntary, sweeping (up to maximum amplitude) contractions
various muscle groups with a significant decrease in muscle tone.
Slow hyperkinesias include athetosis and spastic torticollis.
Athetosis(from Greek atetosis. mobile, unstable) - involuntary,
stereotyped, fluid, worm-like, frilly movements that occur in
as a result of simultaneous motor activation of agonist muscles and
antagonists. Most often, slow, tense movements are observed.
fingers.
Spasmodic torticollis(tilt to one side) is the result
prolonged spasm of the muscles of one side of the neck. Torticollis occurs with edema,
hemorrhage, tumors in the hindbrain, birth trauma.
Movement disorders in cerebellar pathology. When defeated
cerebellum, the following symptoms appear.
Ataxia- disturbed gait with excessive movements, with wide
legs apart (“drunk gait”).
Atony. a sharp decrease in muscle tone.
astasia. inability to maintain a correct, normal position
your body and head in space.
dysarthria- speech disorder, expressed in difficulty
pronunciation of individual words, syllables and sounds.
disequilibration. decreased balance while moving.
Movement disorders are a group of diseases and syndromes that affect the ability to make and control body movements.
Movement disorders: description
It seems simple and easy, but normal movement requires a surprisingly complex control system. Violation of any part of this system can cause movement disorders in a person. Unwanted movements may also occur at rest.
Abnormal movements are symptoms underlying movement disorders. In some cases, abnormalities are the only symptoms. Disorders or conditions that can lead to movement problems include:
- cerebral paralysis,
- choreoathetosis,
- encephalopathy,
- essential tremor,
- hereditary ataxias (Friedreich's ataxia, Machado-Joseph's disease and spinocerebellar ataxia),
- parkinsonism and Parkinson's disease,
- poisoning with carbon monoxide, cyanide, methanol or manganese,
- psychogenic disorders
- restless leg syndrome,
- muscle spasticity,
- stroke,
- Tourette syndrome and other tic disorders,
- Wilson's disease.
Causes of movement disorders
The movements of our body are produced and coordinated by several interacting brain centers, including the cortex, the cerebellum, and a group of structures in the inner parts of the brain called the basal ganglia. Sensory information ensures the accuracy of the current position and speed of parts of the body and spine, nerve cells (neurons) help to prevent contractions of antagonist muscle groups at the same time.
To understand how movement disorders arise, it is helpful to consider any normal movement, such as touching an object with the index finger of the right hand. To achieve the desired movement, the hand must be raised and extended with the participation of the forearm, and the index finger must be extended while the other fingers of the hand remain bent.
Motor start commands originate in the cortex, located on the outer surface of the brain. Movement of the right hand begins with the activity of the left motor cortex, which generates signals for the muscles involved. These electrical signals travel along the upper motor neurons through the midbrain to the spinal cord. Electrical stimulation of the muscles causes contraction, and the force of contraction causes movement of the hand and finger.
Damage or death to any of the neurons along the way causes weakness or paralysis of the affected muscles.
Antagonistic muscle pairs
The previous description of a simple movement, however, is too primitive. One important clarification to it is the consideration of the role of opposite, or antagonistic, pairs of muscles. Contraction of the biceps muscle located on the upper arm affects the forearm to flex the elbow and arm. Contraction of the triceps located on the opposite side engages the elbow and straightens the arm. These muscles, as a rule, work in such a way that the contraction of one group is automatically accompanied by the blocking of the other. In other words, the command to the bicep provokes another command to prevent the contraction of the triceps. Thus, the antagonist muscles are kept from resisting each other.
Spinal cord injuries or traumatic brain injury can lead to damage to the control system and cause involuntary simultaneous contraction and spasticity, and an increase in resistance to movement during muscle work.
Cerebellum
Once the hand movement is initiated, sensory information guides the finger to its precise destination. In addition to the appearance of an object, the most important source of information about an object is its "semantic position", represented by the many sensory neurons located in the limbs (proprioception). Proprioception is what allows a person to touch his nose with his finger even with his eyes closed. The balance organs in the ears provide important information about the position of an object. Proprioceptive information is processed by a structure at the back of the brain called the cerebellum. The cerebellum sends electrical signals to change movements as the finger moves, creating a barrage of commands in the form of a tightly controlled, ever-evolving pattern. Cerebellar disorders cause an inability to control strength, precise positioning, and speed of movement (ataxia). Diseases of the cerebellum can also impair the ability to judge the distance to the target, while the person underestimates or overestimates it (dysmetria). Tremor during voluntary movements can also be the result of cerebellar damage.
Basal ganglia
Both the cerebellum and the cerebral cortex send information to a set of structures deep within the brain that help control the involuntary components of movement. The basal ganglia send output messages to the motor cortex, helping to initiate movements, regulate repetitive or complex movements, and control muscle tone.
The circuits within the basal ganglia are very complex. Within this structure, some groups of cells start the action of other components of the basal ganglia, and some groups of cells block their action. These complex feedback patterns are not entirely clear. Disturbances in the circuits of the basal ganglia cause several types of movement disorders. Part of the basal ganglia, the so-called substantia nigra, sends out signals that block their exit from another structure called the hypothalamic nucleus. The hypothalamic nucleus sends signals to the globus pallidus, which in turn blocks the thalamic nucleus. Finally, the thalamic nucleus sends signals to the motor cortex. The black substance then starts the movement of the pale ball and blocks it. This complex pattern can be broken at several points.
