Pyramidal nervous system. The pyramidal tract is a conductive system of movements. Symptoms of defeat. Levels

Descending tracts of the brain and spinal cord conduct impulses from the cerebral cortex, cerebellum, subcortical and stem centers to the underlying motor nuclei of the brain stem and spinal cord.

Descending paths are divided into two groups:

Pyramid system ensures the execution of precise, purposeful conscious movements, adjusts breathing, ensuring the pronunciation of words. It includes the corticonuclear, anterior and lateral corticospinal (pyramidal) tracts.

Corticonuclear pathway begins in the lower third of the precentral gyrus of the cerebrum. Here pyramidal cells (1 neuron) are located, the axons of which pass through the knee of the internal capsule into the brain stem and are directed in its basal part down to the motor nuclei of the cranial nerves of the opposite side (III–VII, IX–XII). The bodies of the second neurons of this system, which are analogues of the motor neurons of the anterior horns of the spinal cord, are located here. Their axons go as part of the cranial nerves to the innervated muscles of the head and neck.

Anterior and lateral corticospinal(pyramidal) tracts conduct motor impulses from pyramidal cells located in the upper two-thirds of the precentral gyrus to the muscles of the trunk and limbs of the opposite side.

The axons of the first neurons of these pathways go together as part of the corona radiata and pass through hind leg internal capsule into the brain stem, where they are located ventrally. In the medulla oblongata they form pyramidal elevations (pyramids); and from this level these paths diverge. The fibers of the anterior pyramidal tract descend along the ipsilateral side in the anterior cord, forming the corresponding tract of the spinal cord (see Fig. 23), and then at the level of their segment they pass to the opposite side and end on the motor neurons of the anterior horns of the spinal cord (the second neuron of the system). The fibers of the lateral pyramidal tract, in contrast to the anterior one, pass to the opposite side at the level of the medulla oblongata, forming the decussation of the pyramids. Then they go in the back of the lateral cord (see Fig. 23) to “their” segment and end on the motor neurons of the anterior horns of the spinal cord (the second neuron of the system).

Extrapyramidal system carries out involuntary regulation and coordination of movements, regulation of muscle tone, maintaining posture, organizing motor manifestations of emotions. Ensures smooth movements and establishes the starting position for their execution.

The extrapyramidal system includes:

Corticothalamic tract, conducting motor impulses from the cortex to the motor nuclei of the thalamus.

Radiance of the striatum- a group of fibers connecting these subcortical centers with the cerebral cortex and thalamus.

Cortico-red nuclear tract, conducts impulses from the cerebral cortex to the red nucleus, which is the motor center of the midbrain.

Red nuclear spinal tract(Fig. 58) conducts motor impulses from the red nucleus to the motor neurons of the anterior horns on the opposite side (for more details, see Section 5.3.2.).

Tectospinal tract. Its passage in general outline similar to the previous path, with the difference that it does not begin in the red nuclei, in the nuclei of the roof of the midbrain. The first neurons of this system are located in the tubercles of the quadrigeminal midbrain. Their axons move to the opposite side and, as part of the anterior cord of the spinal cord, descend to the corresponding segments of the spinal cord (see Fig. 23). Then they enter the anterior horns and end on the motor neurons of the spinal cord (the second neuron of the system).

vestibulospinal tract connects the vestibular nuclei of the hindbrain (pons) and provides regulation of body muscle tone (see Section 5.3.2.).

Reticulospinal tract connects RF neurons and spinal cord neurons, providing regulation of their sensitivity to control impulses (see Section 5.3.2.).

Corticopontine-cerebellar tract allow the cortex to control the functions of the cerebellum. The first neurons of this system are located in the cortex of the frontal, temporal, occipital or parietal lobe. Their neurons (corticopontine fibers) pass through the internal capsule and are directed to the basilar part of the pons, to the intrinsic nuclei of the pons. Here there is a switch to the second neurons of this system. Their axons (pontocerebellar fibers) pass to the opposite side and are directed through the middle cerebellar peduncle to the contralateral cerebellar hemisphere.

Main ascending paths.

Ascending to the hindbrain: posterior spinocerebellar tract of Flexig, anterior spinocerebellar tract of Govers. Both spinocerebellar tracts conduct unconscious impulses (unconscious coordination of movements).

Risingto the midbrain: lateral spinal-midcerebral (spinotectal) tract

TO diencephalon : lateral spinothalamic tract. It conducts temperature irritations and pain; the anterior spinothalamic is the pathway for conducting impulses of touch and touch.

Some of them are fibers of primary afferent (sensitive) neurons running without interruption. These fibers - thin (Gaull's bundle) and wedge-shaped (Burdach's bundle) bundles are part of the dorsal funiculi of the white matter and end in the medulla oblongata near the neutron relay nuclei, called the nuclei of the dorsal funiculus, or the nuclei of Gaulle and Burdach. The fibers of the dorsal cord are conductors of skin-mechanical sensitivity.

The remaining ascending pathways begin from neurons located in the gray matter of the spinal cord. Because these neurons receive synaptic inputs from primary afferent neurons, they are commonly referred to as second-order neurons, or secondary afferent neurons. The bulk of fibers from secondary afferent neurons pass within the lateral funiculus of the white matter. The spinothalamic tract is located here. The axons of spinothalamic neurons cross and reach without interruption through the medulla oblongata and midbrain to the thalamic nuclei, where they form synapses with thalamic neurons. By spinothalamic tracts impulses come from skin receptors.

The lateral funiculi contain fibers of the spinocerebellar tracts, dorsal and ventral, carrying impulses from skin and muscle receptors to the cerebellar cortex.

The lateral cord also includes fibers of the spinocervical tract, the ends of which form synapses with relay neurons of the cervical spinal cord - neurons of the cervical nucleus. After switching in the cervical nucleus, this pathway goes to the cerebellum and brainstem nuclei.

The pain sensitivity pathway is localized in the ventral columns of white matter. In addition, the spinal cord’s own pathways pass through the posterior, lateral and anterior columns, ensuring the integration of functions and reflex activity of its centers.

3.1. Pyramid system

There are two main types of movements: involuntary And arbitrary.

Involuntary movements include simple automatic movements carried out by the segmental apparatus of the spinal cord and brain stem as a simple reflex act. Voluntary purposeful movements are acts of human motor behavior. Special voluntary movements (behavioral, labor, etc.) are carried out with the leading participation of the cerebral cortex, as well as the extrapyramidal system and the segmental apparatus of the spinal cord. In humans and higher animals, the implementation of voluntary movements is associated with the pyramidal system. In this case, the impulse from the cerebral cortex to the muscle occurs through a chain consisting of two neurons: central and peripheral.

Central motor neuron. Voluntary muscle movements occur due to impulses traveling along long nerve fibers from the cerebral cortex to the cells of the anterior horns of the spinal cord. These fibers form the motor ( corticospinal), or pyramidal, path. They are the axons of neurons located in the precentral gyrus, in cytoarchitectonic area 4. This zone is a narrow field that stretches along the central fissure from the lateral (or Sylvian) fissure to the anterior part of the paracentral lobule on the medial surface of the hemisphere, parallel to the sensitive area of the postcentral gyrus cortex .

Neurons innervating the pharynx and larynx are located in the lower part of the precentral gyrus. Next, in ascending order, come the neurons innervating the face, arm, torso, and leg. Thus, all parts of the human body are projected in the precentral gyrus, as if upside down. Motor neurons are located not only in area 4, they are also found in neighboring cortical fields. At the same time, the vast majority of them occupy the 5th cortical layer of the 4th field. They are “responsible” for precise, targeted single movements. These neurons also include Betz giant pyramidal cells, which have axons with thick myelin sheaths. These fast-conducting fibers make up only 3.4-4% of all fibers of the pyramidal tract. Most of the fibers of the pyramidal tract come from small pyramidal, or fusiform (fusiform), cells in motor fields 4 and 6. Cells of field 4 provide about 40% of the fibers of the pyramidal tract, the rest come from cells of other fields of the sensorimotor zone.

Area 4 motor neurons control fine voluntary movements skeletal muscles the opposite half of the body, since most of the pyramidal fibers pass to the opposite side in the lower part of the medulla oblongata.

The impulses of the pyramidal cells of the motor cortex follow two paths. One, the corticonuclear pathway, ends in the nuclei of the cranial nerves, the second, more powerful, the corticospinal tract, switches in the anterior horn of the spinal cord on interneurons, which in turn end on large motor neurons of the anterior horns. These cells transmit impulses through the ventral roots and peripheral nerves to the motor end plates of skeletal muscles.

