Pyramidal and extrapyramidal systems of the brain. Extrapyramidal tracts Pyramidal and extrapyramidal systems briefly

Extrapyramidal system – This is a system of cortical, subcortical and stem nuclei of the brain and pathways connecting them to each other, as well as with the motor nuclei of the cranial nerves of the brain stem and anterior columns of the spinal cord, which carries out involuntary automatic regulation and coordination of complex motor acts, regulation of muscle tone, maintenance postures, organization of motor manifestations of emotions.

Composition of the extrapyramidal system:

    Cerebral cortex;

    Basal ganglia of the telencephalon: caudate and lenticular;

    Subthalamic nucleus and thalamic nuclei of the diencephalon;

    Red nucleus and substantia nigra, nuclei of the midbrain roof;

    Vestibular nuclei;

    Inferior olive kernels;

    Cerebellum;

    Nuclei of the reticular formation;

    Conducting pathways.

Functions of the extrapyramidal system:

    Providing complex automated movements (crawling, swimming, running, walking, spitting, chewing and others);

    Maintaining muscle tone and its redistribution during movement;

    Participation in speech articulation and facial expressive movements;

    Maintaining the segmental apparatus in readiness for action.

25. Limbic system.

Limbic system- a nonspecific brain system associated with the olfactory analyzer, the main function of which is the organization of holistic behavior and the integration of physiological activity processes.

Functions of the limbic system:

    Emotional and motivational behavior and adaptation to external and internal environmental conditions;

    Complex forms of behavior: instincts, food, sexual, defensive, changes in phases of sleep and wakefulness;

    Regulatory influence on the cortex and subcortical formations to establish the necessary correspondence of activity levels.

Composition of the limbic system:

    Cortical structures: limbic lobe (cingulate, parahippocampal, dentate and ribbon gyri) and hippocampus;

    Subcortical formations: the basal part of the telencephalon, structures of the diencephalon (papillary bodies, leash nuclei), parts of the midbrain (interpeduncular nucleus, central gray matter) and pathways that provide communication between these structures.

Features of the limbic system– the formation of bilateral connections between the nuclei and many closed circles of different diameters and lengths (large and small).

Greater limbic circle:

    Compound: hippocampus - fornix - mammillary bodies of the hypothalamus - mastoid-thalamic fasciculus of Vic-d'Azir - anterior nuclei of the thalamus - thalamic cingulate radiation - cingulate gyrus - parahippocampal gyrus - hippocampus.

    Function: ensuring memory and learning processes.

Small limbic circle:

    Compound: amygdala – hypothalamus – reticular formation of the midbrain – amygdala.

    Function: regulation of aggressive-defensive, eating and sexual behavior.

26. Regularities in the structure of motor pathways .

Descending, Efferent, Motor, Conscious (Tr. Cortico...), Reflexcore (from subcortical formations).

Among the tracts there are Main PyramidPath, which consists of 3 paths. The first passes from neurons of the precentral gyrus to motor neurons concentrated in the nuclei of the brain stem - this corticonuclearpath. Two other paths: corticospinal front and side go from the precentral gyrus to the nuclei of the anterior horns of the spinal cord. The fibers of each tract cross over in different parts of the brain.

Corticonuclear path of conscious movements crosses over the cranial nerve nuclei in the brain stem. It includes two neural reflex arcs.

Lateral and anterior corticospinal tracts also conduct conscious impulses. The lateral tract crosses at the border of the medulla oblongata and spinal cord, forming pyramidal cross. The anterior tract is crossed at the spinal cord.

Corticopontine-cerebellar the path crosses in the pons at the level of the middle cerebellar peduncles. The first motor neurons are located in the cortex of the frontal, temporal, parietal and occipital lobes. They conduct their axons through the internal capsule (knee). The second neurons lie in the motor nuclei of the pons and the cortex of the cerebellar hemispheres. Axons from the cerebellum exit through the middle peduncle to the motor nuclei of the pons, where they switch.

Descending extrapyramidal tracts of unconscious movements belong to the ancient ways, and they always begin in the subcortical structures of the brain. Their reflex arcs have a two-neuron composition and crossovers at different levels of the brain. Some of them run along only one side, without forming crosses.

Red nuclear spinal the pathway regulating and coordinating muscle tone and automatic muscle contractions crosses in the midbrain.

vestibulospinal way of balance and coordination of movements.

Tectospinal tract visual-auditory unconditioned reflexes.

Olive-spinal automatic way muscle tone A.

Posterior longitudinal fasciculus- a way to coordinate the movements of the eyeballs, head and neck.

The fibers of the bundle connect the motor nuclei with each other III, IV, VI pairs of cranial nerves and the nuclei of the anterior horns of the spinal cord of the cervical and thoracic regions.

    Characteristics of pyramidal tracts.

Pyramid Tractuspyramidalis(volitional, conscious) conduct impulses from the cortex to the motor nuclei and further to the muscles. They are divided into: fibrae corticospinales And fibrae corticonucleares

Fibrae (tractus) corticospinalis

    1 neuron – giant pyramidal cell (Betsa) – neuron of the fifth layer of the cortex of the precentral gyrus

    The pathways pass through the internal capsule in its posterior limb just behind the knee.

    In the midbrain, the fibers of the pathway are located in the cerebral peduncles, in their middle part.

    In the pons area - fibers pass in the ventral part of the pons

    In the medulla oblongata - in the pyramids.

    At the border with the spinal cord, 85% of the tracts cross (decussatio pyramidum), the remaining 15% go into the spinal cord without crossing and pass to the opposite side in the corresponding segment of the spinal cord.

    2 neuron – cell of the motor nucleus of the anterior horn of the spinal cord.

    The axon of the second neuron passes as part of the anterior root, cord and branches of the spinal nerve to the skeletal muscle.

Fibrae (tractus) corticonuclearis (corticobulbaris)

    1 neuron - giant pyramidal cell (Betz) of the fifth layer of the cortex in the precentral gyrus

    The path passes through the knee of the internal capsule

    2 neuron – cells of the somatic motor nuclei of cranial nerves

    The axon of the second neuron passes as part of the cranial nerve to the muscle

    The path gives branches to its own and the opposite side, with the exception of the nuclei of X11 and V11 pairs of cranial nerves

    Characteristics of motor extrapyramidal pathways.

Extrapyramidal The pathways carry impulses to the muscles from the subcortical centers: the basal nuclei of the hemispheres, the dorsal (optic) tubercle, the red nucleus, the substantia nigra, the olive nuclei, the nuclei of the vestibular nerve, the reticular formation. The extrapyramidal system automatically maintains the tone of skeletal muscles and ensures the work of antagonist muscles. The extrapyramidal tracts include: tractus rubrospinalis, tractus tectospinalis, tractus reticulospinalis, tractus olivospinalis, tractus vestibulispinalis. The tracts begin in the corresponding subcortical nuclei (1 neuron). The axons of the first neurons, having previously made the transition to the opposite side, switch to the motor cells of the anterior horns of the spinal cord, the processes of which end in the skeletal muscles. The extrapyramidal system also includes the cortical-cerebellar correlation pathways (tractus cortico-ponto - cerebello - dentato - rubro - spinalis.

    Fundamental morphological differences between central and peripheral paralysis.

PARALYSIS - complete loss of motor functions with lack of muscle strength.

