home Analyzes Peripheral paralysis develops when affected. Difference between central and peripheral paralysis. Hypoglossal nerve syndrome

Peripheral paralysis develops when affected. Difference between central and peripheral paralysis. Hypoglossal nerve syndrome

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.

PARALYSIS, PARESIS(Greek paralysis; syn. plegia; Greek, paresis weakening, relaxation) - loss (paralysis) or weakening (paresis) of motor functions with the absence or decrease in muscle strength as a result of various pathological processes in the nervous system, causing disruption of the structure and function of the motor analyzer.

Types of paralysis and paresis

There are organic, functional and reflex paralysis and paresis. Organic paralysis or paresis can develop as a result of organic changes in the structure of the central or peripheral motor neuron (brain or spinal cord or peripheral nerve), arising under the influence of various pathol processes (trauma, tumors, cerebrovascular accidents, inflammatory and other processes). Organic paralysis or paresis includes, for example, traumatic (including postpartum, obstetric, etc.), eclamptic (see Eclampsia), bulbar palsy (see), recurrent paralysis (see). The occurrence of functions, paralysis or paresis is associated with the influence of psychogenic factors, which lead to neurodynamic disorders of c. n. With. and meet ch. arr. with hysteria (see). Reflex paralysis or paresis is caused by neurodynamic functions, disorders of the nervous system that arise under the influence, as a rule, of an extensive lesion that is not topically related to the developed paralysis or paresis.

According to the prevalence of the lesion, monoplegia (monoparesis) - paralysis (paresis) of the muscles of one limb and diplegia (diparesis) - paralysis (paresis) of the muscles of two limbs are distinguished. Among diplegias, a distinction is made between upper and lower paraplegia (see), when the muscles of both arms or legs are paralyzed; partial paralysis of the muscles of both arms or legs, called upper or lower paraparesis. Paralysis or paresis of the muscles of one half of the body is called hemiplegia (see) or hemiparesis, respectively. Triplegia (triparesis) is paralysis (paresis) of the muscles of three limbs. Tetraplegia (tetraparesis) is paralysis (paresis) of the muscles of both arms and both legs.

Based on the nature of the tone of the affected muscles, flaccid, spastic and rigid paralysis and paresis are distinguished.

Depending on the level of damage to the motor analyzer, paralysis and paresis are divided into central, peripheral and extrapyramidal. In addition, there are traumatic and eclamptic paralysis and paresis, which can be of both central and peripheral origin,

Central paralysis or paresis by the nature of the tone of the affected muscles, as a rule, is spastic and develops as a result of organic damage to the central motor neuron in any part of the corticospinal (pyramidal) tract (in the cerebral cortex, internal capsule, brain stem, spinal cord ). Central paralysis is also called pyramidal palsy. The causes of central paralysis or paresis can be circulatory disorders, trauma, tumors, demyelinating and other processes of the brain or spinal cord that disrupt the structure of the pyramidal tract. Central paralysis is sometimes observed in children due to various brain lesions - in utero, during childbirth, and also during the newborn period (see Infantile paralysis). The most characteristic signs of central paralysis or paresis are muscle hypertension, hyperreflexia, the presence of patol, and protective reflexes, patol, friendly movements, decreased or absent skin reflexes.

Muscle tone in central paralysis and paresis is increased according to the spastic type. Muscle resistance is determined to a greater extent at the beginning of the movement, then sharply decreases (the “jackknife” symptom). With pronounced muscle hypertension, muscle-joint contractures develop. With hemiplegia (hemiparesis), muscle tone increases in the adductor muscles of the shoulder, flexors and pronators of the forearm, flexors of the hand and fingers, extensors of the hip and leg, adductor muscles of the thigh and plantar flexors of the foot. As a result, patients experience a characteristic Wernicke-Mann position: the arm is brought to the body, pronated and bent at the elbow and wrist joints, the fingers are bent, the leg is extended at the hip and knee joints, the foot is bent in the plantar direction. As a result of lengthening contracture of the leg, the gait of patients takes on the character of a mower's gait (the affected leg describes a semicircle with each step). With lower paraparesis, patients walk mainly on their toes, crossing their legs. In acute diseases of the brain or spinal cord (cerebrovascular accidents, injuries, infectious diseases), accompanied by central paralysis, muscle tone can be reduced due to the switching off of the influence of the reticular formation (diaschisal paralysis).

The level of damage to the central motor neuron is established on the basis of the localization of paralysis or paresis and its combination with other neurol symptoms. Thus, when the precentral gyrus of the cerebral cortex is damaged, hemiplegia of the opposite limbs develops with muscle atony in the initial period, followed by slow recovery and increased muscle tone, moderate revitalization of tendon and decreased abdominal reflexes, the presence of extensor pathols, reflexes. When the premotor area is damaged on the side opposite to the patol, the focus, spastic hemiplegia occurs with severe muscle hypertension, a sharp increase in tendon reflexes, clonus, coordination synkinesis, patol, flexion-type reflexes and preservation of abdominal reflexes. When the lesion spreads to the area of the postcentral gyrus of the cerebral cortex, sensitivity disorders occur, the recovery of impaired motor functions slows down, muscle hypertonicity decreases, and imitation synkinesis appears.

