Paralysis and paresis. The reasons for their occurrence

Paralysis is one of the types of impairment of human motor activity and manifests itself in its complete loss (Greek. paralysis- relaxation). This disease is a symptom of many organic diseases of the nervous system.

In the case of not a complete loss of motor function, but only a weakening of it to one degree or another, this disorder will be called paresis(Greek paresis- weakening). Moreover, in both the first and second cases, motor dysfunction is the result of damage to the nervous system, its motor centers and/or pathways of the central and/or peripheral parts.

Paralysis should be distinguished from movement disorders that occur due to muscle inflammation and mechanical damage to the osteoarticular apparatus.

Paresis and paralysis are movement disorders that are caused by the same reasons.

The main causes of these diseases.

Paralysis is not caused by any one specific factor. Any damage to the nervous system can lead to impaired motor function. Congenital, hereditary and degenerative diseases of the central nervous system are usually accompanied by movement disorders.

Birth injuries are a common cause of cerebral palsy, as well as paralysis due to damage to the brachial plexus. Unfortunately, over 15 million patients with cerebral palsy have already been recorded in the world.

A number of diseases of unknown origin (for example, multiple sclerosis) are characterized by movement disorders of varying severity.

Circulatory disorders, inflammatory processes, injuries, tumors of the nervous system can also cause paralysis or paresis.

Often paralysis is of a psychogenic nature and is a manifestation of hysteria.

The causes of paralysis can also be divided into organic, infectious and toxic.

Organic causes include:

1. Malignant neoplasms;
2. Vascular lesions;
3. Metabolic disorders;
4. Intoxication;
5. Eating disorders;
6. Infections;
7. Injuries;
8. Multiple sclerosis;

Infectious causes include:

1. Meningitis;
2. Polio;
3. Viral encephalitis;
4. Tuberculosis;
5. Syphilis.

Toxic causes include:

1. Vitamin B1 deficiency;
2. Nicotinic acid deficiency;
3. Heavy metal poisoning;
4. Alcoholic neuritis.

Paralysis can be observed in one muscle, one limb ( monoplegia), in the arm and leg on one side ( hemiplegia), in both arms or both legs ( paraplegia) (the suffix plegia means paralysis).

By localization lesions distinguish two groups of paralysis, significantly different in clinical manifestations: central ( spastic) and peripheral ( sluggish).

Central paralysis occur when central motor neurons are damaged. They are characterized by:

• hypertonicity (increased muscle tone), for example, the “jackknife” phenomenon;
• hyperreflexia (increased intensity of deep reflexes), especially demonstrably with unilateral damage;
• the presence of pathological reflexes (Babinsky, Bekhterev, Astvatsaturov, etc.);
• the appearance of pathological synkinesias (friendly movements), for example, when a patient voluntarily clenches a healthy hand into a fist and does not voluntarily repeat this movement with the affected hand, but with less force;
• the appearance of clonus (convulsive muscle contractions in response to an impact), for example, foot clonus - when a patient lying on his back, with the affected leg bent at the hip and knee joints, the doctor performs dorsal extension of the foot, and the flexor muscles begin to involuntarily contract rhythmically , the rhythm can persist for a long time or fade out almost immediately.

Peripheral paralysis (flaccid) characterized by a complete lack of movement, a drop in muscle tone, extinction of reflexes, and muscle atrophy. With damage to the peripheral nerve or plexus, which contains both motor and sensory fibers, sensitivity disorders are also detected.

When the subcortical structures of the brain are damaged, extrapyramidal paralysis, automated movements disappear, motor initiative is absent. Muscle tone is characterized by plasticity - the limb is held in a passive position given to it.

Classification

There are two scales for assessing the severity of paralysis (paresis) - by the degree of decrease in muscle strength and by the degree of severity of paralysis (paresis), which are the opposite of each other:

1. 0 points “muscle strength” - no voluntary movements. Paralysis.
2. 1 point - barely noticeable muscle contractions, without movements in the joints.
3. 2 points - the range of movements in the joint is significantly reduced, movements are possible without overcoming the force of gravity (along the plane).
4. 3 points - a significant reduction in the range of movements in the joint, the muscles are able to overcome the force of gravity and friction (in fact, this means the possibility of tearing the limb off the surface).
5. 4 points - slight decrease in muscle strength, with full range of motion.
6. 5 points - normal muscle strength, full range of movements.

The most significant features of peripheral paralysis are:

1. atony (decreased tone) of muscles;

2. muscle atrophy due to decreased nerve trophism;

3. fasciculations (involuntary contractions of individual muscle fibers, perceived by the patient and visible to the doctor’s eye), which develop when large alpha motor neurons of the anterior horns of the spinal cord are damaged.

Determination of the stage of paralysis (paresis.)

An external examination can detect deformities of the spine, joints, feet, hands, asymmetry of skeletal development, and leg length.
Swelling of the legs and arms, changes in the trophism of the nails and skin, the presence of folding of the skin over the spine, stretch marks, varicose veins, areas of skin pigmentation, tumors, and scars from burns are detected.

The most common method of examining muscles, bones and joints is palpation. Palpation of muscles is the main method of determining their tone.

Hypotension(decreased tone) is observed with pure pyramidal paresis, with impaired muscle-articular sensitivity, with a number of neuromuscular diseases, cataplexy, attacks of sudden falling, hysterical paralysis, with lesions of the cerebellum, etc.
With hypotension, the muscle is relaxed, spread out, has no contours, the finger easily sinks into the thickness of the muscle tissue, its tendon is relaxed, and greater mobility is noted in the corresponding joint. Hypotension can be mild, moderate, or severe.

Atony- lack of normal tone of the muscles of the skeleton and internal organs, developing as a result of insufficient general nutrition, disorders of the nervous system, infectious diseases, disorders of the endocrine glands. With atony, movement is not possible.

At hypertonicity the muscle is tense, shortened, prominent, compacted, the finger has difficulty penetrating the muscle tissue, movements in the joint are, as a rule, limited in scope.

Spasticity or spastic paresis.

Paresis is characterized by a peculiar selective increase in tone in the adductor muscles of the shoulder, flexors of the forearm, hand, fingers and pronators of the hand. In the leg, hypertonicity is noted in the extensors of the hip and knee joints, the adductor muscles of the thigh, plantar flexors of the foot and toes (Wernicke-Mann position). With repeated movements, the springy muscle resistance may disappear and the spastic posture is overcome - a “jackknife” symptom.

In conditions of a spinal lesion above the cervical thickening, spastic hemi- or tetraplegia develops; damage at the level of the thoracic segments causes lower paraplegia.

With spastic paresis, a number of accompanying symptoms are noted:

1. Tendon-periosteal hyperreflexia with expansion of the reflex zone, clonus of the feet, hands, and lower jaw.
2. The most reliable of them is the Babinski reflex, which is caused by streak irritation of the outer part of the sole with a pen from the heel to the toes. In response, the first finger extends and the remaining fingers flex and fan out.
3. Hoffman reflex - increased flexion of the fingers of the hanging hand in response to pinch irritation of the nail phalanx of the third finger.
4. Protective reflexes - a triple flexion reflex of the leg when the skin of the foot is irritated by a pinch or a cold object, as well as a reflex of lengthening the leg in response to a thigh prick.
5. The absence of abdominal reflexes and signs of peripheral neuron damage (fibrillary muscle twitching, atrophy) complements the picture of spastic paresis.

Extrapyramidal pseudoparesis, rigidity.

Pseudoparesis manifests itself as uniform hypertonicity in massive muscle groups - agonists and antagonists, flexors and extensors of the limbs, which leads to a plastic increase in tone, freezing of the limb in an uncomfortable position given to it (waxy flexibility).
Stronger flexors give the patient a “petitioner” posture. — The torso and head are tilted forward, the arms are half-bent at the elbow joints and pressed to the body. Movements are slow, awkward, and their initiation is especially difficult. When studying passive movements, intermittent muscle resistance is noted during flexion and extension of the limb. Rhythmic constant tremor of the fingers at rest is often observed.