Paresis– weakening of motor functions with a decrease in muscle strength.

Paralysis and paresis develop as a result of various pathological processes (trauma, hemorrhage, etc.) in the central or peripheral part of the nervous system.

Central paralysis

1.Muscle groups are diffusely affected; there is no damage to individual muscles. Moderate atrophy

2. Spasticity with increased tendon reflexes

3. Extensor plantar reflex, Babinski's symptom

4. There are no fascicular twitches

Peripheral paralysis

1.Individual muscles may be affected

2. Severe atrophy, 70-80% of the total mass

3. Lethargy and hypotonia of the affected muscles with loss of tendon reflexes. Plantar reflex, if evoked, is of the normal, flexion type.

4. There may be fasciculations; Electromyography reveals a decrease in the number of motor units and fibrillation

    Regularities in the structure of sensitive pathways.

Ascending, Centripetal, Afferent, Sensitive (...), Conscious (to the cortex), reflex.

    Characteristics of conscious afferent pathways.

Proprioceptive pathways of cortical direction

Fasciculus gracilis (Goll) and fasciculus cuneatus (Burdach).

    1 neuron

    The axon as part of the dorsal root goes to the spinal cord, without entering the gray matter of the dorsal horn, lies in the dorsal funiculi and goes to the medulla oblongata (tractus gangliobulbaris)

    2 neuron - nucleus gracilis et nucleus cuneati lies in the same-named tubercles of the medulla oblongata

    The axons of the second neurons bend ventrally and move to the opposite side, giving rise to the formation of the medial loop

(Lemniscus medialis – tractus bulbothalamicus)

    3 neuron – cells of the lateral nucleus of the dorsal (optic) thalamus

    The processes of the third neurons (tractus thalamocorticalis) pass through the posterior leg of the internal capsule and reach the precentral and postcentral gyri (cells of the fourth layer of the cortex).

    Characteristics of reflex afferent pathways.

Proprioceptivewayscerebellardirections

Tractus spinocerebellaris anterior (Gowers) et spinocerebellaris posterior (Flechsig)

    1 neuron – pseudounipolar cell of the spinal ganglion

    The dendrite of the first neuron ends with a receptor in muscles, tendons, ligaments, joints

    The axon as part of the dorsal root enters the gray matter of the spinal cord and switches to the body of the second neuron

    2 neuron: for Gowersa – nucleus intermediomedialis

for Flechsiga - nucleus thoracicus

    The axons of the second neuron of the Gowersa pathway through the anterior white commissure are directed to the lateral cord of the opposite side, ascend to the medulla oblongata, the pons, and in the superior medullary velum pass to the opposite side and through the superior cerebellar peduncle reach the vermis cortex. The axons of the second neuron of the Flechsiga pathway are directed to the lateral cord of the same side, ascend into the medulla oblongata and reach the vermis cortex through the inferior cerebellar peduncle.

    Medial loop.

A bundle of white matter fibers formed by the axons of the gracilis and cuneate nuclei conducts the conscious proprioceptive pathways and the pathways of general sensitivity, because the spinothalamic tracts join it.

    Commissural nerve fibers of the brain, their structure.

Commissural nerve fibers connect similar areas of the two hemispheres. The nerve fibers of the brain are divided into associative, commissural and projection - they all form pathways for nerve impulses. Association fibers connect cells within one hemisphere, and in the spinal cord - at the level of one half. Commissural fibers connect the right and left hemispheres, the right and left halves of the spinal cord. Projection fibers connect higher and lower brain structures: cortical cells with nuclear cells and organs. They are divided into ascending (sensory) and descending (motor) pathways or tracts.

Commissural fibers, which are part of the so-called cerebral commissures, or commissures, connect the symmetrical parts of both hemispheres. The largest cerebral commissure is the corpus callosum, corpus callosum , connects the parts of both hemispheres related to neencephalon .

Two brain adhesions comissura anterior And comissura inferior , much smaller in size, belong to rhinencephalon and connect: comissura anterior - olfactory lobes and both parahippocampal gyri, comissura fornicis - hippocampi.

Under the corpus callosum is the so-called fornix, forniх , representing two arched white cords, which, in their middle part, corporis fornicis , are connected to each other, and diverge in front and behind, forming pillars of the vault in front, columnae fornicis , behind - the legs of the arch, crura fornicis . Crura fornicis , heading back, descend into the lower horns of the lateral ventricles and pass there into fimbria hippocampi . Between crura fornicis under splenium corporis callosi transverse bundles of nerve fibers extend, forming commissura fornicis . The anterior ends of the arch columnae fornicis , continue down to the base of the brain, where they end in corpora mamillaria passing through gray matter hypothalamus . Columnae fornicis limit the interventricular foramina lying behind them, connecting the third ventricle with the lateral ventricles. In front of the columns of the arch is the anterior commissure, commissura anterior , having the appearance of a white transverse crossbar consisting of nerve fibers. Between the front of the arch and genu corporis callosi a thin vertical plate of brain tissue is stretched - a transparent septum, septum pellucidum , in the thickness of which there is a small slit-like cavity, cavum septi pellucidi .

    Morphological basis of alternating syndrome.

Alternating syndromes- syndromes that combine damage to the craniocerebral nerves on the side of the lesion with conduction disorders of motor and sensory functions on the opposite side.

They occur when the anatomical components of the brain stem are damaged: peduncles - pedincular crossed syndromes, pons - pontine, medulla oblongata - bulbar. These also include crossed hemiplegia - damage to the pyramidal pathway that crosses at different levels of the brain. Therefore, for example, paralysis or paresis of the right arm and left leg occurs with lesions below the brain stem. With opposite hemianesthesia, the ascending pathways are damaged: spinothalamic and bulbothalamic rhythms, fibers of the medial lemniscus.

The term “extrapyramidal system” refers to subcortical and brainstem extrapyramidal formations and motor pathways that do not pass through the pyramids of the medulla oblongata. Part of this system are also those bundles that connect the cerebral cortex with the extrapyramidal gray structures: the striatum, the red nucleus, the substantia nigra, the cerebellum, the reticular formation and the tegmental nuclei of the trunk.

In these structures, impulses are transmitted to intercalary nerve cells and then descend as tegmental, red nucleus-spinal, reticular and vestibular and other pathways to the motor neurons of the anterior horns of the spinal cord. Through these pathways, the extrapyramidal system influences spinal motor activity. The extrapyramidal system, consisting of projection efferent nerve pathways starting in the cerebral cortex, including the nuclei of the striatum, some nuclei of the brain stem and the cerebellum, regulates movements and muscle tone. It complements the cortical system of voluntary movements; voluntary movements become prepared, finely tuned for execution.

The pyramidal tract (via interneurons) and fibers of the extrapyramidal system ultimately meet on the anterior horn motor neurons, alpha and gamma cells, and influence them through both activation and inhibition.

The extrapyramidal system is phylogenetically more ancient (especially its pallidal part) compared to the pyramidal system. With the development of the pyramidal system, the extrapyramidal system moves into a subordinate position.