If the upper part of the precentral gyrus is damaged, monoplegia of the leg occurs; if its middle part is damaged, monoplegia of the arm occurs (on the side opposite to the lesion). Hemiplegia, observed when the pyramidal tract is damaged in the area of the internal capsule, is usually combined with hemianesthesia, central paresis of the facial and hypoglossal nerves. When the lesion is localized in the brain stem, central paralysis of the limbs opposite to the lesion is combined with dysfunction of the cranial nerves on the affected side and with a sensory conduction disorder in the paralyzed limbs (see Alternating syndromes, Gaze palsy, convulsions).

If there is a lesion in the pons or in the medulla oblongata, the alternating syndrome can be combined with respiratory distress, disturbances in cardiac function and vascular tone, and vomiting (see Bulbar palsy, Pseudobulbar palsy). Damage to the pyramidal tract in the spinal cord is accompanied by central paralysis or paresis, developing below the level of the lesion on the side of the lesion. Damage to half the diameter of the spinal cord is manifested by Broun-Séquard syndrome (see Brown-Séquard syndrome).

Peripheral paralysis or paresis, by the nature of the change in the tone of the affected muscles, is flaccid and is observed with damage to the peripheral motor neuron (cells of the anterior horns of the spinal cord or nuclei of the cranial nerves, anterior roots of the spinal nerves, plexuses, spinal or cranial nerves). The causes of peripheral paralysis or paresis can be infectious, infectious-allergic, degenerative pathol, processes (see Myelitis, Neuritis, Polyneuritis, Poliomyelitis), as well as traumatic injuries of the spinal cord, plexuses and peripheral nerves. The main symptoms of peripheral paralysis or paresis are muscle atrophy (see Muscle atrophy), their hypotension (see Tone, pathology of muscle tone), areflexia (see). Peripheral paralysis and paresis are characterized by changes in the electrical excitability of muscles (the so-called degeneration reaction). Depending on the location of the lesion along the neuron, peripheral paralysis has other features. Thus, when the cells of the anterior horn of the spinal cord are damaged, fibrillary twitching is observed; damage to the anterior roots of the spinal nerves causes movement disorders of the radicular type; movement disorders that occur when a peripheral nerve is damaged are combined with sensory disorders in the area of innervation of the affected nerve, as well as vasomotor and trophic disorders, especially in connection with damage to nerves containing a large number of autonomic fibers (for example, the median, sciatic nerves).

Extrapyramidal paralysis or paresis, due to the nature of the change in the tone of the affected muscles, is rigid and is observed when the pallidicular system of the brain is damaged. It is caused by a change in the influence of this system on the reticular formation (see) and a violation of cortical-subcortical - stem neural connections. Extrapyramidal paralysis and paresis, in contrast to the central (pyramidal) one, is characterized by hl. arr. absence or decrease in motor activity or movement (see Hypokinesia, Movements), decrease in the tempo of movements (see Bradykinesia), loss of friendly and automatic movements. As a result, there is a lack of movement (oligokinesia), slow speech, gait in small steps with the absence of accompanying hand movements (acheirokinesis). Muscle tone in extrapyramidal paralysis and paresis is increased according to the plastic type and is not springy (as in pyramidal paralysis), but waxy in nature (muscle resistance, determined by studying their tone, remains uniformly increased in all phases of movement due to its simultaneous increase in flexors and extensors , pronators and supinators). Often the “gear wheel” phenomenon can be observed (jerk-like rhythmic resistance to passive flexion and extension of the limbs), and the limb freezes in a given position (see Catalepsy). In contrast to pyramidal, with extrapyramidal paralysis or paresis there are no patol, reflexes and there is no sharp increase in tendon and periosteal reflexes. At the same time, an increase in postural reflexes appears (see).

Hysterical paralysis may have an external resemblance to peripheral paralysis, as well as hemiplegia, paraplegia or monoplegia of organic origin. But unlike them, in hysterical paralysis, the lack of movement and decreased strength in the limbs are not accompanied by changes in muscle tone and reflexes, trophic disorders, changes in electrophysiological, morphological, and biochemical indicators.

Traumatic paralysis or paresis develops as a result of injury to the central or peripheral nervous system and can be central or peripheral in nature, respectively. The most common cause of central traumatic paralysis or paresis is contusion or compression of the brain and spinal cord. Due to diaschisis (see) - a special type of shock that develops in the nerve centers in the acute period of injury - this paralysis can have the character of diaschisal paralysis.

Peripheral traumatic paralysis is observed with injuries to the spinal cord, spinal nerve roots, plexuses, and peripheral nerves. In cases associated with birth trauma, it is called obstetric paralysis. Obstetric paralysis occurs as a result of injury, most often to the brachial plexus and the roots that form it, in the fetus, when traction is performed by the hand while providing manual assistance during childbirth. Obstetric arm paralysis can be unilateral or bilateral; in this case, a distinction is made between upper Duchenne-Erb palsy (see Duchenne-Erb palsy), lower Dejerine-Klumpke palsy (see Dejerine-Klumpke palsy) and total paralysis. Obstetric paralysis of the arm is often accompanied by Bernard-Horner syndrome (see Bernard-Horner syndrome).

Peripheral traumatic paralysis or paresis can occur in women during the postpartum period (puerperal paralysis or paresis). It occurs, as a rule, after prolonged complicated labor due to compression of the lumbosacral plexus or its individual branches. In most cases, postpartum paralysis or paresis is unilateral, less often bilateral, but the lesions are asymmetrical. It manifests itself as weakness in the legs, gait disorder, impaired sensitivity in the area of innervation of the affected branches of the plexus and is characterized by a tendency to rapid restoration of impaired functions.