When the pyramidal tract fibers leave the motor cortex, they pass through the corona radiata of the white matter of the brain and converge towards the posterior limb of the internal capsule. In somatotopic order, they pass through the internal capsule (its knee and the anterior two-thirds of the posterior thigh) and go in the middle part of the cerebral peduncles, descending through each half of the base of the pons, being surrounded by numerous nerve cells of the pons nuclei and fibers of various systems. At the level of the pontomedullary junction, the pyramidal tract becomes visible from the outside, its fibers forming elongated pyramids on either side of the midline of the medulla oblongata (hence its name). In the lower part of the medulla oblongata, 80-85% of the fibers of each pyramidal tract pass to the opposite side at the decussation of the pyramids and form lateral pyramidal tract. The remaining fibers continue to descend uncrossed in the anterior funiculi as anterior pyramidal tract. These fibers cross at the segmental level through the anterior commissure of the spinal cord. In the cervical and thoracic parts of the spinal cord, some fibers connect with the cells of the anterior horn of their side, so that the muscles of the neck and trunk receive cortical innervation on both sides.

The crossed fibers descend as part of the lateral pyramidal tract in the lateral funiculi. About 90% of the fibers form synapses with interneurons, which in turn connect with large alpha and gamma neurons of the anterior horn of the spinal cord.

Fibers forming corticonuclear pathway, are directed to the motor nuclei (V, VII, IX, X, XI, XII) of the cranial nerves and provide voluntary innervation of the facial and oral muscles.

Another bundle of fibers, starting in the “eye” area 8, and not in the precentral gyrus, also deserves attention. Impulses traveling along this beam provide friendly movements eyeballs in the opposite direction. The fibers of this bundle at the level of the corona radiata join the pyramidal tract. Then they pass more ventrally in the posterior leg of the internal capsule, turn caudally and go to the nuclei of the III, IV, VI cranial nerves.

Peripheral motor neuron. Fibers of the pyramidal tract and various extrapyramidal tracts (reticular-, tegmental-, vestibular, red-nuclear-spinal, etc.) and afferent fibers entering the spinal cord through the dorsal roots end on the bodies or dendrites of large and small alpha and gamma cells (directly or through intercalary, associative or commissural neurons of the internal neuronal apparatus of the spinal cord) In contrast to the pseudounipolar neurons of the spinal ganglia, the neurons of the anterior horns are multipolar. Their dendrites have multiple synaptic connections with various afferent and efferent systems. Some of them are facilitative, others are inhibitory in their action. In the anterior horns, motoneurons form groups organized into columns and not divided segmentally. These columns have a certain somatotopic order. In the cervical region, the lateral motor neurons of the anterior horn innervate the hand and arm, and the motor neurons of the medial columns innervate the muscles of the neck and chest. In the lumbar region, neurons innervating the foot and leg are also located laterally in the anterior horn, and those innervating the trunk are located medially. The axons of the anterior horn cells exit the spinal cord ventrally as radicular fibers, which gather in segments to form the anterior roots. Each anterior root connects to a posterior one distal to the spinal ganglia and together they form the spinal nerve. Thus, each segment of the spinal cord has its own pair of spinal nerves.

The nerves also include efferent and afferent fibers emanating from the lateral horns of the spinal gray matter.

Well-myelinated, fast-conducting axons of large alpha cells extend directly to the striated muscle.

In addition to alpha motor neurons major and minor, the anterior horn contains numerous gamma motor neurons. Among the interneurons of the anterior horns, Renshaw cells, which inhibit the action of large motor neurons, should be noted. Large alpha cells with thick, fast-conducting axons produce rapid muscle contractions. Small alpha cells with thinner axons perform a tonic function. Gamma cells with thin and slow-conducting axons innervate muscle spindle proprioceptors. Large alpha cells are associated with giant cells of the cerebral cortex. Small alpha cells have connections with the extrapyramidal system. The state of muscle proprioceptors is regulated through gamma cells. Among the various muscle receptors, the most important are the neuromuscular spindles.

Afferent fibers called ring-spiral, or primary endings, have a rather thick myelin coating and belong to fast-conducting fibers.

Many muscle spindles have not only primary but also secondary endings. These endings also respond to stretch stimuli. Their action potential spreads in the central direction along thin fibers communicating with interneurons responsible for the reciprocal actions of the corresponding antagonist muscles. Only a small number of proprioceptive impulses reach the cerebral cortex; most are transmitted through feedback rings and do not reach the cortical level. These are elements of reflexes that serve as the basis for voluntary and other movements, as well as static reflexes that resist gravity.

Extrafusal fibers in a relaxed state have a constant length. When a muscle is stretched, the spindle is stretched. The ring-spiral endings respond to stretching by generating an action potential, which is transmitted to the large motor neuron along fast-conducting afferent fibers, and then again along fast-conducting thick fibers. efferent fibers– extrafusal muscles. The muscle contracts and its original length is restored. Any stretch of the muscle activates this mechanism. Percussion on the muscle tendon causes stretching of this muscle. The spindles react immediately. When the impulse reaches the motor neurons in the anterior horn of the spinal cord, they respond by causing a short contraction. This monosynaptic transmission is basic for all proprioceptive reflexes. The reflex arc covers no more than 1-2 segments of the spinal cord, which is of great importance in determining the location of the lesion.

Gamma neurons are influenced by fibers descending from the motor neurons of the central nervous system as part of tracts such as pyramidal, reticular-spinal, and vestibular-spinal. The efferent influences of gamma fibers make it possible to finely regulate voluntary movements and provide the ability to regulate the strength of the receptor response to stretching. This is called the gamma neuron-spindle system.

Research methodology. Inspect, palpate and measure muscle volume, determine the volume of active and passive movements, muscle strength, muscle tone, rhythm active movements and reflexes. Electrophysiological methods are used to identify the nature and localization of movement disorders, as well as for clinically insignificant symptoms.

The study of motor function begins with an examination of the muscles. Attention is drawn to the presence of atrophy or hypertrophy. By measuring the volume of the limb muscles with a centimeter, the degree of severity of trophic disorders can be determined. When examining some patients, fibrillary and fascicular twitching is noted. By palpation, you can determine the configuration of the muscles and their tension.

Active movements are checked consistently in all joints and performed by the subject. They may be absent or limited in volume and weakened in strength. Complete absence active movements are called paralysis, limitation of movements or weakening of their strength is called paresis. Paralysis or paresis of one limb is called monoplegia or monoparesis. Paralysis or paresis of both arms is called upper paraplegia or paraparesis, paralysis or paraparesis of the legs is called lower paraplegia or paraparesis. Paralysis or paresis of two limbs of the same name is called hemiplegia or hemiparesis, paralysis of three limbs - triplegia, paralysis of four limbs - quadriplegia or tetraplegia.

Passive movements are determined when the subject’s muscles are completely relaxed, which makes it possible to exclude a local process (for example, changes in the joints) that limits active movements. Along with this, determining passive movements is the main method for studying muscle tone.

The volume of passive movements in the joints of the upper limb is examined: shoulder, elbow, wrist (flexion and extension, pronation and supination), finger movements (flexion, extension, abduction, adduction, opposition of the first finger to the little finger), passive movements in the joints of the lower extremities: hip, knee, ankle (flexion and extension, rotation outward and inward), flexion and extension of fingers.

Muscle strength determined consistently in all groups with active resistance of the patient. For example, when studying the strength of the muscles of the shoulder girdle, the patient is asked to raise his arm to a horizontal level, resisting the examiner’s attempt to lower his arm; then they suggest raising both hands above the horizontal line and holding them, offering resistance. To determine the strength of the shoulder muscles, the patient is asked to bend his arm in elbow joint, and the examiner tries to straighten it; The strength of the shoulder abductors and adductors is also examined. To study the strength of the forearm muscles, the patient is instructed to perform pronation, and then supination, flexion and extension of the hand with resistance while performing the movement. To determine the strength of the finger muscles, the patient is asked to make a “ring” from the first finger and each of the others, and the examiner tries to break it. Strength is checked by moving the fifth finger away from the fourth finger and bringing the other fingers together, while clenching the hands into a fist. The strength of the pelvic girdle and hip muscles is examined by performing the task of raising, lowering, adducting, and abducting the hip while exerting resistance. The strength of the thigh muscles is examined by asking the patient to bend and straighten the leg at the knee joint. The strength of the lower leg muscles is checked as follows: the patient is asked to bend the foot, and the examiner holds it straight; then the task is given to straighten the foot bent at the ankle joint, overcoming the resistance of the examiner. The strength of the muscles of the toes is also examined when the examiner tries to bend and straighten the toes and separately bend and straighten the first toe.