The extrapyramidal system consists of the following main structures: the caudate nucleus, the putamen, the lentiform nucleus, the globus pallidus, the subthalamic nucleus, the substantia nigra and the red nucleus. The lower order level of this system is the reticular formation of the tegmentum of the brain stem and the spinal cord. With the further development of the animal world, the paleostriatum (globus pallidus) began to dominate these structures. Then, in higher mammals, the neostriatum (caudate nucleus and putamen) takes on a leading role. As a rule, phylogenetically later centers dominate over earlier ones. This means that in lower animals the innervation of movements belongs to the extrapyramidal system. A classic example of "pallidar" creatures is fish. In birds, a fairly developed neostriatum appears. In higher animals, the role of the extrapyramidal system remains very important, despite the fact that as the cerebral cortex develops, phylogenetically older motor centers (paleostriatum and neostriatum) are increasingly controlled by a new motor system, the pyramidal system.

The striatum is the leading center among the structures that make up the extrapyramidal system. It receives impulses from various areas of the cerebral cortex, especially from the frontal motor cortex, which includes fields 4 and 6. These afferent fibers are organized in a somatotopic projection, run ipsilaterally and are inhibitory in their action. Another system of afferent fibers coming from the thalamus also reaches the striatum. From the caudate nucleus and the putamen of the lentiform nucleus, the main afferent fibers are directed to the lateral and medial segments of the globus pallidus, which are separated from each other by the internal medullary plate. There are connections going from the ipsilateral cerebral cortex to the substantia nigra, red nucleus, subthalamic nucleus, and reticular formation.

The caudate nucleus and the shell of the lentiform nucleus have two “channels” of connections with the substantia nigra. On the one hand, nigrostriatal afferents are described as dopaminergic and reducing the inhibitory function of the striatum. On the other hand, the strionigral pathway is GABAergic and has an inhibitory effect on dopaminergic nigrostriatal neurons. These are closed feedback loops. GABAergic neurons control muscle tone via gamma neurons in the spinal cord.

All other efferent fibers of the striatum pass through the medial segment of the globus pallidus. They form rather thick bundles of fibers. One of these bundles is called the lenticular loop. Its fibers begin in the ventral part of the medial segment of the pallidum and run ventromedially around the posterior limb of the internal capsule to the thalamus and hypothalamus, and also reciprocally to the subthalamic nucleus. After crossing, they connect to the reticular formation of the midbrain, from which a chain of neurons forms the reticular-spinal tract (descending reticular system), ending in the cells of the anterior horns of the spinal cord.

The main part of the efferent fibers of the globus pallidus goes to the thalamus. This is the pallidothalamic fascicle, or Trout area H1. Most of its fibers end in the anterior nucleus of the thalamus, which projects to cortical area 6. Fibers starting in the dentate nucleus of the cerebellum end in the posterior nucleus of the thalamus, which projects to cortical area 4. All these thalamocortical connections transmit impulses in both directions. In the cortex, thalamocortical pathways synapse with corticostriatal neurons and form feedback rings. Reciprocal (coupled) thalamocortical connections facilitate or inhibit the activity of cortical motor fields.

The fibers of the basal ganglia that descend to the spinal cord are relatively few in number and reach the spinal cord only through a chain of neurons. This pattern of connections suggests that the main function of the basal ganglia is to control and regulate the activity of motor and premotor cortical fields, so that voluntary movements can be performed smoothly, continuously.

The pyramidal tract begins in the sensorimotor area of ​​the cerebral cortex (fields 4, 1,2, 3). These are at the same time the fields in which the extrapyramidal motor pathways begin, which include corticostriatal, corticorubral, corticonigral and corticoreticular fibers going to the motor nuclei of the cranial nerves and to the spinal motor nerve cells through descending chains of neurons.

Most of these cortical connections pass through the internal capsule. Consequently, damage to the internal capsule interrupts not only the fibers of the pyramidal tract, but also the extrapyramidal fibers. This break is the cause of muscle spasticity.

Semiotics of extrapyramidal disorders. The main signs of extrapyramidal disorders are disorders of muscle tone (dystonia) and involuntary movements (hyperkinesis, hypokinesis, akinesis), absent during sleep. Two clinical syndromes can be distinguished. One of them is characterized by a combination of hyperkinesis (automatic violent movements due to involuntary muscle contractions) and muscle hypotonia and is caused by damage to the neostriatum. The other is a combination of hypokinesis and muscle hypertension or rigidity and is observed when the medial part of the globus pallidus and substantia nigra are affected.

Akinetic-rigid syndrome (syn.: amyostatic, hypokinetic-hypertensive, pallidonigral). This syndrome in its classical form is found in shaking palsy, or Parkinson's disease. The pathological process in this disease is degenerative, leading to the loss of melanin-containing neurons of the substantia nigra. The lesions in Parkinson's disease are usually bilateral. With unilateral cell loss, clinical signs are observed on the opposite side of the body. In Parkinson's disease, the degenerative process is hereditary. Similar loss of substantia nigra neurons may be due to other causes. In such cases, shaking palsy is referred to as Parkinson's syndrome or parkinsonism. If it is a consequence of encephalitis lethargica, it is called postencephalitic parkinsonism. Other conditions (cerebral atherosclerosis, typhus, cerebral syphilis, primary or secondary involvement of the midbrain due to tumor or injury, intoxication with carbon monoxide, manganese and other substances, long-term use of phenothiazine or reserpine) can also cause parkinsonism.

Clinical manifestations of akinetic-rigid syndrome are characterized by three main signs: hypokinesia (akinesis), rigidity and tremor. With hypokinesia, the patient's mobility slowly decreases. All facial and expressive movements gradually disappear or slow down sharply. Starting movement, such as walking, is very difficult. The patient first takes several short steps. Having started moving, he cannot suddenly stop and takes a few extra steps. This continued activity is called propulsion. The facial expression becomes mask-like (hypomimia, amymia). Speech becomes monotonous and dysarthric, which is partly caused by tongue rigidity and tremor. The body is in a fixed flexion position of anteflexion, all movements are extremely slow and incomplete.

Hands are not involved in the act of walking (acheirokinesis). All facial and friendly expressive movements characteristic of the individual are absent.

In contrast to spastic increases in muscle tone, rigidity can be felt in the extensors as a “waxy” resistance to all passive movements. The muscles cannot be relaxed. With passive movements, you can feel that the tone of the antagonist muscles decreases stepwise, inconsistently (gear wheel symptom). The raised head of a lying patient does not fall if suddenly released, but gradually falls back onto the pillow (head fall test). In contrast to the spastic state, proprioceptive reflexes are not increased, and pathological reflexes and paresis are absent. It is difficult to evoke reflexes and impossible to strengthen the knee reflex with the Jendrasik maneuver.

Most patients exhibit passive tremor of low frequency (4–8 movements per second). Passive tremor is rhythmic and results from the interaction of agonists and antagonists (antagonistic tremor). In contrast to intention tremor, antagonistic tremor stops during goal-directed movements. Rolling pills or counting coins are signs characteristic of parkinsonian tremor.

The mechanism that causes the appearance of the three listed signs is not fully understood. Akinesis may be associated with loss of dopaminergic transmission of impulses to the striatum. Akinesis can be explained as follows: damage to the neurons of the substantia nigra causes the loss of the influence of inhibitory descending nigroreticulospinal impulses on Renshaw cells. Renshaw cells, which have connections with large motor neurons, reduce the activity of the latter with their inhibitory effect, which makes the onset of voluntary movement more difficult.

