- This two-neuron pathway (2 neurons central and peripheral) , connecting the cerebral cortex with the skeletal (striated) muscles (corticomuscular path). The pyramidal path is a pyramidal system, the system that provides voluntary movements.

Central neuron

Central the neuron is located in the Y layer (layer of Betz's large pyramidal cells) of the anterior central gyrus, in the posterior sections of the superior and middle frontal gyri and in the paracentral lobule. There is a clear somatic distribution of these cells. The cells located in the upper part of the precentral gyrus and in the paracentral lobule innervate the lower limb and trunk, located in its middle part - the upper limb. In the lower part of this gyrus there are neurons that send impulses to the face, tongue, pharynx, larynx, and masticatory muscles.

The axons of these cells are in the form of two conductors:

1) corticospinal tract (otherwise called the pyramidal tract) - from the upper two-thirds of the anterior central gyrus

2) corticobulbar tract - from the lower part of the anterior central gyrus) go from the cortex deep into the hemispheres, pass through the internal capsule (the corticobulbar tract - in the knee area, and the corticospinal tract through the anterior two-thirds of the posterior thigh of the internal capsule).

Then the cerebral peduncles, pons, and medulla oblongata pass through, and at the border of the medulla oblongata and spinal cord, the corticospinal tract undergoes an incomplete decussation. The large, crossed part of the tract passes into the lateral column of the spinal cord and is called the main, or lateral, pyramidal fasciculus. The smaller uncrossed part passes into the anterior column of the spinal cord and is called the direct uncrossed fasciculus.

The fibers of the corticobulbar tract end in motor nuclei cranial nerves (Y, YII, IX, X, XI, XII ), and the fibers of the corticospinal tract - in anterior horns of the spinal cord . Moreover, the fibers of the corticobulbar tract undergo decussation sequentially as they approach the corresponding nuclei cranial nerves(“supranuclear” decussation). For the oculomotor, masticatory muscles, muscles of the pharynx, larynx, neck, trunk and perineum, there is bilateral cortical innervation, i.e., fibers of central motor neurons approach part of the motor nuclei of the cranial nerves and some levels of the anterior horns of the spinal cord not only from the opposite side, but also with one’s own, thus ensuring the approach of impulses from the cortex not only of the opposite, but also of one’s hemisphere. The limbs, tongue, and lower part of the facial muscles have unilateral (only from the opposite hemisphere) innervation. The axons of the motor neurons of the spinal cord are directed to the corresponding muscles as part of the anterior roots, then the spinal nerves, plexuses and, finally, the peripheral nerve trunks.

Peripheral neuron

Peripheral neuron starts from the places where the first one ended: the fibers of the cortic-bulbar tract ended at the nuclei of the cranial nerve, which means they go as part of the cranial nerve, and the corticospinal tract ended in the anterior horns of the spinal cord, which means it goes as part of the anterior roots of the spinal nerves, then peripheral nerves, reaching the synapse.

Central and peripheral paralysis develop with neuron damage of the same name.

Exam questions:

1.5. Pyramidal tract (central motor neuron): anatomy, physiology, symptoms of damage.

1.6. Peripheral motor neuron: anatomy, physiology, symptoms of damage.

1.15. Cortical innervation of the motor nuclei of cranial nerves. Symptoms of damage.

Practical skills:

1. Taking anamnesis in patients with diseases of the nervous system.

2. Study of muscle tone and assessment of motor disorders in the patient.

Reflex-motor sphere: general concepts

1. Terminology:

- Reflex- - the body’s reaction to a stimulus, realized with the participation of the nervous system.

- Tone- reflex muscle tension, ensuring the preservation of posture and balance, preparation for movement.

2. Classification of reflexes

- By origin:

1) unconditional (constantly occurring in individuals of a given species and age with adequate stimulation of certain receptors);

2) conditional (acquired during an individual’s life).

- By type of stimulus and receptor:

1) exteroceptive(touch, temperature, light, sound, smell),

2) proprioceptor(deep) are divided into tendon, which arise when muscles are stretched, and tonic, to maintain the position of the body and its parts in space.

3) interoreceptor.

- By arc closure level:spinal; stem; cerebellar; subcortical; cortical.

- By effect caused: motor; vegetative.

3. Types of motor neurons:

- Alpha large motor neurons- performing fast (phasic) movements (from the motor cortex);

- Alpha small motor neurons- maintaining muscle tone (from the extrapyramidal system), are the first link of the gamma loop;

- Gamma motor neurons- maintaining muscle tone (from muscle spindle receptors), are the last link of the gamma loop - participate in the formation of the tonic reflex.

4. Types of proprioceptors:

- Muscle spindles- consist of intrafusal muscle fiber(similar to embryonic fibers) and receptor apparatus, are excited when muscles relax (passively lengthen) and are inhibited when they contract(parallel activation with muscle) :

1) phasic (1 type of receptors - annulo-spiral, “core-chain”), activated in response to sudden lengthening of the muscle - the basis of tendon reflexes,

2) tonic (type 2 receptors - grape-shaped, “bursa-nuclei”), activated in response to slow lengthening of the muscle - the basis for maintaining muscle tone.

- Golgi receptors- afferent fiber located among the connective tissue fibers of the tendon - Excited when the muscle is tense and inhibited when it relaxes(sequential activation with the muscle) - inhibits overstretching of the muscle.

Reflex-motor sphere: morphophysiology

1. General features of two-neuron pathways for movement implementation

- First neuron (central) is located in the cerebral cortex (precentral gyrus).

- Axons of the first neurons cross over to the opposite side.

- Second neuron (peripheral) is located in the anterior horns of the spinal cord or in the motor nuclei of the brainstem (alpha major)

2. Corticospinal (pyramidal) tract

Pair and precentral lobules, posterior sections of the superior and middle frontal gyrus (body I - Betz cells of layer V of the cerebral cortex) - corona radiata - anterior two-thirds of the posterior limb of the internal capsule - base of the brain (cerebral peduncles) - incomplete decussation at the border of the medulla oblongata and spinal cord: crossed fibers (80%) - in the lateral cords of the spinal cord(to alpha major motor neurons of limb muscles) , uncrossed fibers (Turk's bundle, 20%) - in the anterior cords of the spinal cord (to the alpha large motor neurons of the axial muscles).

- Nuclei of the anterior horn of the spinal cord(body II, alpha large motor neurons) of the opposite side - anterior roots - spinal nerves - nerve plexuses - peripheral nerves - skeletal (striated) muscles.

3. Spinalmuscle innervation (Forster):

- Cervical level (C): 1-3 - small muscles of the neck; 4 - rhomboid and diaphragmatic muscles; 5 - mm.supraspinatus, infraspinatus, teres minor, deltoideus, biceps, brachialis, supinator brevis et longis; 6 - mm.serratus anterior, subscapullaris, pectoris major et minor, latissimus dorsi, teres major, pronator teres; 7 - mm.extensor carpi radialis, ext.digitalis communis, triceps, flexor carpi radialis et ulnaris; 8 - mm.extensor carpi ulnaris, abductor pollicis longus, extensor pollicis longus, palmaris longus, flexor digitalis superficialis et profundus, flexor pollicis brevis;

- Thoracic level (Th): 1 - mm.extensor pollicis brevis, adductor pollicis, flexor pollicis brevis intraosseii; 6-7 - pars superior m.rectus abdominis; 8-10 - pars inferior m.rectus abdominis; 8-12 - oblique and transverse abdominal muscles;

- Lumbar level (L): 1 - m.Illiopsoas; 2 - m.sartorius; 2-3 - m.gracillis; 3-4 - hip adductors; 2-4 - m.quadroiceps; 4 - m.fasciae latae, tibialis anterior, tibialis posterior, gluteus medius; 5 - mm.extensor digitorum, ext.hallucis, peroneus brevis et longus, quadratus femorris, obturatorius internus, piriformis, biceps femoris, extensor digitorum et hallucis;

- Sacral level (S): 1-2 - calf muscles, flexors of fingers and thumb; 3 - muscles of the sole, 4-5 - muscles of the perineum.

4. Corticonuclear pathway

- Anterior central gyrus(lower part) (body I - Betz cells of layer V of the cerebral cortex) - corona radiata - knee of the internal capsule - base of the brain (cerebral peduncles) - cross directly above the corresponding nuclei ( incomplete- bilateral innervation for III, IV, V, VI, upper ½ VII, IX, X, XI cranial nerves; full- unilateral innervation for the lower ½ VII and XII cranial nerves - rule 1.5 cores).

- Cranial nerve nuclei(body II, alpha large motor neurons) of the same and/or opposite side - cranial nerves - skeletal (striated) muscles.

5. Reflexarcs of basic reflexes:

- Tendon and periosteal(place and method of evocation, afferent part, level of closure, efferent part, effect) :

1) Superciliary- percussion of the brow ridge - - [ trunk] - - closing the eyelids;

2) Mandibular(Bekhterev) - chin percussion - - [ trunk] - - closing of the jaws;

3) Carporadial- from the styloid process of the radius - - [ C5-C8] - - flexion at the elbow joint and pronation of the forearm;

4) Bicipital- from the biceps tendon - - [ C5-C6] - - flexion at the elbow joint;

5) Tricipital- from the triceps tendon - - [ C7-C8] - - extension at the elbow joint;

6) Knee- with ligamentum patellae - - - [ n.femoralis] - extension in the knee joint;

7) Achilles- from the tendon of the gastrocnemius muscle - - [ S1-S2] - - plantar flexion of the foot.

- Tonic postural reflexes(regulate muscle tone depending on the position of the head):

1) Cervical,

2) Labyrinth;

- From the skin and mucous membranes(Same) :

1) Corneal (corneal)- from the cornea of ​​the eye - - [ trunk

2) Conjunctival- from the conjunctiva of the eye - - [ trunk] - - closing the eyelids;

3) Pharyngeal (palatal)- from the back wall of the pharynx (soft palate) - - [ trunk] - - act of swallowing;

4) Abdominal upper- line irritation of the skin parallel to the costal arch in the direction from the outside to the inside - - [ Th7-Th8

5) Abdominal middle - line irritation of the skin perpendicular to the midline in the direction from outside to inside - - [ Th9-Th10] - - contraction of the abdominal muscle;

6) Abdominal lower- line irritation of the skin parallel to the inguinal fold in the direction from the outside to the inside - - [ Th11-Th12] - - contraction of the abdominal muscle;

7) Cremasteric- line irritation of the skin of the inner thigh in the direction from bottom to top - - [ L1-L2] - - raising the testicle;

8) Plantar- streak irritation of the skin of the outer plantar surface of the foot - - [ L5-S1] - - flexion of the toes;

9) Anal (superficial and deep)- streak irritation of the skin of the perianal zone - - [ S4-S5] - - contraction of the anal sphincter

- Vegetative:

1) Pupillary reflex- eye lighting - [ retina (I and II body) - n.opticus - chiasm - tractus opticus ] - [ lateral geniculate body (III body) - superior colliculus of the quadrigeminal (IV body) - Yakubovich-Edinger-Westphal nucleus (V body) ] - [ n.oculomotorius (preganglionic) - gang.ciliare (VI body) - n.oculomotorius (postganglionic) - sphincter of the pupil ]

2) Reflex for accommodation and convergence- tension of the internal rectus muscles - [ same way ] - miosis (direct and friendly reaction);

3) Cervical-heart(Chermak) - see Autonomic nervous system;

4) Ocular-heart(Danyini-Aschner) - see Autonomic nervous system.