To identify paresis of the limbs, a Barre test is performed: the paretic arm, extended forward or raised upward, gradually lowers, the leg raised above the bed also gradually lowers, while the healthy one is held in its given position. With mild paresis, you have to resort to a test for the rhythm of active movements; pronate and supinate your arms, clench your hands into fists and unclench them, move your legs like on a bicycle; insufficient strength of the limb is manifested in the fact that it gets tired more quickly, movements are performed less quickly and less dexterously than with a healthy limb. Hand strength is measured with a dynamometer.

Muscle tone– reflex muscle tension, which provides preparation for movement, maintaining balance and posture, and the ability of the muscle to resist stretching. There are two components of muscle tone: the muscle’s own tone, which depends on the characteristics of the metabolic processes occurring in it, and neuromuscular tone (reflex), reflex tone is often caused by muscle stretching, i.e. irritation of proprioceptors, determined by the nature of the nerve impulses that reach this muscle. It is this tone that underlies various tonic reactions, including anti-gravity ones, carried out under conditions of maintaining the connection between the muscles and the central nervous system.

Tonic reactions are based on a stretch reflex, the closure of which occurs in the spinal cord.

Muscle tone is influenced by the spinal (segmental) reflex apparatus, afferent innervation, reticular formation, as well as cervical tonic, including vestibular centers, cerebellum, red nucleus system, basal ganglia, etc.

The state of muscle tone is assessed by examining and palpating the muscles: with a decrease in muscle tone, the muscle is flabby, soft, doughy. with increased tone, it has a denser consistency. However, the determining factor is the study of muscle tone through passive movements (flexors and extensors, adductors and abductors, pronators and supinators). Hypotonia is a decrease in muscle tone, atony is its absence. A decrease in muscle tone can be detected by examining Orshansky's symptom: when lifting up (in a patient lying on his back) the leg straightened at the knee joint, hyperextension in this joint is detected. Hypotonia and muscle atony occur with peripheral paralysis or paresis (disturbance of the efferent part of the reflex arc with damage to the nerve, root, cells of the anterior horn of the spinal cord), damage to the cerebellum, brain stem, striatum and posterior cords of the spinal cord. Muscle hypertension is the tension felt by the examiner during passive movements. There are spastic and plastic hypertension. Spastic hypertension - increased tone of the flexors and pronators of the arm and extensors and adductors of the leg (if the pyramidal tract is affected). With spastic hypertension, a “penknife” symptom is observed (an obstacle to passive movement in the initial phase of the study), with plastic hypertension – a “cogwheel” symptom (a feeling of tremors during the study of muscle tone in the limbs). Plastic hypertension is a uniform increase in the tone of muscles, flexors, extensors, pronators and supinators, which occurs when the pallidonigral system is damaged.

Reflexes. A reflex is a reaction that occurs in response to irritation of receptors in the reflexogenic zone: muscle tendons, skin of a certain area of the body, mucous membrane, pupil. The nature of the reflexes is used to judge the condition various departments nervous system. When studying reflexes, their level, uniformity, and asymmetry are determined: with an increased level, a reflexogenic zone is noted. When describing reflexes, the following gradations are used: 1) living reflexes; 2) hyporeflexia; 3) hyperreflexia (with an expanded reflexogenic zone); 4) areflexia (lack of reflexes). Reflexes can be deep, or proprioceptive (tendon, periosteal, articular), and superficial (skin, mucous membranes).

Tendon and periosteal reflexes are caused by percussion with a hammer on the tendon or periosteum: the response is manifested by the motor reaction of the corresponding muscles. To obtain tendon and periosteal reflexes on the upper and lower limbs it is necessary to evoke them in an appropriate position favorable for the reflex reaction (lack of muscle tension, average physiological position).

Upper limbs. Biceps tendon reflex caused by a hammer blow to the tendon of this muscle (the patient’s arm should be bent at the elbow joint at an angle of about 120°, without tension). In response, the forearm flexes. Reflex arc: sensory and motor fibers of the musculocutaneous nerve, CV-CVI. Triceps brachii tendon reflex is caused by a hammer blow on the tendon of this muscle above the olecranon (the patient’s arm should be bent at the elbow joint at almost an angle of 90°). In response, the forearm extends. Reflex arc: radial nerve, CVI-CVI. Radiation reflex caused by percussion of the styloid process radius(the patient’s arm should be bent at the elbow joint at an angle of 90° and be in a position midway between pronation and supination). In response, flexion and pronation of the forearm and flexion of the fingers occur. Reflex arc: fibers of the median, radial and musculocutaneous nerves, CV-CVIII.

Lower limbs. Knee reflex caused by a hammer hitting the quadriceps tendon. In response, the lower leg is extended. Reflex arc: femoral nerve, LII-LIV. When examining the reflex in a horizontal position, the patient’s legs should be bent at the knee joints at an obtuse angle (about 120°) and rest freely on the examiner’s left forearm; when examining the reflex in a sitting position, the patient's legs should be at an angle of 120° to the hips or, if the patient does not rest his feet on the floor, hang freely over the edge of the seat at an angle of 90° to the hips, or one of the patient's legs is thrown over the other. If the reflex cannot be evoked, then the Jendraszik method is used: the reflex is evoked when the patient pulls towards the hand with the fingers tightly clasped. Heel (Achilles) reflex caused by percussion of the calcaneal tendon. In response, plantar flexion of the foot occurs as a result of contraction of the calf muscles. Reflex arc: tibial nerve, SI-SII. For a lying patient, the leg should be bent at the hip and knee joints, foot – at the ankle joint at an angle of 90°. The examiner holds the foot with his left hand, and with his right hand percusses the heel tendon. With the patient lying on his stomach, both legs are bent at the knee and ankle joints at an angle of 90°. The examiner holds the foot or sole with one hand and strikes with the hammer with the other. The reflex is caused by a short blow to the heel tendon or to the sole. The heel reflex can be examined by placing the patient on his knees on the couch so that the feet are bent at an angle of 90°. In a patient sitting on a chair, you can bend your leg at the knee and ankle joints and evoke a reflex by percussing the heel tendon.

Joint reflexes are caused by irritation of receptors in the joints and ligaments of the hands. 1. Mayer - opposition and flexion in the metacarpophalangeal and extension in the interphalangeal joint of the first finger with forced flexion in the main phalanx of the third and fourth fingers. Reflex arc: ulnar and median nerves, СVII-ThI. 2. Leri – flexion of the forearm with forced flexion of the fingers and hand in a supinated position, reflex arc: ulnar and median nerves, CVI-ThI.

Skin reflexes are caused by line irritation with the handle of a neurological hammer in the corresponding skin area in the patient's position on the back with slightly bent legs. Abdominal reflexes: upper (epigastric) are caused by irritation of the skin of the abdomen along the lower edge of the costal arch. Reflex arc: intercostal nerves, ThVII-ThVIII; medium (mesogastric) – with irritation of the skin of the abdomen at the level of the navel. Reflex arc: intercostal nerves, ThIX-ThX; lower (hypogastric) – with skin irritation parallel to the inguinal fold. Reflex arc: iliohypogastric and ilioinguinal nerves, ThXI-ThXII; the abdominal muscles contract at the appropriate level and the navel deviates towards the irritation. The cremasteric reflex is caused by irritation of the inner thigh. In response, the testicle is pulled upward due to contraction of the levator testis muscle, reflex arc: genital femoral nerve, LI-LII. Plantar reflex - plantar flexion of the foot and toes when the outer edge of the sole is stimulated by strokes. Reflex arc: tibial nerve, LV-SII. Anal reflex - contraction of the external sphincter anus with tingling or streak irritation of the skin around it. It is called in the position of the subject on his side with his legs brought to the stomach. Reflex arc: pudendal nerve, SIII-SV.

Pathological reflexes . Pathological reflexes appear when the pyramidal tract is damaged, when spinal automatisms are disrupted. Pathological reflexes, depending on the reflex response, are divided into extension and flexion.