Rigidity may also be explained by loss of substantia nigra neurons. Normally, these neurons have an inhibitory effect on the impulses of the striatum, which in turn inhibit the globus pallidus. Their loss means that efferent pallidal impulses are not inhibited. The descending tract of the globus pallidus forms synapses with reticulospinal neurons; which facilitate the action of interneurons in the circuit of the tonic stretch reflex. In addition, impulses emanating from the medial part of the globus pallidus reach through the thalamic nuclei of area 6a and, through corticospinal fibers, also have a facilitating effect on interneurons in the circuit of the tonic stretch reflex. There is a disturbance in muscle tone called rigidity.

If the efferent cells and fibers of the globus pallidus are destroyed by stereotactic surgery in its medial part or the region of the lenticular loop, or the thalamic nucleus, rigidity decreases.

Stereotactic coagulation operations of the medial part of the globus pallidus, pallidothalamic fibers or dentatothalamic fibers and their terminal thalamic nucleus are indicated in some patients.

Hyperkinetic-hypotonic syndrome. Develops when the striatum is damaged. Hyperkinesis is caused by damage to the inhibitory neurons of the neostriatum, the fibers of which go to the globus pallidus and the substantia nigra. In other words, there is a violation of higher-order neuronal systems, which leads to excessive excitation of neurons in lower-lying systems. As a result, hyperkinesis of various types occurs: athetosis, chorea, spastic torticollis, torsion dystonia, ballism, etc.

Athetosis is usually caused by perinatal damage to the striatum. It is characterized by involuntary slow and worm-like movements with a tendency to hyperextension of the distal parts of the limbs. In addition, there is an irregular, spastic increase in muscle tension in agonists and antagonists. As a result, the postures and movements are quite eccentric. Voluntary movements are significantly impaired due to the spontaneous occurrence of hyperkinetic movements, which can involve the face, tongue and thus cause grimaces with abnormal movements of the tongue. Spastic bursts of laughter or crying are possible. Athetosis can be combined with contralateral paresis. It can also be double-sided.

Facial paraspasm is a tonic symmetrical contraction of the facial muscles of the mouth, cheeks, neck, tongue, eyes. Sometimes blepharospasm is observed - an isolated contraction of the circular muscles of the eyes, which can be combined with clonic spasms of the muscles of the tongue and mouth. Paraspasm sometimes occurs during conversation, eating, or smiling. Intensifies with excitement and bright lighting. Disappears in sleep.

Choreic hyperkinesis is characterized by short, fast, involuntary twitches, randomly developing in the muscles and causing various types of movements, sometimes resembling voluntary ones. The distal parts of the limbs are involved first, then the proximal ones. Involuntary twitching of the facial muscles causes grimaces. In addition to hyperkinesis, a decrease in muscle tone is characteristic. Choreic movements with slow development can be a pathognomonic sign in Huntington's chorea and chorea minor, secondary to other brain diseases (encephalitis, carbon monoxide poisoning, vascular diseases). The striatum is affected.

Spasmodic torticollis and torsion dystonia are the most important dystonia syndromes. In both diseases, the putamen and centromedian nucleus of the thalamus, as well as other extrapyramidal nuclei (globus pallidus, substantia nigra, etc.) are usually affected. Spasmodic torticollis is a tonic disorder expressed in spastic contractions of the muscles of the cervical region, leading to slow, involuntary turns and tilts of the head. Patients often use compensatory techniques to reduce hyperkinesis, in particular supporting their head with their hands. In addition to other neck muscles, the sternocleidomastoid and trapezius muscles are especially often involved in the process.

Spasmodic torticollis may represent an abortive form of torsion dystonia or an early symptom of another extrapyramidal disease (encephalitis, Huntington's chorea, hepatocerebral dystrophy).

Torsion dystonia is characterized by passive rotational movements of the trunk and proximal limb segments. They can be so severe that the patient cannot stand or walk without support. The disease may be symptomatic or idiopathic. In the first case, birth trauma, jaundice, encephalitis, early Huntington's chorea, Hallerwarden-Spatz disease, hepatocerebral dystrophy (Wilson-Westphal-Strumpel disease) are possible.

Ballistic syndrome usually occurs in the form of hemiballismus. Manifested by rapid contractions of the proximal muscles of the extremities of a rotating nature. With hemiballismus, the movement is very powerful, strong (“throwing”, sweeping), since very large muscles contract. It occurs due to damage to the subthalamic nucleus of Lewis and its connections with the lateral segment of the globus pallidus. Hemiballismus develops on the side contralateral to the lesion.

Myoclonic twitching usually indicates damage to the area of ​​the Guillen-Mollare triangle: red nucleus, inferior olive, dentate nucleus of the cerebellum. These are rapid, usually erratic contractions of various muscle groups.

Tics are rapid involuntary contractions of muscles (most often the orbicularis oculi muscle and other facial muscles).

The term “extrapyramidal system” refers to subcortical and brainstem extrapyramidal formations and motor pathways that do not pass through the pyramids of the medulla oblongata. Part of this system are also those bundles that connect the cerebral cortex with the extrapyramidal gray structures: the striatum, the red nucleus, the substantia nigra, the cerebellum, the reticular formation and the tegmental nuclei of the trunk. In these structures, impulses are transmitted to intercalary nerve cells and then descend as tegmental, red-nuclear spinal, reticular and vestibular spinal and other pathways to the motor neurons of the anterior horns of the spinal cord. Through these pathways, the extrapyramidal system influences spinal motor activity. The extrapyramidal system, consisting of projection efferent nerve pathways starting in the cerebral cortex, including the nuclei of the striatum, some nuclei of the brain stem and the cerebellum, regulates movements and muscle tone. It complements the cortical system of voluntary movements; voluntary movements become prepared, finely tuned for execution.

The pyramidal tract (via interneurons) and fibers of the extrapyramidal system ultimately meet on the anterior horn motor neurons, alpha and gamma cells, and influence them through both activation and inhibition.

The extrapyramidal system is phylogenetically more ancient (especially its pallidal part) compared to the pyramidal system. With the development of the pyramidal system, the extrapyramidal system moves into a subordinate position.

The extrapyramidal system consists of the following main structures: the caudate nucleus, the putamen, the lentiform nucleus, the globus pallidus, the subthalamic nucleus, the substantia nigra and the red nucleus. The lower order level of this system is the reticular formation of the tegmentum of the brain stem and the spinal cord. With the further development of the animal world, the paleostriatum (globus pallidus) began to dominate these structures. Then, in higher mammals, the neostriatum (caudate nucleus and putamen) takes on a leading role. As a rule, phylogenetically later centers dominate over earlier ones. This means that in lower animals the innervation of movements belongs to the extrapyramidal system. A classic example of "pallidar" creatures is fish. In birds, a fairly developed neostriatum appears. In higher animals, the role of the extrapyramidal system remains very important, despite the fact that as the cerebral cortex develops, phylogenetically older motor centers (paleostriatum and neostriatum) are increasingly controlled by a new motor system, the pyramidal system.

The striatum is the leading center among the structures that make up the extrapyramidal system. It receives impulses from various areas of the cerebral cortex, especially from the frontal motor cortex, which includes fields 4 and 6. These afferent fibers are organized in a somatotopic projection, run ipsilaterally and are inhibitory in their action. Another system of afferent fibers coming from the thalamus also reaches the striatum. From the caudate nucleus and the putamen of the lentiform nucleus, the main afferent fibers are directed to the lateral and medial segments of the globus pallidus, which are separated from each other by the internal medullary plate. There are connections going from the ipsilateral cerebral cortex to the substantia nigra, red nucleus, subthalamic nucleus, and reticular formation.