6. Peripheral mechanisms for maintaining muscle tone (gamma loop)

- Tonogenic formations of the brain(red nuclei, vestibular nuclei, reticular formation) - rubrospinal, vestibulospinal, reticulospinal tract [inhibitory or excitatory effect]

- gamma neuron(anterior horns of the spinal cord) [intrinsic rhythmic activity] - gamma fiber as part of the anterior roots and nerves

Muscular part of intrafusal fiber - nuclear chains (static, tonic) or nuclear bags (dynamic)

Annulospiral endings - sensory neuron(dorsal ganglion)

- alpha small motor neuron

Extrafusal fibers (contraction).

7. Regulationpelvic organs

- Bladder:

1) parasympathetic center(S2-S4) - contraction of the detrusor, relaxation of the internal sphincter (n.splanchnicus inferior - inferior mesenteric ganglion),

2) sympathetic center(Th12-L2) - contraction of the internal sphincter (n.splanchnicus pelvinus),

3) arbitrary center(sensitive - gyrus of the fornix, motor - paracentral lobule) at the level of S2-S4 (n.pudendus) - contraction of the external sphincter,

4) arc of automatic urination- proprioceptors tensile- spinal ganglia - dorsal roots S2-S4 - parasympathetic center is activated(detrusor contraction) and sympathetic tomositis (relaxation of the internal sphincter) - proprioceptors from the walls of the urethra in the area of ​​the external sphincter- deep sensitivity to the gyrus of the fornix - paracentral lobule - pyramid path(relaxation of the external sphincter) ,

5) defeat - central paralysis(acute urinary retention - periodic incontinence (automatism of MP), or imperative urges), paradoxical ischuria(MP is full, drop by drop due to overstretching of the sphincter), peripheral paralysis(denervation of the sphincters - true urinary incontinence).

- Rectum:

1) parasympathetic center(S2-S4) - increased peristalsis, relaxation of the internal sphincter (n.splanchnicus inferior - inferior mesenteric ganglion),

2) sympathetic center(Th12-L2) - inhibition of peristalsis, contraction of the internal sphincter (n.splanchnicus pelvinus),

3) arbitrary center(sensitive - gyrus of the fornix, motor - paracentral lobule) at the level of S2-S4 (n.pudendus) - contraction of the external sphincter + abdominal muscles,

4) arc of automatic defecation- see MP ,

5) defeat- see MP.

- Genital organs:

1) parasympathetic center(S2-S4) - erection (nn.pudendi),

2) sympathetic center(Th12-L2) - ejaculation (n.splanchnicus pelvinus),

3) automatic arc;)

4) defeat - central neuron- impotence (may be reflex priapism and involuntary ejaculation), peripheral- persistent impotence.

Reflex-motor sphere: research methods

1. Rules for studying the reflex-motor sphere:

Grade subjective the patient’s sensations (weakness, awkwardness in the limbs, etc.),

At objective the study is being assessed absolute[muscle strength, magnitude of reflexes, severity of muscle tone] and relative indicators[symmetry of strength, tone, reflexes (anisoreflexia)].

2. Range of active and passive movements in the main joints

3. Muscle strength study

- Voluntary, active muscle resistance(by volume of active movements, dynamometer and level of resistance to external force on a six-point scale): 5 - complete preservation of motor function, 4 - slight decrease in muscle strength, compliance, 3 - active movements in full in the presence of gravity, the weight of the limb or its segment overcomes, but there is pronounced compliance, 2 - active movements in full while eliminating gravity, 1 - preservation of movement, 0 - complete lack of movement. Paralysis- lack of movement (0 points), paresis- decrease in muscle strength (4 - mild, 3 - moderate, 1-2 - deep).

- Muscle groups(check groups by system ISCSCI with corr.) :

1) proximal group of the hand:

1) raising your arm to the horizontal

2) raising the arm above the horizontal;

2) shoulder muscle group:

1) flexion at the elbow joint

2) extension in the elbow joint ;

3) muscle group of the hand:

1) flexion of the hand

2) extension brushes ,

3) flexion of the distal phalanx III finger ,

4) lead V finger ;

4) proximal leg group:

1) hip flexion ,

2) hip extension,

3) hip abduction;

5) groupmusclesshins:

1) flexion of the lower leg,

2) extension shins ;

6) groupmusclesfeet:

1) rear bending feet ,

2) extension big finger ,

3) plantar bending feet ,

- Correspondence level of spinal cord damage and loss of movements:

1) cervical thickening

1) C5 - flexion at the elbow joint

2) C6 - wrist extension,

3) C7 - extension at the elbow joint;

4) C8 - flexion of the distal phalanx of the third finger

5) Th1 - abduction of the first finger

2) lumbar thickening

1) L2 - hip flexion

2) L3 - leg extension

3) L4 - dorsiflexion of the foot

4) L5 - thumb extension

5) S1 - plantar flexion of the foot

- Tests for hidden paresis:

1) upper Barre sample(straight arms in front of you, slightly above the horizontal - the weak hand “sinks”, i.e. falls below the horizontal),

2) Mingazzini test(similar, but the hands are in a supinated position - the weak hand “sinks”)

3) Panchenko test(arms above your head, palms facing each other - the weak hand “sinks”),

4) lower Barre sample(on the stomach, legs bent at the knee joints 45 degrees - the weak leg “sinks”),

5) Davidenkov's symptom(symptom of the ring, keeping the ring from “breaking” between the index and thumb - muscle weakness leads to low resistance to “breaking” the ring),

6) Venderovich's symptom(holding the little finger while trying to move it away from the fourth finger of the hand - muscle weakness leads to easy abduction of the little finger).

4. Study of reflexes

- Tendon reflexes: carporadial, bicipital, tricipital, knee, Achilles.

- Reflexes from the surface of the skin and mucous membranes: corneal, pharyngeal, upper, middle, lower abdominal, plantar.

5. Study of muscle tone - involuntary muscle resistance is assessed during passive movements in the joints with maximum voluntary relaxation:

Flexion-extension in the elbow joint (tone of the squeezers and extensors of the forearm);

Pronation-supination of the forearm (tone of the pronators and supinators of the forearm);

Flexion-extension in the knee joint (tone of the quadriceps and hamstrings, gluteal muscles, etc.).

6. Change in gait (a set of features of posture and movements when walking).

- Steppage(French “steppage” - trotting, peroneal gait, rooster gait, stork) - high raising of the leg with throwing it forward and sharp lowering - with peripheral paresis of the peroneal muscle group.

- Duck gait- rolling the body from side to side - with paresis of the deep muscles of the pelvic pelvis and hip flexors.

- Hemiplegic gait(mowing, mowing, circumducing) - excessive abduction of the paretic leg to the side, as a result of which it describes a semicircle with each step; in this case, the paretic arm is bent at the elbow and brought to the body - Wernicke-Mann position - with hemiplegia.

Reflex-motor sphere: symptoms of damage

1. Symptoms of loss

- Peripheral paralysis develops when a peripheral motor neuron is damaged in any area, the symptoms are caused by a weakening of the level of segmental reflex activity:

1) decreased muscle strength,

2) muscle areflexia(hyporeflexia) - reduction or complete absence of deep and superficial reflexes.

3) muscle atony- decreased muscle tone,

4) muscle atrophy- decrease in muscle mass,

+ fibrillary or fascicular twitching(symptom of irritation) - spontaneous contractions of muscle fibers (fibrillar) or groups of muscle fibers (fascicular) - a specific sign of damage body peripheral neuron.

- Central paralysis (unilateral lesion of the pyramidal tract) develops when the central motor neuron is damaged in any area, the symptoms are caused by an increase in the level of segmental reflex activity:

1) decreased muscle strength,

2) hyperreflexia of tendon reflexes with expansion of reflexogenic zones.

3) reduction or absence of superficial (abdominal, cremasteric and plantar) reflexes

4) clonus feet, hands and kneecaps - rhythmic muscle contractions in response to stretching of the tendons.

5) pathological reflexes:

- Foot flexion reflexes- reflex flexion of the toes:

- Rossolimo- a short jerky blow to the tips of the 2-5 toes,

- Zhukovsky- a short jerky blow with a hammer in the middle of the patient’s foot,

- Goffman- pinching irritation of the nail phalanx of the II or III toes,

- Bekhtereva- a short jerky blow with a hammer on the back of the foot in the area of ​​4-5 metatarsals,

- Bekhterev calcaneal- a short, jerky blow to the heel with a hammer.

- Foot extensor reflexes- appearance of extension of the big toe and fan-shaped divergence of 2-5 toes:

- Babinsky- moving the handle of the hammer along the outer edge of the foot,

- Oppenheim- running along the anterior edge of the tibia,

- Gordon- compression of the calf muscles,

- Schaeffer- compression of the Achilles tendon,

- Chaddock- streak irritation around the outer ankle,

- Carpal analogues of flexion reflexes- reflex flexion of the fingers (thumb):

- Rossolimo- a jerky blow to the tips of the 2-5 fingers of the hand in a pronated position,

- Goffman- pinching irritation of the nail phalanx of the II or III fingers of the hand (1), IV or V fingers of the hand (2),

- Zhukovsky- a short jerky blow with a hammer in the middle of the patient’s palm,

- Bekhtereva- a short jerky blow with a hammer on the back of the hand,

- Galanta- a short jerky blow with a hammer on the tenar,

- Jacobson-Lask- a short jerky blow with a hammer on the styloid process.

6) protective reflexes: Bekhterev-Marie-Foy- with sharp painful flexion of the toes, “triple flexion” of the leg occurs (in the hip, knee and ankle joints).

7) muscle hypertension - increased muscle tone of the spastic type (the “jackknife” symptom is determined - when passively extending a bent limb, resistance is felt only at the beginning of the movement), development of contractures, Wernicke-Mann pose(arm flexion, leg extension)

8) pathological synkinesis- involuntary friendly movements that accompany the performance of active actions ( physiological- swinging arms while walking, pathological- arise in a paralyzed limb due to the loss of the inhibitory influences of the cortex on intraspinal automatisms:

- global- change in the tone of the injured limbs in response to prolonged muscle tension on the healthy side (sneezing, laughing, coughing) - shortening in the arm (flexion of the fingers and forearm, shoulder abduction), lengthening in the leg (hip adduction, shin extension, foot flexion),

- coordinator- involuntary contractions of paretic muscles with voluntary contraction of the muscles functionally associated with them (Strumpel's tibial phenomenon - dorsiflexion is impossible, but appears when bending the knee joint; Raymist's symptom - does not adduct the leg at the hip, but when the healthy leg is adducted, movement occurs in the paretic one; Babinski phenomenon - standing up without the help of hands - a healthy and paretic leg rises),

- imitation- involuntary movements of a paretic limb, imitating volitional movements of a healthy one.

- Central paralysis (bilateral damage to the pyramidal tract):

+ dysfunction of the pelvic organs of the central type- acute urinary retention when the pyramidal tract is damaged, followed by periodic urinary incontinence (reflex emptying of the bladder during overdistension), accompanied by an imperative urge to urinate.

- Central palsy (unilateral damage to the corticonuclear pathway): according to the rule of 1.5 nuclei, only the lower ½ nucleus of the facial nerve and the nucleus of the hypoglossal nerve have unilateral cortical innervation:

1) smoothness of the nasolabial fold and drooping of the corner of the mouth on the side opposite to the lesion,

2) tongue deviation in the direction opposite to the lesion (deviation is always towards the weak muscles).