Eclamitic paralysis or paresis can be central or peripheral and develops in late pregnancy or during childbirth. Central eclamptic paralysis is caused by an acute circulatory disorder of the brain, often as a hemorrhagic stroke; less often, paralysis is a consequence of thrombosis of the cerebral vessels and sinuses of the dura mater. In this case, paralysis in most cases has the character of hemiplegia. Peripheral paralysis in eclampsia is a consequence of the effects of impaired metabolism products on the peripheral nervous system. More often, these paralysis are observed in late pregnancy, occur as polyneuritis and are characterized by predominant damage to the distal muscles of the extremities, accompanied by sensory disturbances and trophic disorders in the area of innervation of the peripheral nerves.

Diagnosis

Determining the nature of paralysis or paresis and identifying their cause is closely related to establishing the diagnosis of the underlying disease that caused the development of paralysis or paresis. Diagnosis uses various methods of clinical, laboratory, radiological, electrophysiological and other types of special studies.

Treatment of paralysis and paresis

Treatment of paralysis and paresis is part of the complex treatment of the underlying disease. It includes the use of drugs that improve metabolism in nervous tissue, increase the speed of nerve impulses, increase synaptic conductivity, and normalize muscle tone. Physiobalneotherapy, exercise therapy, massage, and orthopedic treatment are widely used.

Physiobalneotherapy helps restore the motor function of affected muscles, has an anti-inflammatory and analgesic effect, stimulates regeneration processes, prevents the development of atrophy of the affected muscles, the formation of contractures, and helps normalize muscle tone.

For peripheral paralysis and paresis, in the first days of treatment, UHF therapy (see) and microwave therapy (see), pulsed currents (see), ultrasound (see), electrophoresis (see) of drugs that provide analgesic effect - calcium, novocaine, etc. (see Electrophoresis), UV irradiation in erythemal doses (see Ultraviolet radiation). In the future, in order to improve the conductivity and excitability of the affected neuromuscular system, electrophoresis of anticholinesterase substances (proserine, galantamine), high-frequency alternating magnetic field, paraffin, ozokerite treatment in combination with electrical stimulation of the affected muscles and the corresponding segments of the spinal cord are used. Electrical stimulation (see), causing muscle contraction, improves their blood supply and trophism, prevents muscle atrophy, enhances afferent impulses, which helps restore impaired motor function of muscles. For electrical stimulation, various pulse currents are used, the parameters of which are selected depending on the severity of the lesion and the state of excitability of the neuromuscular system.

In the late recovery and residual periods, mud therapy (see) and mineral baths (sulfide, radon, sodium chloride, nitrogen-siliceous thermal, etc.) are used, which have a stimulating effect on the regeneration processes.

For central paralysis and paresis, physiobalneotherapy is introduced into complex treatment in the early recovery period: for injuries of the brain and spinal cord - in the 2-3rd week, inflammatory lesions of the c. n. With. - on the 3rd week, cerebrovascular accidents - on the 3-5th week. It is aimed at improving blood circulation in the affected area and stimulating the activity of nerve elements. For this purpose, electrophoresis of drugs (aminophylline, no-shpa, novocaine, magnesium, iodine, calcium) is used on the collar and sinocarotid zones using the general exposure method or the orbital-occipital method. The technique is chosen depending on the nature of the stroke or injury, the state of the cardiovascular system and the age of the patients. With inflammatory lesions c. n. With. UHF and microwave therapy are also prescribed.

Physiotherapy is used to restore impaired motor function, reduce spasticity, eliminate pain and contractures that impede movement. Electrical stimulation is used with pulses of low and high frequencies generated by single- and multi-channel devices. Antagonists of spastic muscles are stimulated predominantly. In this case, it is important to carefully select motor points, parameters and force of influence during the procedure in order to avoid increased spasticity. For mild spasticity, 1-2 courses are recommended, for moderate and severe spasticity - 2-3 courses of electrical stimulation at intervals of 3-6 weeks. With a slight increase in tone, electrical stimulation can be combined with electrophoresis of prozerin or dibazol using the method of local impact on muscles. With an early increase in muscle tone, as well as in the late recovery and residual periods, electrical stimulation is carried out with the simultaneous use of muscle relaxants. To reduce muscle tone, before electrical stimulation, treatment is carried out with heat (mud, paraffin, ozokerite applications) or cold in combination with treatment by positioning the paralyzed limb. Cryotherapy (see) is especially indicated for severe spasticity with contractures in patients aged no older than 60-65 years.

To relieve pain, sinusoidal modulated or diadynamic currents and electrophoresis using novocaine are used locally. For joint and muscle contractures, thermal procedures are prescribed (paraffin, ozokerite, mud applications, local warm baths), electrophoresis of medicinal substances, ultrasound, pulsed currents.

San.-kur. Treatment of patients with paralysis and paresis is carried out in local neurol, sanatoriums, mud and balneological resorts with sulfide, radon, sodium chloride, nitrogen-silicon thermal waters (Evpatoria, Kemeri, Odessa, Pyatigorsk, Sochi-Matsesta, Tskaltubo, etc.) or in specialized sanatoriums for patients with spinal cord lesions. For peripheral paralysis and paresis of dignity. treatment is indicated after 2-6 months. after the end of the acute period; for central paralysis and paresis - after 4-6 months. (see Sanatorium and resort selection).