Peripheral paresis (flaccid).

At flaccid paresis peripheral type pathological signs, synkinesis and protective reflexes are absent.
Nerve damage (neuritis, mononeuropathy) leads to selective atrophy of the muscle group innervated by this nerve.
Polyneuritis contribute to symmetrical paresis of the distal muscles (feet, legs, hands, forearms).
Plexus lesion (plexite) accompanied by unilateral paresis with predominant localization in the upper or lower limbs, in the muscles of the pelvic or shoulder girdle.

Mixed paresis.

In some cases, patients have both signs of flaccid paresis and symptoms of damage to the central motor neuron. This type of paresis is called mixed.
It causes damage to the cells of the anterior horn and pyramidal tract.
The mixed type of paresis includes central type defects after strokes, with tumors (hematomas) with compression on this area. This category of patients presents together with hemiparkinsonism and spastic hemiparesis.

The treatment of such patients must be approached individually. Treatments for this disease include sulfur and radon baths, segmental and acupressure massage, balance therapy, and stem cell treatment. But the main method of treatment is special therapeutic exercises.

Peripheral paralysis is characterized by the following main symptoms: absence of reflexes or their decrease (hyporeflexia, areflexia), decrease or absence of muscle tone (atony or hypotonia), muscle atrophy. In addition, changes in electrical excitability, called the degeneration reaction, develop in paralyzed muscles and affected nerves. The depth of changes in electrical excitability allows one to judge the severity of the lesion in peripheral paralysis and the prognosis. Loss of reflexes and atony are explained by interruption of the reflex arc; such a break in the arc leads to loss of muscle tone. For the same reason, the corresponding reflex cannot be evoked. Muscle atrophy, or sudden weight loss, develops due to the disconnection of the muscle from the neurons of the spinal cord; from these neurons, impulses flow through the peripheral nerve to the muscle, stimulating normal metabolism in muscle tissue. With peripheral paralysis, fibrillar twitching may be observed in atrophied muscles in the form of rapid contractions of individual muscle fibers or bundles of muscle fibers (fascicular twitching). They are observed in chronic progressive pathological processes in the cells of peripheral motor neurons.

Damage to a peripheral nerve leads to peripheral paralysis of the muscles innervated by this nerve. In this case, sensory disturbances and autonomic disorders are also observed in the same area, since the peripheral nerve is mixed - motor and sensory fibers pass through it. As a result of damage to the anterior roots, peripheral paralysis of the muscles innervated by this root occurs. Damage to the anterior horns of the spinal cord causes peripheral paralysis of the muscles in the areas of innervation by this segment.

Thus, damage to the anterior horns of the spinal cord in the area of ​​the cervical thickening (the fifth - eighth cervical segments and the first thoracic) leads to peripheral paralysis of the arm. Damage to the anterior horns of the spinal cord at the level of the lumbar enlargement (all lumbar and first and second sacral segments) causes peripheral paralysis of the leg. If the cervical or lumbar thickening is affected on both sides, then upper or lower paraplegia develops.

An example of peripheral limb paralysis is the paralysis that occurs due to polio. With polio, paralysis of the legs, arms, and respiratory muscles can develop. When the cervical and thoracic segments of the spinal cord are affected, peripheral paralysis of the diaphragm and intercostal muscles is observed, leading to respiratory failure. Damage to the upper thickening of the spinal cord leads to peripheral paralysis of the arms, and the lower (lumbar thickening) leads to paralysis of the legs.

Facial nerve syndrome

In children, inflammatory lesions of the facial nerve often occur, leading to peripheral paralysis of the facial muscles. On the side of the lesion of the facial nerve, the folds in the forehead are smoothed, the eyebrow is slightly lowered, the palpebral fissure does not close, the cheek hangs down, the nasolabial fold is smoothed, and the corner of the mouth is lowered. The patient cannot stretch his lips forward, blow out a burning match, or puff out his cheeks. When eating, liquid food pours out through the lowered corner of the mouth. Paresis of the facial muscles is most pronounced when crying and laughing. These disorders can sometimes be accompanied by lacrimation, increased sensitivity to auditory stimuli (hyperacusis), and taste disturbance in the anterior two-thirds of the tongue.

Less commonly, peripheral paresis of the facial muscles is caused by underdevelopment of the nuclei of the facial nerve. In such cases, the lesion is usually bilateral and symmetrical; symptoms are observed from birth and are often combined with other developmental defects.

Bilateral damage to the facial nerve, most often its roots, can also be observed with multiple neuritis (polyneuritis), inflammation of the meninges (meningitis), fractures of the bones of the base of the skull and other skull injuries.

Oculomotor nerve syndrome

Damage to the oculomotor and abducens nerves leads to paralysis of the muscles they innervate and the occurrence of strabismus. in patients with damage to the oculomotor nerve, divergent strabismus occurs, since the healthy external rectus muscle, innervated by the abducens nerve, pulls the eyeball in its direction. When the abducens nerve is damaged, convergent strabismus develops for the same reason (the healthy internal rectus muscle, innervated by the oculomotor nerve, is pulled). When the trochlear nerve is damaged, strabismus, as a rule, does not occur. There may be a slight convergent squint when looking down. If the oculomotor nerve is damaged, drooping of the upper eyelid (ptosis) may occur due to paralysis of the muscle that lifts the upper eyelid, as well as dilation of the pupil (mydriasis) due to paralysis of the muscle that constricts the pupil, and impaired accommodation (deterioration of near vision).

With paralysis of the extraocular muscles, the eyeball may protrude from the orbit due to a decrease in their tone (exophthalmos). When looking to the side with a paralyzed muscle, double vision (diplopia) occurs.

Hypoglossal nerve syndrome

Damage to the hypoglossal nerve or its nucleus in the brain stem causes peripheral paralysis of the corresponding half of the tongue. Atrophy of the tongue muscles (thinning of the paralyzed half of the tongue), hypotonia (the tongue is thin, spread out, elongated), deviation of the tongue when it protrudes towards the paralysis, and fibrillary twitching are observed. Movement of the tongue in the affected direction is limited or impossible. Possible disturbance of sound pronunciation - dysarthria.

Accessory nerve syndrome

When the accessory nerve or its nucleus is damaged in the brain stem, peripheral paralysis of the sternocleidomastoid and trapezius muscles develops. As a result, the patient experiences difficulty turning his head to the healthy side and, if necessary, raising his shoulder. Raising the arm above the horizontal line is limited. Shoulder drooping is observed on the affected side. The lower angle of the scapula extends from the spine.

Syndrome of combined lesions of the glossopharyngeal, vagus and hypoglossal nerves (bulbar syndrome)

When the glossopharyngeal and vagus nerves are damaged, motor disorders are characterized by peripheral paralysis of the muscles of the pharynx, larynx, soft palate, trachea, and tongue. This condition is called bulbar palsy. Paralysis of the muscles of the pharynx leads to difficulty swallowing. When swallowing, patients choke. Paralysis of the muscles of the epiglottis leads to the entry of liquid food into the larynx and trachea, and paralysis of the soft palate leads to the flow of food into the nasal cavity. Paralysis of the mouse larynx leads to sagging of the ligaments and to aphonia or hypophonia (the voice becomes silent). Due to the sagging of the soft palate, the voice may take on a nasal tone. The tongue deviates to the healthy side. Due to tongue paralysis, chewing is impaired. The tongue deviates to the affected side, its movements are difficult. Atrophy and hypotonia of the tongue are observed. There is a violation of sound pronunciation: bulbar dysarthria develops. The palatal and pharyngeal reflexes disappear.

The vagus nerve provides autonomic (parasympathetic) innervation of blood vessels and internal organs (including the heart). Its bilateral defeat causes death due to cardiac and respiratory arrest.