Extensor pathological reflexes in the lower extremities. The most important is the Babinski reflex - extension of the first toe when the skin of the outer edge of the sole is irritated by strokes; in children under 2-2.5 years old - a physiological reflex. Oppenheim reflex - extension of the first toe in response to running the fingers along the crest of the tibia down to the ankle joint. Gordon's reflex - slow extension of the first toe and fan-shaped divergence of the other toes when the calf muscles are compressed. Schaefer reflex - extension of the first toe when the heel tendon is compressed.

Flexion pathological reflexes in the lower extremities. The most important reflex is the Rossolimo reflex - flexion of the toes during a quick tangential blow to the pads of the toes. Bekhterev-Mendel reflex - flexion of the toes when struck with a hammer on its dorsal surface. The Zhukovsky reflex is the flexion of the toes when a hammer hits the plantar surface directly under the toes. Ankylosing spondylitis reflex - flexion of the toes when hitting the plantar surface of the heel with a hammer. It should be borne in mind that the Babinski reflex appears with acute damage to the pyramidal system, for example with hemiplegia in the case of cerebral stroke, and the Rossolimo reflex is a later manifestation of spastic paralysis or paresis.

Pathological flexion reflexes in the upper limbs. Tremner reflex - flexion of the fingers in response to rapid tangential stimulation with the fingers of the examiner examining the palmar surface of the terminal phalanges of the patient's II-IV fingers. The Jacobson-Weasel reflex is a combined flexion of the forearm and fingers in response to a blow with a hammer on the styloid process of the radius. The Zhukovsky reflex is the flexion of the fingers of the hand when hitting the palmar surface with a hammer. Carpal-digital ankylosing spondylitis reflex - flexion of the fingers during percussion of the back of the hand with a hammer.

Pathological protective, or spinal automatism, reflexes on the upper and lower extremities– involuntary shortening or lengthening of a paralyzed limb during injection, pinching, cooling with ether or proprioceptive stimulation according to the Bekhterev-Marie-Foy method, when the examiner performs a sharp active flexion of the toes. Protective reflexes are more often of a flexion nature (involuntary flexion of the leg at the ankle, knee and hip joints). The extensor protective reflex is characterized by involuntary extension of the leg at the hip and knee joints and plantar flexion of the foot. Cross defensive reflexes– flexion of the irritated leg and extension of the other are usually observed with combined damage to the pyramidal and extrapyramidal tracts, mainly at the level of the spinal cord. When describing protective reflexes, the form of the reflex response, the reflexogenic zone, is noted. area of evocation of the reflex and intensity of the stimulus.

Cervical tonic reflexes arise in response to irritations associated with changes in the position of the head in relation to the body. Magnus-Klein reflex - when the head is turned, the extensor tone in the muscles of the arm and leg, towards which the head is turned with the chin, increases, and the flexor tone in the muscles of the opposite limbs; flexion of the head causes an increase in flexor tone, and extension of the head - extensor tone in the muscles of the limbs.

Gordon reflex– delay of the lower leg in the extension position while inducing the knee reflex. Foot phenomenon (Westphalian)– “freezing” of the foot during passive dorsiflexion. Foix-Thevenard tibia phenomenon– incomplete extension of the lower leg in the knee joint in a patient lying on his stomach, after the lower leg was held in extreme flexion for some time; manifestation of extrapyramidal rigidity.

Janiszewski's grasp reflex on the upper limbs - involuntary grasping of objects in contact with the palm; on the lower extremities - increased flexion of the fingers and toes when moving or other irritation of the sole. The distant grasping reflex is an attempt to grasp an object shown at a distance. It is observed with damage to the frontal lobe.

Expression sharp increase tendon reflexes serve clonus, manifested by a series of rapid rhythmic contractions of a muscle or group of muscles in response to their stretching. Foot clonus is caused by the patient lying on his back. The examiner bends the patient's leg at the hip and knee joints, holds it with one hand, and with the other grabs the foot and, after maximum plantar flexion, jerks the foot into dorsiflexion. In response, rhythmic clonic movements of the foot occur while the heel tendon is stretched. Clonus of the patella is caused by a patient lying on his back with straightened legs: fingers I and II grasp the apex of the patella, pull it up, then sharply shift it in the distal direction and hold it in this position; in response, there is a series of rhythmic contractions and relaxations of the quadriceps femoris muscle and twitching of the patella.

Synkinesis– a reflex friendly movement of a limb or other part of the body, accompanying the voluntary movement of another limb (part of the body). Pathological synkinesis is divided into global, imitation and coordinator.

Global, or spastic, is called pathological synkinesis in the form of increased flexion contracture in a paralyzed arm and extension contracture in a paralyzed leg when trying to move paralyzed limbs or during active movements with healthy limbs, tension in the muscles of the trunk and neck, when coughing or sneezing. Imitative synkinesis is the involuntary repetition by paralyzed limbs of voluntary movements of healthy limbs on the other side of the body. Coordinative synkinesis manifests itself in the form of additional movements performed by paretic limbs in the process of a complex, purposeful motor act.

Contractures. Persistent tonic muscle tension, causing limited movement in the joint, is called contracture. They are distinguished by shape as flexion, extension, pronator; by localization - contractures of the hand, foot; monoparaplegic, tri- and quadriplegic; according to the method of manifestation - persistent and unstable in the form of tonic spasms; according to the period of occurrence after the development of the pathological process - early and late; in connection with pain – protective-reflex, antalgic; depending on the damage to various parts of the nervous system - pyramidal (hemiplegic), extrapyramidal, spinal (paraplegic), meningeal, with damage to peripheral nerves, such as the facial nerve. Early contracture – hormetonia. It is characterized by periodic tonic spasms in all extremities, the appearance of pronounced protective reflexes, and dependence on intero- and exteroceptive stimuli. Late hemiplegic contracture (Wernicke-Mann position) – adduction of the shoulder to the body, flexion of the forearm, flexion and pronation of the hand, extension of the hip, lower leg and plantar flexion of the foot; when walking, the leg describes a semicircle.

Semiotics of movement disorders. Having identified, based on a study of the volume of active movements and their strength, the presence of paralysis or paresis caused by a disease of the nervous system, its nature is determined: whether it occurs due to damage to central or peripheral motor neurons. Damage to central motor neurons at any level of the corticospinal tract causes the occurrence of central, or spastic, paralysis. When peripheral motor neurons are damaged at any site (anterior horn, root, plexus and peripheral nerve), peripheral, or sluggish, paralysis.

Central motor neuron : damage to the motor area of the cerebral cortex or pyramidal tract leads to the cessation of the transmission of all impulses for voluntary movements from this part of the cortex to the anterior horns of the spinal cord. The result is paralysis of the corresponding muscles. If the pyramidal tract is interrupted suddenly, the muscle stretch reflex is suppressed. This means that the paralysis is initially flaccid. It may take days or weeks for this reflex to return.

When this happens, the muscle spindles will become more sensitive to stretching than before. This is especially evident in the arm flexors and leg extensors. Stretch receptor hypersensitivity is caused by damage to the extrapyramidal tracts, which terminate in the anterior horn cells and activate gamma motor neurons that innervate intrafusal muscle fibers. As a result of this phenomenon, the impulse through the feedback rings that regulate muscle length changes so that the arm flexors and leg extensors are fixed in the shortest possible state (minimum length position). The patient loses the ability to voluntarily inhibit overactive muscles.

Spastic paralysis always indicates damage to the central nervous system, i.e. brain or spinal cord. The result of damage to the pyramidal tract is the loss of the most subtle voluntary movements, which is best seen in the hands, fingers, and face.

The main symptoms of central paralysis are: 1) decreased strength combined with loss of fine movements; 2) spastic increase in tone (hypertonicity); 3) increased proprioceptive reflexes with or without clonus; 4) reduction or loss of exteroceptive reflexes (abdominal, cremasteric, plantar); 5) the appearance of pathological reflexes (Babinsky, Rossolimo, etc.); 6) protective reflexes; 7) pathological friendly movements; 8) absence of degeneration reaction.