Therapeutic exercise and massage for central and peripheral paralysis and paresis improve blood circulation and muscle trophism in the affected limbs, prevent the development of contractures, restore movement, develop compensatory motor skills, and have a healing effect on the patient’s body. Exercise therapy and massage are indicated in the early stages of the disease. From the first days they begin to use special positioning for paralyzed limbs. For hemiplegia and hemiparesis that arise as a result of an ischemic stroke, treatment with positioning begins on the 2-4th day of illness; for cerebral hemorrhage - on the 6th-8th day (if the patient’s condition allows this treatment). Laying on the back is carried out in a position opposite to the Wernicke-Mann position: the shoulder is moved to the side at an angle of 90°, the elbow and fingers are extended, the hand is supinated and held on the palm side with a splint; the entire limb is fixed in position using sandbags. The paralyzed leg is bent at the knee joint at an angle of 15-20°, and a roll of cotton wool and gauze is placed under the knee. The foot is placed in dorsiflexion at an angle of 90° and held in this position with a wooden stand. Laying on the back is periodically alternated with laying on the healthy side; in this case, the paralyzed limbs are bent at the elbow, hip, knee and ankle joints and placed on pillows. The position of the patient on the back and healthy side is changed every 1–2 hours. Simultaneously with positional treatment, massage is prescribed. Among the massage techniques (see), stroking, rubbing, light kneading and continuous vibration are recommended. Massage for central paralysis should be selective: muscles with increased tone are massaged using stroking at a slow pace, and their antagonists - by stroking, rubbing and light shallow kneading at a faster pace. In case of peripheral paralysis, the entire limb is first stroked, then the paralyzed muscles are massaged, and their antagonists are only stroked. The massage begins with the proximal parts of the limbs and is carried out daily for 10-15 days, and its duration gradually increases from 10 to 20 minutes; course of treatment - 30-40 sessions (if necessary, it can be repeated after 2 weeks). Acupressure and reflex-segmental massage are also shown. Passive movements are used simultaneously with the massage. They are carried out separately for each joint (5-10 movements in full and at a slow pace), starting from the proximal parts of the limbs on both the healthy and the affected side. Passive movements are carried out by the methodologist or the patient himself with the help of a healthy limb.

To restore motor function, active gymnastics is of primary importance. In case of central paralysis and paresis, it is started on the 7-10th day from the onset of the disease in case of ischemic stroke, in case of cerebral hemorrhage - on the 15-20th day. It is advisable to begin with exercises in holding the limb in its given position. After the patient learns to perform these exercises and hold the limb, active gymnastics is performed first for those muscles whose tone is not increased. The development of active movements is carried out with the help of lightweight exercises using special devices: frames with a system of blocks and hammocks, slippery surfaces, spring traction, gymnastic apparatus. Then active free exercises are prescribed for healthy and affected limbs, including the use of special devices for fastening and unbuttoning buttons, tying and untying ribbons, etc.

Teaching patients to sit begins in case of ischemic stroke 10 days from the onset of the disease, and in case of cerebral hemorrhage - after 3-4 weeks. Preparing the patient for walking begins with him lying down, and then sitting, and exercises that simulate walking are practiced. When the condition of the patients allows them to get out of bed, they begin to be taught to stand on both legs, alternately on the healthy and sore leg, walk in place, with an instructor, then in a special wheelchair, using a three-legged crutch, along a track, stairs. During the entire course of exercise therapy for central paralysis, a set of exercises is also carried out aimed at eliminating patol and synkinesis. It is advisable to perform gymnastic exercises for peripheral paralysis in a bath or pool with warm water. The duration of the exercise therapy course is individual in each individual case and can vary from 3-4 weeks. up to 2-3 months and more, and sometimes several years, which depends on the nature of the pathol, the process that caused the occurrence of paralysis or paresis.

Orthopedic treatment can be conservative or surgical. Conservative treatment as an independent treatment is usually indicated in the absence of evidence of interruption or compression of the nerve trunk and is carried out using prosthetic and orthopedic devices, shoes, plaster, plastic and other removable splints, special beds and other means. Its goal is partial compensation of lost motor function. Surgical treatment of paralysis is carried out by Ch. arr. in case of anatomical interruption of the nerve (partial or complete), compression or crushing of the nerve trunk and in case of ineffectiveness of conservative treatment. Surgical interventions are performed directly on the nerves with the application of a primary or secondary nerve suture (see), performing neurolysis (see); on tendons and muscles - grafting, muscle plasty, transosseous tenodesis (see); on joints - operations to secure the joint in a permanent fixed position (see Arthrodesis) and to form an artificial bone brake in order to limit mobility in the joint (see Arthrosis).

In case of persistent pronounced loss of nerve function in the period of St. 2 years after the injury and the impossibility or ineffectiveness of surgical intervention on the nerves, orthopedic surgery is indicated. So, for example, in order to replace the function of a paralyzed deltoid muscle in children over 6 years of age, trapezius muscle myolavsanoplasty is performed. The operation consists of cutting off the trapezius muscle from the clavicle and scapular spine along with the periosteum, suturing a Mylar prosthesis to it, the other end of which is fixed in the upper third of the humerus. Pronation contracture of the limb is eliminated using detorsion osteotomies of the shoulder and forearm bones. For peripheral paralysis of the limb, tenodesis of the wrist joint is sometimes performed.