With severe damage to the first or second motor neurons, the central ordecrease in volume and strength of movements) - central orperipheral paralysis, with partial damage (onlyspherical paralysis or paresis has one common symptom - the inability to make voluntary movements or difficulty in performing movements due to weakness in the limbs. For a range of symptoms, the centraland peripheral paralysis are different from each other,which is of great diagnostic importance, as it helps to establish the topic of damage to the nervous system.

Symptoms of central (or spastic) paralysis, which occurs when the central motor neuron is damaged at any level (precentral gyrus, internal capsule, brain stem, spinal cord), are as follows.

1.Increased muscle tone - muscle hypertension.

2.Increased tendon and periosteal reflexes - hyperreflexia.

3.Rhythmic, long-lasting contractions of any group muscles with certain summoning techniques - to a clone sy.

4. Extensor and flexion pathological reflexes.

Extensor ones are manifested by extension of the big toe when applying line irritation along the outer edge of the sole (Babinsky) (Fig. 24) or along the front surface of the leg (Oppenheim), when squeezing the calf muscle (Gordon), squeezing the Achilles tendon (Schaeffer reflex), holding the handle of a hammer near the external condyle (Chadok reflex) 12).

Extensor pathological reflexes (Babinsky, Oppenheim, etc.) can also be caused by cold stimulation (ethyl chloride). Babinsky himself pointed out the possibility of extending the zone of evocation of the reflex he described to the lower leg, thigh, and even torso. Therefore, the symptoms of Oppenheim, Schöffer, Chadok and others can be considered as variants of the Babinski reflex.

Flexion pathological reflexes are manifested by reflex flexion of the fingers or toes in response to a short extension blow to their tips (Rossolimo reflex) or when struck on the back of the hand or foot (Bechterew reflex I), a blow to the heel (Bechterew reflex II), in the middle of the sole or palms (Zhukovsky reflex), along the area of ​​the styloid process (Jacobson-Lask reflex).

5.Defensive reflexes, i.e. involuntary movements, expressed in flexion or extension of the paralyzed limb when it is irritated (injection, cooling).

6.Synkinesias are various kinds of involuntary cooperative movements in paralyzed limbs, observed in response to some purposeful or involuntary movement.

7. Adductor symptoms - adduction of the paralyzed leg during percussion along the iliac crest (Razdolsky's symptom) or along the tibia (Marie's symptom), or along the sole (Bal's symptom) Ducci).

All symptoms of central paralysis indicate damage to the first motor neuron - pyramidal cells in the cortex or any part of the corticonuclear or corticospinal (pyramidal) tracts from the cortex to the motor neurons of the brain stem and spinal cord.

The large extent of the pyramidal tract causes the frequent appearance of symptoms of central paralysis when the process is localized at different levels of the nervous system - in the cortex, subcortex, internal capsule, trunk,

spinal cord. Early symptoms are as follows: slight hyperreflexia (anisoreflexia), unstable pathological Babinski reflex, slight increase in muscle tone. Moreover, they can appear not only with focal lesions of the nervous system, but also with exogenous and endogenous intoxications (poisoning with neuroleptics and sleeping pills, anesthesia, eclampsia, uremia, etc.).

The pathophysiological basis of the symptoms of central paralysis is the loss of the inhibitory influences of the cerebral cortex on intraspinal automatisms.

Symptoms of peripheral (or flaccid) paralysis, which occurs when a peripheral motor neuron is damaged at any level (motoneurons of the trunk or spinal cord, anterior roots, plexuses, nerves), are as follows. 1. Loss or decrease in muscle tone - muscle atony or hypotonia.

2.Absence or decreased tendon reflexes - areflexia or hyporeflexia.

3.Muscle malnutrition - muscle atrophy.

4.Violation of electrical excitability - reaction I rebirth (cathode closure contraction - KZS - equal to or less than anode closure contraction - AZS).

It should be taken into account that lesions of the anterior horn are more characterized by fibrillary twitching, early appearance of muscle atrophy and degeneration reactions, while lesions of the anterior roots are characterized by fascicular twitching, areflexia and atony of muscles in the innervation zone, etc.

The symptomatology of peripheral paralysis is due to complete or partial efferent denervation of muscles - their disconnection from the motor neurons of the anterior horns of the spinal cord. Tendon reflexes are closed in the cells of the anterior horn; from them, impulses supporting tone and trophism, etc., are constantly supplied to the muscles.

Diagnosis of central and peripheral paralysis should be carried out taking into account all its signs. The development of muscle atrophy and tone disorders occurs whendiseases that do not directly affect motor neurons: myopathy, myotonia, thyrotoxicosis, dermatomyositis, rheumatoid arthritis, scleroderma. Decreased or increased tendon reflexes may be congenital, etc.

Topical diagnostics. Cerebral cortex. For outbreaks in the precentral gyrus paralysis (complete lack of movement) or paresis (decreased strength and range of movement) develops on the opposite half of the body. Due to the large extent of the precentral gyrus, it is more often necessary to observe not hemiplegia (lack of movement in one half of the body), but monoplegia (lack of movement in one of the limbs) of the arms or legs or hemiplegia with predominant damage to the muscles of the face (with foci in the lower part of the precentral gyrus), arms (for lesions in the middle section of the precentral gyrus) or legs (for lesions in the upper sections of the precentral gyrus). If any process does not turn on, but only irritates the motor cells of the precentral gyrus (this is usually observed in the initial phase of the disease), clonic convulsions occur, i.e., seizures of cortical (Jacksonian) epilepsy.

For outbreaks in premotor zone complex motor acts are upset - professional skills, for example, playing the piano, typing. Isolated movements of the arm, hand and individual fingers are preserved.

During processes in parietal lobe Afferent paresis with muscle atrophy may develop, i.e., a movement disorder due to loss of sensory information necessary for this.

At the outbreak in the knee and hind leg In the internal capsule, where the pyramidal tract passes, hemiplegia or hemiparesis develops with damage to the VII or XII nerves of the central type. In case of defeat ventral parts of the brain stem (passage of the pyramidal tract) central hemiplegia (hemiparesis) occurs on the opposite side. In this case, more dorsally located nuclei of the cranial nerves may also be involved with the development of peripheral paralysis of the corresponding muscles of the eyeball, face, tongue on the side of the lesion, i.e., the so-called.

Alternating syndrome. Whenbilateral involvement corticonuclear pathway develops to the IX-X-XII nervespseudobulbar paralysis, and in case of defeatcores these nerves (their roots or nerve trunks) -tabloid paralysis (see topical diagnostics section).

Defeat area pyramid intersection leads to paralysis of the arm on the side of the lesion and the leg on the opposite side (syndrome hemiplegia cruciatus). Defeat lateral funiculus spinal cord leads to central paralysis of the muscles below the localization of the lesion, and both lateral cords spinal cord on upper cervical level causes central tetraplegia. If the outbreak is at the thoracic level, lower central paraplegia appears. When involved lateral funiculi and anterior horns on level of cervical thickening peripheral paralysis of the arms and central paralysis of the legs develops.

Defeat area pyramidal cross leads to flaccid paraplegia, anterior horns, anterior roots And peripheral nerves causes peripheral paralysis in the corresponding innervation zone (segmental, radicular, peripheral nerve).

It must be taken into account that when the internal capsule, brain stem, spinal cord and peripheral nerves are damaged, complex combined syndromes of disorders develop, including not only disorders of motor function, but also sensitivity, statics, gait, and coordination of movements.

Article on the topic Central peripheral paralysis

Considering organic paralysis and paresis, it is necessary to imagine the path that the nerve impulse takes. It originates in the cerebral cortex brain and runs throughout two sections: central and peripheral. The central section is located from the anterior central gyrus of the brain brain to the anterior horns of the dorsal brain Peripheral area - from the dorsal brain and to the muscle. This distinction is essential because defines type of organic paralysis- peripheral or central, respectively, which have different external manifestations, treatment methods and prognosis. (In the case of the facial muscles, the central segment of the path ends not in the spinal cord, but in the nuclei of the cranial nerves).