The caudate nucleus and the shell of the lentiform nucleus have two “channels” of connections with the substantia nigra. On the one hand, nigrostriatal afferents are described as dopaminergic and reducing the inhibitory function of the striatum. On the other hand, the strionigral pathway is GABAergic and has an inhibitory effect on dopaminergic nigrostriatal neurons. These are closed feedback loops. GABAergic neurons, via gamma neurons in the spinal cord, control muscle tone.

All other efferent fibers of the striatum pass through the medial segment of the globus pallidus. They form rather thick bundles of fibers. One of these bundles is called the lenticular loop. Its fibers begin in the ventral part of the medial segment of the pallidum and run ventromedially around the posterior limb of the internal capsule to the thalamus and hypothalamus, and also reciprocally to the subthalamic nucleus. After crossing, they connect to the reticular formation of the midbrain, from which a chain of neurons forms the reticular spinal tract (descending reticular system), ending in the cells of the anterior horns of the spinal cord.

The main part of the efferent fibers of the globus pallidus goes to the thalamus. This is the pallidothalamic fascicle, or Trout area H1. Most of its fibers end in the anterior nucleus of the thalamus, which projects to cortical area 6. Fibers starting in the dentate nucleus of the cerebellum end in the posterior nucleus of the thalamus, which projects to cortical area 4. All these thalamocortical connections transmit impulses in both directions. In the cortex, thalamocortical pathways synapse with corticostriatal neurons and form feedback rings. Reciprocal (coupled) thalamocortical connections facilitate or inhibit the activity of cortical motor fields.

The fibers of the basal ganglia that descend to the spinal cord are relatively few in number and reach the spinal cord only through a chain of neurons. This pattern of connections suggests that the main function of the basal ganglia is to control and regulate the activity of motor and premotor cortical fields, so that voluntary movements can be performed smoothly, continuously.

The pyramidal tract begins in the sensorimotor area of ​​the cerebral cortex (fields 4, 1,2, 3). These are at the same time the fields in which the extrapyramidal motor pathways begin, which include corticostriatal, corticorubral, corticonigral and corticoreticular fibers going to the motor nuclei of the cranial nerves and to the spinal motor nerve cells through descending chains of neurons.

Most of these cortical connections pass through the internal capsule. Consequently, damage to the internal capsule interrupts not only the fibers of the pyramidal tract, but also the extrapyramidal fibers. This break is the cause of muscle spasticity.

Semiotics of extrapyramidal disorders. The main signs of extrapyramidal disorders are disorders of muscle tone (dystonia) and involuntary movements (hyperkinesis, hypokinesis, akinesis), absent during sleep. Two clinical syndromes can be distinguished. One of them is characterized by a combination of hyperkinesis (automatic violent movements due to involuntary muscle contractions) and muscle hypotonia and is caused by damage to the neostriatum. The other is a combination of hypokinesis and muscle hypertension or rigidity and is observed when the medial part of the globus pallidus and substantia nigra are affected.

Akinetic-rigid syndrome (syn.: amyostatic, hypokinetic hypertonic, pallidonigral). This syndrome in its classical form is found in shaking palsy, or Parkinson's disease. The pathological process in this disease is degenerative, leading to the loss of melanin-containing neurons of the substantia nigra. The lesions in Parkinson's disease are usually bilateral. With unilateral cell loss, clinical signs are observed on the opposite side of the body. In Parkinson's disease, the degenerative process is hereditary. Similar loss of substantia nigra neurons may be due to other causes. In such cases, shaking palsy is referred to as Parkinson's syndrome or parkinsonism. If it is a consequence of encephalitis lethargica, it is called postencephalitic parkinsonism. Other conditions (cerebral atherosclerosis, typhus, cerebral syphilis, primary or secondary involvement of the midbrain due to tumor or injury, intoxication with carbon monoxide, manganese and other substances, long-term use of phenothiazine or reserpine) can also cause parkinsonism.

Clinical manifestations of akinetic-rigid syndrome are characterized by three main signs: hypokinesia (akinesis), rigidity and tremor. With hypokinesia, the patient's mobility slowly decreases. All facial and expressive movements gradually disappear or slow down sharply. Starting movement, such as walking, is very difficult. The patient first takes several short steps. Having started moving, he cannot suddenly stop and takes a few extra steps. This continued activity is called propulsion. The facial expression becomes mask-like (hypomimia, amymia). Speech becomes monotonous and dysarthric, which is partly caused by tongue rigidity and tremor. The body is in a fixed flexion position of anteflexion, all movements are extremely slow and incomplete. Hands are not involved in the act of walking (acheirokinesis). All facial and friendly expressive movements characteristic of the individual are absent.

In contrast to spastic increases in muscle tone, rigidity can be felt in the extensors as a “waxy” resistance to all passive movements. The muscles cannot be relaxed. With passive movements, you can feel that the muscle tone of the antagonists decreases stepwise, inconsistently (gear wheel symptom). The raised head of a lying patient does not fall if suddenly released, but gradually falls back onto the pillow (head fall test). In contrast to the spastic state, proprioceptive reflexes are not increased, and pathological reflexes and paresis are absent. It is difficult to evoke reflexes and impossible to strengthen the knee reflex with the Jendrasik maneuver.

Most patients exhibit passive tremor of low frequency (4–8 movements per second). Passive tremor is rhythmic and results from the interaction of agonists and antagonists (antagonistic tremor). In contrast to intention tremor, antagonistic tremor stops during goal-directed movements. Rolling pills or counting coins are signs characteristic of parkinsonian tremor.

The mechanism that causes the appearance of the three listed signs is not fully understood. Akinesis may be associated with loss of dopaminergic transmission of impulses to the striatum. Akinesis can be explained as follows: damage to the neurons of the substantia nigra causes the loss of the influence of inhibitory descending nigroreticulospinal impulses on Renshaw cells. Renshaw cells having a connection with large ones? motor neurons, their inhibitory effect reduces the activity of the latter, which makes the onset of voluntary movement more difficult.

Rigidity may also be explained by loss of substantia nigra neurons. Normally, these neurons have an inhibitory effect on the impulses of the striatum, which in turn inhibit the globus pallidus. Their loss means that efferent pallidal impulses are not inhibited. The descending tract of the globus pallidus forms synapses with reticulospinal neurons; which facilitate the action of interneurons in the circuit of the tonic stretch reflex. In addition, impulses emanating from the medial part of the globus pallidus reach through the thalamic nuclei of area 6a and, through corticospinal fibers, also have a facilitating effect on interneurons in the circuit of the tonic stretch reflex. There is a disturbance in muscle tone called rigidity.

If the efferent cells and fibers of the globus pallidus are destroyed by stereotactic surgery in its medial part or the region of the lenticular loop, or the thalamic nucleus, rigidity decreases.

Stereotactic coagulation operations of the medial part of the globus pallidus, pallidothalamic fibers or dentatothalamic fibers and their terminal thalamic nucleus are indicated in some patients.