With high damage to the sciatic nerve, the function of the muscles innervated by the tibial and common peroneal nerves is lost. In this case, the ligamentous apparatus of the foot is weakened, pronounced bone atrophy and excessive mobility in the ankle and small joints of the foot occur. To restore the weight-bearing ability of the limb, arthrodesis, arthrorrhiza, and tenodesis of the foot joints are used. For example, with pronounced valgus or varus alignment of the foot, arthrodesis of the ankle joint is used, in some cases combined with subtalar arthrodesis.

Wreden's bridging arthrodesis involves the simultaneous closure of the ankle joint and the transverse tarsal joint (Schopart's joint) while maintaining mobility in the tarsometatarsal joints (Lisfranc joint) using a sliding bone graft from the tibial crest. Oppel-Dzhanelidze-Lortiuar arthrodesis consists of closing the ankle, subtalar and talocaleonavicular joints. To limit excessive mobility with a dangling cauda equina, Campbell's posterior arthrorrhiza is recommended; with a calcaneal foot - anterior arthrorrhiza according to Mitbrait.

Damage to the superficial peroneal nerve leads to loss of function of the peroneal muscle group. In these cases, transplantation of the tibialis anterior tendon to the outer edge of the foot is indicated. Damage to the deep peroneal nerve leads to loss of function of the muscles that extend and supinate the foot. To compensate for them, transplantation of the peroneus longus tendon to the inner edge of the foot is indicated. Damage to the common peroneal nerve entails loss of function of the muscles that extend, supinate and pronate the foot. In this case, they most often resort to tenodesis using the tendons of the same paralyzed muscles, which are fixed in the lower third of the tibia. The operation of separate transplantation of the gastrocnemius muscle to the dorsum of the foot consists of isolating the tendon of the soleus muscle, cutting it off at the site of attachment to the tubercle of the heel bone and fixing it to the dorsum of the second or third metatarsal bones. The tendon of this muscle is lengthened using Dacron tape.

In cases of radial nerve palsy, the flexor carpi ulnaris tendon can be transplanted onto the extensor digitorum tendon, and the flexor carpi radialis tendon can be transplanted separately into the extensor and abductor pollicis tendons. This operation was first performed by F. Frank in 1898. One of its modifications is the Osten-Sakena-Dzhanelidze operation: cross-transplantation of the flexor carpi ulnaris tendon to the extensor pollicis longus and abductor pollicis longus, and the flexor carpi radialis tendon to the extensor digitorum.

In the postoperative period, the limb is immobilized with the help of splints, splints, functional orthopedic devices (see), and in some cases - distraction-compression devices (see). A feature of immobilization is the fixation of the limb in a position that ensures minimal tension on the operated nerves, muscles or tendons. Its duration is determined by the timing of fusion of these formations or the timing of the formation of ankylosis or callus (during operations on bones).

Forecast

The prognosis depends on the nature of the patol. the process, depth and extent of damage to the motor analyzer and the compensatory capabilities of the body. With central paralysis and paresis that developed as a result of circulatory disorders, the range of movements increases as blood flow is restored. With central paralysis and paresis caused by a cortical lesion, movements are restored faster and more fully compared to paralysis caused by damage to the internal capsule. In case of peripheral paralysis and paresis that developed as a result of injury to the brachial plexus during childbirth, movements in the affected limbs are restored within 1-2 years.

In case of peripheral paralysis and paresis caused by damage to the peripheral nerves, if conservative treatment is ineffective, reconstructive surgery is resorted to. After operations on the nerves, restoration of their conductivity occurs no earlier than after 5-6 months.

Orthopedic operations on joints, muscles and tendons provide only partial restoration of the function of a paralyzed limb.

Bibliography: Badalyan L. O. Children's neurology, M., 1975; Bogolepov N.K. Impaired motor functions in vascular lesions of the brain, M., 1953; B about r o-dinsky D. K., Cor om ed A. A. and Shvarev A. I. Guide to practical training in nervous diseases, p. 27, JI., 1977; Vreden R.R. Practical guide to orthopedics, JI., 1936; Kolesnikov G. F. Electrical stimulation of the neuromuscular system, Kyiv, 1977; Kreimer A. Ya. and G o l d e l m a n M. G. Clinic and complex therapy of diseases of the nervous system, p. 69 and others, Tomsk, 1978 - Krol M. B. and Fedorova E. A. Basic neuropathological syndromes, M., 1966; Livshits A.V., V about l-kov G.M. and Gelfand V.B. Clinical and electrophysiological studies of spastic syndrome and its neurosurgical treatment in patients with spinal cord lesions, Vopr, neurosurgeon., V. 5, p. 36, 1976; Multi-volume guide to surgery, ed. B.V. Petrovsky, vol. 10, p. 79, M., 1964; Moshkov V. N. Therapeutic physical training in the clinic of nervous diseases, M., 1972; Experience of Soviet medicine in the Great Patriotic War of 1941 -1945, vol. 20, p. 442, M., 1952; Stolyarova L. G. and Tkacheva G. R. Rehabilitation of patients with post-stroke movement disorders, M., 1978; Triumphov A.V. Topical diagnosis of diseases of the nervous system, L., 1974; Tsivyan Ya. L. On the surgical treatment of paresis and paralysis in scoliotic disease, Vopr, neurokhir., No. 2, p. 29, 1973; Chaklin V.D. Fundamentals of operative orthopedics and traumatology, p. 595, M., 1964; Ch e r-face M. D. and Mikhailova T. A. Organization and some features of orthopedic treatment of children with cerebral spastic palsy, in the book: Issues, trauma, and orthotics, ed. Ya. N. Rodina et al., p. 38, Saratov, 1972; Shmidt E. V. Syndromes of damage to the premotor and motor zones with gunshot wounds of the skull, Vopr, neurokhir., vol. 6, no. 3, p. 40, 1942; Sh t e p e n-g e r c A. E. Therapeutic physical education for paralytic diseases in children and adolescents, Kyiv, 1972; Bailey H. a. Love R. J. Short practice of surgery, p. 284, 466, L., 1975; Colton S. L., Ransford A. O. a. Lloyd-Ro-b e r t s G. C. Transposition of the tendon of pronator teres in cerebral palsy, J. Bone Jt Surg., y. 58-B, p. 220, 1976; Gilroy J. a. Meyer J. S. Medical neurology, p. 455 N. Y. a. o., 1975; Hamilton D. Some experience with paraplegia in a small hospital in Nepal, Paraplegia, v. 15, p. 293, 1978; Handbook of clinical neurology, ed. by P. J. Yinken a. G. W. Bruyn, v. 1-2, Amsterdam a. o., 1975; Rainer H. t)ber die Behandlung spastischer Lahmungen am Unterschen-kel mit Schwellstromimpulsen, Therapie-woche, Bd 25, S. 5576, 1975; V a n G i j n J. The Babinski sign and the pyramidal syndrome, J. Neurol. Neurosurg. Psychiat., v. 41, p. 865, 1978; Die zereb-ralen Durchblutungsstorungen des Erwach-senenalters, hrsg. v. J. Quandt, S. 308, 793, B., 1969.