- Central palsy (bilateral damage to the corticonuclear pathway):

1) decreased muscle strength muscles of the pharynx, larynx, tongue (dysphagia, dysphonia, dysarthria);

2) strengthening of the chin reflex;

3) pathological reflexes = oral automatism reflexes:

- Sucking(Oppenheim) - sucking movements with line irritation of the lips,

- Proboscis- hitting the upper lip with a hammer causes the lips to be pulled forward or the orbicularis oris muscle to contract,

- Nasolabial(Astvatsaturova) - a blow with a hammer to the back of the nose causes the lips to be pulled forward or the orbicularis oris muscle to contract,

- Distance-oral(Karchikyan) - bringing the hammer to the lips causes the lips to be pulled forward,

- Palmomental(Marinescu-Radovici) - line irritation of the thenar skin causes contraction of the mental muscle on the same side.

2. Symptoms of irritation

- Jacksonian epilepsy - paroxysmal clonic spasms of individual muscle groups, with possible spread and secondary generalization (most often from the thumb (maximum zone of representation in the precentral gyrus) - other fingers - hand - upper limb - face - whole body = Jacksonian march)

- Kozhevnikovskaya epilepsy (epilepsypartialiscontinua)- constant convulsions (myoclonus in combination with torsion dystonia, choreoathetosis) with periodic generalization (chronic tick-borne encephalitis)

Reflex-motor sphere: levels of damage

1. Levels of damage in central paralysis:

- Prefrontal cortex - area 6(monoparesis in the contralateral arm or leg, normal tone with rapid increase),

- Precentral gyrus - area 4(monoparesis in the contralateral arm or leg, low tone with long recovery, Jacksonian march - a symptom of irritation),

- Inner capsule(contralateral hemiparesis with damage to the corticonuclear tract, more pronounced in the arm, marked increase in muscle tone),

- Brain stem(contralateral hemiparesis in combination with lesions of the brain stem nuclei - alternating syndromes)

- Pyramid Crossing(complete lesion - tetraplegia, lesion of the external parts - alternating hemiplegia [contralateral paresis in the leg, ipsilateral paresis in the arm]),

- Lateral and anterior cord of the spinal cord(ipsilateral paralysis below the level of injury).

2. Levels of damage in peripheral paralysis:

- Procorneal(muscle paresis in the segment area + fasciculations).

- Koreshkovy(paresis of muscles in the area of ​​innervation of the root),

- Polyneuritic(muscle paresis in distal sections limbs),

- Mononeuritic(paresis of muscles in the area of ​​innervation of the nerve, plexus).

Differential diagnosis of motor syndromes

1. Central or mixed hemiparesis- muscle paralysis that has developed in the arm and leg on one side.

- suddenly developing or rapidly progressing:

1) Acute cerebrovascular accident (stroke)

2) Traumatic brain injury and trauma cervical region spine

3) Brain tumor (with pseudo-stroke course)

4) Encephalitis

5) Postictal state (after an epileptic seizure, Todd's palsy)

6) Multiple sclerosis

7) Migraine with aura (hemiplegic migraine)

8) Brain abscess;

- slowly progressive

1) Acute cerebrovascular accident (atherothrombotic stroke)

2) Brain tumor

3) Subacute and chronic subdural hematoma

4) Brain abscess;

5) Encephalitis

6) Multiple sclerosis

- required examination methods:

1) clinical minimum (OAC, OAM, ECG)

2) neuroimaging (MRI, CT)

3) electroencephalography

4) hemostasiogram / coagulogram

2. Lower spastic paraparesis- paralysis of the muscles of the lower extremities, symmetrical or almost symmetrical:

- spinal cord compression (combined with sensory disturbances)

1) Tumors of the spinal cord and cranio-vertebral junction

2) Spinal diseases (spondylitis, disc herniation)

3) Epidural abscess

4) Arnold-Chiari malformation

5) Syringomyelia

- hereditary diseases

1) Strumpel's familial spastic paraplegia

2) Spinocerebellar degenerations

- infectious diseases

1) Spirochetoses (neurosyphilis, neuroborreliosis)

2) Vacuolar myelopathy (AIDS)

3) Acute transverse myelitis (including post-vaccination)

4) Tropical spastic paraparesis

- autoimmune diseases

1) Multiple sclerosis

2) Systemic lupus erythematosus

3) Devic's optomyelitis

- vascular diseases

1) Lacunar conditions (occlusion of the anterior spinal artery)

2) Epidural hematoma

3) Cervical myelopathy

- other diseases

1) Funicular myelosis

2) Motor neuron disease

3) Radiation myelopathy

Reflex-motor sphere: characteristics of young children

1. Volume of active and passive movements:

Volume of active movements - by visual assessment: symmetry and completeness of range of motion

Range of passive movements - flexion and extension of limbs

2. Muscle strength- assessed by observing spontaneous activity and testing unconditioned reflexes.

3. Study of reflexes:

- Reflexes of “adults”- appear and are saved in the future:

1) from birth - knee, bicipital, anal

2) from 6 months - tricipital and abdominal (from the moment of sitting down)

- Reflexes " childhood» - present at birth and normally disappear by a certain age:

1) oral group of reflexes= oral automatism reflexes:

- Sucking- with line irritation of the lips - sucking movements (up to 12 months),

- Proboscis- touching the lips - pulling the lips forward (up to 3 months),

- Search engine(Kussmaul) - when stroking the corner of the mouth - turn the head in this direction and open the mouth slightly (up to 1.5 months)

- Palmo-oral(Babkina) - pressing on both palms - opening the mouth and slightly bringing the head to the chest (up to 2-3 months)

2) spinal group of reflexes:

- on the back:

- grasping(Robinson) - pressing on the palms - grasping the fingers (symmetry is important) (up to 2-3 months)

- grasping(Moro) - raising the arms with a sharp lowering (or hitting the table) - 1st phase: raising the arms - 2nd phase: clasping one’s own torso (up to 3-4 months)

- plantar- pressing on the foot - sharp plantar flexion of the toes (up to 3 months)

- Babinsky- irritation of the outer edge of the foot - fan-shaped extension of the toes (up to 24 months)

- cervical tonic symmetric reflex (CTSR)- flexion of the head - flexion in the arms and extension in the legs (up to 1.5-2.5 months)

- cervical tonic asymmetric reflex (ASTR, Magnus-Klein)- turning the head - straightening the arm and leg on the side of the turn, bending on the opposite side - “fencing pose” (visually disappears by 2 months, but when testing the tone, traces of it can be felt up to 6 months).

- on the stomach:

- protective- when lying on the stomach - turning the head to the side (up to 1.5-2 months), then it is replaced by voluntary holding of the head with the crown of the head up),

- labyrinthine tonic(LTR) - when positioned on the stomach - flexion of the arms and legs, then after 20-30 s swimming movements (up to 1-1.5 months),

- crawling(Bauer) - resting the feet in the palm of the researcher - extension of the leg (“crawling”) (up to 3 months),

- Galanta- line irritation paraventrally - flexion in the direction of irritation, flexion of the arm and leg on the same side (up to 3 months),

- Pereza- line irritation along the spinous processes from the coccyx to the neck - extension of the spine, elevation of the head and pelvis, movements of the limbs (up to 3 months),

- vertically:

- supports- feet on the table - 1st phase: withdrawal with flexion, 2nd phase: support on the table - straightens the legs, torso and slightly throws back the head, the researcher has a feeling of a “straightening spring” (up to 3 months, but only the “spring” phenomenon disappears, and the actual support on the foot does not disappear and subsequently becomes the basis for the formation of independent walking),

- automatic walking- when bending to the sides - phase 3: flexion/extension of the legs (“walking”) (up to 2 months).

3) chain symmetrical reflexes- steps towards verticalization:

- straightening from the body to the head- feet on support - straightening of the head (from 1 month to 1 year),

- cervical erector- turn the head - turn the body in the same direction (allows you to turn from back to side, from 2-3 months - up to 1 year)

- straightening the torso- the same, but with rotation between the shoulders and pelvis (allows you to roll over from back to side, from 5-6 months to 1 year)

- Upper Landau- in the position on the stomach - emphasis on the arms and raising the upper half of the body (from 3-4 months - to 6-7 months)

- Landau lower- the same + extension in the back in the form of strengthening of lumbar lordosis (from 5-6 months - to 8-9 months)

4. Muscle tone:

- Peculiarities: In children of the first year of life, the flexor tone is increased (“embryonic position”); the correct examination technique is important during the examination (comfortable ambient temperature, painless contact).

- Variants of pathological changes in tone in children:

1) opisthotonus- on the side, head thrown back, limbs straightened and tense,

2) “frog” pose(muscular hypotonia) - limbs in a state of extension and abduction, "seal feet"- drooping hands, "heel feet"- the toes are brought to the front surface of the shin.

3) “fencer” pose(central hemiparesis) - on the affected side - the arm is extended, internally rotated in the shoulder, pronated in the forearm, bent in the palm; on the opposite side - the arm and leg are bent.

4.1. Pyramid system

There are two main types of movements - involuntary and voluntary. 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 a pyramidal system consisting of two neurons - central and peripheral.

Central motor neuron. Voluntary muscle movements occur as a result of 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 tract.

The bodies of central motor neurons are located in the precentral gyrus in cytoarchitectonic areas 4 and 6 (Fig. 4.1). This narrow zone stretches along central slit from the lateral (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. The vast majority of motor neurons lie in the 5th cortical layer of area 4, although they are also found in adjacent cortical areas. Small pyramidal, or fusiform (spindle-shaped) cells predominate, providing the basis for 40% of the fibers of the pyramidal tract. Betz's giant pyramidal cells have axons with thick myelin sheaths that allow precise, well-coordinated movements.

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.

Rice. 4.1. Pyramid system (diagram).

A- Pyramidal tract: 1 - cerebral cortex; 2 - internal capsule; 3 - cerebral peduncle; 4 - bridge; 5 - intersection of pyramids; 6 - lateral corticospinal (pyramidal) tract; 7 - spinal cord; 8 - anterior corticospinal tract; 9 - peripheral nerve; III, VI, VII, IX, X, XI, XII - cranial nerves. B- Convexital surface of the cerebral cortex (fields 4 and 6); topographic projection of motor functions: 1 - leg; 2 - torso; 3 - hand; 4 - brush; 5 - face. IN- Horizontal section through the internal capsule, location of the main pathways: 6 - visual and auditory radiation; 7 - temporopontine fibers and parieto-occipital-pontine fascicle; 8 - thalamic fibers; 9 - corticospinal fibers to the lower limb; 10 - corticospinal fibers to the muscles of the trunk; 11 - corticospinal fibers to the upper limb; 12 - cortical-nuclear pathway; 13 - frontal-pontine tract; 14 - corticothalamic tract; 15 - anterior leg of the internal capsule; 16 - elbow of the internal capsule; 17 - posterior leg of the internal capsule. G- Anterior surface of the brain stem: 18 - decussation of pyramids

The axons of motor neurons form two descending pathways - the corticonuclear, heading to the nuclei of the cranial nerves, and the more powerful corticospinal tract, going to the anterior horns of the spinal cord. Fibers of the pyramidal tract, leaving the motor cortex, pass through the corona radiata white matter brain and converge to the internal capsule. In somatotopic order, they pass through the internal capsule (in the knee - the corticonuclear tract, in the anterior 2/3 of the posterior thigh - the corticospinal tract) and go in the middle part of the cerebral peduncles, descending through each half of the base of the bridge, being surrounded by numerous nerve cells of the nuclei bridge and fibers of various systems.