It has now been established that:

1) central paralysis occurs when the central segment of the nerve pathway in the brain or spinal cord is damaged;

2) peripheral paralysis occurs when the peripheral segment in the anterior horns of the spinal cord is damaged brain, in individual nerves, in nervous

muscle junctions (synapses) and muscles;

3) in certain diseases, isolated damage to the anterior horn of the dorsal brain, in which both the central and peripheral segments suffer - there is mixed type of paralysis.

Central paralysis (paresis) is characterized by three main symptoms:

1) increased muscle tone - hypertonicity or muscle spasticity;

2) increased reflexes - hyperreflexia;

3) the appearance of pathological reflexes and accompanying movements.

All these manifestations are a consequence of increased activity of the spinal cord. brain, which is a much more ancient formation in historical terms than the head one. Therefore, it contains more ancient “programs” of behavior and reflexes consisting of immediate action, i.e. muscle contraction, since the restraining influence of the cerebral cortex brain interrupted, the muscles begin to act according to the “spinal cord program”, they are constantly tense. Suffice it to recall the freshwater hydra from several biology textbooks: to any irritation - mechanical or chemical (an injection or a drop of a chemical), it reacts in the same way - with a general contraction.

For central paralysis the muscles involved become like this hydra - they are contracted (tense). Depending on the location where the passage of nerve impulses is interrupted, different muscle groups may be involved. In its own way prevalence of central palsy divided into monoplegia (one is paralyzed limb), hemiplegia (paralysis one half body), paraplegia (paralysis two symmetrical limbs, upper or lower), tetraplegia (all four limbs are paralyzed).

For peripheral paralysis a completely different picture is observed. It is also characterized by three signs, but completely opposite ones:

1) decrease in muscle tone, up to its complete loss - atony or hypotension;

2) loss or decrease in reflexes - areflexia or hyporeflexia;

3) muscle atrophy as a consequence of impaired muscle tissue metabolism due to the lack of neurotrophic influence.

If with central paralysis the muscle receives nerve impulses, but not completely, but only from the spinal brain, That with peripheral paralysis the muscle receives nothing. Therefore, if in the first case there is perverted muscle activity (constant tension or spasm), then in the second there is no activity at all. Due to these causes of central paralysis also called spastic, and peripheral flaccid.

It was mentioned above about isolated lesions of the anterior horns of the dorsal brain There are diseases (for example, amyotrophic lateral sclerosis) with pathology only of these formations. Here both the central and peripheral sections of the path will be involved in the process. Type of paralysis experienced will be mixed, i.e. having signs of the first and second types. Of course, three signs will come to the fore: flaccid (peripheral) paralysis: atony, atrophy, areflexia. But thanks to the influences of the spinal brain from neighboring areas, a fourth feature is added, which is already characteristic of spastic (central) paralysis. These are pathological, i.e. reflexes that do not occur normally, since muscle tone and activity are reduced, they will manifest themselves to a rather weak degree and over time, as a result of the development of the disease, they will fade away completely.

The second large group, as already mentioned, is - functional paralysis. As follows from the definition, there is no organic damage to the neuromuscular pathway, and only the function suffers. They occur in various types of neuroses, usually in hysteria.

Origin of functional paralysis, According to the theory of Academician Pavlov, it is explained by the emergence in the cerebral cortex brain individual foci of inhibition.

Depending on the location of the outbreak, different areas will be paralyzed. So in some cases, during severe mental shocks, a person can freeze and become immobilized - fall into a stupor, which will be a consequence of extensive diffuse inhibition in the cerebral cortex brain Therefore, stupor can, with some stretch, be attributed to temporary paralysis functional type.

In hysteria there may be clinical picture of peripheral paralysis, hemiplegia, paralegia, monoplegia are of organic origin, but the similarity remains purely external and there are no objective signs that can be obtained through instrumental examination. Paralysis can take various forms, appear and disappear, change. As a rule, it is always possible to identify their “benefit” for the patient. There is also a special form of movement disorder characteristic of hysteria - astasia-abasia - the inability to walk and stand with the organic integrity of the supporting apparatus, muscular and nervous system.

Another feature that has very specific features, but is not mentioned above and paralytic peripheral type. It manifests itself in a neuromuscular disease, myasthenia gravis, and consists of “pathological fatigue” of the muscles. The essence of this phenomenon is the increase in the degree of paresis during functioning, i.e. work. The muscles seem to get tired quickly, but recover after rest. Since there is damage to the neuromuscular junction, in everything else is paralyzed have signs of a peripheral type.

Professor Balyazin Viktor Aleksandrovich, Honored Doctor of the Russian Federation, Professor, Doctor of Medical Sciences, Head of the Department of Nervous Diseases and Neurosurgery, Rostov State Medical University, Rostov-on-Don.

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Martirosyan Vazgen Vartanovich

Professor,Doctor of Medical Sciences,Assistant at the Department of Nervous Diseases of Rostov State Medical University since 1958,Neurologist of the highest qualification category

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Fomina-Chertousova Neonila Anatolyevna, Candidate of Medical Sciences,Assistant at the Department of Nervous Diseases and Neurosurgery,Neurologist, epileptologist of the highest qualification category

Peripheral paralysis occurs when a peripheral motor neuron (nerve cell, axon, ending in a synaptic plaque through which efferent impulses are transmitted to the muscle) is damaged. Afferent impulses to the cell enter through dendrites. Peripheral neurons include the nuclei of the motor cranial nerves with the nerves extending from them and the cells of the anterior horns of the spinal cord, from which the anterior roots extend, forming plexuses that pass into the peripheral nerves ending in the muscles. In order to understand the essence of nervous processes, it is necessary to take into account bioelectrical phenomena (the cell membrane and axon are electrically polarized) and biochemical processes (the synapse contains a chemical mediator - acetylcholine, which is subject to the action of cholinesterase). The dynamics of bioelectrical and biochemical processes are associated with the processes of excitation and inhibition; if the excitation processes in the synapse are disrupted, the transmission of impulses stops, and asynapsia develops.

In the cells of the anterior horns of the spinal cord, transformation of various impulses occurs: 1) arriving through the dorsal roots and dorsal horns (extero- andproprioceptive impulses); 2) from the motor area of ​​the cerebral cortex (cytoarchitectonic fields 4 and 6) along the pyramidal tract; 3) from the thalamus, striopallidal system and cerebellum through the red nucleus as part of the rubrospinal tract; 4) from the reticular formation of the brain stem along the reticulospinal tract; 5) from the vestibular nuclei of the brain stem and cerebellum; 6) from the front andposterior quadrigeminal tract along the tectospinal tract (for the implementation of adjustment reflexes to visual and auditory stimuli). From the cells of the anterior horns of the spinal cord, impulses pass through the axons to carry out motor functions (movements, strength and muscle tone), to perform reflexes from muscles and joints in response to proprioceptive stimuli, motor reflex reactions in response to nociceptive and interoceptive stimuli (muscle tension during pathologies of internal organs), as well as segmental skin reactions carried out with the participation of autonomic innervation (vasomotor, pilomotor, temperature, etc.).

According to the latest scientific data (Granite), alpha and gamma pathways are distinguished for the innervation of muscles (Fig. 9). The path of slowly conducting impulses provides regulation of muscle tone, the “position reflex” or “postural reflex”; the fast-conducting pathway causes muscle contraction. Skeletal muscles contain fibers called muscle spindles that contain stretch receptors. Skeletal muscle fibers receive neuromotor innervation from the anterior horn cells and carry out tonic function (slow-acting fibers) and physical activity (fast-acting fibers). Posture is associated with tonic activity, and movement is associated with phasic activity. Accordingly, there is a tonic stretch reflex and a phasic tendon reflex. In the act of walking, reciprocal innervation is important: excitation of the hip flexors causes reciprocal inhibition of the extensors of the same hip and the hip flexors on the opposite leg, and before raising one leg, the person moves the center of gravity to the other leg. An essential factor in the activity of a peripheral neuron is the implementation of muscle trophism.