L. O. Badalyan; M. I. Antropova (cur.), M. V. Volkov, P. Ya. Fishchenko (injury), G. S. Fedorova (physical therapy).

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Paralysis is the absence of movement in a muscle or muscle group as a result of interruption of the motor reflex pathway. Incomplete loss of movement (limitation of its volume and strength) is called paresis.

Depending on the prevalence of paralysis, there are monoplegia (paralysis of one limb), hemiplegia (paralysis of one half of the body), paraplegia (paralysis of both arms or legs), tetraplegia (paralysis of all four limbs).

When the peripheral motor neuron and its connections to the muscle (peripheral nerve) are damaged, peripheral paralysis occurs. When the central motor neuron and its connection with the peripheral neuron are damaged, central paralysis develops.

Clinical characteristics of central and peripheral paralysis

Symptoms of paralysis	Central paralysis	Peripheral paralysis
muscle tone
reflexes	tendon reflexes are increased, abdominal reflexes are decreased or lost	tendon and skin reflexes are lost or reduced
pathological reflexes		none
friendly movements (syncinesis)		none
amyotrophy	absent	expressed
degeneration reaction	absent

Central paralysis

Central paralysis occurs when the central motor neuron is damaged in any part of it (motor zone of the cerebral cortex, brain stem, spinal cord). A break in the pyramidal tract removes the influence of the cerebral cortex on the segmental reflex apparatus of the spinal cord; his own apparatus is disinhibited. In this regard, all the main signs of central paralysis are, in one way or another, associated with increased excitability of the peripheral segmental apparatus. The main signs of central paralysis are muscle hypertension, hyperreflexia, expansion of the zone of evoking reflexes, clonus of the feet and kneecaps, pathological reflexes, protective reflexes and pathological synkinesis.

With muscular hypertension, the muscles are tense and dense to the touch; Their resistance during passive movement is felt more at the beginning of the movement. Severe muscle hypertension leads to the development of contractures - a sharp limitation of active and passive movements in the joints, due to which the limbs can “freeze” in an incorrect position. Hyperreflexia is accompanied by an expansion of the zone of evocation of reflexes. Clonus of the feet, kneecaps and hands are rhythmic muscle contractions in response to stretching of the tendons. They are a consequence of a sharp increase in tendon reflexes. Foot clonus is caused by rapid dorsiflexion of the feet. In response to this, rhythmic twitching of the feet occurs. Sometimes foot clonus is also noted when inducing a reflex from the heel tendon. Patella clonus is caused by sudden downward abduction of the kneecap.

Pathological reflexes appear when the pyramidal tract is damaged at any of its levels.

The Babinski reflex is caused by line irritation of the foot closer to its outer edge. In this case, a fan-shaped spread of the fingers and extension of the thumb occurs (perverted plantar reflex). A distinct extension of the thumb and a fan-shaped spread of all other fingers occurs when the hand is vigorously drawn from top to bottom along the inner edge of the tibia (Oppenheim reflex), pressing on the calf muscle (Gordon reflex), and squeezing the Achilles tendon (Schaeffer reflex). The listed pathological symptoms are the extensor group of pathological reflexes.

There are also flexion reflexes. When the flesh of the tips of the toes is abruptly struck, they bend (Rossolimo reflex). The same effect is observed when hitting the dorsum of the foot with a hammer in the area of the base of the II-IV toes (Bekhterev reflex) or in the middle of the sole at the base of the toes (Zhukovsky reflex).

Protective reflexes occur in response to pain or temperature stimulation of a paralyzed limb. At the same time, she involuntarily withdraws.

Synkinesis - involuntary friendly movements that occur, accompanied by active movements (for example, waving your arms while walking). With central paralysis, pathological synkinesis is observed. So, when the muscles of a healthy limb on the paralyzed side are tense, the arm is bent at the elbow and brought to the body, and the leg is extended.