At the border of the medulla oblongata and the spinal cord, 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, forming the lateral pyramidal tract. The remaining fibers continue to descend in the homolateral anterior funiculi as part of the anterior pyramidal tract. In the cervical and thoracic sections of the spinal cord, its fibers connect with motor neurons, providing bilateral innervation to the muscles of the neck, torso, and respiratory muscles, due to which breathing remains intact even with severe unilateral damage.

The fibers that have passed to the opposite side 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 α- and γ-motoneurons of the anterior horn of the spinal cord.

The fibers forming the corticonuclear tract are directed to motor nuclei, located in the brain stem (V, VII, IX, X, XI, XII) cranial nerves, and provide motor innervation to the facial muscles. The motor nuclei of the cranial nerves are homologues of the anterior horns of the spinal cord.

Another bundle of fibers also deserves attention, starting in area 8, which provides cortical innervation of gaze, and not in the precentral gyrus. 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.

It should be borne in mind that only part of the fibers of the pyramidal tract constitutes an oligosynaptic two-neuron pathway. A significant part of the descending fibers forms polysynaptic pathways that carry information from various parts of the nervous system. Along with afferent fibers entering the spinal cord through the dorsal roots and carrying information from receptors, oligo- and polysynaptic fibers modulate the activity of motor neurons (Fig. 4.2, 4.3).

Peripheral motor neuron. The anterior horns of the spinal cord contain motor neurons - large and small a- and 7-cells. The neurons of the anterior horns are multipolar. Their dendrites have multiple synaptic

connections with various afferent and efferent systems.

Large α-cells with thick and rapidly conducting axons carry out rapid muscle contractions and are associated with giant cells of the cerebral cortex. Small a-cells with thinner axons perform a tonic function and receive information from the extrapyramidal system. 7-Cells with a thin and slowly conducting axon innervate proprioceptive muscle spindles, regulating their functional state. 7-Motoneurons are influenced by the descending pyramidal, reticular-spinal, and vestibulospinal tracts. The efferent influences of 7-fibers provide fine regulation of voluntary movements and the ability to regulate the strength of the receptor response to stretching (7-motoneuron-spindle system).

In addition to the motor neurons themselves, in the anterior horns of the spinal cord there is a system of interneurons that provide

Rice. 4.2. Conducting tracts of the spinal cord (diagram).

1 - wedge-shaped bundle; 2 - thin beam; 3 - posterior spinocerebellar tract; 4 - anterior spinocerebellar tract; 5 - lateral spinothalamic tract; 6 - dorsal tegmental tract; 7 - dorso-olive tract; 8 - anterior spinothalamic tract; 9 - anterior own bundles; 10 - anterior corticospinal tract; 11 - tegnospinal tract; 12 - vestibulospinal tract; 13 - olivo-spinal tract; 14 - red nuclear spinal tract; 15 - lateral corticospinal tract; 16 - rear own beams

Rice. 4.3. Topography of the white matter of the spinal cord (diagram). 1 - anterior cord: blue indicates the paths from the cervical, thoracic and lumbar segments, purple - from the sacral; 2 - lateral cord: blue indicates the paths from the cervical segments, blue - from the thoracic, purple - from the lumbar; 3 - posterior cord: blue indicates the paths from the cervical segments, blue - from the thoracic, dark blue - from the lumbar, purple - from the sacral

regulation of signal transmission from the upper parts of the central nervous system, peripheral receptors responsible for the interaction of adjacent segments of the spinal cord. Some of them have a facilitating effect, others have an inhibitory effect (Renshaw cells).

In the anterior horns, motor neurons form groups organized into columns in several segments. These columns have a certain somatotopic order (Fig. 4.4). In the cervical region, the laterally located motor neurons of the anterior horn innervate the hand and arm, and the motor neurons of the distal columns innervate the muscles of the neck and chest. In the lumbar region, motor neurons innervating the foot and leg are also located laterally, and those innervating the muscles of the trunk are medially.

The axons of motor neurons leave the spinal cord as part of the anterior roots, unite with the posterior roots, forming a common root, and, as part of the peripheral nerves, are directed to the striated muscles (Fig. 4.5). Well-myelinated, rapidly conducting axons of large α-cells extend directly to striated muscle, forming neuromuscular junctions, or end plates. The nerves also include efferent and afferent fibers emanating from the lateral horns of the spinal cord.

A skeletal muscle fiber is innervated by the axon of only one α-motoneuron, but each α-motoneuron can innervate a different number of skeletal muscle fibers. The number of muscle fibers innervated by one α-motoneuron depends on the nature of regulation: for example, in muscles with fine motor skills (for example, ocular, articular muscles), one α-motoneuron innervates only a few fibers, and in

Rice. 4.4. Topography of motor nuclei in the anterior horns of the spinal cord at the level of the cervical segment (diagram). On the left is the general distribution of anterior horn cells; on the right - nuclei: 1 - posteromedial; 2 - anteromedial; 3 - front; 4 - central; 5 - anterolateral; 6 - posterolateral; 7 - posterolateral; I - gamma efferent fibers from small cells of the anterior horns to the neuromuscular spindles; II - somatic efferent fibers, giving collaterals to medially located Renshaw cells; III - gelatinous substance

Rice. 4.5. Cross section of the spine and spinal cord (diagram). 1 - spinous process of the vertebra; 2 - synapse; 3 - skin receptor; 4 - afferent (sensitive) fibers; 5 - muscle; 6 - efferent (motor) fibers; 7 - vertebral body; 8 - node of the sympathetic trunk; 9 - spinal (sensitive) node; 10 - gray matter of the spinal cord; 11 - white matter of the spinal cord

muscles of the proximal limbs or in the rectus dorsi muscles, one α-motoneuron innervates thousands of fibers.

The α-motoneuron, its motor axon and all the muscle fibers innervated by it form the so-called motor unit, which is the main element of the motor act. Under physiological conditions, the discharge of an α-motoneuron leads to contraction of all muscle fibers of the motor unit.

The skeletal muscle fibers of one motor unit are called a muscle unit. All fibers of one muscle unit belong to the same histochemical type: I, IIB or IIA. Motor units that contract slowly and are resistant to fatigue are classified as slow (S - slow) and consist of type I fibers. Group S muscle units provide energy through oxidative metabolism and are characterized by weak contractions. motor units,

leading to fast phasic single muscle contractions, are divided into two groups: fast fatigue (FF - fastfatigable) and fast, fatigue-resistant (FR - fast fatigue resistant). The FF group contains type IIB muscle fibers with glycolytic energy metabolism and strong contractions but fatigue. The FR group includes type IIA muscle fibers with oxidative metabolism and high resistance to fatigue, and their contractile strength is intermediate.

In addition to large and small α-motoneurons, the anterior horns contain numerous 7-motoneurons - smaller cells with a soma diameter of up to 35 μm. The dendrites of γ-motoneurons are less branched and oriented predominantly in the transverse plane. 7-Motoneurons projecting to a specific muscle are located in the same motor nucleus as α-motoneurons. The thin, slow-conducting axon of γ-motoneurons innervates the intrafusal muscle fibers that make up the proprioceptors of the muscle spindle.

Large a-cells are associated with giant cells of the cerebral cortex. Small a-cells have a connection with the extrapyramidal system. The state of muscle proprioceptors is regulated through 7-cells. Among the various muscle receptors, the most important are the neuromuscular spindles.

Afferent fibers, called ring-spiral or primary endings, have a fairly thick myelin coating and are 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 along fast-conducting afferent fibers, and then again through 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. Tapping a muscle tendon causes it to stretch. 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 important when determining the location of the lesion.

Many muscle spindles have not only primary but also secondary endings. These endings also respond to stretch stimuli. Their action potential extends 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 counteract the force of gravity.

Both during voluntary effort and during reflex movement, the thinnest axons come into activity first. Their motor units generate very weak contractions, which allows fine regulation of the initial phase of muscle contraction. As motor units are recruited, α-motoneurons with increasingly larger diameter axons are gradually recruited, which is accompanied by an increase in muscle tension. The order of involvement of motor units corresponds to the order of increase in the diameter of their axon (the principle of proportionality).

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. To establish the nature and localization of motor disorders with clinically insignificant severe symptoms use electrophysiological methods.

The study of motor function begins with an examination of the muscles. Pay attention to atrophy or hypertrophy. By measuring the muscle circumference with a centimeter tape, you can assess the severity of trophic disorders. Sometimes fibrillar and fascicular twitching can be noticed.

Active movements are checked sequentially in all joints (Table 4.1) and are performed by the subject. They may be absent or limited in volume and weakened. The complete absence of active movements is called paralysis, or plegia, while limitation of the range of movements or a decrease in 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 - 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.

Table 4.1. Peripheral and segmental innervation of muscles

Continuation of Table 4.1.

Continuation of Table 4.1.

End of table 4.1.

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. The study of 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 i 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 is 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 forearm muscles, the patient is asked to bend his arm at the elbow joint, and the examiner tries to straighten it; The strength of the abductors and adductors of the shoulder is also assessed. To assess the strength of the forearm muscles, the patient is given the task

allowing you to perform pronation and supination, flexion and extension of the hand with resistance during the movement. To determine the strength of the finger muscles, the patient is asked to make a “ring” from the first finger and successively each of the others, and the examiner tries to break it. Strength is checked by moving the V finger away from the IV and bringing the other fingers together, while clenching the hand 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. To test the strength of the lower leg muscles, the patient is asked to bend the foot, and the examiner holds it straight; then they are given the task 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 determined when the examiner tries to bend and straighten the fingers and separately bend and straighten the i finger.

To identify paresis of the limbs, a Barre test is performed: the paretic arm, extended forward or raised upward, is gradually lowered, the leg raised above the bed is also gradually lowered, and the healthy one is held in its given position (Fig. 4.6). Mild paresis can be detected by testing the rhythm of active movements: the patient is asked to pronate and supinate his arms, clench his hands into fists and unclench them, move his legs, as when riding 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.

Muscle tone is a reflex muscle tension that ensures preparation for performing a movement, maintaining balance and posture, and the ability of a 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), which is caused by muscle stretching, i.e. irritation of proprioceptors and is determined by the nerve impulses that reach this muscle. Tonic reactions are based on a stretch reflex, the arc of which closes in the spinal cord. It is this tone that lies in

Rice. 4.6. Barre test.

A paretic leg descends faster

the basis of various tonic reactions, including anti-gravity ones, carried out under conditions of maintaining the connection between the muscles and the central nervous system.

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 and etc.

Muscle tone is assessed by feeling 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 rhythmic passive movements (flexors and extensors, adductors and abductors, pronators and supinators), performed with maximum relaxation of the subject. Hypotonia is a decrease in muscle tone, while atony is its absence. A decrease in muscle tone is accompanied by the appearance of Orshansky's symptom: when lifting upward (in a patient lying on his back) the leg straightened at the knee joint, it hyperextends in this joint. 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 due to damage to the pyramidal tract. With spastic hypertension, during repeated movements of the limb, muscle tone does not change or decreases. With spastic hypertension, a “penknife” symptom is observed (an obstacle to passive movement in the initial phase of the study).

Plastic hypertension - a uniform increase in the tone of muscles, flexors, extensors, pronators and supinators occurs when the pallidonigral system is damaged. During the examination of plastic hypertension, muscle tone increases, and the “cogwheel” symptom is noted (a feeling of jerky, intermittent movement during examination of muscle tone in the limbs).