Hyperkinetic hypotonic syndrome. Develops when the striatum is damaged. Hyperkinesis is caused by damage to the inhibitory neurons of the neostriatum, the fibers of which go to the globus pallidus and the substantia nigra. In other words, there is a violation of higher-order neuronal systems, which leads to excessive excitation of neurons in lower-lying systems. As a result, hyperkinesis of various types occurs: athetosis, chorea, spastic torticollis, torsion dystonia, ballism, etc.

Athetosis is usually caused by perinatal damage to the striatum. It is characterized by involuntary slow and worm-like movements with a tendency to hyperextension of the distal parts of the limbs. In addition, there is an irregular, spastic increase in muscle tension in agonists and antagonists. As a result, the postures and movements are quite eccentric. Voluntary movements are significantly impaired due to the spontaneous occurrence of hyperkinetic movements, which can involve the face, tongue and thus cause grimaces with abnormal movements of the tongue. Spastic bursts of laughter or crying are possible. Athetosis can be combined with contralateral paresis. It can also be double-sided.

Facial paraspasm is a tonic symmetrical contraction of the facial muscles of the mouth, cheeks, neck, tongue, eyes. Sometimes blepharospasm is observed - an isolated contraction of the circular muscles of the eyes, which can be combined with clonic spasms of the muscles of the tongue and mouth. Paraspasm sometimes occurs during conversation, eating, or smiling. Intensifies with excitement and bright lighting. Disappears in sleep.

Choreic hyperkinesis is characterized by short, fast, involuntary twitches, randomly developing in the muscles and causing various types of movements, sometimes resembling voluntary ones. The distal parts of the limbs are involved first, then the proximal ones. Involuntary twitching of the facial muscles causes grimaces. In addition to hyperkinesis, a decrease in muscle tone is characteristic. Choreic movements with slow development can be a pathognomonic sign in Huntington's chorea and chorea minor, secondary to other brain diseases (encephalitis, carbon monoxide poisoning, vascular diseases). The striatum is affected.

Spasmodic torticollis and torsion dystonia are the most important dystonia syndromes. In both diseases, the putamen and centromedian nucleus of the thalamus, as well as other extrapyramidal nuclei (globus pallidus, substantia nigra, etc.) are usually affected. Spasmodic torticollis is a tonic disorder expressed in spastic contractions of the muscles of the cervical region, leading to slow, involuntary turns and tilts of the head. Patients often use compensatory techniques to reduce hyperkinesis, in particular supporting their head with their hands. In addition to other neck muscles, the sternocleidomastoid and trapezius muscles are especially often involved in the process.

Spasmodic torticollis may represent an abortive form of torsion dystonia or an early symptom of another extrapyramidal disease (encephalitis, Huntington's chorea, hepatocerebral dystrophy).

Torsion dystonia is characterized by passive rotational movements of the trunk and proximal limb segments. They can be so severe that the patient cannot stand or walk without support. The disease may be symptomatic or idiopathic. In the first case, birth trauma, jaundice, encephalitis, early Huntington's chorea, Hallerwarden-Spatz disease, hepatocerebral dystrophy (Wilson-Westphal-Strumpel disease) are possible.

Ballistic syndrome usually occurs in the form of hemiballismus. Manifested by rapid contractions of the proximal muscles of the extremities of a rotating nature. With hemiballismus, the movement is very powerful, strong (“throwing”, sweeping), since very large muscles contract. It occurs due to damage to the subthalamic nucleus of Lewis and its connections with the lateral segment of the globus pallidus. Hemiballismus develops on the side contralateral to the lesion.

Myoclonic twitching usually indicates damage to the area of ​​the Guillen-Mollare triangle: red nucleus, inferior olive, dentate nucleus of the cerebellum. These are rapid, usually erratic contractions of various muscle groups.

Tics are rapid involuntary contractions of muscles (most often the orbicularis oculi muscle and other facial muscles).

Hyperkinesis presumably develops as a result of the loss of the inhibitory effect of the striatum on the underlying neuronal systems (globus pallidus, substantia nigra).

Pathological impulses go to the thalamus, to the motor cortex and then along efferent cortical neurons.

In elderly patients with cerebral atherosclerosis, one can often find signs of Parkinson-like disorders or hyperkinesis, especially tremor, a tendency to repeat words and phrases, final syllables of words (logoclonia) and movements (polykinesia). There may be a tendency toward pseudospontaneous movements, but true choreiform or athetoid movements are relatively rare. In most cases, symptoms are due to miliary and somewhat large necrotic lesions of the striatum and globus pallidus, which are found in the form of scars and very small cysts. This condition is known as lacunar status. The tendency to repetition and logoclonus is considered to be due to similar lesions of the caudate nucleus, and tremor - to the putamen.

Automated actions are complex motor acts and other sequential actions that occur without conscious control. Occurs with hemispheric lesions that destroy the connections of the cortex with the basal ganglia while their connection with the brain stem is preserved; appear in the limbs of the same name as the lesion.

Each person performs conscious actions; the pyramidal system of the brain is directly responsible for these processes. How are involuntary reactions triggered? These processes occur due to the functioning of the extrapyramidal system. This article will discuss its structure, main functions and possible complications in case of serious violations.

General concept of ES

So, the pyramidal system is responsible for all conscious movements (walking, speaking, hand movements, etc.). However, deep in the human brain there is a special extrapyramidal system that is responsible for all our new skills and capabilities.

Scientists divided its formation (evolution) into two separate periods:

  • non-ostrianary;
  • palleostriatal.

The first arose much earlier than the palleostriatal one; together they complement each other. Due to it, processes of slowing down motor activity occur, which in turn are triggered by the second system.

ES originates in the brain (in the area of ​​the pons and protongus) and is directed to the spinal cord. It is considered one of the first to be responsible for human motor activity.

ES functions

The pyramidal system is responsible for conscious movements in the human body. For example, in order for a person to be able to bring a spoon or fork to his mouth while eating, he needs to think about it in advance. What processes are considered unconscious and do not require the participation of the cerebral cortex to run? You can get the answer only by studying in detail the functions of the extrapyramidal structure. So, she is responsible for:

  • regulatory processes of tone in muscle muscles. There is a muscle group that does not relax even during a period of rest. However, a person never thinks twice before “preparing” them for physical activity; this is what ES does;
  • protective reflexes of the body. For example, when there is a loud clap or sound, a person involuntarily closes his eyes or flinches;
  • maintaining balance. In this case, when a person slips on ice: the tilt of the body changes, and the hands are involved. This is all done on an unconscious level with the participation of the ES;
  • skills that are acquired throughout the life cycle and are reinforced. In this case, they talk about the “Caesar” syndrome, which performed several actions at the same time. A person can work calmly and at the same time talk on the phone. All this was made possible with the help of a unique extrapyramidal complex.

If one of the areas of this structure is damaged, a person develops serious impairments in coordination, etc. To understand these processes in more detail, let us consider its structure in detail.

