Descending pyramidal tracts. pyramid path

There are two main types of movements: involuntary and voluntary.

Involuntary include simple automatic movements carried out by the segmental apparatus of the spinal cord and brain stem in the form of a simple reflex act. Arbitrary 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 conduction of an impulse from the cerebral cortex to the muscle occurs along 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, pathway. They are axons of neurons located in the precentral gyrus, in cytoarchitectonic field 4. This zone is a narrow field that stretches along the central fissure from the lateral (or Sylvian) groove to the anterior part of the paracentral lobule on the medial surface of the hemisphere, parallel to the sensory area of ​​the postcentral gyrus cortex .

The neurons that innervate the pharynx and larynx are located in the lower part of the precentral gyrus. Next in ascending order are the neurons that innervate the face, arm, torso, and leg. Thus, all parts of the human body are projected in the precentral gyrus, as it were, upside down. Motor neurons are located not only in field 4, they are also found in neighboring cortical fields. At the same time, the vast majority of them are occupied by 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 a thick myelin sheath. 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 originate from small pyramidal, or fusiform (fusiform) cells in motor fields 4 and 6. The cells of field 4 give about 40% of the fibers of the pyramidal tract, the rest originate from cells of other fields of the sensorimotor zone.

Motoneurons of field 4 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 medulla oblongata.

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

When the fibers of the pyramidal tract leave the motor cortex, they pass through the corona radiata of the white matter of the brain and converge towards the posterior leg 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 to the middle part of the legs of the brain, descend through each half of the base of the bridge, being surrounded by numerous nerve cells of the nuclei of the bridge and fibers of various systems. At the level of the pontomedullary articulation, the pyramidal tract becomes visible from the outside, its fibers form elongated pyramids on both sides of middle line 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 pyramidal decussation and form the lateral pyramidal tract. The remaining fibers continue to descend uncrossed in the anterior cords as the 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 from both sides.

Crossed fibers descend as part of the lateral pyramidal tract in the lateral cords. 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.

The fibers that form the cortical nuclear pathway are sent to the motor nuclei (V, VII, IX, X, XI, XII) of the cranial nerves and provide voluntary innervation of the facial and oral muscles.

Noteworthy is another bundle of fibers, starting in the "eye" field 8, and not in the precentral gyrus. The impulses going along this bundle provide friendly movements of the eyeballs in the opposite direction. The fibers of this bundle at the level of the radiant crown join the pyramidal pathway. Then they pass more ventrally in the posterior crus 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, vestibulo, red nuclear spinal, etc.) and afferent fibers entering the spinal cord through the posterior roots terminate on the bodies or dendrites of large and small alpha and gamma cells (directly or through intercalary , association or commissural neurons of the internal neuronal apparatus of the spinal cord) In contrast to the pseudo-unipolar neurons of the spinal nodes, the neurons of the anterior horns are multipolar. Their dendrites have multiple synaptic connections with various afferent and efferent systems. Some of them are facilitating, others are inhibitory in their action. In the anterior horns, motor neurons form groups organized in columns and not divided into segments. There is a certain somatotopic order in these columns. In the cervical part, 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, the neurons innervating the foot and leg are also located laterally in the anterior horn, while those innervating the trunk are medial. 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 the posterior root distally to the spinal nodes and together they form the spinal nerve. Thus, each segment of the spinal cord has its own pair spinal nerves.

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

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

In addition to large and small alpha motor neurons, the anterior horns contain numerous gamma motor neurons. Among the intercalary neurons of the anterior horns, Renshaw cells, which inhibit the action of large motor neurons, should be noted. Large alpha cells with a thick and fast-conducting axon fast cuts muscles. Small alpha cells with a thinner axon perform a tonic function. Gamma cells with a thin and slow-conducting axon innervate the proprioceptors of the muscle spindle. Large alpha cells are associated with giant cells in the cerebral cortex. Small alpha cells have a connection with the extrapyramidal system. Gamma cells regulate the state of muscle proprioceptors. Among the various muscle receptors, the most important are neuromuscular muscle spindles.

Afferent fibers, called annular, or primary, endings, have a fairly thick myelin coating and are fast-conducting fibers.

Many muscle spindles have not only primary but also secondary endings. These endings also respond to stretch stimuli. Their action potential propagates in the central direction along thin fibers that communicate with the intercalary neurons 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 loops and do not reach the cortical level. These are the elements of reflexes that serve as the basis for voluntary and other movements, as well as static reflexes that oppose gravity.

Extrafusal fibers in a relaxed state have a constant length. When the 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 efferent fibers - extrafusal muscles. The muscle contracts, its original length is restored. Any stretching of the muscle activates this mechanism. Percussion along the tendon of a muscle causes stretching of this muscle. The spindles react immediately. When the impulse reaches the motor neurons of the anterior horn of the spinal cord, they react by causing a short contraction. This monosynaptic transmission is the basis 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 localization of the lesion.

Gamma neurons are under the influence of fibers descending from the motor neurons of the CNS as part of such pathways as pyramidal, reticular spinal, vestibulo 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 response of receptors to stretch. This is called the gamma neuron-spindle system.

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 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 muscles of the limb with a centimeter, it is possible to identify the severity of trophic disorders. When examining some patients, fibrillar and fascicular twitches are noted. With the help of palpation, you can determine the configuration of the muscles, their tension.

Active movements are checked sequentially in all joints and performed by the subject. They may be absent or limited in scope and weakened in strength. Complete absence active movements are called paralysis, restriction of movements or weakening of their strength - 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 with complete relaxation of the muscles of the subject, which makes it possible to exclude a local process (for example, changes in the joints), which limits active movements. Along with this, the definition of passive movements is the main method for studying muscle tone.

Investigate the volume of passive movements in the joints of the upper limb: 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 the fingers.

Muscle strength is determined consistently in all groups with active resistance of the patient. For example, when examining 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 offer to raise both hands above the horizontal line and hold them, offering resistance. To determine the strength of the shoulder muscles, the patient is asked to bend the arm at the elbow joint, and the examiner tries to straighten it; the strength of the abductors and adductors of the shoulder is also examined. To study the strength of the muscles of the forearm, the patient is given the task to perform pronation, and then supination, flexion and extension of the hand with resistance during the movement. To determine the strength of the muscles of the fingers, the patient is offered to make a “ring” of the first finger and each of the others, and the examiner tries to break it. They check the strength when the V finger is abducted from the IV and the other fingers are brought together, when the hands are clenched into a fist. The strength of the muscles of the pelvic girdle and thigh is examined when asked to raise, lower, adduct and abduct the thigh, while providing resistance. The strength of the thigh muscles is examined, inviting the patient to bend and straighten the leg at the knee joint. The strength of the calf muscles is checked as follows: the patient is asked to bend the foot, and the examiner keeps it extended; then the task is given to unbend 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 unbend the fingers and separately bend and unbend the first finger.