Symptoms vary depending on the location of the lesion in the central motor neuron. Damage to the precentral gyrus is characterized by two symptoms: focal epileptic seizures (Jacksonian epilepsy) in the form of clonic seizures and central paresis (or paralysis) of the limb on the opposite side. Paresis of the leg indicates damage to the upper third of the gyrus, the arm to its middle third, half of the face and tongue to its lower third. It is diagnostically important to determine where clonic seizures begin. Often, convulsions, starting in one limb, then move to other parts of the same half of the body. This transition occurs in the order in which the centers are located in the precentral gyrus. Subcortical (corona radiata) lesion, contralateral hemiparesis in the arm or leg, depending on which part of the precentral gyrus the lesion is closer to: if it is in the lower half, then the arm will suffer more, and in the upper half, the leg. Damage to the internal capsule: contralateral hemiplegia. Due to the involvement of corticonuclear fibers, there is a disruption of innervation in the area of the contralateral facial and hypoglossal nerves. Most cranial motor nuclei receive pyramidal innervation on both sides, either completely or partially. Rapid damage to the pyramidal tract causes contralateral paralysis, initially flaccid, as the lesion has a shock-like effect on peripheral neurons. It becomes spastic after a few hours or days.

Damage to the brain stem (cerebral peduncle, pons, medulla oblongata) is accompanied by damage to the cranial nerves on the side of the lesion and hemiplegia on the opposite side. Cerebral peduncle: Lesions in this area result in contralateral spastic hemiplegia or hemiparesis, which can be combined with ipsilateral (on the side of the lesion) lesion of the oculomotor nerve (Weber syndrome). Pontine cerebri: If this area is affected, contralateral and possibly bilateral hemiplegia develops. Often not all pyramidal fibers are affected.

Since the fibers descending to the nuclei of the VII and XII nerves are located more dorsally, these nerves may be spared. Possible ipsilateral involvement of the abducens or trigeminal nerve. Damage to the pyramids of the medulla oblongata: contralateral hemiparesis. Hemiplegia does not develop, since only the pyramidal fibers are damaged. The extrapyramidal tracts are located dorsally in the medulla oblongata and remain intact. When the pyramidal decussation is damaged, it develops rare syndrome Cruciant (or alternating) hemiplegia (right arm and left leg and vice versa).

To recognize focal brain lesions in patients in a comatose state, the symptom of an outwardly rotated foot is important. On the side opposite to the lesion, the foot is turned outward, as a result of which it rests not on the heel, but on outer surface. To determine this symptom, you can use the technique of maximum outward rotation of the feet - Bogolepov's symptom. On the healthy side, the foot immediately returns to its original position, while the foot on the hemiparesis side remains turned outward.

If the pyramidal tract is damaged below the chiasm in the region of the brain stem or upper cervical segments of the spinal cord, hemiplegia occurs with involvement of the ipsilateral limbs or, in the case of bilateral damage, tetraplegia. Lesions of the thoracic spinal cord (involvement of the lateral pyramidal tract) cause spastic ipsilateral monoplegia of the leg; bilateral damage leads to lower spastic paraplegia.

Peripheral motor neuron : damage can involve the anterior horns, anterior roots, peripheral nerves. Neither voluntary nor reflex activity is detected in the affected muscles. The muscles are not only paralyzed, but also hypotonic; areflexia is observed due to interruption of the monosynaptic arc of the stretch reflex. After a few weeks, atrophy occurs, as well as a reaction of degeneration of paralyzed muscles. This indicates that the cells of the anterior horns have a trophic effect on muscle fibers, which is the basis for normal muscle function.

It is important to determine exactly where the pathological process is localized - in the anterior horns, roots, plexuses or peripheral nerves. When the anterior horn is damaged, the muscles innervated from this segment suffer. Often, in atrophying muscles, rapid contractions of individual muscle fibers and their bundles are observed - fibrillar and fascicular twitching, which are a consequence of irritation by the pathological process of neurons that have not yet died. Since muscle innervation is polysegmental, complete paralysis requires damage to several adjacent segments. Involvement of all muscles of the limb is rarely observed, since the cells of the anterior horn, supplying various muscles, are grouped into columns located at some distance from each other. The anterior horns may be involved in the pathological process in acute polio, lateral amyotrophic sclerosis, progressive spinal muscle atrophy, syringomyelia, hematomyelia, myelitis, disorders of the blood supply to the spinal cord. When the anterior roots are affected, almost the same picture is observed as when the anterior horns are affected, because the occurrence of paralysis here is also segmental. Radicular paralysis develops only when several adjacent roots are affected.

Each motor root at the same time has its own “indicator” muscle, which makes it possible to diagnose its lesion by fasciculations in this muscle on the electromyogram, especially if the cervical or lumbar region is involved in the process. Since damage to the anterior roots is often caused by pathological processes in the membranes or vertebrae, which simultaneously involve the posterior roots, movement disorders are often combined with sensory disturbances and pain. Damage to the nerve plexus is characterized by peripheral paralysis of one limb in combination with pain and anesthesia, as well as autonomic disorders in this limb, since the trunks of the plexus contain motor, sensory and autonomic nerve fibers. Often observed partial lesions plexus. When the mixed peripheral nerve is damaged, peripheral paralysis of the muscles innervated by this nerve occurs, combined with sensory disturbances caused by interruption of afferent fibers. Damage to a single nerve can usually be explained mechanical reasons(chronic compression, trauma). Depending on whether the nerve is completely sensory, motor or mixed, disturbances occur, respectively, sensory, motor or autonomic. A damaged axon does not regenerate in the central nervous system, but can regenerate in peripheral nerves, which is ensured by the preservation of the nerve sheath, which can guide the growing axon. Even if the nerve is completely severed, bringing its ends together with a suture can lead to complete regeneration. Damage to many peripheral nerves leads to widespread sensory, motor and autonomic disorders, most often bilateral, mainly in the distal segments of the limbs. Patients complain of paresthesia and pain. Sensitive disturbances of the “socks” or “gloves” type, flaccid muscle paralysis with atrophy, and trophic skin lesions are detected. Polyneuritis or polyneuropathy are noted, arising due to many reasons: intoxication (lead, arsenic, etc.), nutritional deficiencies (alcoholism, cachexia, cancer internal organs etc.), infectious (diphtheria, typhus, etc.), metabolic (diabetes mellitus, porphyria, pellagra, uremia, etc.). Sometimes the cause cannot be determined and this condition is regarded as idiopathic polyneuropathy.

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Definition Pyramid system, pyramidal path (lat. tractus pyramidales, PNA) system of nervous structures. Supports complex and fine coordination of movements. The pyramidal system is a system of efferent neurons, the bodies of which are located in the cerebral cortex, ending in the motor nuclei of the cranial nerves and the gray matter of the spinal cord. The pyramid system is one of the later acquisitions of evolution. Lower vertebrates do not have a pyramidal system; it appears only in mammals, and reaches its greatest development in monkeys and especially in humans.

Pyramidal tract The cerebral cortex in layer V contains Betz cells (or giant pyramidal cells). In 1874, scientist Vladimir Alekseevich Betz discovered and described giant pyramidal cells of the cerebral cortex (Betz cells). Corticospinal (pyramidal) tract, lat. tractus corticospinalis

The pyramidal tract is carried out by nerve fibers that emanate from these Betz cells and descend into the spinal cord without interruption. The pyramidal tract passes through the internal capsule, the brain stem, giving off branches (collaterals) along its path with the extrapyramidal system, as well as with the subcortical nuclei (motor nuclei of the cranial nerves). The fibers intersect at the border of the brain and spinal cord (most in the medulla oblongata, smaller in the spinal cord). They then pass through the spinal cord (anterior and lateral columns of the spinal cord). In each segment of the spinal cord, these fibers form synaptic endings (see Synapse), which are responsible for a specific area of the body ( cervical region the spinal cord for the innervation of the arms, the thoracic for the torso, and the lumbar for the legs).

Direct irritation of certain areas of the cerebral cortex leads to muscle spasms corresponding to the area of the cortex in the projection motor zone. When the upper third of the anterior central gyrus is irritated, a cramp of the leg muscles occurs, mediocre, lower face, and on the side opposite to the source of irritation in the hemisphere. These seizures are called partial (Jacksonian). They were discovered by the English neurologist D.H. Jackson (). In the projection motor zone of each cerebral hemisphere, all the muscles of the opposite half of the body are represented.

Types of nerve fibers The human pyramidal system contains about 1 million nerve fibers. The following types of fibers are distinguished: Type of nerve fibers Diameter Conduction speed Function Thick, fast-conducting 16 µm up to 80 m/s provide fast phase movements Thin, slow-conducting 4 µm from 25 to 7 m/s are responsible for the tonic state of the muscles The largest number of pyramidal cells (Benz cells) innervate small muscles , responsible for subtle differentiated movements of the hand, facial expressions and speech acts. A significantly smaller number of them innervate the muscles of the trunk and lower extremities.