Reflexes

A reflex is a reaction to stimulation of receptors in the reflexogenic zone: muscle tendons, skin of a certain area of ​​the body.

la, mucous membrane, pupil. The nature of the reflexes is used to judge the state of various parts of the nervous system. When examining reflexes, their level, uniformity, and asymmetry are determined; at elevated levels, a reflexogenic zone is noted. When describing reflexes, the following gradations are used: living reflexes; hyporeflexia; hyperreflexia (with an expanded reflexogenic zone); areflexia (lack of reflexes). There are deep or proprioceptive (tendon, periosteal, articular) and superficial (skin, mucous membrane) reflexes.

Tendon and periosteal reflexes (Fig. 4.7) are evoked by tapping the tendon or periosteum with a hammer: the response is manifested by the motor reaction of the corresponding muscles. It is necessary to study reflexes on the upper and lower extremities in a position favorable for the reflex reaction (lack of muscle tension, average physiological position).

Upper limbs: the reflex from the tendon of the biceps brachii muscle (Fig. 4.8) is caused by tapping the tendon of this muscle with a hammer (the patient’s arm should be bent at the elbow joint at an angle of about 120°). In response, the forearm flexes. Reflex arc - sensory and motor fibers of the musculocutaneous nerves. The closure of the arc occurs at the level of segments C v -C vi. The reflex from the tendon of the triceps brachii muscle (Fig. 4.9) is caused by hitting the tendon of this muscle above the olecranon with a hammer (the patient’s arm should be bent at the elbow joint at an angle of 90°). In response, the forearm extends. Reflex arc: radial nerve, segments C vi -C vii. The radial reflex (carporadial) (Fig. 4.10) 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, C v -C viii.

Lower limbs: the knee reflex (Fig. 4.11) is caused by hitting the quadriceps tendon with a hammer. In response, the lower leg is extended. Reflex arc: femoral nerve, L ii -L iv. When examining the reflex in a supine position, the patient’s legs should be bent at the knee joints at an obtuse angle (about 120°) and the forearm should be supported by the examiner in the area of ​​the popliteal fossa; when examining the reflex in a sitting position, the patient’s shins should be at an angle of 120° to the hips, or, if the patient does not rest his feet on the floor, free

Rice. 4.7. Tendon reflex (diagram). 1 - central gamma path; 2 - central alpha path; 3 - spinal (sensitive) node; 4 - Renshaw cell; 5 - spinal cord; 6 - alphamotoneuron of the spinal cord; 7 - gamma motor neuron of the spinal cord; 8 - alpha efferent nerve; 9 - gamma efferent nerve; 10 - primary afferent nerve of the muscle spindle; 11 - afferent nerve of the tendon; 12 - muscle; 13 - muscle spindle; 14 - nuclear bag; 15 - spindle pole.

The sign “+” (plus) indicates the process of excitation, the sign “-” (minus) indicates inhibition.

Rice. 4.8. Inducing the elbow-flexion reflex

Rice. 4.9. Inducing the ulnar extension reflex

but hang over the edge of the seat at a 90° angle 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 while the patient stretches his tightly clasped hands to the sides. The heel (Achilles) reflex (Fig. 4.12) is caused by tapping the Achilles tendon. In response,

Rice. 4.10. Inducing the metacarpal radial reflex

promotes plantar flexion of the foot as a result of contraction of the calf muscles. For a patient lying on his back, the leg should be bent at the hip, knee and ankle joints at an angle of 90°. The examiner holds the foot with his left hand and taps the Achilles tendon with his right hand. 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 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 tapping the heel tendon. Reflex arc: tibial nerve, segments S I -S II.

Joint reflexes are caused by irritation of the receptors of the joints and ligaments on the hands: 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, segments C VIII - Th I. Leri - flexion of the forearm with forced flexion of the fingers and hand in a supinated position. Reflex arc: ulnar and median nerves, segments C VI -Th I.

Skin reflexes. Abdominal reflexes (Fig. 4.13) are caused by rapid line stimulation from the periphery to the center in the corresponding skin area with the patient lying on his back with slightly legs bent. They are manifested by unilateral contraction of the muscles of the anterior abdominal wall. The superior (epigastric) reflex is caused by irritation along the edge of the costal arch. Reflex arc - segments Th VII - Th VIII. Medium (mesogastric) - with irritation at the level of the navel. Reflex arc - segments Th IX -Th X. Lower (hypogastric) when irritation is applied parallel to the inguinal fold. Reflex arc - ilioinguinal and iliohypogastric nerves, segments Th IX -Th X.

Rice. 4.11. Inducing the knee reflex with the patient sitting (A) and lying down (6)

Rice. 4.12. Inducing the heel reflex with the patient kneeling (A) and lying down (6)

Rice. 4.13. Inducing abdominal reflexes

The cremasteric reflex is caused by stroke stimulation of the inner surface of the thigh. In response, the testicle is pulled upward due to contraction of the levator testis muscle. Reflex arc - genital femoral nerve, segments L I - L II. Plantar reflex - plantar flexion of the foot and toes upon stroke stimulation of the outer edge of the sole. Reflex arc - tibial nerve, segments L V - S III. 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 lying on his side with his legs brought to the stomach. Reflex arc - pudendal nerve, segments S III -S V.

Pathological reflexes appear when the pyramidal tract is damaged. Depending on the nature of the response, extensor and flexion reflexes are distinguished.

Extensor pathological reflexes in the lower extremities. The most important is the Babinski reflex (Fig. 4.14) - extension of the first toe when the outer edge of the sole is irritated by strokes. In children under the age of 2-2.5 years, it is a physiological reflex. Oppenheim reflex (Fig. 4.15) - extension of the first toe in response to the researcher’s fingers running along the crest of the tibia down to the ankle joint. Gordon's reflex (Fig. 4.16) - slow extension of the first toe and fan-shaped spreading of the other toes when the calf muscles are compressed. Schaefer reflex (Fig. 4.17) - extension of the first toe when the Achilles tendon is compressed.

Flexion pathological reflexes in the lower extremities. The Rossolimo reflex (Fig. 4.18) is most often detected - flexion of the toes with a quick tangential blow to the pads of the toes. Bekhterev-Mendel reflex (Fig. 4.19) - flexion of the toes when struck with a hammer on its dorsal surface. Zhukovsky reflex (Fig. 4.20) - folded

Rice. 4.14. Inducing the Babinski reflex (A) and its diagram (b)

Banging of the toes when hitting the plantar surface of the foot with a hammer directly under the toes. Bekhterev reflex (Fig. 4.21) - 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, and the Rossolimo reflex is a later manifestation of spastic paralysis or paresis.

Flexion pathological 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-Lask 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 when tapping the back of the hand with a hammer.

Pathological protective reflexes, or reflexes of spinal automatism, on the upper and lower extremities - involuntary shortening or lengthening of a paralyzed limb during an 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 flexion (involuntary flexion of the leg at the ankle, knee and hip joints). The extensor protective reflex is manifested by involuntary extension

Rice. 4.15. Inducing the Oppenheim reflex

Rice. 4.16. Inducing the Gordon reflex

Rice. 4.17. Inducing the Schaefer reflex

Rice. 4.18. Inducing the Rossolimo reflex

Rice. 4.19. Inducing the Bekhterev-Mendel reflex

Rice. 4.20. Inducing the Zhukovsky reflex

Rice. 4.21. Inducing the heel reflex of Bekhterev

I eat my legs at the hip, 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, note the form of the reflex response, the reflexogenic zone, i.e. area of ​​evocation of the reflex and intensity of the stimulus.

Cervical tonic reflexes occur in response to irritation associated with a change 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's reflex - holding the lower leg in the extension position while inducing the knee reflex. Foot phenomenon (Westphalian) - “freezing” of the foot during passive dorsiflexion. The Foix-Thevenard tibia phenomenon (Fig. 4.22) is incomplete extension of the tibia at the knee joint in a patient lying on his stomach after the tibia has been held in extreme flexion for some time; manifestation of extrapyramidal rigidity.

Janiszewski's grasp reflex on the upper extremities - 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. Distant grasping reflex - an attempt to grab an object shown at a distance; observed with damage to the frontal lobe.

A sharp increase in tendon reflexes appears clonus- a series of rapid rhythmic contractions of a muscle or group of muscles in response to their stretching (Fig. 4.23). 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

Rice. 4.22. Postural reflex study (shin phenomenon)

Rice. 4.23. Inducing clonus of the patella (A) and feet (b)

he grasps 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.

Patellar clonus is caused in 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 distally

direction and hold in this position; in response, rhythmic contractions and relaxations of the quadriceps femoris muscle and twitching of the patella appear.

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

Global(spastic) - synkinesis of the tone of the flexors of the paralyzed arm and extensors of the leg when trying to move paralyzed limbs, with active movements of healthy limbs, tension in the muscles of the trunk and neck, when coughing or sneezing. Imitation synkinesis - involuntary repetition by paralyzed limbs of voluntary movements of healthy limbs on the other side of the body. Coordinating synkinesis - the performance of additional movements by paretic limbs in the process of a complex purposeful motor act (for example, flexion at the wrist and elbow joints when trying to clench the fingers into a fist).

Contractures

Persistent tonic muscle tension, causing limited movement in the joint, is called contracture. There are flexion, extension, pronator contractures; by localization - contractures of the hand, foot; mono-, para-, 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). 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 (Fig. 4.24).

Hormetonia is characterized by periodic tonic spasms mainly in the flexors of the upper and extensors of the lower extremities, and is characterized by dependence on intero- and exteroceptive stimuli. At the same time, there are pronounced protective reflexes.

Semiotics of movement disorders

There are two main syndromes of damage to the pyramidal tract - caused by the involvement of central or peripheral motor neurons in the pathological process. Damage to central motor neurons at any level of the corticospinal tract causes central (spastic) paralysis, and damage to peripheral motor neurons causes peripheral (flaccid) paralysis.

Peripheral paralysis(paresis) occurs when peripheral motor neurons are damaged at any level (neuron body in the anterior horn of the spinal cord or motor nucleus of the cranial nerve in the brainstem, anterior root of the spinal cord or motor root of the cranial nerve, plexus and peripheral nerve). Damage may involve the anterior horns, anterior roots, and peripheral nerves. The affected muscles lack both voluntary and reflex activity. The muscles are not only paralyzed, but also hypotonic (muscle hypoor atony). There is inhibition of tendon and periosteal reflexes (areflexia or hyporeflexia) due to interruption of the monosynaptic arc of the stretch reflex. After a few weeks, atrophy develops, 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.

Along with the general features of peripheral paresis, there are features of the clinical picture that make it possible to accurately determine 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

Rice. 4.24. Wernicke-Mann pose

In the muscles, rapid involuntary contractions of individual muscle fibers and their bundles are observed - fibrillar and fascicular twitching, which is a consequence of irritation by the pathological process of neurons that have not yet died. Since the innervation of the muscles is polysegmental, complete paralysis is observed only when several adjacent segments are affected. Damage to all muscles of the limb (monoparesis) 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 (radiculopathy, radiculitis), the clinical picture is similar to that when the anterior horn is affected. Segmental spread of paralysis also occurs. Paralysis of radicular origin develops only when several adjacent roots are simultaneously affected. Since damage to the anterior roots is often caused by pathological processes, simultaneously involving the posterior (sensitive) roots, movement disorders are often combined with sensory disturbances and pain in the area of ​​innervation of the corresponding roots. The cause is degenerative diseases of the spine (osteochondrosis, spondylosis deformans), neoplasms, and inflammatory diseases.

Damage to the nerve plexus (plexopathy, plexitis) is manifested by peripheral paralysis of a 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. Plexopathies are usually caused by local traumatic injuries, infectious, and toxic effects.