To detect paresis of the extremities, 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 the given position. With mild paresis, one has to resort to a test for the rhythm of active movements; pronate and supinate hands, clench hands into fists and unclench them, move legs like on a bicycle; the insufficiency of the strength of the limb is manifested in the fact that it is more likely to get tired, the movements are performed not so quickly and less dexterously than with a healthy limb. The strength of the hands is measured with a dynamometer.

Muscle tone - reflex muscle tension, which provides preparation for movement, maintaining balance and posture, 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 most often caused by muscle stretching, i.e. irritation of proprioreceptors, determined by the nature of the nerve impulses that reach this muscle. It is this tone that underlies various tonic reactions, including antigravitational ones, carried out under conditions of maintaining the connection of muscles with the central nervous system.

The basis of tonic reactions is the 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 nuclei, etc.

The state of muscle tone is assessed during examination and palpation of the muscles: with a decrease in muscle tone, the muscle is flabby, soft, pasty. with increased tone, it has a denser texture. However, the determining factor is the study of muscle tone through passive movements (flexors and extensors, adductors and abductors, pronators and supinators). Hypotension is a decrease in muscle tone, atony is its absence. A decrease in muscle tone can be detected when examining Orshansky's symptom: when lifting up (in a patient lying on his back) a leg extended at the knee joint, its overextension in this joint is revealed. Hypotension and muscle atony occur with peripheral paralysis or paresis (violation of the efferent section 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 spinal cord. Muscle hypertension is the tension felt by the examiner during passive movements. There are spastic and plastic hypertension. Spastic hypertension - an increase in the tone of the flexors and pronators of the arm and extensor and adductors of the leg (with damage to the pyramidal tract). With spastic hypertension, there is a symptom of a "penknife" (obstacle to passive movement in the initial phase of the study), with plastic hypertension - a symptom of " gear wheel» (feeling of shocks 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 part of the body, mucous membrane, pupil. The nature of the reflexes judge the state various departments nervous system. In the study of reflexes, their level, uniformity, asymmetry are determined: at an increased level, a reflexogenic zone is noted. When describing reflexes, the following gradations are used: 1) live reflexes; 2) hyporeflexia; 3) hyperreflexia (with an extended reflex zone); 4) areflexia (absence of reflexes). Reflexes can be deep, or proprioceptive (tendon, periosteal, articular), and superficial (skin, mucous membranes).

Tendon and periosteal reflexes are evoked 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 extremities, it is necessary to call them in an appropriate position favorable for the reflex reaction (lack of muscle tension, average physiological position).

Upper limbs. The reflex from the tendon of the biceps muscle of the shoulder is caused by a blow of the hammer on 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. The reflex from the tendon of the triceps muscle of the shoulder is caused by a blow of the hammer on the tendon of this muscle above the olecranon (the patient's arm should be bent at the elbow joint almost at an angle of 90 °). In response, the forearm extends. Reflex arc: radial nerve, СVI СVII. The radial 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 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. The patellar reflex is caused by the impact of the hammer on the tendon of the quadriceps muscle. In response, the 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 lie freely on the examiner's left forearm; when examining the reflex in the sitting position, the patient's legs should be at an angle of 120 ° to the hips or, if the patient does not rest with his feet on the floor, freely hang over the edge of the seat at an angle of 90 ° to the hips or one leg of the patient is thrown over the other. If the reflex cannot be evoked, then the Endrashik method is used: the reflex is evoked at the time when the patient pulls towards the hand with tightly clasped fingers. Calcaneal (Achilles) reflex is caused by percussion on the calcaneal tendon. In response, plantar flexion of the foot occurs as a result of contraction calf muscles. Reflex arc: tibial nerve, SI SII. In a lying patient, the leg should be bent at the hip and knee joints, the foot at the ankle joint at an angle of 90 °. The examiner holds the foot with the left hand, and the calcaneal tendon is percussed with the right hand. In the position of the patient on the 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 a hammer with the other. The reflex is caused by a short blow to the heel tendon or sole. The study of the heel reflex can be done 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 the leg at the knee and ankle joints and cause a reflex by percussing the calcaneal tendon.

Articular reflexes are caused by irritation of the receptors of the joints and ligaments on the hands. 1. Mayer - opposition and flexion in the metacarpophalangeal and extension in the interphalangeal articulation of the first finger with forced flexion in the main phalanx of the III and IV fingers. Reflex arc: ulnar and median nerve, СVII ThI. 2. Leri - flexion of the forearm with forced flexion of the fingers and the hand in the supination position, reflex arc: ulnar and median nerves, CVI ThI.

Skin reflexes are caused by stroke stimulation with the handle of the neurological malleus in the corresponding skin zone in the patient's position on the back with slightly bent legs. Abdominal reflexes: upper (epigastric) is caused by irritation of the abdominal skin 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: iliac hypogastric and iliac inguinal nerves, ThXI ThXII; there is a contraction of the abdominal muscles at the appropriate level and the deviation of the navel in the direction of irritation. The cremaster reflex is triggered by stimulation inner surface hips. In response, the testicle is pulled up due to contraction of the muscle that lifts the testicle, reflex arc: femoral pudendal nerve, LI LII. Plantar reflex - plantar flexion of the foot and fingers with dashed irritation of the outer edge of the sole. Reflex arc: tibial nerve, LV SII. Anal reflex - contraction of the external sphincter of the anus with tingling or dashed irritation of the skin around it. Called in the position of the subject on the side with the 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 disturbed. Pathological reflexes, depending on the reflex response, are divided into extensor and flexion.

Pathological extensor reflexes in the lower extremities. Highest value has a Babinsky reflex - extension of the first toe with dashed skin irritation of the outer edge of the sole, in children under 2–2.5 years old - a physiological reflex. Oppenheim reflex - extension of the first toe in response to running fingers along the tibial crest down to the ankle joint. Gordon's reflex - slow extension of the first toe and fan-shaped divergence of other fingers during compression of the calf muscles. Schaefer's reflex - extension of the first toe with compression of the calcaneal tendon.

Flexion pathological reflexes on the lower extremities. The most important is the Rossolimo reflex - flexion of the toes with a quick tangential blow to the balls of the fingers. Ankylosing spondylitis - Mendel's reflex - flexion of the toes when a hammer strikes it dorsal surface. Zhukovsky reflex - flexion of the toes when struck with a hammer on its plantar surface directly under the fingers. Ankylosing spondylitis reflex - flexion of the toes when struck with a hammer on the plantar surface of the heel. It should be borne in mind that the Babinski reflex appears with an acute lesion of the pyramidal system, for example, with hemiplegia in the case of a cerebral stroke, and the Rossolimo reflex is a late manifestation of spastic paralysis or paresis.