Pathology Damage to the pyramidal system is manifested by paralysis, paresis, and pathological reflexes. Damage to the pyramidal system can be caused by inflammation (see Encephalitis), a violation cerebral circulation(see Stroke), tumor, traumatic brain injury and other causes. Depending on the location of the pathological process, the following manifestations are distinguished.

Localization of the pathological process of the pyramidal tract Symptoms projection zones of the cerebral cortex central paralysis (or paresis), see below. in the area of the internal capsule there is hemiplegia, paralysis of the arm and leg on the side opposite to the localization of the lesion. in the region of the brainstem Alternating syndromes are a combination of hemiplegia on the side opposite to the lesion with signs of dysfunction of the cranial nerve on the affected side. in the spinal cord, hemiplegia or paralysis of the leg on the side of the injury, the crossover of the fibers remained higher.

Diagnostic methods pyramidal insufficiency Magnetic resonance imaging (MRI) is a mandatory examination method for epilepsy and seizures. CT scan brain (according to the recommendation of the International League Against Epilepsy, CT is performed as additional method examinations, or when it is not possible to do an MRI). Electromyography is a method for studying the neuromuscular system by recording electrical potentials of muscles. Electroencephalography (EEG study) can detect seizures. More than 65% of seizures occur during sleep, so EEG recording is necessary during physiological, natural sleep. Due to the intermittent nature of seizures, long-term monitoring (video or Holter) is performed. The study reveals the appearance of diffuse delta waves, as well as the synchronization of Tata waves. Epileptiform activity may occur.

Treatment of pyramidal insufficiency Ultrasonography(Ultrasound) of the brain reveals signs of increased pressure in the brain, which creates an irritating effect and can cause central paralysis. Treatment is aimed at the underlying disease, as well as at restoring motor functions in case of paralysis. In treatment, they adhere to the principle of increasing physical activity.

Pyramid system- a system of efferent neurons, the bodies of which are located in the cerebral cortex, ending in the motor nuclei of the cranial nerves and the gray matter of the spinal cord. The pyramidal tract (tractus pyramidalis) consists of corticonuclear fibers (fibrae corticonucleares) and corticospinal fibers (fibrae corticospinales). Both are axons of nerve cells of the inner, pyramidal layer cerebral cortex . They are located in the precentral gyrus and adjacent fields of the frontal and parietal lobes. The primary motor field is localized in the precentral gyrus, where pyramidal neurons that control individual muscles and muscle groups. In this gyrus there is a somatotopic representation of the muscles. Neurons that control the muscles of the pharynx, tongue, and head occupy the lower part of the gyrus; higher are the areas associated with the muscles of the upper limb and torso; the projection of the muscles of the lower limb is located in the upper part of the precentral gyrus and passes to the medial surface of the hemisphere.

The pyramidal tract is formed predominantly by thin nerve fibers that pass through the white matter of the hemisphere and converge to the internal capsule ( rice. 1 ). Corticonuclear fibers form the knee, and corticospinal fibers form the anterior 2/3 of the posterior limb of the internal capsule. From here the pyramidal tract continues to the base of the cerebral peduncle and further to the anterior part of the pons (see. Brain ). Along the brain stem, corticonuclear fibers move to the opposite side to the dorsolateral parts of the reticular formation, where they switch to motor nuclei III, IV, V, VI, VII, IX, X, XI, XII cranial nerves ; only to the upper third of the nucleus of the facial nerve are uncrossed fibers. Some of the fibers of the pyramidal tract pass from the brain stem to the cerebellum.

In the medulla oblongata, the pyramidal tract is located in pyramids, which form a decussation (decussatio pyramidum) at the border with the spinal cord. Above the chiasm, the pyramidal tract contains from 700,000 to 1,300,000 nerve fibers on one side. As a result of the crossing, 80% of the fibers move to the opposite side and form in the lateral cord spinal cord lateral corticospinal (pyramidal) tract. Uncrossed fibers from the medulla oblongata continue into the anterior cord of the spinal cord in the form of the anterior corticospinal (pyramidal) tract. The fibers of this path pass to the opposite side along the spinal cord in its white commissure (segmentally). Most of the corticospinal fibers end in the intermediate gray matter of the spinal cord on its interneurons; only some of them form synapses directly with the motor neurons of the anterior horns, which give rise to the motor fibers of the spinal cords. nerves . About 55% of the corticospinal fibers terminate in the cervical segments of the spinal cord, 20% in the thoracic segments, and 25% in the lumbar segments. The anterior corticospinal tract continues only to the middle thoracic segments. Thanks to the intersection of fibers in P. s. left hemisphere The brain controls the movements of the right half of the body, and the right hemisphere controls the movements of the left half of the body, but the muscles of the trunk and upper third of the face receive fibers of the pyramidal tract from both hemispheres.

Function P. s. consists of perceiving a program of voluntary movement and conducting impulses from this program to the segmental apparatus of the brain stem and spinal cord.

In clinical practice, P.’s condition s. determined by the nature of voluntary movements. The range of movements and the strength of contraction of the striated muscles are assessed using a six-point system (full muscle strength - 5 points, “yielding” muscle strength - 4 points, a moderate decrease in strength with a full range of active movements - 3 points, the possibility of a full range of movements only after the relative elimination of gravity limbs - 2 points, preservation of movement with barely noticeable muscle contraction - 1 point and absence of voluntary movement - 0). The strength of muscle contraction can be quantitatively assessed using a dynamometer. To assess the safety of the pyramidal corticonuclear tract to the motor nuclei of the cranial nerves, tests are used to determine the function of the head and neck muscles innervated by these nuclei, and the corticospinal tract when examining the muscles of the trunk and limbs. Damage to the pyramidal system is also judged by the state of muscle tone and muscle trophism.

Pathology. Dysfunction of P. s. observed in many pathological processes. In P.'s neurons and their long axons, disturbances in metabolic processes often occur, which lead to degenerative-dystrophic changes in these structures. Disorders can be genetically determined or are a consequence of intoxication (endogenous, exogenous), as well as viral damage to the genetic apparatus of neurons. Degeneration is characterized by a gradual, symmetrical and increasing disorder of the function of pyramidal neurons, primarily those with the longest axons, i.e. ending at the peripheral motor neurons of the lumbar enlargement. Therefore, pyramidal in such cases is first detected in the lower extremities. This group of diseases includes Strumpell's familial spastic paraplegia (see. Paraplegia ), portocaval encephalomyelopathy, funicular myelosis , as well as Mills syndrome - unilateral ascending unknown etiology. It usually begins between the ages of 35-40 and 60 years in the central region of the distal parts of the lower limb,

which is gradually spreading to proximal parts the lower, and then the entire upper limb and turns into spastic hemiplegia with vegetative and trophic disorders in the paralyzed limbs. P.S. often affected by slow viral infections, such as amyotrophic lateral , absent-minded etc. Almost always in clinical picture focal lesions of the brain and spinal cord there are signs of dysfunction of the pyramidal system. With vascular lesions of the brain (hemorrhage,) pyramidal disorders develop acutely or subacutely with progression in chronic cerebral circulatory failure. P.S. may be involved in the pathological process when encephalitis And myelitis , at traumatic brain injury And spinal cord injury , for tumors of the central nervous system, etc.

When P. is affected. central s and paralysis with characteristic disturbances of voluntary movements. Muscle tone increases according to the spastic type (muscle trophism usually does not change) and deep reflexes on the limbs, skin reflexes (abdominal, cremasteric) decrease or disappear, pathological reflexes appear on the hands - Rossolimo - Venderovich, Jacobson - Lask, Bekhterev, Zhukovsky, Hoffmann, on the legs - Babinsky, Oppenheim, Chaddock, Rossolimo, Bekhterev, etc. (see. Reflexes ). Characteristic of pyramidal insufficiency is Juster's symptom: a pin prick of the skin in the area of elevation thumb The hand causes flexion of the thumb and bringing it to the index finger while simultaneously extending the remaining fingers and dorsiflexing the hand and forearm. The jackknife symptom is often detected: when passively extending the spastic upper limb and flexing the lower limb, the examiner first experiences a sharp springy resistance, which then suddenly weakens. When P. is affected. global, coordinating and imitative functions are often noted synkinesis .

Diagnosis of P.'s lesion. established on the basis of a study of the patient’s movements and identification of signs of pyramidal insufficiency (presence of a or a, increased muscle tone, increased deep reflexes, clonus, pathological hand and foot signs), features of the clinical course and the results of special studies (electroneuromyography, electroencephalography, tomography, etc.). ).