Symptoms of peripheral paralysis (paresis) are as follows: 1) absence or limitation of range of motion of the corresponding muscles; 2) whether there is a decrease in muscle tone - hypotension or atony, which determines the name “flaccid” paralysis; 3) weakening of muscle strength; 4) absence or decrease in tendon and periosteal reflexes as a result of damage to the effector section of the reflex arc; 5) degenerative muscle atrophy, which occurs as a result of muscle denervation and is characterized by a violation of electrical excitability with a degeneration reaction. Disturbances in electrical excitability are expressed in quantitative (muscle contraction requires a greater current) and qualitative (perversion of reaction) changes. Changes in electrical excitability are detected by studying the faradic and galvanic current of the nerve and muscles. With a complete reaction of degeneration, irritation by faradic current of the muscles and nerves does not cause contraction. When the nerve is irritated by galvanic current, muscle contraction also does not occur. Irritation by galvanic current of the muscles causes sluggish, worm-like contractions; shorting the anode causes a stronger contraction than shorting the cathode (AZSZhZS). In case of incomplete disruption of nerve conduction, a partial degeneration reaction is observed, characterized by varying degrees of disruption of faradic and galvanic excitability; 6) violation of muscle chronaxy; 7) changes in muscle biocurrents, determined by electromyography.

The symptoms of peripheral paralysis vary depending on the level of damage to the peripheral motor neuron: anterior horn cells, anterior roots, plexuses or peripheral nerves.

When the cells of the anterior horns are damaged, muscle paralysis of the poliomyelitis type occurs, depending on the localization of the pathological process. Each muscle receives innervation from 1-3 adjacent segments. The cells innervating the muscles of the trunk lie medially, the cells for the muscles of the limbs are located laterally, dorsal for the flexor group, ventral for the extensor group. With partial damage to the cells of the anterior horns of the spinal cord, muscle function is not completely impaired, since the innervation of the muscles is preserved due to the intact cells of the anterior horns. For the diagnosis of damage to the cells of the anterior horns, uneven damage to individual fibers in the muscle is important, detected during electrodiagnostics and indicating the segmental nature of the process. In a chronic pathological process, fibrillar muscle twitching is sometimes observed in the cells of the anterior horn. They arise when the cells of the anterior horns are irritated in the case when the neurons that have not yet died are in a state of irritation by the pathological process. For the differential diagnosis, the distribution of paralysis and atrophy plays an important role. In the anterior horns there is a somatotopic distribution of nerve cells. The relationship between the segments and the corresponding muscles of the trunk and limbs is as follows: Ci-Civ segments innervate the muscles of the neck, Cv-Sch and Di - Du - muscles of the upper extremities, Dm - Dxn and Li - muscles of the trunk, Li - Lv and Si - Sn - muscles lower extremities, Siii -Sv - muscles of the perineum and genitourinary organs. Poliomyelitis-type paralysis is characterized by a proximal type of lesion: on the arms - the muscles of the shoulder girdle (deltoidmuscle, shoulder muscles, flexors and extensors of the forearm), on the legs - muscles of the pelvic girdle, thigh, and less often the lower leg. Paresis is often unilateral.

Peripheral paralysis or paresis as a result of damage to the cells of the anterior horns of the spinal cord (Fig. 10) occurs with poliomyelitis, spring-summer tick-borne encephalitis, ascending Landry's paralysis, paralytic form of rabies, rabies encephalomyelitis, spinal cord tumor, syphilitic process, due to blockage of the anterior spinal artery , amyotrophic lateral sclerosis. Peripheral paralysis of the muscles of the hands and fingers is observed with syringomyelia (anterior horn form) as a result of damage to the cells of the anterior horns. In this case, paralysis is combined with a dissociated sensitivity disorder: impaired pain and temperature sensitivity while maintaining tactile and deep sensitivity. A special form of peripheral paralysis is paroxysmal muscle weakness, paresis or paralysis caused by electrolyte disturbances (dyskalemic paralysis) due to metabolic disorders in acute renal failure. The disturbance in the conduction of impulses through synapses is leveled out with the introduction of anticholinesterase drugs (prozerin, nivalin).

The diagnostic value of each symptom becomes more definite when comparing symptoms and syndromes of dysfunction with anamnesis, with data indicating the duration of the disease, the course of the disease and the dynamics of symptoms.

Patient S., 15 years old, complains of limited movements in his left hand. At the age of 10 he suffered from polio. Upon examination, limited movement was found in the left shoulder and elbow joints. Sharp loss of left shoulder muscles, loss of forearm muscles. Slight weakness in the fingers of the left hand. The tone and strength of the muscles of the left arm are reduced. The electromyogram shows changes characteristic of peripheral paralysis. A study of electrical excitability revealed a reaction of degeneration of the muscles of the left hand. Sensitivity is not impaired. There are no tendon reflexes. Diagnosis: residual effects of polio. In this case, there are residual phenomena of paralysis, which are caused by a persistent disruption of the structure of the cells of the anterior horns of the spinal cord after polio suffered many years ago.

Rice. 10. Peripheral paralysis of the left hand (a), muscles of the shoulder girdle (b).

When the anterior roots are affected, paralysis occurs, which resembles paralysis when the anterior horns of the spinal cord are affected, but unlike the latter, atrophy when the anterior roots are affected is not accompanied by fibrillar twitching (sometimes there are fascicular twitching). The anterior roots are rarely affected in isolation; usually their damage is combined with damage to the dorsal roots. Damage to the anterior roots of the spinal cord can occur due to trauma, tumor, tuberculosis or osteomyelitis of the spine, pachymennitis, epiduritis. When the upper cervical roots are affected, upper cervical radicular syndrome occurs. When the process is localized in the Cv - Cyi area, atrophy and paralysis involve the deltoid, biceps, brachioradialis, and brachialis muscles. When the process is localized in the lower cervical roots, lower cervical radicular syndrome occurs, in which the triceps brachii muscle atrophies,If the muscles of the hand and forearm are damaged, Horner's syndrome develops. When the anterior roots are damaged in the thoracic region, weakness of the abdominal muscles (paresis) occurs: Dvn - Dxn innervate the rectus abdominis muscles; Dvii - Lj innervate the transverse abdominal muscles. When the anterior roots are affected in the lumbosacral region, limited movements, weakness in the legs, weight loss and flabbiness of the corresponding muscles are observed. When the pathological process is localized in the roots Li - Lts, the hip flexors are affected, bn - Liv - the quadriceps femoris muscle, Liv - Lv - peroneal group, Lv - Si - gastrocnemius, Liv - Si - gluteal, Shi - Sv - perineal muscles. When the cauda equina is affected, asymmetric peripheral paralysis of the feet with atrophy occurs.

When the plexuses are damaged, motor and sensory disorders are observed, the symptoms vary depending on the localization of the pathological process. When the cervical plexus, which is formed from the anterior branches of the first four cervical nerves, is damaged, paralysis of the deep cervical muscles and paralysis or irritation of the phrenic nerve occurs. Irritation of the diaphragm manifests itself as hiccups. Damage to the cervical plexus can occur due to tumors, enlarged lymph glands, tuberculous, purulent and other processes in the area of ​​the upper cervical vertebrae. When the brachial plexus, formed by the V, VI, VII and VIII cervical and I thoracic roots, is damaged, paralysis occurs in the deltoid, biceps, brachialis, coracoid, rhomboid, suprascapular and subscapularis muscles (upper type of Erb's palsy), small muscles of the hand, palmar surface of the forearm ( Dejerine-Klumpke lower palsy). Damage to the brachial plexus occurs with cervical lymphadenitis, tumor (carcinoma of the apex of the lung), aneurysm of the aorta and subclavian artery, trauma (dislocation of the head of the humerus, fracture of the clavicle, stretching of the plexus with a sharp abduction of the raised arm outward and backward), in the presence of a cervical rib, etc. When the lumbosacral plexus, formed by the branches of the lumbar and sacral roots, is damaged, a combined lesion of the femoral and sciatic nerves occurs.