Flexion pathological reflexes on the upper limbs. Tremner's reflex - flexion of the fingers of the hand in response to rapid tangential irritations by the fingers of the examiner of the palmar surface of the terminal phalanges of the II IV fingers of the patient. Jacobson's reflex - Weasel - combined flexion of the forearm and fingers in response to a hammer blow on the styloid process of the radius. Zhukovsky reflex - flexion of the fingers of the hand when struck with a hammer on its palmar surface. Ankylosing spondylitis - flexion of the fingers during percussion with the hammer of the back of the hand.

Pathological protective, or spinal automatism, reflexes on the upper and lower extremities - involuntary shortening or lengthening of a paralyzed limb when pricked, pinched, cooled with ether or proprioceptive irritation according to the Bekhterev-Marie-Foy method, when the researcher produces a sharp active flexion of the toes. Protective reflexes are often flexion in 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 in 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 noted with a combined lesion of 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. the reflex evoking area and the intensity of the stimulus.

Neck tonic reflexes occur in response to stimuli associated with a change in the position of the head in relation to the body. Magnus-Klein reflex - increased extensor tone in the muscles of the arm and leg, towards which the head is turned with the chin, flexor tone in the muscles of opposite limbs when turning the head; flexion of the head causes an increase in flexor, and extension of the head - extensor tone in the muscles of the limbs.

Gordon's reflex - delaying the lower leg in the extension position when evoking a knee jerk. The phenomenon of the foot (Westphal) is the “freezing” of the foot during its passive dorsiflexion. Foix-Thevenard's shin phenomenon - incomplete extension of the shin in the knee joint in a patient lying on his stomach, after the shin was kept in the position of extreme flexion for some time; manifestation of extrapyramidal rigidity.

Yanishevsky's grasping reflex on the upper limbs - involuntary grasping of objects in contact with the palm; on the lower extremities - increased flexion of the fingers and feet during movement or other irritation of the sole. Distant grasping reflex - an attempt to capture an object shown at a distance. It is observed with damage to the frontal lobe.

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

Synkinesia is 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 coordinating.

Global, or spastic, is called pathological synkinesis in the form of increased flexion contracture in the paralyzed arm and extensor contracture in a paralyzed leg when trying to move paralyzed limbs or during active movements with healthy limbs, tension of the muscles of the trunk and neck, when coughing or sneezing. Imitative synkinesis is an involuntary repetition by paralyzed limbs of voluntary movements of healthy limbs on the other side of the body. Coordinator 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 limitation of movement in the joint, is called contracture. Distinguish in shape flexion, extensor, 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; by the time 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 one. Early contracture - hormetonia. It is characterized by periodic tonic spasms in all limbs, the appearance of pronounced protective reflexes, dependence on intero- and exteroceptive stimuli. Late hemiplegic contracture (Wernicke-Mann posture) - bringing the shoulder to the body, flexion of the forearm, flexion and pronation of the hand, extension of the thigh, lower leg and plantar flexion of the foot; when walking, the foot describes a semicircle.

Semiotics of movement disorders. Having revealed, on the basis of 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, determine its nature: whether it occurs due to damage to the central or peripheral motor neurons. The defeat of the central motor neurons at any level of the cortical spinal tract causes the occurrence of central, or spastic, paralysis. With the defeat of peripheral motor neurons in any area (anterior horn, root, plexus and peripheral nerve), peripheral, or flaccid, paralysis occurs.

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 the implementation of 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 interruption of the pyramidal tract occurs suddenly, the stretch reflex is suppressed. This means that the paralysis is initially flaccid. It may take days or weeks for this reflex to recover.

When this happens, the muscle spindles will become more sensitive to stretch than before. This is especially evident in the flexors of the arm and extensors of the leg. Hypersensitivity of stretch receptors is caused by damage to the extrapyramidal pathways that terminate in the cells of the anterior horns and activate gamma motor neurons that innervate intrafusal muscle fibers. As a result of this phenomenon, the impulses along the feedback rings that regulate the length of the muscles change so that the flexors of the arm and the extensors of the leg are fixed in the shortest possible state (the position of the minimum length). The patient loses the ability to voluntarily inhibit hyperactive 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) a decrease in strength combined with a loss of fine movements; 2) spastic increase in tone (hypertonicity); 3) increased proprioceptive reflexes with or without clonus; 4) decrease 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) the absence of the reaction of rebirth.

Symptoms vary depending on the location of the lesion in the central motor neuron. The defeat of the precentral gyrus is characterized by two symptoms: focal epileptic seizures(Jacksonian epilepsy) in the form of clonic convulsions and central paresis (or paralysis) of the limb on the opposite side. Paresis of the leg indicates a lesion of the upper third of the gyrus, the hand - its middle third, half of the face and tongue - its lower third. It is diagnostically important to determine where clonic convulsions begin. Often, convulsions, starting in one limb, then move to other parts of the same half of the body. This transition is made in the order in which the centers are located in the precentral gyrus. Subcortical (radiant crown) lesion, contralateral hemiparesis in the arm or leg, depending on which part of the precentral gyrus the focus is closer to: if to the lower half, then the arm will suffer more, to the upper - the leg. Damage to the internal capsule: contralateral hemiplegia. Due to the involvement of cortical nuclear fibers, there is a violation of innervation in the area of ​​the contralateral facial and hypoglossal nerves. Most cranial motor nuclei receive pyramidal innervation from both sides in whole or in part. 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 (brain stem, pons, medulla oblongata) is accompanied by damage to the cranial nerves on the side of the focus and hemiplegia on the opposite side. Cerebral peduncle: A lesion in this area results in contralateral spastic hemiplegia or hemiparesis, which may be associated with ipsilateral (on the side of the lesion) oculomotor nerve lesion (Weber's syndrome). Brain pons: If affected in this area, 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 intact. Possible ipsilateral involvement of the abducens or trigeminal nerve. The defeat of the pyramids of the medulla oblongata: contralateral hemiparesis. Hemiplegia does not develop, since only the pyramidal fibers are damaged. The extrapyramidal pathways are located dorsally in the medulla oblongata and remain intact. If the chiasm of the pyramids is damaged, a rare syndrome of cruciant (or alternating) hemiplegia develops (right arm and left leg and vice versa).