When the mixed peripheral nerve is damaged, peripheral paralysis of the muscles innervated by this nerve occurs (neuropathy, neuritis). Sensory and autonomic disorders caused by interruption of afferent and efferent fibers are also possible. Damage to a single nerve is usually associated with mechanical stress (compression, acute injury, ischemia). Simultaneous damage to many peripheral nerves leads to the development of peripheral paresis, most often bilateral, mainly in the distal

tal segments of the extremities (polyneuropathy, polyneuritis). At the same time, motor and autonomic disorders may occur. Patients note paresthesia, pain, a decrease in sensitivity of the “socks” or “gloves” type, and trophic skin lesions are detected. The disease is usually caused by intoxication (alcohol, organic solvents, heavy metal salts), systemic diseases (cancer of internal organs, diabetes, porphyria, pellagra), exposure to physical factors, etc.

Clarification of the nature, severity and localization of the pathological process is possible using electrophysiological research methods - electromyography, electroneurography.

At central paralysis damage to the motor area of ​​the cerebral cortex or the pyramidal tract leads to the cessation of the transmission of 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.

The main symptoms of central paralysis are a decrease in strength in combination with a limitation in the range of active movements (hemi-, para-, tetraparesis; spastic increase in muscle tone (hypertonicity); increased proprioceptive reflexes with increased tendon and periosteal reflexes, expansion of reflexogenic zones, the appearance of clonus; decreased or loss of skin reflexes (abdominal, cremasteric, plantar); the appearance of pathological reflexes (Babinsky, Rossolimo, etc.); the appearance of protective reflexes; the occurrence of pathological synkinesis; lack of degeneration reaction.

Symptoms may vary depending on the location of the lesion in the central motor neuron. Damage to the precentral gyrus is manifested by a combination of partial motor epileptic seizures (Jacksonian epilepsy) and central paresis (or paralysis) of the opposite limb. Paresis of the leg, as a rule, corresponds to damage to the upper third of the gyrus, the arm to its middle third, half of the face and tongue to the lower third. Convulsions, starting in one limb, often spread to other parts of the same half of the body. This transition corresponds to the order of location of the motor representation in the precentral gyrus.

Subcortical lesion (corona radiata) is accompanied by contralateral hemiparesis. If the focus is located closer to the lower half of the precentral gyrus, then the arm is more affected, if it is closer to the upper half, the leg is more affected.

Damage to the internal capsule leads to the development of contralateral hemiplegia. Due to the simultaneous involvement of corticonuclear fibers, central paresis of the contralateral facial and hypoglossal nerves. Damage to the ascending sensory pathways passing in the internal capsule is accompanied by the development of contralateral hemihypesthesia. In addition, conduction along the optic tract is disrupted with loss of the contralateral visual fields. Thus, damage to the internal capsule can be clinically described by the “three hemi syndrome” - hemiparesis, hemihypesthesia and hemianopsia on the side opposite to the lesion.

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 - the development of alternating syndromes. When the cerebral peduncle is damaged, there is damage to the oculomotor nerve on the side of the lesion, and on the opposite side there is spastic hemiplegia or hemiparesis (Weber syndrome). Damage to the pons of the brain is manifested by the development of alternating syndromes involving the V, VI, VII cranial nerves. When the pyramids of the medulla oblongata are affected, contralateral hemiparesis is detected, while the bulbar group of cranial nerves may remain intact. When the pyramidal decussation is damaged, a rare syndrome of cruciant (alternating) hemiplegia develops (right arm and left leg or vice versa). In the case of unilateral lesions of the pyramidal tracts in the spinal cord below the level of the lesion, spastic hemiparesis (or monoparesis) is detected, while the cranial nerves remain intact. Bilateral damage to the pyramidal tracts in the spinal cord is accompanied by spastic tetraplegia (paraplegia). At the same time, sensory and trophic disorders are detected.

To recognize focal brain lesions in patients in a comatose state, the symptom of an outwardly rotated foot is important (Fig. 4.25). 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 must be borne in mind that if the pyramidal tract is interrupted suddenly, the muscle stretch reflex is suppressed. This means that we-

Rice. 4.25. Rotation of the foot with hemiplegia

cervical tone, tendon and periosteal reflexes may initially be reduced (diaschisis stage). It may take days or weeks before they recover. 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. Gi-

Stretch receptor sensitivity is caused by damage to the extrapyramidal tracts that terminate in the anterior horn cells and activate γ-motoneurons that innervate intrafusal muscle fibers. As a result, 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.

4.2. Extrapyramidal system

The term “extrapyramidal system” (Fig. 4.26) refers to subcortical and stem extrapyramidal formations, the motor pathways from which do not pass through the pyramids of the medulla oblongata. The most important source of afferentation for them is the motor zone of the cerebral cortex.

The main elements of the extrapyramidal system are the lenticular nucleus (consists of the globus pallidus and putamen), the caudate nucleus, the amygdala complex, the subthalamic nucleus, and the substantia nigra. The extrapyramidal system includes the reticular formation, the tegmental nuclei, the vestibular nuclei and the inferior olive, the red nucleus.

In these structures, impulses are transmitted to intercalary nerve cells and then descend as tegmental, red nuclear, reticular, vestibulospinal and other pathways to the motor neurons of the anterior horns of the spinal cord. Through these pathways, the extrapyramidal system influences spinal motor activity. The extrapyramidal system, consisting of projection efferent nerve pathways starting in the cerebral cortex, including the nuclei of the striatum, some

Rice. 4.26. Extrapyramidal system (scheme).

1 - motor area of ​​the cerebrum (fields 4 and 6) on the left; 2 - corticopallidal fibers; 3 - frontal region of the cerebral cortex; 4 - striopallidal fibers; 5 - shell; 6 - globus pallidus; 7 - caudate nucleus; 8 - thalamus; 9 - subthalamic nucleus; 10 - frontal-pontine tract; 11 - red nuclear-thalamic tract; 12 - midbrain; 13 - red core; 14 - black substance; 15 - dentate-thalamic tract; 16 - dentate-red nuclear pathway; 17 - superior cerebellar peduncle; 18 - cerebellum; 19 - dentate core; 20 - middle cerebellar peduncle; 21 - lower cerebellar peduncle; 22 - olive; 23 - proprioceptive and vestibular information; 24 - tectal-spinal, reticular-spinal and red-nucleus-spinal tracts

These nuclei of the brain stem and cerebellum regulate movements and muscle tone. It complements the cortical system of voluntary movements. The voluntary movement becomes prepared, finely tuned for execution.

The pyramidal tract (via interneurons) and fibers of the extrapyramidal system ultimately meet on the anterior horn motor neurons, α- and γ-cells and influence them through both activation and inhibition. The pyramidal tract begins in the sensorimotor area of ​​the cerebral cortex (fields 4, 1, 2, 3). At the same time, extrapyramidal motor pathways begin in these fields, which include corticostriatal, corticorubral, corticonigral and corticoreticular fibers, going to the motor nuclei of the cranial nerves and to the spinal motor nerve cells through descending chains of neurons.

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

The lower order level of this system, the most ancient phylo- and genetically structures are reti-

cular formation of the tegmentum of the brain stem and spinal cord. With the development of the animal world, the paleostriatum (globus pallidus) began to dominate these structures. Then, in higher mammals, the neostriatum (caudate nucleus and putamen) acquired a leading role. As a rule, phylogenetically later centers dominate over earlier ones. This means that in lower animals the innervation of movements belongs to the extrapyramidal system. A classic example of "pallidar" creatures is fish. In birds, a fairly developed neostriatum appears. In higher animals, the role of the extrapyramidal system remains very important, although as the cerebral cortex develops, phylogenetically older motor centers (paleostriatum and neostriatum) are increasingly controlled by a new motor system - the pyramidal system.

The striatum receives impulses from various areas of the cerebral cortex, primarily the motor cortex (fields 4 and 6). These afferent fibers, somatotopically organized, run ipsilaterally and are inhibitory (inhibitory) in action. The striatum is also reached by another system of afferent fibers coming from the thalamus. From the caudate nucleus and putamen of the lentiform nucleus, the main afferent pathways are directed to the lateral and medial segments of the globus pallidus. There are connections between the ipsilateral cerebral cortex and the substantia nigra, red nucleus, subthalamic nucleus, and reticular formation.

The caudate nucleus and the shell of the lentiform nucleus have two channels of connections with the substantia nigra. Nigrostriatal dopaminergic neurons have an inhibitory effect on striatal function. At the same time, the GABAergic strionigral pathway has an inhibitory effect on the function of dopaminergic nigrostriatal neurons. These are closed feedback loops.

A mass of efferent fibers from the striatum passes through the medial segment of the globus pallidus. They form thick bundles of fibers, one of which is called the lenticular loop. Its fibers pass ventromedially around the posterior limb of the internal capsule, heading to the thalamus and hypothalamus, and also reciprocally to the subthalamic nucleus. After decussation, they connect with the reticular formation of the midbrain; the chain of neurons descending from it forms the reticular-spinal tract (descending reticular system), ending in the cells of the anterior horns of the spinal cord.

The main part of the efferent fibers of the globus pallidus goes to the thalamus. This is the pallidothalamic fasciculus, or Trout area HI. Most of it

fibers end in the anterior nuclei of the thalamus, which project to cortical field 6. Fibers starting in the dentate nucleus of the cerebellum end in the posterior nucleus of the thalamus, which projects to cortical field 4. In the cortex, thalamocortical pathways form synapses with corticostriatal neurons and form feedback rings. Reciprocal (coupled) thalamocortical connections facilitate or inhibit the activity of cortical motor fields.

Semiotics of extrapyramidal disorders

The main signs of extrapyramidal disorders are disorders of muscle tone and involuntary movements. Two groups of main clinical syndromes can be distinguished. One group is a combination of hypokinesis and muscle hypertension, the other is hyperkinesis, in some cases in combination with muscle hypotonia.

Akinetic-rigid syndrome(syn.: amyostatic, hypokinetic-hypertensive, pallidonigral syndrome). This syndrome in its classical form is found in Parkinson's disease. Clinical manifestations presented by hypokinesia, rigidity, tremor. With hypokinesia, all facial and expressive movements slow down sharply (bradykinesia) and are gradually lost. Starting movement, such as walking, switching from one motor act to another is very difficult. The patient first takes several short steps; Having started moving, he cannot suddenly stop and takes a few extra steps. This continued activity is called propulsion. Retropulsion or lateropulsion is also possible.

The entire range of movements turns out to be impoverished (oligokinesia): when walking, the torso is in a fixed position of anteflexion (Fig. 4.27), the arms do not participate in the act of walking (acheirokinesis). All facial (hypomimia, amymia) and friendly expressive movements are limited or absent. Speech becomes quiet, poorly modulated, monotonous and dysarthric.

Muscle rigidity is noted - a uniform increase in tone in all muscle groups (plastic tone); possible “waxy” resistance to all passive movements. A symptom of a gear wheel is revealed - during the study, the tone of the antagonist muscles decreases stepwise, inconsistently. The head of a lying patient, carefully raised by the examiner, does not fall if it is suddenly released, but gradually lowers. In contrast to spastic

paralysis, proprioceptive reflexes are not increased, and pathological reflexes and paresis are absent.

Small-scale, rhythmic tremor of the hands, head, and lower jaw has a low frequency (4-8 movements per second). Tremor occurs at rest and becomes the result of the interaction of muscle agonists and antagonists (antagonistic tremor). It has been described as a "pill rolling" or "coin counting" tremor.