When peripheral nerves are damaged, muscle paresis is observed according to the innervation of a certain nerve (Fig. 11), sensitivity disorders in the area of ​​innervation of the nerve, pain, degenerative muscle atrophy, vasomotor and trophic disorders, especially when nerves are damaged, abundantly containing autonomic fibers. When the radial nerve is damaged (Fig. 12), paralysis of the triceps, brachioradialis, extensors of the hand and fingers, and abductor pollicis longus occurs; The longest fibers are the most vulnerable. There is a “sagging” of the hand at rest. When you stretch your arms forward, the sore hand assumes a posture of flexion and pronation (flexion of the fingers). Extension of the hand and main phalanges of the fingers is limited or absent, supination of the hand and abduction of the thumb are impaired, impossibilityyou can spread your fingers. Damage to the radial nerve occurs due to intoxication (alcohol, lead), injuries of moderatethird of the shoulder (the nerve is located close to the bone and when pressed
this area is easily injured).

With ulnar nerve palsy, atrophic paralysis of the small muscles of the hand, interosseous, lumbrical muscles of the fourth and fifth fingers, the hypothenar muscles, the deep head of the short

flexor digitorum, adductor pollicis, flexor carpi ulnaris, flexor digitorum profundus. Due to paralysis of the interosseous muscles, the hand becomes “clawed”.

Damage to the femoral nerve is characterized by atrophy of the quadriceps muscle, hypotonia of the muscles of the anterior surface of the thigh, the inability to straighten the leg at the knee joint and the absence of

Rice. 12. Position of the hand and fingers in case of nerve damage: ulnar (a),
radial (b) and median (c).

lazy reflex. If the sciatic nerve is damaged in the upper part, flexion of the leg and dorsiflexion of the foot are limited, and the Achilles reflex is reduced. In the popliteal region, the sciatic nerve divides into the tibial and peroneal nerves. If the tibial nerve is damaged (Fig. 13, a), thinning of the calf muscles is noted. The patient cannot stand on his toes, the toes have a claw shape, and the Achilles reflex is absent. Vasomotor-trophic disorders are detected in the foot. When the peroneal nerve is damaged (Fig. 13, b), there is a limitation in the dorsiflexion of the foot, as a result of which the foot sag and the gait is “cock-like,” that is, the patient raises the leg higher than usual so as not to touch the floor with the ends of the toes.

The polyneuritic type of peripheral paralysis is characterized by multiple and symmetrical distribution of paralysis in the distal limbs (Fig. 13, c), the presence of degenerative atrophies, the absence of tendon reflexes and impaired sensitivity in the distal limbs.

Patient G. suffered a febrile state with high temperature, after which he began to notice weakness in the legs, feet and weakness of the hands. On examination: symmetrical paresis of the feet and hands with degenerative muscle atrophy, absence of tendon reflexes, autonomic disorders (cyanosis, coldness) and impairment of all types of sensitivity in the distal extremities. Diagnosis: polyneuritis after viral flu.

Treatment. Exercise therapy (passive and active movements of paretic muscles) - kinesiotherapy, massage, biostimulants that improve synaptic conduction (prozerin, dibazol, galantamine), as well as strychnine, securinine, vitamins.

The motor cranial nerves begin from the motor cells of the nuclei of the cranial nerves of the brain stem (homologues of the anterior horns of the spinal cord) and extend to the base of the brain as part of the cranial nerve root. Damage to the nucleus or root of the cranial nerve causes peripheral paralysis syndrome. In Fig. Figure 16 (see color insert, pp. 96-97) shows a diagram of the location of the nuclei of the cranial nerves in the brain stem.

Oculomotor nerve (III pair). The nuclei of the third nerve (paired magnocellular nucleus, paired small-celled parasympathetic nucleus of Yakubovich and unpaired nucleus of Perlia) are located in the gray matter under the bottom of the Sylvian aqueduct at the level of the anterior colliculus. In the anterior section of the external paired magnocellular nucleus there are cells innervating the muscle that lifts the upper eyelid, below there are cells for the superior rectus and inferior oblique muscles, inwards there are cells for the internal rectus muscle of the eye, and most posteriorly there are cells for the inferior rectus muscle of the eye. The Yakubovich nucleus innervates the sphincter of the pupil and the ciliary muscle. The Perlia core performs convergence. The fibers of the oculomotor nerve extend to the base of the brain along the inner surface of the cerebral peduncles, then pass above the cavernous sinus. The oculomotor nerve exits the cranial cavity through the superior orbital fissure. The oculomotor nerve innervates 5 striated muscles: the levator superior eyelid, the superior rectus (turns the eyeball upward and somewhat inward), the internal rectus (moves the eyeball inward), the inferior oblique (turns the eyeball upward and outward), the inferior rectus (turns the eyeball downward). and somewhat medially) and 2 smooth muscles: the sphincter of the pupil and the ciliary, or accommodative, muscle. Parasympathetic fibers to smooth muscle are interrupted in the ciliary ganglion. Convergence occurs with simultaneous contraction of both internal rectus muscles of the eye. With an isolated lesion of the Yakubovich nucleus, internal ophthalmoplegia is observed (dilation of the pupil, lack of direct and friendly reaction of the pupil to light and impaired accommodation). When the magnocellular nuclei are affected, external ophthalmoplegia, diplopia, ptosis, divergent strabismus, and lack of upward, downward and inward movements of the eyeball are observed. Ophthalmoplegia (Fig. 17, a, b) can be expressed differently when the nucleus and root of the oculomotor nerve are affected.

Symptoms are different when the nucleus and nerve are affected. If the nucleus is damaged: ptosis is less pronounced, pupil function and accommodation are relatively preserved. In case of nerve damage: ptosis appears early, since the fibers are located in the lateral parts of the nerve, paralytic mydriasis and impaired accommodation are noted.

Nuclear damage is observed in polioencephalitis, nerve damage is observed in basal meningitis.

Damage to the oculomotor nerve is observed with compression of the cerebral peduncle, circulatory disorders in the midbrain (Weber's alternating syndrome), aneurysm of the posterior communicating artery, tumors in the area of ​​the bottom of the Sylvian aqueduct, pituitary gland or superior orbital fissure, and with syphilitic meningitis. Recurrent paralysis of the oculomotor nerve is observed in migraine (ophthalmoplegic form) and multiple sclerosis. Paresis of the eye muscles is observed with diphtheria polyneuritis, encephalitis, poliomyelitis, tabes spinal cord, myasthenia gravis, intoxication and after traumatic brain injury. Mild ptosis and mydriasis can occur when the oculomotor nerve is compressed at the edge of the Blumenbach clivus with an aneurysm of the posterior communicating artery, during processes in the cavernous sinus or thickening of the dura mater at the exit site of the oculomotor nerve inporus oculomotorii. In a pathological process in the quadrigeminal region, paresis of the third pair can be combined with gaze paresis and vertical nystagmus, and Parinovertical syndrome developsparesis of gaze, impaired convergence and pupillary reaction to light. Mydriasis is observed with drug intoxication (broom, santonine, atropine, belladonna, scopolamine, phenamine, quinine).

Trochlear nerve (IV pair). The nucleus of the trochlear nerve is located in the central gray matter of the Sylvian aqueduct at the level of the posterior colliculus. The root extends to the base of the brain along the outer edge of the cerebral peduncle and enters the orbit through the superior orbital fissure, innervating the superior oblique muscle of the eye, which rotates the eyeball outward and downward. With isolated damage to the trochlear nerve, diplopia is observed when looking down.