For the recognition of focal lesions of the brain in patients in a coma, the symptom of a rotated outward foot is important. On the side opposite the lesion, the foot is turned outward, as a result of which it rests not on the heel, but on outer surface. In order to determine this symptom, you can use the method of maximum turn of the feet outward - Bogolepov's symptom. On the healthy side, the foot immediately returns to its original position, and the foot on the side of hemiparesis remains turned outward.

If the pyramidal tract is damaged below the decussation in the brainstem or upper cervical segments of the spinal cord, hemiplegia occurs involving the ipsilateral limbs or, in the case of bilateral damage, tetraplegia. Damage to the thoracic spinal cord (involvement of the lateral pyramidal tract) causes spastic ipsilateral monoplegia of the leg; bilateral involvement leads to lower spastic paraplegia.

Peripheral motor neuron: damage can involve anterior horns, anterior roots, peripheral nerves. In the affected muscles, neither voluntary nor reflex activity is detected. Muscles are not only paralyzed, but also hypotonic; there is an areflexia due to interruption of the monosynaptic arc of the stretch reflex. After a few weeks, atrophy sets in, as well as the reaction of the 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 function muscles.

It is important to determine exactly where the pathological process is localized - in the anterior horns, roots, plexuses or in peripheral nerves. When the anterior horn is affected, the muscles innervated from this segment suffer. Often in atrophying muscles, rapid contractions of individual muscle fibers and their bundles - fibrillar and fascicular twitches, which are the result of irritation by the pathological process of neurons that have not yet died. Since the innervation of the muscles is polysegmental, complete paralysis requires the defeat of several neighboring segments. Involvement of all the muscles of the limb is rarely observed, since the cells of the anterior horn, supplying various muscles, are grouped in 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 circulatory disorders of the spinal cord. With damage to the anterior roots, almost the same picture is observed as with the defeat of the anterior horns, because the occurrence of paralysis here is also segmental. Paralysis of the radicular character develops only with the defeat of several adjacent roots.

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 an electromyogram, especially if the cervical or lumbar region is involved in the process. Since the defeat of the anterior roots is often due to pathological processes in the membranes or vertebrae, simultaneously involving the posterior roots, then movement disorders often associated 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 plexus trunks contain motor, sensory and autonomic nerve fibers. Often there are partial lesions of the plexuses. When a mixed peripheral nerve is damaged, peripheral paralysis of the muscles innervated by this nerve occurs, in combination with sensory disturbances caused by a break in the afferent fibers. Injury to a single nerve can usually be explained mechanical causes(chronic compression, trauma). Depending on whether the nerve is completely sensory, motor or mixed, sensory, motor or autonomic disturbances occur, respectively. The damaged axon does not regenerate in the CNS, but can regenerate in the 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. The defeat of many peripheral nerves leads to widespread sensory, motor and autonomic disorders, most often bilateral, mainly in the distal segments of the extremities. Patients complain of paresthesia and pain. Sensitive disorders such as "socks" or "gloves", flaccid muscle paralysis with atrophy, and trophic skin lesions are revealed. Polyneuritis or polyneuropathy is noted, arising from many reasons: intoxication (lead, arsenic, etc.), nutritionally deficient (alcoholism, cachexia, cancer internal organs etc.), infectious (diphtheria, typhoid, etc.), metabolic ( diabetes, porphyria, pellagra, uremia, etc.). Sometimes it is not possible to establish the cause and this condition is regarded as idiopathic polyneuropathy.

The descending pathways 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.

The highest motor center in humans is the cerebral cortex. It controls the motor neurons of the brain stem and spinal cord in two ways: directly through the cortical-nuclear, anterior and lateral cortical-spinal (pyramidal) pathways, or indirectly, through the underlying motor centers. In the latter case, the role of the cortex is reduced to the launch, maintenance, or termination of the execution of motor programs stored in these centers. 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 cortico-nuclear, anterior and lateral cortico-spinal (pyramidal) pathways.

Cortico-nuclear pathway begins in the lower third of the precentral gyrus of the brain. Pyramidal cells (1 neuron) are located here, the axons of which pass through the knee of the internal capsule to the brainstem and are directed in its basal part down to the motor nuclei of the cranial nerves of the opposite side (III–VII, IX–XII). Here are the bodies of the second neurons of this system, which are analogues of the motor neurons of the anterior horns of the spinal cord. 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 radiant crown, pass through the posterior leg of the internal capsule to the brainstem, 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 pathway, in contrast to the anterior one, pass to the opposite side at the level of the medulla oblongata, forming the cross of the pyramids. Then they go in the back of the lateral cord (see Fig. 23) to their "own" segment and end on the motor neurons of the anterior horns of the spinal cord (the second neuron of the system).

    Extrapyramidal system performs involuntary regulation and coordination of movements, regulation of muscle tone, maintenance of posture, organization of motor manifestations of emotions. Provides smooth movements, sets the initial posture for their implementation.

The extrapyramidal system includes:

cortico-thalamic pathway, conducts motor impulses from the cortex to the motor nuclei of the thalamus.

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

Cortical-red nuclear pathway, 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 motoneurons of the anterior horns on the opposite side (for more details, see Section 5.3.2.).

Covering-spinal tract. His passage in in general terms 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 quadrigemina of the midbrain. Their axons pass to the opposite side and, as part of the anterior cords 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).

Vestibulo-spinal tract connects the vestibular nuclei of the hindbrain (pons) and regulates the tone of the muscles of the body (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.).

Cortical-bridge-cerebellar pathway 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 (cortical-bridge fibers) pass through the internal capsule and go to the basilar part of the bridge, to their own nuclei of the bridge. Here there is a switch to the second neurons of this system. Their axons (bridge-cerebellar fibers) pass to the opposite side and go through the middle cerebellar peduncle to the contralateral hemisphere of the cerebellum.

    Main ascending paths.

A. Ascending to the hindbrain: Flexig's posterior spinal cerebellar tract, Gowers' anterior cerebellar tract. Both spinal cerebellar tracts conduct unconscious impulses (unconscious coordination of movements).

Ascending to the midbrain: lateral dorsal-middle cerebral (spinal-tectal) pathway

To the diencephalon: lateral dorsal-thalamic pathway. It conducts temperature irritations and pain; the anterior dorsal-thalamic is the way of conducting impulses of touch, touch.

Some of them are continuous fibers of primary afferent (sensory) neurons. These fibers - thin (Gaulle's bundle) and wedge-shaped (Burdach's bundle) bundles go as 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 cord, or the nuclei of Gaulle and Burdach. The fibers of the dorsal cord are conductors of skin-mechanical sensitivity.