Malfunctions in other parts of the basal ganglia are thought to cause tics, tremors, dystonia, and a host of other movement disorders, although the exact mechanisms by which these disorders occur are not well understood.
Some movement disorders, including Huntington's disease and inherited ataxias, are caused by hereditary genetic defects. Some diseases that cause prolonged muscle contraction are limited to a specific muscle group (focal dystonia), others are caused by trauma. The causes of most cases of Parkinson's disease are unknown.
Symptoms of movement disorders
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Movement disorders are classified as hyperkinetic (many movements) and hypokinetic (little movements).
Hyperkinetic movement disorders
Dystonia- sustained muscle contractions, often causing twisting or repetitive movements and incorrect postures. Dystonia may be limited to one area (focal) or may affect the entire body (general). Focal dystonia may affect the neck (cervical dystonia); face (unilateral or hemifacial spasm, narrowing of the eyelid or blepharospasm, contraction of the mouth and jaw, simultaneous spasm of the chin and eyelid); vocal cords (dystonia of the larynx); arms and legs (writer's spasm or occupational cramps). Dystonia can be a painful condition.
Tremor- uncontrolled (involuntary) shaking of a part of the body. Tremors can only occur when the muscles are in a relaxed state or only during activity.
Teak- involuntary, fast, non-rhythmic movements or sounds. Tics can be controlled to a certain extent.
myoclonus- sudden, short, jerky, involuntary muscle contraction. Myoclonic contractions may occur separately or repeatedly. Unlike tics, myoclonus cannot be controlled even for a short time.
spasticity- an abnormal increase in muscle tone. Spasticity may be associated with involuntary muscle spasms, constant muscle contractions, and exaggerated deep tendon reflexes that make movement difficult or uncontrollable.
Chorea- fast, irregular, uncontrolled convulsive movements, most often of the arms and legs. Chorea can affect the arms, legs, trunk, neck, and face. Choreoathetosis is a syndrome of continuous random movements that usually occurs at rest and can manifest itself in various forms.
Convulsive twitches- similar to chorea, but the movements are much larger, more explosive and occur more often in the arms or legs. This condition can affect both sides of the body, or only one (hemiballismus).
Akathisia- Restlessness and a desire to move to reduce discomfort, which may include a feeling of itching or stretching, usually in the legs.
Athetosis- slow, continuous, uncontrolled movements of the arms and legs.
Hypokinetic movement disorders
Bradykinesia- extreme slowness and stiffness of movements.
Freezing- inability to start movement or involuntary cessation of movement before its completion.
Rigidity- an increase in muscle tension when an arm or leg moves under the influence of an external force.
Postural instability is the loss of the ability to maintain an upright position caused by slow recovery or lack of recovery of reflexes.
Diagnosis of movement disorders
Diagnosis of movement disorders requires a thorough medical history and a complete physical and neurological examination.
The medical history helps the doctor evaluate the presence of other conditions or disorders that may be contributing to or causing the disorder. Family history is assessed for muscle or neurological disorders. Genetic testing may also be done for some forms of movement disorders.
Physical and neurological tests may include assessment of the patient's motor reflexes, including muscle tone, mobility, strength, balance, and endurance; work of the heart and lungs; nerve functions; examination of the abdomen, spine, throat and ears. Blood pressure is measured, blood and urine tests are performed.
Brain studies typically involve imaging modalities, including computed tomography (CT), positron emission tomography (PET), or magnetic resonance imaging (MRI). A lumbar puncture may also be needed. Video recording of abnormal movements is often used to analyze their nature and monitor the course of the disease and treatment.
Other tests may include x-rays of the spine and hip, or diagnostic blocks with local anesthetics to provide information about the effectiveness of possible treatments.
In some cases, nerve conduction studies and electromyography are ordered to assess muscle activity and provide a comprehensive assessment of nerve and muscle function.
An electroencephalogram (EEG) is needed to analyze the overall functioning of the brain, and measure the activity of its parts associated with movement or sensations. This test measures the electrical signals in the brain.
Movement Disorders: Treatment
Treatment of movement disorders begins with a correct diagnostic assessment. Treatment options include physical and occupational therapies, medications, surgery, or combinations of these.
The goals of treatment are to increase patient comfort, reduce pain, ease mobility, assist with daily activities, rehabilitation procedures, and prevent or reduce the risk of developing contractures. The type of treatment recommended depends on the severity of the disease, the general health of the patient, the potential benefits, limitations and side effects of therapy, and its impact on the patient's quality of life.
Treatment for movement disorders is provided by a movement disorder specialist, or a specially trained pediatric neurologist in the case of a child, and a multidisciplinary team of specialists that may include a physical therapist, occupational therapist, orthopedic or neurosurgeon, and others.
Denial of responsibility: The information provided in this article on movement disorders is intended to inform the reader only. It cannot be a substitute for the advice of a health professional.