Hyperkinetic-hypotonic syndrome- the appearance of excessive, uncontrolled movements in various muscle groups. There are local hyperkinesis involving individual muscle fibers or muscles, segmental and generalized hyperkinesis. There are fast and slow hyperkinesis, with persistent tonic tension of individual muscles

Athetosis(Fig. 4.28) is usually caused by damage to the striatum. Slow worm-like movements occur with a tendency to hyperextension of the distal parts of the limbs. In addition, there is an irregular increase in muscle tension in agonists and antagonists. As a result, the patient's postures and movements become pretentious. Voluntary movements are significantly impaired due to the spontaneous occurrence of hyperkinetic movements, which can involve the face, tongue and thus cause grimaces with abnormal movements of the tongue and difficulty speaking. Athetosis can be combined with contralateral paresis. It can also be double-sided.

Facial paraspasm- local hyperkinesis, manifested by tonic symmetrical contractions of facial muscles, muscles of the tongue, and eyelids. Sometimes he watches

Rice. 4.27. Parkinsonism

Rice. 4.28. Athetosis (a-e)

isolated blepharospasm (Fig. 4.29) - isolated contraction of the circular muscles of the eyes. It is provoked by talking, eating, smiling, intensifies with excitement, bright lighting and disappears in sleep.

Choreic hyperkinesis- short, fast, random involuntary twitches in the muscles, causing various movements, sometimes resembling voluntary ones. The distal parts of the limbs are involved first, then the proximal ones. Involuntary twitching of the facial muscles causes grimaces. The sound-producing muscles may be involved with involuntary screams and sighs. In addition to hyperkinesis, there is a decrease in muscle tone.

Spasmodic torticollis(rice.

4.30) and torsion dystonia (Fig.

4.31) are the most common forms of muscular dystonia. In both diseases, the putamen and centromedian nucleus of the thalamus, as well as other extrapyramidal nuclei (globus pallidus, substantia nigra, etc.) are usually affected. Spastic

torticollis is a tonic disorder expressed in spastic contractions of the muscles of the cervical region, leading to slow, involuntary turns and tilts of the head. Patients often use compensatory techniques to reduce hyperkinesis, in particular supporting the head with a hand. In addition to other neck muscles, the sternocleidomastoid and trapezius muscles are especially often involved in the process.

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

Rice. 4.29. Blepharospasm

Rice. 4.30. Spasmodic torticollis

Torsion dystonia- involvement in the pathological process of the muscles of the trunk, chest with rotational movements of the trunk and proximal segments of the limbs. They can be so severe that the patient cannot stand or walk without support. Possible idiopathic torsion dystonia or dystonia as a manifestation of encephalitis, Huntington's chorea, Hallervoorden-Spatz disease, hepatocerebral dystrophy.

Ballistic syndrome(ballism) is manifested by rapid contractions of the proximal muscles of the limbs, rotational contractions of the axial muscles. The most common form is unilateral - hemiballismus. With hemiballismus, movements have greater amplitude and strength (“throwing”, sweeping), since very large muscle groups are contracted. The cause is damage to the subthalamic Lewis nucleus and its connections with the lateral segment of the globus pallidus on the side contralateral to the lesion.

Myoclonic jerks- rapid, erratic contractions of individual muscles or various muscle groups. They occur, as a rule, with damage to the red nucleus, inferior olives, dentate nucleus of the cerebellum, and less often with damage to the sensorimotor cortex.

Tiki- fast, stereotypical, fairly coordinated muscle contractions (most often the orbicularis oculi muscle and other facial muscles). Complex motor tics are possible - sequences of complex motor acts. There are also simple (smacking, coughing, sobbing) and complex (involuntary

muttering of words, obscene language) vocal tics. Tics develop as a result of the loss of the inhibitory effect of the striatum on the underlying neuronal systems (globus pallidus, substantia nigra).

Automated Actions- complex motor acts and other sequential actions that occur without conscious control. Occurs with lesions located in the cerebral hemispheres, destroying the connections of the cortex with the basal ganglia while maintaining their connection with the brain stem; appear in the limbs of the same name as the lesion (Fig. 4.32).

Rice. 4.31. Torsion spasm (a-c)

Rice. 4.32. Automated Actions (a, b)

4.3. Cerebellar system

The functions of the cerebellum are to ensure coordination of movements, regulate muscle tone, coordinate the actions of agonist and antagonist muscles, and maintain balance. The cerebellum and brain stem occupy the posterior cranial fossa, delimited from the cerebral hemispheres by the tentorium cerebellum. The cerebellum is connected to the brain stem by three pairs of peduncles: the superior cerebellar peduncles connect the cerebellum to the midbrain, the middle peduncles pass into the pons, and the inferior cerebellar peduncles connect the cerebellum to the medulla oblongata.

In structural, functional and phylogenetic terms, archicerebellum, paleocerebellum and neocerebellum are distinguished. The archicerebellum (zona flocculonodosa) is an ancient part of the cerebellum, which consists of a nodule and a flocculus vermis, closely connected with the vestibular

system. Thanks to this, the cerebellum is able to synergistically modulate spinal motor impulses, which ensures the maintenance of balance regardless of body position or movement.

The paleocerebellum (old cerebellum) consists of the anterior lobe, the simple lobule and the posterior part of the body of the cerebellum. Afferent fibers enter the paleocerebellum mainly from the homonymous half of the spinal cord through the anterior and posterior spinocerebellar and from the accessory sphenoid nucleus through the sphenocerebellar tract. Efferent impulses from the paleocerebellum modulate the activity of the antigravity muscles and provide muscle tone sufficient for upright standing and upright walking.

The neocerebellum (new cerebellum) consists of the vermis and the region of the hemispheres located between the first and posterior lateral fissure. This is the largest part of the cerebellum. Its development is closely related to the development of the cerebral cortex and the performance of fine, well-coordinated movements. Depending on the main sources of afferentation, these cerebellar regions can be characterized as the vestibulocerebellum, spinocerebellum, and pontocerebellum.

Each cerebellar hemisphere has 4 pairs of nuclei: the tent nucleus, globose, cortical and dentate (Fig. 4.33). The first three nuclei are located in the lid of the fourth ventricle. The tent core is phylogenetically the oldest and is related to the Archcerebellum. Its efferent fibers travel through the inferior cerebellar peduncles to the vestibular nuclei. The spherical and corky nuclei are connected to the adjacent cher-

Rice. 4.33. Cerebellar nuclei and their connections (diagram).

1 - cerebral cortex; 2 - ventrolateral nucleus of the thalamus; 3 - red core; 4 - tent core; 5 - spherical nucleus; 6 - corky core; 7 - dentate core; 8 - dentate-red nuclear and dentate-thalamic pathways; 9 - vestibulocerebellar tract; 10 - paths from the cerebellar vermis (tent nucleus) to the thin and sphenoid nuclei, the inferior olive; 11 - anterior spinocerebellar tract; 12 - posterior spinocerebellar tract

wem areas of the paleocerebellum. Their efferent fibers go to the contralateral red nuclei through the superior cerebellar peduncles.

The dentate nucleus is the largest and is located in the central part of the white matter of the cerebellar hemispheres. It receives impulses from the Purkinje cells of the cortex of the entire neocerebellum and part of the paleocerebellum. Efferent fibers pass through the superior cerebellar peduncles and pass to the opposite side to the border of the pons and midbrain. Their bulk ends in the contralateral red nucleus and the ventrolateral nucleus of the thalamus. Fibers from the thalamus are sent to the motor cortex (fields 4 and 6).

The cerebellum receives information from receptors located in muscles, tendons, joint capsules and deep tissues along the anterior and posterior spinocerebellar tracts (Fig. 4.34). The peripheral processes of the cells of the spinal ganglion extend from the muscle spindles to the Golgi-Mazzoni bodies, and the central processes of these cells through the posterior

Rice. 4.34. Pathways of proprioceptive sensitivity of the cerebellum (diagram). 1 - receptors; 2 - posterior cord; 3 - anterior spinocerebellar tract (uncrossed part); 4 - posterior spinocerebellar tract; 5 - dorso-olive tract; 6 - anterior spinocerebellar tract (crossed part); 7 - olivocerebellar tract; 8 - inferior cerebellar peduncle; 9 - superior cerebellar peduncle; 10 - to the cerebellum; 11 - medial loop; 12 - thalamus; 13 - third neuron (deep sensitivity); 14 - cerebral cortex

These roots enter the spinal cord and split into several collaterals. A significant part of the collaterals connects with neurons of the Clark-Stilling nucleus, located in the medial part of the base of the dorsal horn and extending along the length of the spinal cord from C VII to L II. These cells represent the second neuron. Their axons, which are fast-conducting fibers, create the posterior spinocerebellar tract (Flexiga). They ascend ipsilaterally in the outer parts of the lateral funiculi, which, after passing through the cerebral peduncle, enters the cerebellum through its inferior peduncle.

Some of the fibers emerging from the Clark-Stilling nucleus pass through the anterior white commissure to the opposite side and form the anterior spinocerebellar tract (Gowers). As part of the anterior peripheral part of the lateral funiculi, it rises to the tegmentum of the medulla oblongata and the pons; Having reached the midbrain, it returns to the side of the same name in the superior medullary velum and enters the cerebellum through its superior peduncles. On the way to the cerebellum, the fibers undergo a second decussation.

In addition, part of the fiber collaterals arriving from the proprioceptors in the spinal cord is directed to the large α-motoneurons of the anterior horns, forming the afferent link of the monosynaptic reflex arc.

The cerebellum has connections with other parts of the nervous system. Afferent pathways from:

1) vestibular nuclei (vestibulocerebellar tract ending in the flocculo-nodular zone associated with the tent core);

2) inferior olives (olivocerebellar tract, starting in the contralateral olives and ending on the Purkinje cells of the cerebellum);

3) spinal nodes of the same side (posterior spinocerebellar tract);

4) reticular formation of the brain stem (reticular-cerebellar);

5) accessory cuneate nucleus, fibers from which join the posterior spinocerebellar tract.

The efferent cerebellobulbar pathway passes through the inferior cerebellar peduncles and goes to the vestibular nuclei. Its fibers represent the efferent part of the vestibulocerebellar modulating feedback ring, through which the cerebellum influences the state of the spinal cord through the vestibulocerebellar tract and the medial longitudinal fasciculus.

The cerebellum receives information from the cerebral cortex. Fibers from the cortex of the frontal, parietal, temporal and occipital lobes are sent to the pons, forming the corticocerebellar tract. The frontopontine fibers are localized in the anterior limb of the internal capsule. In the midbrain they occupy the medial quarter of the cerebral peduncles near the interpeduncular fossa. Fibers coming from the parietal, temporal and occipital lobes of the cortex pass through the posterior part of the posterior limb of the internal capsule and the posterolateral part of the cerebral peduncles. All corticopontine fibers form synapses with neurons at the base of the pons, where the bodies of second neurons are located, sending axons to the contralateral cerebellar cortex, entering it through the middle cerebellar peduncles (corticopontine tract).

The superior cerebellar peduncles contain efferent fibers that originate in the neurons of the cerebellar nuclei. The bulk of the fibers are directed to the contralateral red nucleus (Forel's decussation), some of them to the thalamus, reticular formation and brain stem. Fibers from the red nucleus make a second decussation (Werneckin) in the tegmentum, forming the cerebellar-rednuclear-spinal cord (dentorubrospinal) tract, heading to the anterior horns of the same half of the spinal cord. In the spinal cord, this pathway is located in the lateral columns.