The remaining ascending pathways start from neurons located in the gray matter of the spinal cord. Since 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 the fibers from the secondary afferent neurons pass through the lateral funiculus of the white matter. This is where the spinothalamic pathway is located. The axons of the spinothalamic neurons cross and reach without interruption through the medulla oblongata and midbrain to the thalamic nuclei, where they form synapses with thalamic neurons. The spinothalamic pathways receive impulses from skin receptors.

In the lateral cords, fibers of the spinal cerebellar tracts, dorsal and ventral, pass, conducting impulses from skin and muscle receptors to the cerebellar cortex.

As part of the lateral funiculus, there are also fibers of the spinocervical tract, the endings 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 is directed to the cerebellum and the brainstem nuclei.

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

pyramid system- a system of efferent neurons, whose bodies are located in the cerebral cortex, terminate in the motor nuclei of the cranial nerves and the gray matter of the spinal cord. As part of the pyramidal path (tractus pyramidalis), cortical-nuclear fibers (fibrae corticonucleares) and cortical-spinal fibers (fibrae corticospinales) are isolated. Both those and others 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. In the precentral gyrus, the primary motor field is localized, where pyramidal neurons are located that control individual muscles and muscle groups. In this gyrus there is a somatotopic representation of the musculature. The neurons that control the muscles of the pharynx, tongue and head occupy the lower part of the gyrus; above are areas associated with the muscles of the upper limb and trunk; muscle projection lower limb located in the upper part of the precentral gyrus and passes to the medial surface of the hemisphere.

The pyramidal pathway is formed mainly by thin nerve fibers that pass through the white matter of the hemisphere and converge to the internal capsule ( rice. 1 ). Cortical-nuclear fibers form the knee, and cortical-spinal fibers form the anterior 2/3 of the posterior leg of the internal capsule. From here, the pyramidal pathway continues to the base of the brain stem and further to the anterior part of the pons (see Fig. Brain ). Throughout the brainstem, cortical-nuclear fibers pass to the opposite side to the dorsolateral areas of the reticular formation, where they switch to motor nuclei III, IV, V, VI, VII, IX, X, XI, XII cranial nerves ; only uncrossed fibers go to the upper third of the nucleus of the facial nerve. Part of the fibers of the pyramidal pathway passes from the brain stem to the cerebellum.

In the medulla oblongata, the pyramidal path is located in the pyramids, which form a cross (decussatio pyramidum) on the border with the spinal cord. Above the crossroads, the pyramidal pathway contains 700,000 to 1,300,000 nerve fibers On the one side. As a result of crossing, 80% of the fibers pass to the opposite side and form in the lateral funiculus spinal cord lateral cortical-spinal (pyramidal) path. Non-crossed fibers from the medulla oblongata continue into the anterior funiculus of the spinal cord in the form of an anterior cortical-spinal (pyramidal) path. The fibers of this path pass to the opposite side throughout the spinal cord in its white commissure (segmentally). Most of the cortical-spinal fibers terminate in the intermediate gray matter of the spinal cord on its intercalary neurons, only a part of them form synapses directly with the motor neurons of the anterior horns, which give rise to the motor fibers of the spinal cord. nerves . About 55% of the cortical-spinal 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. Due 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, however, the muscles of the trunk and the upper third of the face receive fibers from the pyramidal pathway from both hemispheres.

P.'s function with. consists in the perception of a program of voluntary movement and the conduction of impulses from this program to the segmental apparatus of the brain stem and spinal cord.

IN clinical practice P.'s condition with. determined by the nature of arbitrary movements. Assess the range of motion and the force of contraction of the striated muscles according to a six-point system (full muscle strength - 5 points, "compliance" of muscle strength - 4 points, a moderate decrease in strength with in full active movements - 3 points, the possibility of a full range of movements only after the relative elimination of the force of gravity of the limb - 2 points, the safety of movement with a barely noticeable muscle contraction - 1 point and the absence of voluntary movement - 0). The strength of muscle contraction can be quantitatively assessed using a dynamometer. To assess the safety of the pyramidal cortical-nuclear pathway to the motor nuclei of the cranial nerves, tests are used that determine the function of the muscles of the head and neck innervated by these nuclei, the corticospinal tract - in the study of the muscles of the trunk and limbs. The defeat of the pyramidal system is also judged by the state of muscle tone and muscle trophism.

Pathology. Violations of P.'s function with. observed in many pathological processes. In P.'s neurons with and their long axons, metabolic disturbances often occur, which lead to degenerative-dystrophic changes in these structures. Violations are genetically determined or are the result of intoxication (endogenous, exogenous), as well as viral infection genetic apparatus of neurons. Degeneration is characterized by a gradual, symmetrical and progressive dysfunction of pyramidal neurons, primarily those with the longest axons, i.e. ending at the peripheral motor neurons of the lumbar thickening. Therefore, the pyramidal in such cases is first detected in the lower extremities. Strumpell's family spastic paraplegia belongs to this group of diseases (see. Paraplegia ), portocaval encephalomyelopathy, funicular myelosis , as well as Mills syndrome - unilateral ascending of unclear etiology. It usually begins at the age of 35-40 to 60 years with a central thorax of the distal parts of the lower limb,

which gradually spreads to the proximal parts of the lower, and then to the entire upper limb and turns into spastic hemiplegia with autonomic and trophic disorders in the paralyzed limbs. P. s. often affected by slow viral infections, such as amyotrophic lateral , scattered and others. Almost always in the clinical picture of 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 insufficiency cerebral circulation. P. s. may be involved in the pathological process encephalitis And myelitis , at traumatic brain injury And spinal cord injury , with tumors of the central nervous system, etc.

At P.'s defeat with. central s and paralysis With characteristic disorders 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, Yakobson - Lask, Bekhterev, Zhukovsky, Hoffmann, on the feet - Babinsky, Oppenheim, Chaddock, Rossolimo, Bekhterev, etc. (see. reflexes ). Juster's symptom is characteristic of pyramidal insufficiency: a pin prick of the skin in the area of ​​​​the eminence of the thumb causes the thumb to flex and bring it to the index finger while simultaneously extending the remaining fingers and dorsiflexing the hand and forearm. Quite often, a symptom of a folding knife is revealed: with passive extension of the spastic upper limb and flexion of the lower limb, the examiner first experiences a sharp springy resistance, which then suddenly weakens. At P.'s defeat with. global, coordinating and imitation synkinesis .

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

The differential diagnosis of pyramidal paralysis is carried out with peripheral ami and ami,

that develop with damage to peripheral motor neurons. The latter are also characterized by paretic muscles, a decrease in muscle tone (hypo- and atony), a weakening or absence of deep reflexes, changes in the electrical excitability of muscles and nerves (rebirth reaction). At acute development P.'s defeats with. in the first few hours or days, there is often a decrease in muscle tone and deep reflexes in paralyzed limbs. It is related to the state diaschiza , after the elimination of which there is an increase in muscle tone and deep reflexes. At the same time, pyramidal signs (Babinski's symptom, etc.) are also detected against the background of signs of diaschisis.