Abducens nerve (VI pair). The nucleus of the abducens nerve is located in the posterior part of the pons under the bottom of the rhomboid fossa, under the loop of the facial nerve. The fibers of the abducens nerve pass through the entire diameter of the bridge and exit it at the border with the continuation

Rice. 17. Functional disorders of the oculomotor nerves; ptosis (a), divergent strabismus (b), left abducens nerve palsy (c), convergent strabismus (d), bilateral ptosis (e), upward gaze palsy (f), anisocoria (g),left gaze paralysis (h).

with the brain in the region of the anterior lateral sulcus. The abducens nerve exits the cranial cavity through the superior orbital fissure. Innervates the external rectus muscle of the eye, which rotates the eyeball outward. With damage to the abducens nerveThere is an isolated paralysis of the external rectus muscle of the eye, which causes convergent strabismus (Fig. 17, c, d), double vision (especially when looking towards the affected muscle), and limitation of outward movements of the eyeball. The role of the abducens nerve is revealed in phylogenesis, since in animals the nucleus of the abducens nerve is highly developed to ensure that, with the help of the external rectus muscle of the eye, it can capture signals for protective and defensive movements and correctly orient itself in space.

Isolated abducens nerve palsy occurs with lesions of the pons, and lesions of the abducens nerve nucleus are often combined with lesions of the facial nerve root. Paralysis of the abducens nerve is observed with circulatory disorders in the brain stem, with demyelinating encephalitis, meningitis, tumors of the base of the brain, aneurysms of the posterior cerebral or superior cerebellar arteries. Lesions in the pons involving the abducens nucleus often cause gaze paralysis in the direction of the affected muscle. Thus, when the left nucleus of the abducens nerve is damaged, the eyeballs are turned to the right (left-sided gaze palsy occurs). Gaze paralysis is observed with lesions of the posterior longitudinal fasciculus: paresis of gaze up or down - with lesions of the posterior longitudinal fasciculus at the level of the midbrain, paresis to the sides - with lesions of the posterior longitudinal fasciculus in the pons or lesions of the corticonuclear tracts coming from the frontal lobe (cytoarchitectonic field 8) through the knee of the internal capsule to the nuclei of Darkshevich and Cajal, from which the posterior longitudinal fasciculus begins.

Facial nerve (VII pair) (Fig. 18). The nucleus of the facial nerve is located in the posterior part of the pons in the depth of the tire. The fibers of the facial nerve, heading upward and inward, form a genus surrounding the nucleus of the abducens nerve, then descend down and exit in the area of ​​the cerebellopontine angle. The nerve then passes through the internal auditory canal, the fallopian canal of the facial nerve and exits through the stylomastoid foramen, dividing into a number of branches (“crow’s foot”). The facial nerve innervates the muscles of facial expression, the muscles of the auricle, the cranial roof, the posterior belly of the digastric muscle, the stylohyoid muscle and the platysma. The facial nerve partially includes tear and salivary fibers, taste fibers, and fibers to the inner ear. When the facial nerve is damaged, peripheral paralysis of the facial muscles occurs. In this case, a sharp asymmetry of the face is observed: the affected side is motionless, the folds of the forehead and nasolabial fold are smoothed, the palpebral fissure is wider, the corner of the mouth is lowered. When the forehead is wrinkled, no folds form on the side of paralysis; when the eyes are closed, an open palpebral fissure remains (Bell's symptom) and the eyeball is visible upward and outward, lagophthalmos (incomplete closure of the eyelids). Brickner's symptom (absence or incomplete closure of the eyelids with strong auditory irritation), Marie-Foy's symptom (absence of muscle contractions on the side of the facial nerve paralysis with pressure on the sun) are noted.extending branch of the lower jaw), Monrad-Crohn's symptom (facial movements on a task are performed worse than spontaneous ones), orbicular Revillot's symptom (inability to close the eye on the affected side in isolation). The grin of the teeth is asymmetrical, whistling is impossible, speech is difficult due to damage to the orbicularis muscle

mouth When there is hypotonia of the muscles on the affected side of the facial nerve, a “sail” symptom is observed: the cheek puffs out and seems to “sail” in time with breathing.

Trophic functions are disrupted (weight loss of facial muscles and degeneration reaction). The superciliary and corneal reflexes fade away (Fig. 19). With paralysis of the facial nerve, hyperacusis (n. stapedius), dry eyes and lack of lacrimation (n. petrosus superficialis major) and salivation (n. salivatorius), and taste on the anterior 2/3 tongue (chordae tympani) appear. In a chronic process, fibrillary muscle twitching appears in the nucleus of the facial nerve. With peripheral facial paralysis, sometimes at the onset of the disease there is pain in the mastoid area. When the facial nerve is irritated, a spasm of the facial muscles (spasmus facialis) appears.

Peripheral paralysis of the facial nerve occurs when it is neuritis. In the long-term period after neuritis, tics of paretic muscles, friendly movements of the upper lip and oral muscles with the muscles of the upper eyelid (Hun's synkinesis), and contracture of paretic facial muscles may appear. Facial nerve damage

Rice. 19. Symptoms of left facial paralysis
nerve (a, b, c, d).

Accessory nerve (XI pair). The nucleus is located in the anterior horns of the spinal cord at the level of the I-V cervical segment. The roots emerge on the lateral surface of the spinal cord and, merging into one trunk, enter the cranial cavity through the foramen magnum, and then exit the skull through the large jugular foramen. Innervates the sternocleidomastoid and trapezius muscles. The function of the accessory nerve is to turn the head in the opposite direction, lift the shoulder, scapula and acromial part of the clavicle upward, pull the shoulder girdle posteriorly and bring the scapula to the spine. When the XIth nerve is damaged, the head deviates to the side (torticollis). There is a drooping of the shoulder girdle and clavicle, and an outward deviation of the upper edge of the scapula (paralysis of the trapezius muscle). There is atrophy of the sternocleidomastoid and trapezius muscles. Damage to the accessory nerve is manifested by difficulty raising the shoulders and turning the head in the healthy direction; in this case, drooping of the shoulder and departure of the lower edge of the scapula on the side of the affected nerve are noted. It is observed with neuritis, tumors of the craniospinal localization, trauma to the neck or base of the skull, tick-borne encephalitis, poliomyelitis, anomalies of the base of the skull, syringomyelia. Bilateral lesions occur in polyneuritis, poliomyelitis, myopathy and myotonic dystrophy.

Hypoglossal nerve (XII pair). The nucleus of the hypoglossal nerve is located at the bottom of the rhomboid fossa in the area of ​​trigonum n. hypoglossi. The roots extend to the base of the brain between the pyramids and olives of the medulla oblongata. Merging, they form a common stem, which exits the skull through the foramen hypoglossi. The nucleus of the XII pair is connected to the opposite hemisphere of the brain (the lower part of the anterior central gyrus), where the center of tongue movement is located. The hypoglossal nerve innervates the muscles of the tongue. Function m. genioglossus - protruding the tongue forward and in the opposite direction. Normally, the tongue is located in the midline. With paralysis of m. genioglossus tongue deviates towards the affected muscle, since m. genioglossus of the healthy side pushes the tongue in the opposite direction.

When the hypoglossal nerve is damaged, peripheral paralysis or paresis of the corresponding half of the tongue develops with atrophy and thinning of the muscles (Fig. 20, d). A degeneration reaction and fibrillar twitching are observed (if the nucleus is damaged). With bilateral damage, paralysis of the entire tongue develops, dysarthria (or anarthria) appears, and it becomes difficult to take fluids and food. It is observed with amyotrophic lateral sclerosis, circulatory disorders in the medulla oblongata (alternating Jackson syndrome), encephalitis, tumors in the brain stem, syringomyelia, anomaly of the foramen magnum, polioencephalomyelitis, trauma to the base of the skull, bulbar palsy. With central paralysis, which occurs with unilateral damage to the corticonuclear pathways due to the fact that the nucleus of the hypoglossal nerve is connected only with the opposite sexcerebral ball, the tongue deviates in the direction opposite to the lesion. There is no atrophy of the tongue muscles.

Among the cranial nerves there are mixed ones.