Lesion of the pyramidal tract in the lateral column of the spinal cord causes central paralysis of the muscles below the level of the lesion. If the lesion is localized in the upper cervical segments of the spinal cord, then central hemiplegia develops, and if in the thoracic spinal cord, then central leg plegia.

Damage to the pyramidal tract in the region of the brain stem leads to central hemiplegia on the opposite side. At the same time, the nuclei or roots of the cranial nerves may be affected. In this case, cross syndromes may occur: central hemiplegia on the opposite side and peripheral paralysis of the muscles of the tongue, face, and eyeball on the affected side. Cross syndromes make it possible to accurately determine the location of the lesion. Lesion of the pyramidal tract in the internal capsule is characterized by central hemiplegia on the opposite side with central paralysis of the muscles of the tongue and face on the same side. Damage to the anterior central gyrus most often leads to monoplegia on the opposite side.

Central paralysis of the facial muscles differs from peripheral paralysis observed with neuritis of the facial nerve or with crossed Millard-Gubler syndrome in that only the muscles of the lower half of the face are affected. The patient cannot extend his lips forward and grin his teeth on the affected side. His nasolabial fold is smoothed and the corner of his mouth is lowered. However, the forehead muscles remain intact, and the palpebral fissure closes completely. There are no lacrimation, hyperacusis (sound phobia, hypersensitivity to loud sounds) or taste disorders.

With central paralysis of the tongue muscles, tongue atrophy does not develop.

Peripheral paralysis

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.

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.

An example of peripheral paralysis of the limbs is the paralysis that occurs with polio, an acute infectious disease of the nervous system. 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.

Paresis is a decrease in muscle strength caused by damage to the nerve pathways connecting the brain to a muscle or group of muscles. This symptom occurs as a result of the same reasons as paralysis.

Paresis does not have one clear cause. It can occur with any type of damage to the brain, spinal cord, or peripheral nerves. Depending on the level of damage, there are central(at the level of the brain and spinal cord) and peripheral (at the level of peripheral nerves) paresis.

Central paresis

Central paresis occurs when the brain or spinal cord is damaged. Disorders develop below the site of injury and usually affect the right or left half of the body (this condition is called hemiparesis). Most often, such a picture can be observed in a patient.

Sometimes central paresis causes problems in both arms or both legs ( paraparesis), and in the most severe cases - in all 4 limbs ( tetraparesis).

Main causes of central paresis:

stroke;
traumatic brain injuries, spinal cord injuries;
encephalitis;
tumors of the brain and spinal cord;
osteochondrosis, intervertebral hernia;
cerebral circulatory insufficiency due to atherosclerosis, arterial hypertension or other causes;
amyotrophic lateral sclerosis;
cerebral palsy (CP).

With central paresis, the decrease in muscle strength is expressed to varying degrees. In some cases it manifests itself in the form of rapid fatigue and awkwardness, while in others there is an almost complete loss of movement.

With central paresis, the part of the spinal cord below the site of injury remains intact - it tries to compensate for the disturbance. This leads to an increase in the tone of the affected muscles, strengthening of normal reflexes and the appearance of new, pathological ones, which do not occur in a healthy person. Thus, in a patient who has suffered a stroke, the tone of the forearm flexor muscles increases. Therefore, the arm is always bent at the elbow. On the leg, on the contrary, the tone of the extensors increases - due to this, it bends at the knee worse. Neurologists even have a figurative expression: “the hand asks, but the foot mows.”

Due to increased muscle tone and impaired movement, central paresis can lead to contractures (restriction of movement in the joints).

Peripheral paresis

Peripheral paresis occurs when the nerve is directly damaged. In this case, disorders develop in one group of muscles that this nerve innervates. For example, muscle weakness may be present in only one arm or leg (monoparesis). The larger the nerve is damaged, the larger part of the body the paresis covers.

The main causes of peripheral paresis:

degenerative diseases of the spine, radiculitis;
demyelinating diseases;
nerve damage due to vasculitis and connective tissue diseases;
compression of nerves (“tunnel syndromes”);
nerve injuries;
poisoning with alcohol and other substances.

Peripheral paresis is also called flaccid. Muscle weakness, decreased tone, and weakened reflexes occur. Involuntary muscle twitching is noted. Over time, the muscles decrease in volume (atrophy develops), and contractures occur.

Diagnosis of paresis

Paresis and paralysis are identified by a neurologist during an examination. The doctor asks the patient to make various movements, then tries to flex or straighten the affected limb and asks the patient to resist. A test is performed during which the patient must hold both legs or arms suspended. If muscle strength is reduced in one of the limbs, then after 20 seconds it will noticeably drop down.

After the examination, the doctor prescribes an examination that helps to identify the cause of the paresis.

Treatment and rehabilitation for paresis

Treatment depends on the cause of the paresis. Rehabilitation treatment is of great importance for restoring movements and preventing contractures. Unfortunately, today in many Russian clinics little attention is paid to this issue due to the lack of special equipment and trained specialists.

Rehabilitation treatment for paresis includes:

At the Yusupov Hospital, increased attention is paid to the rehabilitation of neurological patients. After all, the restoration of function, performance, and quality of life of the patient in the future depends on this.