Treatment of P.'s defeats with. directed 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 (point) and reflexology are widely used, aimed at reducing muscle tone; physio- and balneotherapy, orthopedic measures. Neurosurgical treatment is performed for tumors and injuries of the brain and spinal cord, as well as for a number of acute cerebrovascular accidents (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; Granite R. Fundamentals of regulation of movements, translated from English, M., 1973; Gusev E.I., Grechko V.E. and Burd G.S. Nervous diseases, With. 66, M., 1988; Dzugaeva S.B. Pathways of the human brain (in ontogeny), p. 92, M., 1975; Kostyuk P.K. Structure and function of the descending systems of the spinal cord, L. 1973; Lunev D.K. Violation of muscle tone in cerebral e, M. 1974; Multi-volume guide to neurology, ed. N.I. Grashchenkova, vol. 1, book. 2, p. 182, Moscow, 1960; Skoromets D.D. Topical diagnosis of diseases of the nervous system, p. 47, L., 1989; Turygin V.V. Pathways of the brain and spinal cord, Omsk. 1977.

Exist following descending pathways:
cortical-spinal pathway (pyramidal pathway);
reticulospinal pathway (extrapyramidal pathway);
vestibulo-spinal pathway;
tegmental-spinal pathway;
suture-spinal pathway;
pathways of aminergic systems of the CNS;
pathways of the autonomic nervous system.

Cortico-spinal tract

It is a major pathway for voluntary motor activity. About 40% of its fibers originate from the primary motor cortex of the precentral gyrus. The remaining fibers originate from the accessory motor area on the medial side of the hemisphere, the premotor cortex on the lateral side of the hemisphere, the somatic sensory cortex, the parietal cortex, and the cingulate cortex. The fibers from the two sensory centers mentioned above terminate at the sensory nuclei of the brainstem and spinal cord, where they regulate the transmission of sensory impulses.

Cortico-spinal tract descends through the radiant crown and the posterior leg of the internal capsule to the brain stem. It then passes in the peduncle (cerebrum) at the level of the midbrain and basilar part of the pons, reaching the medulla oblongata. Here it forms a pyramid (hence the name - the pyramidal pathway).

Passing through the brainstem, the corticospinal pathway gives off fibers that activate the motor nuclei of the cranial nerves, in particular those that innervate the muscles of the face, jaw, and tongue. These fibers are called cortical-bulbar. (The term "corticonuclear" is also used, since the term "bulbar" can be interpreted in different ways.)

Demonstration of the course of the fibers of the pyramidal tract on the left side.
Additional motor area on the medial side of the hemisphere.
The arrow shows the level of the cross of the pyramids. Sensory neurons are highlighted in blue.

Coronal section of the patient's embalmed brain followed by copper sulfate treatment (Mulligan stain),
showing unstained corticospinal fibers running through the pontine nuclei towards the pyramids.

Characteristics of the fibers of the cortical-spinal tract above the level of the spinal junction:

About 80% (70-90%) of the fibers pass to the opposite side at the level of the pyramidal decussation;

These fibers descend on the opposite side of the spinal cord and make up the lateral cortical-spinal pathway (crossing cortical-spinal pathway); the remaining 20% ​​of the fibers do not cross and continue down in the anterior part of the spinal cord;

Half of these non-decussing fibers enter the anterior/ventral corticospinal pathway and are located in the ventral/anterior funiculus of the spinal cord at the cervical and upper thoracic levels; these fibers pass to the opposite side at the level of the white commissure and innervate the muscles of the anterior and posterior walls of the abdominal cavity;

The other half enters the lateral cortico-spinal pathway on its own half of the spinal cord.

It is believed that the cortical-spinal pathway contains about 1 million nerve fibers. The average conduction velocity is 60 m/s, which indicates an average fiber diameter of 10 µm (the "rule of six"). About 3% of the fibers are very large (up to 20 microns); they depart from giant neurons (Betz cells), located mainly in the region of the motor cortex, which is responsible for the innervation of the lower extremities. All fibers of the cortical-spinal tract are excitatory and use glutamate as a mediator.

Pyramidal pathway.
CSP - cortical-spinal pathway;
PCST - anterior cortical-spinal pathway;
LKSP - lateral cortical-spinal pathway.
Note that only the motor component is shown; components of the parietal lobe are omitted.

Target cells of the lateral corticospinal tract:

A) Motoneurons of the distal limbs. In the anterior horns of the gray matter of the spinal cord, axons of the lateral corticospinal tract can directly synapse on the dendrites of α- and γ-motoneurons innervating the muscles of the extremities, especially the upper ones (however, as a rule, this occurs through interneurons within the gray matter of the spinal cord). Individual axons of the lateral corticospinal tract can activate "large" or "small" motor units.

A motor unit is a complex consisting of a neuron of the anterior horn of the spinal cord and all the muscle fibers that this neuron innervates. Small motor unit neurons selectively innervate a small number of muscle fibers and are involved in performing fine and precise movements (for example, when playing the piano). The neurons of the anterior horn that innervate large muscles (for example, the gluteus maximus) can individually cause hundreds of muscle cells to contract at once, since these muscles are responsible for gross and simple movements.

The unique property of these corticomoneuronal fibers of the lateral corticospinal tract is demonstrated by the concept of "fractionation" referring to the variable activity of interneurons, whereby small groups of neurons can be selectively activated to perform a specific general function. This is easily shown in the index finger, which can be flexed or extended regardless of the position of the other fingers (although three of its long tendons have a common origin with the muscle beds of all four fingers).

Fractionation is of great importance when performing habitual movements, such as buttoning up a coat or tying shoelaces. Traumatic or other damage to the cortical motor neuron system at any level entails the loss of the skills to perform habitual movements, which are then rarely recoverable.

When performing these movements, α- and γ-motoneurons are activated together through the lateral cortical-spinal pathway in such a way that the spindles of the muscles primarily involved in the movement send impulses about active stretching, and the spindles of antagonist muscles - about passive stretching.


medulla oblongata and upper divisions spinal cord, front view.
Three groups of nerve fibers of the left pyramid are shown.

b) Renshaw Cells. The functions of the synapses of the lateral cortical-spinal tract on Renshaw cells are quite numerous, since inhibition on some cell synapses mainly occurs due to type Ia interneurons; on other synapses, this function is performed by Renshaw cells. Probably the most important function- control of the joint contraction of the main moving muscles and their antagonists to fix one or more joints, for example, when working with kitchen knife or a shovel. Joint contraction occurs due to the inactivation of inhibitory Ia interneurons by Renshaw cells.