Differential diagnosis of pyramidal palsy is carried out with peripheral muscles and muscles,

which develop when peripheral motor neurons are damaged. The latter are also characterized by paretic muscles, decreased muscle tone (hypo- and atony), weakened or absent deep reflexes, changes in the electrical excitability of muscles and nerves (degeneration reaction). With the acute development of P.'s lesions. in the first few hours or days, a decrease in muscle tone and deep reflexes in paralyzed limbs is often observed. This is due to the condition diaschisis , after its elimination, an increase in muscle tone and deep reflexes occurs. At the same time, pyramidal signs (Babinsky's symptom, etc.) are also detected against the background of signs of diaschisis.

Treatment of lesions of P. s. aimed at the underlying disease. Apply medications, improving metabolism in nerve cells (nootropil, cerebrolysin, encephabol, glutamic acid, aminalon), nerve impulse conduction (prozerin, dibazol), microcirculation (vasoactive drugs), normalizing muscle tone (mydocalm, baclofen, lioresal), vitamins B, E Exercise therapy, massage (acupressure) and reflexology aimed at reducing muscle tone are widely used; physiotherapy and balneotherapy, orthopedic measures. Neurosurgical treatment is carried out for tumors and injuries of the brain and spinal cord, as well as for a number of acute disorders of cerebral circulation (with e or e extracerebral arteries, intracerebral hematoma, malformations of cerebral vessels, etc.).

Bibliography: Blinkov S.M. and Glezer I.I. The human brain in figures and tables, p. 82, L., 1964; Diseases of the nervous system, ed. P.V. Melnichuk, vol. 1, p. 39, M., 1982; Granit R. Fundamentals of movement regulation, translated from English, M., 1973; Gusev E.I., Grechko V.E. and Burd G.S. Nervous diseases, p. 66, M., 1988; Dzugaeva S.B. Conducting pathways of the human brain (in ontogenesis), p. 92, M., 1975; Kostyuk P.K. Structure and function of descending systems of the spinal cord, L. 1973; Lunev D.K. Violation of muscle tone in brain e, M. 1974; Multi-volume guide to neurology, ed. N.I. Grashchenkova, vol. 1, book. 2, p. 182, M., 1960; Skoromets D.D. Topical diagnosis of diseases of the nervous system, p. 47, L., 1989; Turygin V.V. Conducting pathways of the brain and spinal cord, Omsk. 1977.

Neurology and neurosurgery Evgeniy Ivanovich Gusev

3.1. Pyramid system

There are two main types of movements: involuntary And arbitrary.

Area 4 motor neurons control fine voluntary movements of the skeletal muscles of the opposite half of the body, since most of the pyramidal fibers pass to the opposite side in the lower part of the medulla oblongata.

Fibers forming corticonuclear pathway, are directed to the motor nuclei (V, VII, IX, X, XI, XII) of the cranial nerves and provide voluntary innervation of the facial and oral muscles.

Another bundle of fibers, starting in the “eye” area 8, and not in the precentral gyrus, also deserves attention. The impulses traveling along this bundle provide friendly movements of the eyeballs in the opposite direction. The fibers of this bundle at the level of the corona radiata join the pyramidal tract. Then they pass more ventrally in the posterior leg of the internal capsule, turn caudally and go to the nuclei of the III, IV, VI cranial nerves.

The nerves also include efferent and afferent fibers emanating from the lateral horns of the spinal gray matter.

Well-myelinated, fast-conducting axons of large alpha cells extend directly to the striated muscle.

Afferent fibers called ring-spiral, or primary endings, have a rather thick myelin coating and belong to fast-conducting fibers.

Extrafusal fibers in a relaxed state have a constant length. When a muscle is stretched, the spindle is stretched. The ring-spiral endings respond to stretching by generating an action potential, which is transmitted to the large motor neuron via fast-conducting afferent fibers, and then again via fast-conducting thick efferent fibers - the extrafusal muscles. The muscle contracts and its original length is restored. Any stretch of the muscle activates this mechanism. Percussion on the muscle tendon causes stretching of this muscle. The spindles react immediately. When the impulse reaches the motor neurons in the anterior horn of the spinal cord, they respond by causing a short contraction. This monosynaptic transmission is basic for all proprioceptive reflexes. The reflex arc covers no more than 1-2 segments of the spinal cord, which is of great importance in determining the location of the lesion.

Research methodology. Inspection, palpation and measurement of muscle volume are carried out, the volume of active and passive movements, muscle strength, muscle tone, rhythm of active movements and reflexes are determined. Electrophysiological methods are used to identify the nature and localization of movement disorders, as well as for clinically insignificant symptoms.

Active movements are checked consistently in all joints and performed by the subject. They may be absent or limited in volume and weakened in strength. The complete absence of active movements is called paralysis, limitation of movements or weakening of their strength is called paresis. Paralysis or paresis of one limb is called monoplegia or monoparesis. Paralysis or paresis of both arms is called upper paraplegia or paraparesis, paralysis or paraparesis of the legs is called lower paraplegia or paraparesis. Paralysis or paresis of two limbs of the same name is called hemiplegia or hemiparesis, paralysis of three limbs - triplegia, paralysis of four limbs - quadriplegia or tetraplegia.

Muscle strength determined consistently in all groups with active resistance of the patient. For example, when studying the strength of the muscles of the shoulder girdle, the patient is asked to raise his arm to a horizontal level, resisting the examiner’s attempt to lower his arm; then they suggest raising both hands above the horizontal line and holding them, offering resistance. To determine the strength of the shoulder muscles, the patient is asked to bend his arm at the elbow joint, and the examiner tries to straighten it; The strength of the shoulder abductors and adductors is also examined. To study the strength of the forearm muscles, the patient is instructed to perform pronation, and then supination, flexion and extension of the hand with resistance while performing the movement. To determine the strength of the finger muscles, the patient is asked to make a “ring” from the first finger and each of the others, and the examiner tries to break it. Strength is checked by moving the fifth finger away from the fourth finger and bringing the other fingers together, while clenching the hands into a fist. The strength of the pelvic girdle and hip muscles is examined by performing the task of raising, lowering, adducting, and abducting the hip while exerting resistance. The strength of the thigh muscles is examined by asking the patient to bend and straighten the leg at the knee joint. The strength of the lower leg muscles is checked as follows: the patient is asked to bend the foot, and the examiner holds it straight; then the task is given to straighten the foot bent at the ankle joint, overcoming the resistance of the examiner. The strength of the muscles of the toes is also examined when the examiner tries to bend and straighten the toes and separately bend and straighten the first toe.

Tonic reactions are based on a stretch reflex, the closure of which occurs in the spinal cord.

Muscle tone is influenced by the spinal (segmental) reflex apparatus, afferent innervation, reticular formation, as well as cervical tonic centers, including vestibular centers, the cerebellum, the red nucleus system, basal ganglia, etc.

Reflexes. A reflex is a reaction that occurs in response to irritation of receptors in the reflexogenic zone: muscle tendons, skin of a certain area of the body, mucous membrane, pupil. The nature of the reflexes is used to judge the state of various parts of the nervous system. When studying reflexes, their level, uniformity, and asymmetry are determined: with an increased level, a reflexogenic zone is noted. When describing reflexes, the following gradations are used: 1) living reflexes; 2) hyporeflexia; 3) hyperreflexia (with an expanded reflexogenic zone); 4) areflexia (lack of reflexes). Reflexes can be deep, or proprioceptive (tendon, periosteal, articular), and superficial (skin, mucous membranes).

Tendon and periosteal reflexes are caused by percussion with a hammer on the tendon or periosteum: the response is manifested by the motor reaction of the corresponding muscles. To obtain tendon and periosteal reflexes in the upper and lower extremities, it is necessary to evoke them in an appropriate position favorable for the reflex reaction (lack of muscle tension, average physiological position).

Upper limbs. Biceps tendon reflex caused by a hammer blow to the tendon of this muscle (the patient’s arm should be bent at the elbow joint at an angle of about 120°, without tension). In response, the forearm flexes. Reflex arc: sensory and motor fibers of the musculocutaneous nerve, CV-CVI. Triceps brachii tendon reflex is caused by a hammer blow on the tendon of this muscle above the olecranon (the patient’s arm should be bent at the elbow joint at almost an angle of 90°). In response, the forearm extends. Reflex arc: radial nerve, CVI-CVI. Radiation reflex is caused by percussion of the styloid process of the radius (the patient’s arm should be bent at the elbow joint at an angle of 90° and be in a position intermediate between pronation and supination). In response, flexion and pronation of the forearm and flexion of the fingers occur. Reflex arc: fibers of the median, radial and musculocutaneous nerves, CV-CVIII.