Advantages of Yusupov Hospital

The average experience of our neurologists is 14 years. Many have an academic degree and are doctors of the highest category;
Well-developed area of rehabilitation treatment - modern equipment for mechanotherapy, experienced instructors;
We adhere exclusively to the principles of evidence-based medicine and use the best practices of foreign colleagues;
We did everything to make the patient feel comfortable in the clinic, to create a positive attitude toward recovery.

All this serves one goal - to achieve the maximum therapeutic effect in each patient, the fastest and most complete restoration of impaired functions, and improve the quality of life.

Bibliography

ICD-10 (International Classification of Diseases)
Yusupov Hospital
Batueva E.A., Kaygorodova N.B., Karakulova Yu.V. The influence of neurotrophic therapy on neuropathic pain and the psycho-vegetative status of patients with diabetic neuropathy // Russian Journal of Pain. 2011. No. 2. P. 46.
Boyko A.N., Batysheva T.T., Kostenko E.V., Pivovarchik E.M., Ganzhula P.A., Ismailov A.M., Lisinker L.N., Khozova A.A., Otcheskaya O .V., Kamchatnov P.R. Neurodiclovit: possibility of use in patients with back pain // Farmateka. 2010. No. 7. pp. 63–68.
Morozova O.G. Polyneuropathy in somatic practice // Internal medicine. 2007. No. 4 (4). pp. 37–39.

The consequence of damage, disruption of the functioning of peripheral motor neurons (cells of the spinal cord, motor fibers of the spinal and cerebral nerves) is dangerous peripheral paralysis. With this paralysis, there is a significant loss of normal reflexes, hypotonia, and degenerative muscle atrophy, which is accompanied by a transformation reaction.

The loss of reflexes (or dullness if they are partially damaged) becomes clearer if we remember that the function of the peripheral motor neuron is a certain transmission of information on the reflex arc. If there is a failure in such transmission, then the reflected reflex is not possible or is quite weakened during a short break.

Muscle flaccidity or hypotonia also indicates inactive intervals of the reflex arc. In this case, the muscles lose their characteristic constant tone, which is normally maintained by the same reflected arc. In addition, it can significantly increase with the onset of muscle mass atrophy.

Muscle atony

Relaxed muscles on palpation are flabby, apathetic, inert movements are unnecessary, “loose” joints. Because of this state of the muscles, peripheral paralysis is also called flaccid or atonic.

Muscle wasting occurs due to an imbalance with the anterior horn cell, because it is from there that motor nerve fibers transmit the necessary nerve impulses to the muscles, which clearly stimulate the natural metabolism of the muscles. When motor nerve fibers degenerate and die, muscle “denervation” occurs, resulting in muscle loss.

As a result, motor fibers disappear in the nerves from the site of the disorder, and a specific process of degeneration is formed in the muscle mass. It is caused by muscle transformations, their disappearance, and the production of connective and adipose tissue. Transformations of the electrical interactions of the affected nerves and muscles, typical of peripheral paralysis, appear, the so-called reaction of degeneration or degeneration.

With degeneration, nerves lose their function as conductors of current into the muscle due to the death of motor centrifugal fibers. The muscle inevitably loses certain contraction skills when irritated by faradic current and reacts exclusively to galvanic current. However, even such compression is done slowly. This is a transformation reaction that occurs 12-15 days after the disruption or death of the anterior horn cells.

The absolute transformation reaction does not yet represent a bad prognostic sign. If the nerve fiber is subject to regeneration, it is possible to replace the incomplete response phase with ordinary electrical excitability. But when a muscle is denervated for more than 12-14 months, its fibers completely die, being replaced by adipose tissue. Dangerous muscle cirrhosis begins, the reaction to galvanic current is lost, that is, an irreversible process occurs in the muscles.

Other processes of muscle wasting (inactivity, muscle diseases) are not accompanied by a degeneration reaction. Clinical studies make it possible to perform a distinctive diagnosis of muscle wasting in various forms. In addition, the study of electrical excitability provides a unique opportunity to determine in advance the diagnosis of pathologies of nerve conduction and the ability of muscles to contract. Based on the results of such modern research, one can see noticeable dynamics of the process.

In the course of studying the electrical excitability of nerve fibers, it turned out that a normal contraction is easier and comes out better from specific areas of muscles and nerves - points of irritation.

The change reflex, characteristic of peripheral paralysis, is classified as a group of qualitative transformations of electrical excitability. This group also includes myotonia and myasthenia. Myotonia - the sensibility of the nerve is typical, the muscles weaken rather slowly after the resulting contraction. Myasthenia gravis is characterized by fairly severe muscle fatigue, which can also be seen in the active depletion of their ability to contract when subjected to repeated electric stimulation.

Chronaximetry

Chronaximetry is a newer and noticeably more sensitive way of studying the electrical excitability of nerve fibers and muscles. This method made it possible to establish new and interesting patterns in the pathologies and physiology of nerve endings and the system as a whole. Chronaximetry is considered a very delicate method of study, especially in cases of damage to the peripheral nervous system.

In specific clinical studies, in addition to the electrical excitability of nerves and muscles, mechanical excitability is also studied, which in certain diseases can be overestimated or underestimated. Muscle contraction is always checked by hitting it with a hammer. The mechanical sensitivity of nerve endings is studied either using the same hammer, or by palpation, “rolling” the nerve trunk in a place where it can be easily felt and pressed against the bone.

The level of mechanical excitability of nerve fibers is determined due to certain contractions of the innervated muscles.