V) Excitatory interneurons. The lateral cortical-spinal pathway influences the activity of motor neurons located in the middle part of the gray matter and at the base of the anterior horn of the spinal cord, innervating the axial (vertebral) muscles and muscles of the proximal limbs through excitatory interneurons. d) la-inhibiting interneurons. These neurons are also located in the middle part of the gray matter of the spinal cord and are activated by the lateral corticospinal tract, primarily during voluntary movements.

The activity of Ia-interneurons promotes relaxation of antagonist muscles before agonists begin to contract. In addition, they cause refractoriness of motor neurons of antagonist muscles to stimulation of the neuromuscular spindle by afferents when they are passively stretched during movement. Sequence of processes for arbitrary bending knee joint shown in the figure below.

(Note the terminology: in a relaxed standing position, the person's knees are "closed" in slight hyperextension, and the quadriceps femoris is inactive, as evidenced by the "free" position of the patella. When trying to bend one or both knees, the quadriceps femoris twitches in a response to passive stretching of dozens of muscle spindles in it.Since flexion is resisted in this way, the reflex is called a resistance reflex.

On the other hand, during voluntary flexion of the knee joint, the muscles contribute to this movement using the same mechanism, but through the help reflex. The change in sign from negative to positive is called the reversal reflex.)

e) Presynaptic inhibitory neurons that mediate the stretch reflex. Consider the movements of the sprinter. With each step, gravity pulls his body down onto the straightened quadriceps knee. At the moment of contact with the ground, all neuromuscular spindles in the contracted quadriceps muscle are sharply stretched, as a result of which there is a danger of rupture of the muscle. The Golgi tendon organ provides some protection through internal inhibition, but the main defense mechanism provides a lateral cortical-spinal pathway through presynaptic inhibition of spindle afferents near their contact with motor neurons.

At the same time, the lengthening of the pause to the Achilles reflex serves as an advantage in this situation, since the motor neurons that innervate the back of the leg are restored for the next jerk. It is assumed that the degree of suppression of the stretch reflex from the side of the lateral cortical-spinal tract depends on the specific movements.

e) Presynaptic inhibition of first-order sensory neurons. In the posterior horn of the gray matter of the spinal cord, there is some suppression of the transmission of sensory impulses to the spinothalamic pathway during voluntary movements. It does this by activating synapses formed by inhibitory interneurons and primary sensory nerve endings.

Even finer regulation is observed at the level of the subtle and wedge-shaped nuclei, where the fibers of the pyramidal tract (after crossing) are able to increase the transmission of sensitive impulses during slow, accurate movements or weaken it during fast movements.


The sequence of events when performing a voluntary movement (knee flexion). MN - motor neurons.
(1) Activation of la interneurons inhibits their α-motoneuron antagonists.
(2) Activation of α- and γ-motoneuron agonists.
(3) Activation of extrafusal and intrafusal muscle fibers.
(4) Impulse from actively stretched neuromuscular spindles increases the activity of the a-motoneuron agonist and reduces the activity of its antagonists.
(5) Ia fibers from passively stretched antagonist neuromuscular spindles are sent to the corresponding refractory a-motoneurons.
Note that the sequence "γ-motor neuron-Ia-fiber-α-motor neuron" forms a γ-loop.

Video lesson anatomy of the pyramidal tract - tractus corticospinalis et corticonuclearis

pyramid system- this is a system of efferent neurons, the bodies of which are located in the cerebral cortex, terminate in the motor nuclei of the cranial nerves and the gray matter of the spinal cord. As part of the pyramidal path (tractus pyramidalis), cortical-nuclear fibers (fibrae corticonucleares) and cortical-spinal fibers (fibrae corticospinales) are isolated. Both those and others are axons of nerve cells of the inner, pyramidal, layer of the cerebral cortex.

They are located in the precentral gyrus and adjacent fields of the frontal and parietal lobes. In the precentral gyrus, the primary motor field is localized, where pyramidal neurons are located that control individual muscles and muscle groups. In this gyrus there is a somatotopic representation of the musculature.

The neurons that control the muscles of the pharynx, tongue and head occupy the lower part of the gyrus; above are areas associated with the muscles of the upper limb and trunk; 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 pathway is formed mainly by thin nerve fibers that pass through the white matter of the hemisphere and converge to the internal capsule.
Cortical-nuclear fibers form the knee, and cortical-spinal fibers form the anterior 2/3 of the posterior leg of the internal capsule. From here, the pyramidal pathway continues into the base of the brain stem and further into the anterior part of the pons.

Throughout the brainstem, the cortical-nuclear fibers pass to the opposite side to the dorsolateral areas of the reticular formation, where they switch to the motor nuclei III, IV, V, VI, VII, IX, X, XI, XII of the cranial nerves; only to the upper third of the nucleus facial nerve uncrossed fibers. Part of the fibers of the pyramidal pathway passes from the brain stem to the cerebellum.

In the medulla oblongata, the pyramidal path is located in the pyramids, which form a cross (decussatio pyramidum) on the border with the spinal cord. Above the decussation, the pyramidal pathway contains 700,000 to 1,300,000 nerve fibers on one side. As a result of crossing, 80% of the fibers pass to the opposite side and form a lateral cortical-spinal (pyramidal) path in the lateral funiculus of the spinal cord.
Non-crossed fibers from the medulla oblongata continue into the anterior funiculus of the spinal cord in the form of an anterior cortical-spinal (pyramidal) pathway. The fibers of this path pass to the opposite side throughout the spinal cord in its white commissure (segmentally).

Most of the cortical-spinal fibers terminate in the intermediate gray matter of the spinal cord on its intercalary neurons, only a part of them form synapses directly with the motor neurons of the anterior horns, which give rise to the motor fibers of the spinal nerves. About 55% of the cortical-spinal 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. Due to the intersection of fibers in the pyramidal system, the left hemisphere of 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, however, the muscles of the trunk and upper third of the face receive fibers of the pyramidal pathway from both hemispheres.

The function of the pyramidal system is to perceive the program of voluntary movement and conduct the impulses of this program to the segmental apparatus of the brainstem and spinal cord.

In clinical practice, the state of the pyramidal system is determined by the nature of voluntary movements.
The range of motion and the force of contraction of the striated muscles are assessed according to a six-point system (full muscle strength - 5 points, "compliance" of 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, the safety of movement with a barely noticeable muscle contraction - 1 point and the absence of voluntary movement - 0).