Lower limbs. Knee reflex caused by a hammer hitting the quadriceps tendon. In response, the lower leg is extended. Reflex arc: femoral nerve, LII-LIV. When examining the reflex in a horizontal position, the patient’s legs should be bent at the knee joints at an obtuse angle (about 120°) and rest freely on the examiner’s left forearm; when examining the reflex in a sitting position, the patient's legs should be at an angle of 120° to the hips or, if the patient does not rest his feet on the floor, hang freely over the edge of the seat at an angle of 90° to the hips, or one of the patient's legs is thrown over the other. If the reflex cannot be evoked, then the Jendraszik method is used: the reflex is evoked when the patient pulls towards the hand with the fingers tightly clasped. Heel (Achilles) reflex caused by percussion of the calcaneal tendon. In response, plantar flexion of the foot occurs as a result of contraction of the calf muscles. Reflex arc: tibial nerve, SI-SII. For a lying patient, the leg should be bent at the hip and knee joints, the foot should be bent at the ankle joint at an angle of 90°. The examiner holds the foot with his left hand, and with his right hand percusses the heel tendon. With the patient lying on his stomach, both legs are bent at the knee and ankle joints at an angle of 90°. The examiner holds the foot or sole with one hand and strikes with the hammer with the other. The reflex is caused by a short blow to the heel tendon or to the sole. The heel reflex can be examined by placing the patient on his knees on the couch so that the feet are bent at an angle of 90°. In a patient sitting on a chair, you can bend your leg at the knee and ankle joints and evoke a reflex by percussing the heel tendon.

Skin reflexes are caused by line irritation with the handle of a neurological hammer in the corresponding skin area in the patient's position on the back with slightly bent legs. Abdominal reflexes: upper (epigastric) are caused by irritation of the skin of the abdomen along the lower edge of the costal arch. Reflex arc: intercostal nerves, ThVII-ThVIII; medium (mesogastric) – with irritation of the skin of the abdomen at the level of the navel. Reflex arc: intercostal nerves, ThIX-ThX; lower (hypogastric) – with skin irritation parallel to the inguinal fold. Reflex arc: iliohypogastric and ilioinguinal nerves, ThXI-ThXII; the abdominal muscles contract at the appropriate level and the navel deviates towards the irritation. The cremasteric reflex is caused by irritation of the inner thigh. In response, the testicle is pulled upward due to contraction of the levator testis muscle, reflex arc: genital femoral nerve, LI-LII. Plantar reflex - plantar flexion of the foot and toes when the outer edge of the sole is stimulated by strokes. Reflex arc: tibial nerve, LV-SII. Anal reflex - contraction of the external anal sphincter when the skin around it tingles or is irritated. It is called in the position of the subject on his side with his legs brought to the stomach. Reflex arc: pudendal nerve, SIII-SV.

Pathological protective, or spinal automatism, reflexes in the upper and lower extremities– involuntary shortening or lengthening of a paralyzed limb during injection, pinching, cooling with ether or proprioceptive stimulation according to the Bekhterev-Marie-Foy method, when the examiner performs a sharp active flexion of the toes. Protective reflexes are often of a flexion nature (involuntary flexion of the leg at the ankle, knee and hip joints). The extensor protective reflex is characterized by involuntary extension of the leg at the hip and knee joints and plantar flexion of the foot. Cross protective reflexes - flexion of the irritated leg and extension of the other - are usually observed with combined damage to the pyramidal and extrapyramidal tracts, mainly at the level of the spinal cord. When describing protective reflexes, the form of the reflex response, the reflexogenic zone, is noted. area of evocation of the reflex and intensity of the stimulus.

An expression of a sharp increase in tendon reflexes is clonus, manifested by a series of rapid rhythmic contractions of a muscle or group of muscles in response to their stretching. Foot clonus is caused by the patient lying on his back. The examiner bends the patient's leg at the hip and knee joints, holds it with one hand, and with the other grabs the foot and, after maximum plantar flexion, jerks the foot into dorsiflexion. In response, rhythmic clonic movements of the foot occur while the heel tendon is stretched. Clonus of the patella is caused by a patient lying on his back with straightened legs: fingers I and II grasp the apex of the patella, pull it up, then sharply shift it in the distal direction and hold it in this position; in response, there is a series of rhythmic contractions and relaxations of the quadriceps femoris muscle and twitching of the patella.

Since the fibers descending to the nuclei of the VII and XII nerves are located more dorsally, these nerves may be spared. Possible ipsilateral involvement of the abducens or trigeminal nerve. Damage to the pyramids of the medulla oblongata: contralateral hemiparesis. Hemiplegia does not develop, since only the pyramidal fibers are damaged. The extrapyramidal tracts are located dorsally in the medulla oblongata and remain intact. When the pyramidal decussation is damaged, a rare syndrome of cruciant (or alternating) hemiplegia develops (right arm and left leg and vice versa).

To recognize focal brain lesions in patients in a comatose state, the symptom of an outwardly rotated foot is important. On the side opposite to the lesion, the foot is turned outward, as a result of which it rests not on the heel, but on the outer surface. To determine this symptom, you can use the technique of maximum outward rotation of the feet - Bogolepov's symptom. On the healthy side, the foot immediately returns to its original position, while the foot on the hemiparesis side remains turned outward.

It is important to determine exactly where the pathological process is localized - in the anterior horns, roots, plexuses or peripheral nerves. When the anterior horn is damaged, the muscles innervated from this segment suffer. Often, in atrophying muscles, rapid contractions of individual muscle fibers and their bundles are observed - fibrillar and fascicular twitching, which are a consequence of irritation by the pathological process of neurons that have not yet died. Since muscle innervation is polysegmental, complete paralysis requires damage to several adjacent segments. Involvement of all muscles of the limb is rarely observed, since the cells of the anterior horn, supplying various muscles, are grouped into columns located at some distance from each other. The anterior horns can be involved in the pathological process in acute poliomyelitis, amyotrophic lateral sclerosis, progressive spinal muscular atrophy, syringomyelia, hematomyelia, myelitis, and disorders of the blood supply to the spinal cord. When the anterior roots are affected, almost the same picture is observed as when the anterior horns are affected, because the occurrence of paralysis here is also segmental. Radicular paralysis develops only when several adjacent roots are affected.

Each motor root at the same time has its own “indicator” muscle, which makes it possible to diagnose its lesion by fasciculations in this muscle on the electromyogram, especially if the cervical or lumbar region is involved in the process. Since damage to the anterior roots is often caused by pathological processes in the membranes or vertebrae, which simultaneously involve the posterior roots, movement disorders are often combined with sensory disturbances and pain. Damage to the nerve plexus is characterized by peripheral paralysis of one limb in combination with pain and anesthesia, as well as autonomic disorders in this limb, since the trunks of the plexus contain motor, sensory and autonomic nerve fibers. Partial lesions of the plexuses are often observed. When the mixed peripheral nerve is damaged, peripheral paralysis of the muscles innervated by this nerve occurs, combined with sensory disturbances caused by interruption of afferent fibers. Damage to a single nerve can usually be explained by mechanical causes (chronic compression, trauma). Depending on whether the nerve is completely sensory, motor or mixed, disturbances occur, respectively, sensory, motor or autonomic. A damaged axon does not regenerate in the central nervous system, but can regenerate in peripheral nerves, which is ensured by the preservation of the nerve sheath, which can guide the growing axon. Even if the nerve is completely severed, bringing its ends together with a suture can lead to complete regeneration. Damage to many peripheral nerves leads to widespread sensory, motor and autonomic disorders, most often bilateral, mainly in the distal segments of the limbs. Patients complain of paresthesia and pain. Sensitive disturbances of the “socks” or “gloves” type, flaccid muscle paralysis with atrophy, and trophic skin lesions are detected. Polyneuritis or polyneuropathy are noted, arising due to many reasons: intoxication (lead, arsenic, etc.), nutritional deficiency (alcoholism, cachexia, cancer of internal organs, etc.), infectious (diphtheria, typhoid, etc.), metabolic ( diabetes mellitus, porphyria, pellagra, uremia, etc.). Sometimes the cause cannot be determined and this condition is regarded as idiopathic polyneuropathy.

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