It consists of separate areas that are found deep in the cerebral cortex. Since this structure is considered one of the oldest, it is characterized by the formation of a nucleus. Detailed study of ES began in the second half of the 19th century. Then scientists found that the core consists of three components:

  • the striatum (stiatrum), which is divided into two separate sections: the caudate and the lenticular. The latter consists of a pale layer and a shell;
  • the fence that lies between the layers of gray matter. There is little information about it, its functions have not been fully studied by scientists;
  • the amygdala region, which is directly connected to the subcortical olfactory system and the limbometric system;
  • red nuclei, which are of a paired nature. It is from this area that unconscious impulses originate and are directed to the muscular muscles of the skeleton. There is a concept of Trout cross, thanks to which all processes are launched from both sides. The red tint is due to the presence of blood capillaries and a high ferrum content;
  • the cerebellum does not belong to the extrapyramidal system, but it is fully involved in all unconscious processes of the human body;
  • black content, which is characterized by pairing. It got its name due to the high content of melanin pigment. Anatomical location - between the peduncle and the tegmentum of the brain. Supplied with a large number of blood vessels, it is directly connected to parts of the brain.

Relationships between the structures of the extrapyramidal system

Until now, the interaction processes remain incompletely studied. The ES is directly connected to the thalamus, reticulatory nuclei, pons, cerebellum, etc. For full functioning, gamma motor neutrons from the spinal cord are added to all of these structures.

This system is closely related to the pyramidal structure. Thanks to this interaction, a person organizes all movements that are provoked by parts of the pyramidal system. The processes of the red nucleus of the extrapyramidal system form the so-called rubrospinal tract. It is responsible for the motor processes of the human upper limbs.

The vestibular region of the ES is closely connected with the area of ​​the inner ear, cerebellum and some parts of the spinal cord. Thanks to this, a person makes movements with his neck, torso, head and limbs. In addition, the relationship with various structures of the brain provides the functions of blinking, turning the head and controlling muscle contractions. When one of the processes is disrupted, a person experiences various complications.

ES malfunctions

When the human body is exposed to a number of negative factors or diseases, the functioning of the extrapyramidal system is disrupted. This is accompanied by increased or decreased muscle tone, curvature of posture, and reflex disorders. Such disorders were recorded with long-term use of antipsychotic drugs (they have a direct effect on areas of the brain).

Among the most well-known disorders of the extrapyramidal system are dyskinesia, dystonia, etc. For example, with long-term use of antipsychotic drugs, a patient is diagnosed with “rabbit syndrome”. This is a condition that is accompanied by involuntary contractions of the perioral muscles. Treatment of this pathology is very complex and lengthy. A person may also experience involuntary muscle contractions in the face or neck.

It is important to note that disruption of the extrapyramidal system is associated with a person having traumatic brain injuries, brain diseases (mennitis, etc.), problems with blood vessels in the brain, genetic diseases, trauma to the child during childbirth, the presence of tumors in the brain and etc. Parkinson's disease is the result of a disorder of the ES. The patient experiences severe tremors of the limbs, speech becomes monotonous, and facial expressions are disrupted.

In the case of damage to the substantia nigra of the ES, the patient's reflex functions significantly increase from the time of taking the initial certain posture. When palladium is affected, the patient is diagnosed with muscle hypertension, which is also called waxy hypertension. In this case, when performing movements, the person’s posture remains unchanged. Such patients are characterized by stiffness in movements, facial expressions are completely absent (the expression resembles a mask). To make a particular movement (for example, straighten an arm) requires a lot of effort.

Treatment of problems associated with ES disorders is long and complex. Elderly people are susceptible to such pathologies; they are prescribed supportive drug therapy.

Conclusion

Until recently, problems with disorders of the extrapyramidal system remain incompletely studied. They are varied: from increased flexibility to complete stupor, the disappearance of necessary functions and the appearance of new ones, the development of tremors or nervous tics, chorea or hyperkinesis of various types.

These pathologies develop in a person both throughout life and have a one-time nature; they are the result of poor heredity. At the first unpleasant symptoms, it is recommended to immediately undergo a diagnosis. Treatment lasts a lifetime, and the person is not a full-fledged member of society. However, scientists are able to create new modern drugs that help eliminate these problems.

Extrapyramidal system

unites the motor centers of the cerebral cortex, its nuclei and pathways that do not pass through the pyramids of the medulla oblongata; regulates involuntary components of motor skills (muscle tone, coordination of movements, posture).

From the pyramidal system (Pyramid system) E. s. differs in the localization of nuclei in the subcortical region of the hemispheres and the brain stem and the multi-link nature of the pathways (Conducting pathways). The primary centers of the system are the caudate and lenticular nuclei of the striatum, the subthalamic nucleus, the red nucleus and the substantia nigra of the midbrain (see Brain, Brain stem). In addition, in E. s. are included as integration centers of the cerebral cortex (cerebral cortex), thalamic nuclei, cerebellum, vestibular and olivary nuclei, reticular formation. Part of E. s. is the striopallidal system, which unites the nuclei of the striatum and their afferent and efferent pathways. In the striopallidar system, a phylogenetically new part is distinguished - the striatum, which includes the caudate nucleus and the shell of the lenticular nucleus, and a phylogenetically old part - the pallidum (globus pallidus). The striatum and pallidum differ in their neuroarchitecture, connections and functions.

The striatum receives fibers from the cerebral cortex, the central nucleus of the thalamus and the substantia nigra. Efferent fibers from the striatum are sent to the pallidum, as well as to the substantia nigra. From the pallidum, fibers go to the thalamus, hypothalamus, to the subthalamic nucleus and to the brain stem. The latter form a lenticular loop and partly end in the reticular formation, partly go to the red nucleus, vestibular and olivary nuclei. The next links of the extrapyramidal tracts are the reticular spinal cord, red nucleus spinal cord, vestibulospinal cord and olivospinal cord, ending in the anterior columns and the intermediate gray matter of the spinal cord (Spinal cord). The cerebellum is included in E. s. through pathways connecting it to the thalamus, red nucleus and olivary nuclei.

Functionally E. s. inseparable from the pyramid system. It provides an orderly course of voluntary movements regulated by the pyramidal system; regulates congenital and acquired automatic motor acts (see Movements), ensures the establishment of muscle tone and maintaining body balance; regulates accompanying movements (for example, hand movements when walking) and expressive movements (facial expressions).

Research methods. Various methods of studying the brain help identify pathology: Electroencephalography, Rheoencephalography, pneumoencephalography, Angiography, radionuclide Scintigraphy, computer X-ray and positron emission tomography; registration of the state of the neuromuscular system (Electromyography, myotonometry, gramography, kymography of hyperkinesis at rest and during stimulation, film recording of movements in accelerated filming with slow-motion projection, etc.), study of the content of catecholamines and other neurotransmitters in the blood and cerebrospinal fluid.

Pathology. Pathological syndromes arise when various nuclei and connections of E. are damaged. Motor functions, muscle tone, posture, coordination, emotional manifestations, and vegetative-vascular reactions are impaired. Disturbances can manifest themselves as an excess of movements and postures, the appearance of hyperkinesis (Hyperkinesis), excessive gesticulation, synkinesis (Synkinesis), and a deficiency of movements - akinesia.

In humans, there is a close phylogenetic relationship between motor skills and muscle tone, therefore, in the pathology of E. s. There are combined disorders of motor skills and muscle tone. For example, “pallidal rigidity”, which occurs when the globus pallidus and its connections are damaged (Parkinsonism, atherosclerotic muscle rigidity of Förster), is characterized, on the one hand, by increased postural reflexes and postures, the appearance of plastic muscle tone, stepwise muscle contraction, and on the other hand, loss of extrapyramidal kineses , immobility. In striatal hyperkinetic-hypotonic syndromes, hyperkinesis, pretentious postures, grimaces, gestures, disturbances in speech, writing, and gait appear against the background of muscle hypotonia or dystonia (Gordon's symptom).