The strength of muscle contraction can be quantitatively assessed using a dynamometer. To assess the safety of the pyramidal cortical-nuclear pathway to the motor nuclei of the cranial nerves, tests are used that determine the function of the muscles of the head and neck innervated by these nuclei, the corticospinal tract - in the study of the muscles of the trunk and limbs. The defeat of the pyramidal system is also judged by the state of muscle tone and muscle trophism.

Pathology:

Dysfunctions of the pyramidal system are observed in many pathological processes.
In the neurons of the pyramidal system and their long axons, metabolic disturbances often occur, which lead to degenerative-dystrophic changes in these structures. Violations are genetically determined or are the result of intoxication (endogenous, exogenous), as well as viral damage to the genetic apparatus of neurons.

Degeneration is characterized by a gradual, symmetrical and progressive dysfunction of pyramidal neurons, primarily those with the longest axons, i.e. ending at the peripheral motor neurons of the lumbar thickening. Therefore, pyramidal insufficiency in such cases is first detected in the lower extremities. This group of diseases includes Strümpell's familial spastic paraplegia, portocaval encephalomyelopathy, funicular myelosis, and Mills syndrome - unilateral ascending paralysis of unclear etiology.

It usually begins at the age of 35-40 to 60 years with central paresis of the distal parts of the lower limb, which gradually spreads to the proximal parts of the lower, and then to the entire upper limb and turns into spastic hemiplegia with autonomic and trophic disorders in the paralyzed limbs.

The pyramidal system is often affected by slow viral infections, such as amyotrophic lateral sclerosis, multiple sclerosis, etc. Almost always, in the clinical picture of focal lesions of the brain and spinal cord, there are signs of dysfunction of the pyramidal system. With vascular lesions of the brain (hemorrhage, ischemia), pyramidal disorders develop acutely or subacutely with progression in chronic cerebrovascular insufficiency. The pyramidal system can be involved in the pathological process in encephalitis and myelitis, in traumatic brain injury and spinal cord injury, in tumors of the central nervous system, etc.

When the pyramidal system is damaged, central paresis 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, Yakobson - Lask, Bekhterev, Zhukovsky, Hoffmann, on the legs - Babinsky, Oppenheim, Chaddock, Rossolimo, Bekhterev, etc.

Juster's symptom is characteristic of pyramidal insufficiency: a pin prick of the skin in the area of ​​​​the eminence of the thumb causes the thumb to flex and bring it to the index finger while simultaneously extending the remaining fingers and dorsiflexing the hand and forearm. Quite often, a symptom of a folding knife is revealed: with passive extension of the spastic upper limb and flexion of the lower limb, the examiner first experiences a sharp springy resistance, which then suddenly weakens. With the defeat of the pyramidal system, global, coordinating and imitation synkinesis are often noted.

To detect mild paresis, special tests are used: the Venderovich motor ulnar reflex (the ability to take the little finger away from the ring finger when it is pinched), the Barre test (with closed eyes raise up and fix both hands with palms inward with spread fingers; on the side of pyramidal insufficiency, the arm gets tired faster, lowers and bends at the elbow and wrist joints), etc.

Depending on the localization of the pathological focus and its size, there are various options clinical picture of dysfunction of the pyramidal system. With damage to the cortex of the precentral gyrus, spastic monoplegia develops - paralysis of one upper or lower limb, hand or foot, or even individual fingers. Perhaps an isolated lesion of pyramidal neurons associated with the nuclei of the facial and hypoglossal nerves. At the same time, central paralysis (paresis) of the mimic muscles of the lower part of the face, which has unilateral supranuclear innervation, and the muscles of one half of the tongue develops. With an extensive cortical focus on the outer surface of the precentral gyrus, faciolinguobrachial paralysis develops. When intact neurons are irritated, paroxysms of Jacksonian epilepsy or Kozhevnikov epilepsy occur.

Most often the pyramidal system is affected at the level of the internal capsule. At the same time, spastic paralysis of the limbs develops on the side opposite to the pathological focus. Such capsular hemiplegia is characterized by a complete loss of voluntary movements in the distal parts of the limbs (in the hand and foot), the Wernicke-Mann position is typical: the arm is bent at the elbow, wrist and interphalangeal joints, brought to the body, the thigh and lower leg are unbent, the foot is in the position of the plantar flexed and turned inward. When walking, the paretic leg is carried forward, describing a semicircle (the so-called squinting gait). Spasticity, and then contracture of paralyzed muscles, arise as a result of simultaneous damage to the axons of the pyramidal and extrapyramidal systems in the internal capsule.

The destruction of the pyramidal system at the level of the brain stem is manifested by various alternating syndromes: Weber (with damage to one leg of the brain), Fauville or Miyar-Gubler (with damage to half of the bridge of the brain), Avellis, Jackson (with damage to the medulla oblongata), etc.

With the destruction of the spinal cord above the cervical thickening, spastic tetraplegia develops, and below the cervical thickening (but above the lumbar thickening), spastic paraplegia develops. Bilateral damage to the cortical-nuclear tracts leads to pseudobulbar palsy(paresis), one half of the diameter of the spinal cord (right or left) - to the development of Brown-Séquard syndrome.

Diagnosis of lesions of the pyramidal system:

The diagnosis of damage to the pyramidal system is established on the basis of a study of the patient's movements and the identification of signs of pyramidal insufficiency (the presence of paresis or paralysis, increased muscle tone, increased deep reflexes, clonuses, pathological hand and foot signs), clinical course and results special studies(electroneuromyography, electroencephalography, tomography, etc.).

The differential diagnosis of pyramidal paralysis is carried out with peripheral paresis and paralysis, which develop with damage to peripheral motor neurons. The latter are characterized by malnutrition and atrophy of the paretic muscles, decreased muscle tone (hypo- and atony), weakening or absence of deep reflexes, changes in the electrical excitability of muscles and nerves (degeneration reaction). With the acute development of damage to the pyramidal system 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 state of diaschisis, after the elimination of which there is an increase in muscle tone and deep reflexes. At the same time, pyramidal signs (Babinski's symptom, etc.) are also detected against the background of signs of diaschisis.

Treatment of lesions of the pyramidal system:

Treatment of lesions of the pyramidal system is aimed at the underlying disease. Drugs are used that improve 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 of the group C, E. Exercise therapy, massage (point) and reflexotherapy are widely used to reduce muscle tone; physio- and balneotherapy, orthopedic measures. Neurosurgical treatment is performed for tumors and injuries of the brain and spinal cord, as well as for a number of acute cerebrovascular accidents (with thrombosis or stenosis of extracerebral arteries, intracerebral hematoma, malformations of cerebral vessels, etc.).