Trigeminal nerve (V pair) (Fig. 21). The motor and sensory nuclei of the trigeminal nerve are located in the pons (in the lateral part of the tegmentum). The motor fibers of the trigeminal nerve begin from the motor nucleus (nucleus motorius) and the mesencephalic root, located in the dorsolateral part of the pontine tegmentum. The fibers emerge in the form of a thin root and join the third branch of the trigeminal nerve. They innervate the masticatory muscles. Sensitive fibers start from the Gasserian ganglion and form three branches: orbital, maxillary and mandibular, innervating the corresponding areas of the face. Sensory fibers end in two nuclei: 1) fibers conducting superficial sensitivity - in the descending root of the trigeminal nerve (comes from the pons to the cervical spinal cord); 2) fibers conducting deep sensitivity in the sensitive core. In the descending root of the trigeminal nerve, fibers from the orbital branch pass ventro-laterally, from the mandibular branch - dorsomedially, from the maxillary branch - in the interval between them. The lower part of the descending root has a segmental structure: the cranial position is occupied by the cells where the fibers from the inner part of the face end, and the lowest - from the outer part of the face. Some of the fibers conducting superficial sensitivity contact the nuclei of the VII, IX and X nerves and pass as an independent bundle between the descending root and the Burdach bundle. The trigeminal nerve anastomoses with the plexus of the internal carotid artery in the cavernous sinus, with the facial nerve, chorda tympani, greater occipital, hypoglossal and glossopharyngeal nerves. In the zone of innervation of the trigeminal nerve, repercussive pain syndromes occur: in the area of ​​the upper branch, reflected pain during intracranial processes, as well as with pathology of internal organs and a repercussive phenomenon in syringomyelia. Rice. 21 (see color plate p. 96_______ 97)

When the motor fibers of the trigeminal nerve are damaged, the lower jaw (when opening the mouth) deviates in the direction of the lesion, the strength and tone of the masticatory muscles are reduced (mm. masseter, temporalis, pterygoideus lateralis et pterygoideus medialis; m. tensor tympani, m. tensor veli palatini, m. mylohyodeus et venter anterior, m. digastrici), atrophy of the temporal and masticatory muscles, a decrease in the masseter reflex, a degeneration reaction in the study of electrical excitability, and a change in oscillations on the electromyogram are noted. When the V pair is irritated, convulsive clenching of the jaws (trismus) appears. Observed in tetanus, meningitis, rabies. With bilateral supranuclear lesions, central paralysis develops (symptoms of pseudobulbar palsy), sagging of the lower jaw, and weakening of the mandibular reflex.

When the trigeminal nerve is damaged, shooting pains and sensitivity disorders occur in the innervation zone. To amazetion of the descending root of the trigeminal nerve is characterized by a segmental sensitivity disorder (disorder of surface sensitivity in the Zelder zones). When the upper branch (n. ophthalmicus) is affected, pain occurs in the area of ​​the eye, forehead and temple. When the middle branch (n. maxillaris) is affected, the pain is localized in the upper jaw. The lower branch (n. mandibularis) is characterized by localization of pain in the lower jaw and chin area. With trigeminal neuralgia, painful hyperkinesis occurs; the patient swallows air, coughs, blows his nose, closes his eyes, etc. Painful hyperkinesis is one of the symptoms of trigeminal neuralgia and is realized with the participation of the reticular formation. With the participation of afferent fibers of the trigeminal nerve (sensitive innervation of the mucous membranes of the mouth, tongue, nose, eyes), the following reflexes are carried out: corneal and conjunctival, from the mucous membranes of the nose and the mandibular reflex.

Damage to the trigeminal nerve occurs due to neuritis, pathological processes (tumor or inflammatory process, circulatory disorders in the trunk) at the site of the nerve, in the cerebellopontine angle or in the pons.

The glossopharyngeal nerve (IX pair) (Fig. 22, A) contains motor, sensory, gustatory and secretory fibers. The motor nucleus (nuel. ambiguus), common with the vagus nerve, is located in the tegmentum of the medulla oblongata, the roots extend to the surface of the brain outward from the inferior olive, in the posterior lateral sulcus. The glossopharyngeal nerve has two ganglia (ganglion superius and ganglion petrosum). Sensitive fibers end in two nuclei (nucl. alae cinereae and nucl. tractus solitarii). Salivatory fibers begin from nucl. salivatorius (common nucleus with XIII nerve). Motor nuclei IX and X pairs have bilateral connections with the cerebral cortex.

When the glossopharyngeal nerve is damaged, there is a violation of the taste for bitter on the same side of the tongue, anesthesia of the mucous membrane of the upper half of the pharynx and sometimes dry mouth, fasciculations of the soft palate.

With neuralgia of the glossopharyngeal nerve, “jerking” pain occurs, especially when eating, talking, swallowing, sometimes the pain begins in the tonsils, radiates to the ear, and is accompanied by salivation. When the IX nerve is irritated, a spasm of the pharyngeal muscles occurs (pharyngospasm).

The vagus nerve (X pair) (Fig. 22, B) is somatic and autonomic (visceral). The vagus nerve has motor fibers for striated and smooth muscles, sensory and secretory fibers. The vagus nerve has two ganglia (ganglion jugulare, ganglion nodosum). The nuclei are located in the medulla oblongata. The roots emerge on the surface of the brain in the amount of 12-16 between the inferior olive and the rope body below the roots of the glossopharyngeal nerve. Sensitive fibers end in nucl. alae cinereae, motor fibers start from two nuclei (nucl. ambiguus, nucl. dorsalis), the dorsal nucleus is visceral motor, the somatic nucleus innervates the muscles of the soft palate, pharynx, larynx, epiglottis. Motor visceral fibers innervate the smooth muscles of the trachea and bronchi, lungs, gastrointestinal tract and other abdominal organs.

Sensitive fibers of the vagus nerve end in the meninges, in the depths of the external auditory canal, pharynx, larynx, trachea, bronchi, lungs, gastrointestinal tract and other abdominal organs. Secretory fibers go to the stomach and pancreas, vasomotor fibers go to the vessels.

With unilateral damage to the vagus nerve, there is a drooping of the soft palate on the affected side, limited mobility on the affected side during phonation, deviation of the uvula to the healthy side, fibrillary twitching (with damage to the nucleus), paralysis of the vocal cord, dysarthria, dysphagia and dysphonia, decreased pharyngeal and palatal reflexes (bulbar palsy). With bilateral damage to the vagus nerve, aphonia, lack of swallowing, tachycardia, and slow irregular breathing are observed. If both vagus nerves are damaged, the patient cannot swallow, and cardiac activity and breathing are impaired. When swallowing, food enters the nose or windpipe and can sometimes cause asphyxia or aspiration pneumonia.

When the vagus nerve is irritated, convulsions of the laryngeal muscles, pharyngo-, esophago-, cardio-, pylorospasm, and cardiac dysfunction may occur.

These disorders are sometimes observed with neuritis of the vagus nerve, syringobulbia, encephalitis, tabes dorsalis, enlarged cervical lymph nodes, and amyotrophic lateral sclerosis.

When corticobulbar neurons are damaged bilaterally, pseudobulbar palsy occurs. Functional impairments are similar to bulbar palsy, but the pharyngeal and palatal reflexes are preserved, there is no muscle atrophy, reflexes of oral automatism, violent crying and laughter are pronounced. Pseudobulbar palsy is observed in cerebral atherosclerosis, atherosclerotic parkinsonism, and amyotrophic lateral sclerosis. Unilateral paralysis of the vagus nerve is observed with neuritis of the vagus nerve, poliomyelitis, brainstem encephalitis, diphtheria, botulism, circulatory disorders in the medulla oblongata (part of the Wallenberg-Zakharchenko syndrome), syringobulbia, tumors and other processes in the brain stem, included in Avellis syndrome, enlarged lymphatic nodes at the level of the jugular foramen.

Damage to the recurrent nerve occurs with mediastinal tumors, aortic aneurysm, cervical lymphadenitis, struma, trauma and neck surgery.