Thalamocortical fibers reach the cerebral cortex, from which corticopontine fibers descend, thus completing an important feedback loop from the cerebral cortex to the pontine nuclei, cerebellar cortex, dentate nucleus, and from there back to the thalamus and cerebral cortex. An additional feedback loop goes from the red nucleus to the inferior olive through the central tegmental tract, from there to the cerebellar cortex, the dentate nucleus, back to the red nucleus. Thus, the cerebellum indirectly modulates the motor activity of the spinal cord through its connections with the red nucleus and reticular formation, from which the descending red nucleus-spinal and reticular-spinal tracts begin. Due to the double decussation of fibers in this system, the cerebellum exerts an ipsilateral effect on the striated muscles.

All impulses arriving in the cerebellum reach its cortex, undergo processing and multiple recoding due to repeated switching of neural circuits in the cortex and cerebellar nuclei. Due to this, and also due to the close connections of the cerebellum with various structures of the brain and spinal cord, it carries out its functions relatively independently of the cerebral cortex.

Research methodology

They examine coordination, smoothness, clarity and consistency of movements, muscle tone. Coordination of movements is the finely differentiated sequential participation of a number of muscle groups in any motor act. Coordination of movements is carried out on the basis of information received from proprioceptors. Impaired coordination of movements is manifested by ataxia - loss of the ability to perform targeted differentiated movements with preserved muscle strength. There are dynamic ataxia (impaired performance of voluntary movements of the limbs, especially the upper ones), static (impaired ability to maintain balance in a standing and sitting position) and static-locomotor (disorders of standing and walking). Cerebellar ataxia develops with preserved deep sensitivity and can be dynamic or static.

Tests to identify dynamic ataxia.Finger test(Fig. 4.35): the patient, sitting or standing with his arms extended in front of him, is asked to touch the tip of his nose with his index finger with his eyes closed. Heel-knee test(Fig. 4.36): the patient, lying on his back, is asked to place the heel of one leg on the knee of the other with his eyes closed and move the heel down the shin of the other leg. Finger-finger test: the patient is offered the tips index fingers touch the fingertips of the examiner who is sitting opposite. First, the patient performs tests with with open eyes, then - with closed ones. Cerebellar ataxia does not worsen with the eyes closed, in contrast to ataxia caused by damage to the posterior cord of the spinal cord. Need to install

Rice. 4.35. Finger test

Fig.4.36. Heel-knee test

does the patient accurately hit the intended target (is there a miss or miss) and is there any intention tremor?

Tests for the detection of static and static-locomotor ataxia: the patient walks with his legs spread wide, staggering from side to side and deviating from the line of walking - “a drunken gait” (Fig. 4.37), cannot stand, deviating to the side.

Romberg test(Fig. 4.38): the patient is asked to stand with his eyes closed, his toes and heels pulled together, and attention is paid to the direction in which the torso deviates. There are several options for the Romberg test:

1) the patient stands with his arms extended forward; trunk deviation increases if the patient is standing, closing your eyes, stretching your arms forward and placing your legs one in front of the other in a straight line;

2) the patient stands with his eyes closed and his head thrown back, while the deviation of the torso is more pronounced. A deviation to the side, and in severe cases, a fall when walking or performing the Romberg test, is observed in the direction of the cerebellar lesion.

Violation of smoothness, clarity, and coherence of movements is manifested in tests to identify dysmetria (hypermetry). Dysmetria is a disproportion of movements. The movement has an excessive amplitude, ends too late, is performed impulsively, with excessive speed. First appointment: the patient is asked to take objects of various sizes. He cannot arrange his fingers in advance according to the volume of the object that needs to be taken. If the patient is offered an object of small volume, he spreads his fingers too wide and closes them much later than required. Second technique: the patient is asked to stretch his arms forward with his palms up and, at the doctor’s command, synchronously rotate his arms with his palms up and down. On the affected side, movements are performed more slowly and with excessive amplitude, i.e. Adiadochokinesis is detected.

Other samples.Asynergy Babinsky(Fig. 4.39). The patient is asked to sit from a supine position with his arms crossed over his chest. If the cerebellum is damaged, it is impossible to sit down without the help of hands, while the patient makes a number of auxiliary movements to the side, raises both legs due to incoordination of movements.

Schilder's test. The patient is asked to stretch out his hands in front of him, closing his eyes, raise one hand vertically up, and then lower it to the level of the other hand and repeat the test with the other hand. If the cerebellum is damaged, it is impossible to accurately perform the test; the raised hand will fall below the outstretched one.

Rice. 4.37. A patient with an ataxic gait (A), uneven handwriting and macrography (b)

Rice. 4.38. Romberg test

Rice. 4.39. Asynergy Babinsky

When the cerebellum is damaged, it appears intentional tremors(tremor), when performing voluntary purposeful movements, it intensifies with maximum approach to the object (for example, when performing a finger-nose test, as the finger approaches the nose, the tremor intensifies).

Impaired coordination of fine movements and tremors are also manifested by handwriting disorders. The handwriting becomes uneven, the lines become zigzag, some letters are too small, others, on the contrary, are large (megalography).

Myoclonus- rapid clonic twitching of muscles or their individual bundles, in particular the muscles of the tongue, pharynx, soft palate, occur when the stem formations and their connections with the cerebellum are involved in the pathological process due to a violation of the system of connections between the dentate nuclei - red nuclei - inferior olives.

The speech of patients with cerebellar damage becomes slow, drawn out, and individual syllables are pronounced louder than others (become stressed). This kind of speech is called chanted.

Nystagmus- involuntary rhythmic biphasic (with fast and slow phases) movements of the eyeballs with damage to the cerebellum. As a rule, nystagmus has a horizontal direction.

Hypotension muscle pain is manifested by lethargy, flabbiness of muscles, excessive excursion in the joints. Tendon reflexes may be decreased. Hypotonia can be manifested by a symptom of the absence of a reverse impulse: the patient holds his arm in front of him, bending it at the elbow joint, in which he experiences resistance. When the resistance suddenly stops, the patient's hand hits the chest with force. In a healthy person, this does not happen, since the antagonists - the extensors of the forearm - quickly come into action (reverse push). Hypotension also causes pendulum-like reflexes: when examining the knee reflex in the patient's sitting position with the shins freely hanging from the couch, several rocking movements of the shin are observed after being hit with a hammer.

Changes in postural reflexes is also one of the symptoms of cerebellar damage. Doinikov's finger phenomenon: if a sitting patient is asked to hold his hands in a supinated position with his fingers apart (kneeling position), then on the side of the cerebellar lesion flexion of the fingers and pronation of the hand occur.

Underestimating the weight of an object held by the hand, is also a peculiar symptom on the side of the cerebellar lesion.

Semiotics of cerebellar disorders When the worm is affected, imbalance and instability when standing (astasia) and walking (abasia), ataxia of the trunk, impaired statics, and the patient falls forward or backward are noted.

Due to the common functions of the paleocerebellum and neocerebellum, their defeat causes a single clinical picture. In this regard, in many cases it is impossible to consider this or that clinical symptomatology as a manifestation of damage to a limited area of ​​the cerebellum.

Damage to the cerebellar hemispheres leads to impaired performance of locomotor tests (finger-to-nose, heel-knee), intention tremor on the affected side, and muscle hypotonia. Damage to the cerebellar peduncles is accompanied by the development of clinical symptoms caused by damage to the corresponding connections. If the lower legs are affected, nystagmus and myoclonus of the soft palate are observed; if the middle legs are affected, locomotor tests are impaired; if the upper legs are affected, choreoathetosis and rubral tremor appear.

Having established that a patient has paralysis (or paresis) caused by a disease of the nervous system, they try first of all to find out the nature of the paralysis (or paresis): does it depend on lesions of the central motor neuron paths or peripheral. Let us remind you that central neuron the main path for voluntary movements begins in motor zone of the cerebral cortex, near pyramidal cells, passes through the internal bursa and brain stem and ends at the cells of the anterior horns of the spinal cord or at the nuclei motor cranial nerves.

Peripheral neuron goes from the cell of the anterior horn of the spinal cord or the nucleus of the cranial nerve to the muscle.

Wherever this was interrupted motor path, paralysis will occur. Defeat central neuron will give central paralysis, peripheral neuron damage- peripheral paralysis.

Clinical features central And peripheral paralysis are so different from each other that in the vast majority of cases it is possible to easily differentiate one type of paralysis from another.

Signs central paralysis - increased tendon and periosteal reflexes, muscle tone, the appearance of pathological, protective reflexes, clonus and unusual friendly movements - are easily explained by the essence of the process.

The intensity of Paresis can be very different. In mild cases, it is necessary to resort to some special techniques to identify the existing weakness of the limb. Suspecting, for example, the subject has weakness in one hand, you can ask him to clench his hands into fists and unclench them many times in a row, repeatedly finger the fingers of both hands with his thumb.

1. Semiotics of peripheral motor neuron lesions.

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 central, or spastic, paralysis. When peripheral motor neurons are damaged at any site (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 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. Leg paresis indicates defeat upper third gyri, hands - its middle third, half of the face and tongue - 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, since the lesion has a shock-like effect on the peripheral

1. Syndrome of transverse lesion of the cervical thickening of the SM.

When the spinal cord is interrupted at the upper cervical level (C I– C IV) appear:

• spastic tetraplegia (spastic paralysis of all four limbs) due to bilateral damage to the descending motor tracts, bilateral peripheral (flaccid) paralysis of the muscles of the corresponding myotome (muscles of the occipital region) due to damage to the peripheral motor neurons of the anterior horns, as well as flaccid paralysis of the sternocleidomastoid muscles and upper sections trapezius muscles as a result of damage to the spinal portion of the nucleus of the XI pair (n. accesorius), bilateral peripheral paralysis of the diaphragm due to damage to the peripheral motor neurons of the anterior horns of the spinal cord at level C III–C IV, the axons of which form the phrenic nerve (n. phrenicus) with the development of acute syndrome respiratory failure or the appearance paradoxical type of breathing(when inhaling, the anterior abdominal wall retracts, and when exhaling, it protrudes;
• loss of all types of sensitivity of the conductor type, i.e. below the level of the lesion according to the principle of “everything below” with bilateral damage to all sensitive conductors, as well as of the segmental type in the corresponding sclerotomes (the scalp of the occipital region);
• bilateral dissociated anesthesia of the lateral areas of the face, i.e. loss of superficial types of sensitivity – temperature ( thermaneesthesia) and pain ( analgesia) with preservation of deep types of sensitivity (spatial skin sensitivity) in the posterior Zelder dermatomes("bulbous" type sensory disorders) with damage to the lower segment of the nucleus of the spinal tract of the trigeminal nerve (nucl. spinalis n. trigemini);
• dysfunction of the pelvic organs of the central type, which are manifested by acute retention of urine (retentio urinae), feces (retentio alvi) or periodic incontinence of urine (incontinentio intermittens urinae) and feces (incontinentio intermittens alvi). This occurs because the influence of the central neurons of the precentral gyrus, located on the medial surface of the frontal lobe, in the paracentral lobule, is lost, and the peripheral somatic regulation of the function of the pelvic organs is carried out at the level of segments S III - S V of the spinal cord, where motor neurons are located in the anterior horns of the gray matter , innervating the striated muscles of the pelvic organs (external sphincters). Moreover, with a complete transverse lesion of the spinal cord, the principle of bilateral cortical innervation of the pelvic organs is lost.

Neurology and neurosurgery Evgeniy Ivanovich Gusev

3.1. Pyramid system

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 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.

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. 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.

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 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.

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. 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.

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. 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.

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 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.

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 centers, including vestibular centers, the cerebellum, the 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 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.

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 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 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 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.

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.

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.

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, 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.

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 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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