Lesions of E. s. occur in various diseases of the brain: encephalitis (Encephalitis) (epidemic, rheumatic, etc.), vascular diseases, traumatic brain injury (traumatic brain injury), intoxication (carbon monoxide, lead, mercury, etc.), tumors, etc. Long-term use of antipsychotic drugs (neuroleptic drugs) with a change in tolerance to the drug can lead to damage to E. s. Extrapyramidal syndromes can also be the result of more rare causes, for example, severe forms of allergies, hyperventilation, asphyxia, polyglobulia, etc. It is possible that such syndromes may develop after stereotactic surgery. There are known diseases associated with congenital insufficiency of the basal ganglia (myoclonus-epilepsy, double athetosis, etc.).

In the pathogenesis of E.'s diseases. great importance is attached to neurochemical mechanisms. In the subcortical areas of the brain, specialized neurotransmitters function, the action of which is disrupted under pathological conditions. For example, motor and emotional disorders in Parkinsonism are caused by a decrease in the activity of two systems of dopaminergic neurons: in the nigrostriatal pathway (decreased motor activity) and in the mesolimbic pathway (decreased emotional reactions). When dopamine activity in the striatum is weakened (impaired input of the dopamine system to the receptors of cholinergic neurons), an excess of acetylcholine occurs, which leads to the appearance of tremors.

One of the clinical forms of extrapyramidal disorders is trembling (tremor), in which the involvement of the red nucleus system - the reticular formation of the dentate nucleus of the cerebellum has been established. Trembling is variable in amplitude, frequency, localization (fingers, neck, head, hemitremor, etc.). Static trembling of the fingers (resting tremor) in the form of rolling pills or counting coins is an important sign of Parkinson's disease (shaking palsy). In combination with muscle rigidity and hypomimia, it forms tremulous-rigid forms of parkinsonism. Statodynamic tremors are characteristic of essential tremor (Minor tremor), hepatocerebral dystrophy. The cerebellar type of tremor (dynamic, intention tremor) is characteristic of multiple sclerosis and encephalitis. Impaired motor reactions due to damage to the tegmentum of the brain stem. reticular formation, substantia nigra leads to the appearance of fixed postural postures, strengthening of flexor or extensor position reflexes. Postural localized postures such as “torsion” include spastic torticollis. The syndrome occurs after encephalitis, intoxication, and is caused by the release of cervical-tonic and labyrinthine reflexes at the level of the oral parts of the brain stem. It can be combined with other extrapyramidal hyperkinesis (tremor, torsion dystonia, etc.), which distinguishes torticollis of an extrapyramidal nature from reflex torticollis (with accessory ribs, cervical radiculitis, osteochondrosis).

Short, rapid spasms of a muscle or part of it, resembling large fasciculations, are considered Friedreich's paramyoclonus. Muscle contractions involving synergistic muscles with movement of body parts and limbs are classified as myoclonic hyperkinesis. Rubrodentoolivary myoclonus is more common, developing after encephalitis, rheumatism, toxoplasmosis, etc. Hereditary myoclonus can be combined with epilepsy (Unferricht-Lundborg myoclonus epilepsy) or with cerebellar asynergia (Hunt's cerebellar asynergia). The myorhythmia described by G. Mannescu, which is localized mainly in the muscles of the soft palate and auditory tube, is classified as the lower olivary type.

When E. is affected, tics of the muscles of the face, abdominal wall, diaphragm, and vocal folds may develop (stuttering). Generalized tics in combination with speech tics in children are called Tourette's disease; There is a diaphragm tic that causes hiccups. Hyperkinesis with respiratory paroxysms arise as a result of contraction of the muscles of the diaphragm and abdominal wall and are manifested by attacks of rapid convulsive exhalations, accompanied by screams and coughing. During paroxysmal respiratory hyperkinesis, the pulse quickens and vasomotor disorders are observed.

The clinical group of thalamostriatal disorders consists of various forms of chorea (minor chorea, Huntington's chorea, atherosclerotic chorea, etc.). Convulsions during chorea are scattered, fast, powerful, appear in all parts of the body and limbs, and are accompanied by grimacing. Chorea minor is a symptom of rheumatic encephalitis. Huntington's chorea is a hereditary chronic disease that occurs with increasing dementia. After acute cerebrovascular accidents, hemichorea may appear in the area of ​​the internal capsule and striatal bodies. Variants of choreic hyperkinesis include hemiballismus, characterized by throwing rotational movements in the arm or leg of one side of the body in combination with muscle hypotonia. Develops with damage to the subthalamic nucleus of Lewis and its connection with the globus pallidus.

Pathological movements in the distal extremities, extending to the muscles of the face and neck, can be observed with athetosis. They are changeable, occur as if overcoming an obstacle, are asynchronous, and create the impression of a continuous wave-like spasm, reminiscent of the movements of the tentacles of an octopus. Muscle tone is altered according to the dystonic type. Double athetosis, as a type of childhood forms of athetosis, is associated with symmetrical atrophy of the basal ganglia of the brain, manifested by a kind of hyperkinesis of the facial muscles and symmetrical athetosis in the hands and feet. Athetotic hyperkinesis can be combined with cerebral palsy, be a consequence of encephalitis, vascular diseases of the brain, etc. It often forms mixed forms: choreathetosis, athetosis with the thalamic hand, etc. Extrapyramidal hyperkinesis is a torsion spasm, which is characterized by widespread spasms of large muscle groups. Convulsive-tonic body postures appear in the form of opisthotonus, “torsion arc”. Hyperkinesis during torsion spasm resembles the circular movements of a boa constrictor. There is torsion dystonia, combined with hemiballismus, chorea, tremors, etc.

Tonic-clonic spasms of the facial muscles are observed with facial paraspasm. Limited paraspasm is localized in the upper part of the face (closing of the eyelids); with widespread spasm, all facial muscles contract, as well as the muscles of the neck and limbs. Paraspasm, like many extrapyramidal syndromes, is characterized by voluntary attitudes and postures that are used by patients to reduce or stop hyperkinesis. When E. is affected. Tonic spasms of gaze, blepharospasm, uncontrollable bouts of laughter, crying, and oral-mandibular dyskinesia are often encountered.

Complex paroxysmal hyperkinesis occurs during forced crying. They occur in cycles (2-3 minutes each) in the form of waving a hand in front of the face, rhythmic rubbing of the heart area, face. A peculiar extrapyramidal syndrome is subcortical epilepsy.

Treatment of extrapyramidal syndromes is difficult. Etiotropic, symptomatic, and restorative medications are used. In some cases, acupuncture and auto-training are indicated. Surgical treatment of extrapyramidal syndromes is carried out using stereotactic operations on the subcortical nodes.

Bibliography: Granit R. Fundamentals of movement regulation, trans. from English, M., 1973; Gusev E.I. Grechko V.E. and Kurya G.G. Nervous diseases, p. 66, M., 1988; Kandel E.I. and Voityna S.V. Deforming muscular torsion dystonia, M., 1971.

Encyclopedic Dictionary of Medical Terms M. SE-1982-84, PMP: BRE-94, MME: ME.91-96.