Central spastic paralysis: analysis of causes and symptoms. Central paralysis - how it manifests itself, why it is dangerous, treatment When central paralysis is observed

To carry out a motor act, it is necessary that an impulse from the motor area of ​​the cortex be unhindered to the muscle. If the cortico-muscular tract is damaged in any part of it (the motor zone of the cerebral cortex, the pyramidal tract, the motor cells of the spinal cord, the anterior root, the peripheral nerve), the conduction of the impulse becomes impossible, and the corresponding muscles can no longer take part in the movement - it becomes paralyzed. Thus, paralysis or plegia , - This lack of movement in a muscle or muscle groups 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(one limb paralyzed) 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 with the muscle (peripheral nerve) are damaged, peripheral paralysis. When the central motor neuron and its connection with the peripheral neuron are damaged, central paralysis. The qualitative characteristics of these paralysis are different (Table 1).

Table 1

Clinical characteristics of central and peripheral paralysis

Peripheral paralysis

Peripheral paralysis is characterized by the following main symptoms:

absence of reflexes or their decrease (hyporeflexia, areflexia),

decreased or absent muscle tone (atony or hypotension),

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.

So, damage to the anterior horns of the spinal cord in the area of ​​the cervical thickening(fifth - eighth cervical segments and 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 leg paralysis . If the cervical or lumbar thickening is affected on both sides, then upper or lower paraplegia develops.

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.

Facial nerve syndrome

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 (Fig. 57). 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.

Rice. 57. Peripheral paralysis of facial muscles

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.

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 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.

Central paralysis

Central paralysis occurs when the central nutrient neuron is damaged in any part of it ( motor 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. Due to this 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.

The difference between central and peripheral paralysis is characterized by the data presented in table. Table 1.

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, and therefore the limbs can “freeze” in an incorrect position. Hyperreflexia is accompanied by an expansion of the zone of evocation of reflexes. Clonus feet, kneecaps and hands - these 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. There are hand and foot reflexes. Pathological reflexes on the foot are of greatest diagnostic importance: reflexes of Babinsky, Oppenheim, Gordon, Schaeffer, Rossolimo, Zhukovsky.

When studying reflexes, it should be taken into account that these reflexes are normally found in newborns and young children.

Babinski reflex cause streak 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 fan-shaped spread of all other fingers occurs when the hand is vigorously passed from top to bottom along the inner edge of the tibia ( Oppenheim reflex) (Fig. 59), pressing the calf muscle ( Gordon's reflex) (Fig. 60), compression of the Achilles tendon ( Schaeffer reflex) (Fig. 61). 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) (Fig. 62). 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 ( ankylosing spondylitis reflex) (Fig. 63) or in the middle of the sole at the base of the toes ( Zhukovsky reflex) (Fig. 64).

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, 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.

Rice. 67. Characteristic posture of a patient with capsular paralysis (Wernicke-Mann posture)

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, there may be cross syndromes: central hemiplegia on the opposite side and peripheral paralysis of the muscles of the tongue, face, and eyeball on the affected side (Fig. 65). 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 (Fig. 66, 67). 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 Maillard-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 is no lacrimation, hyperacusis or taste disorder.

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

Pseudobulbar palsy syndrome

With bilateral damage to the corticonuclear tracts with the nuclei of the hypoglossal, glossopharyngeal and vagus nerves, central paralysis of the muscles of the tongue, pharynx, soft palate and larynx develops. This syndrome is called pseudobulbar palsy.

The symptoms of pseudobulbar palsy are the same as with bulbar palsy, but the palatal and pharyngeal reflexes remain intact and pathological pseudobulbar reflexes are detected - reflexes of oral automatism (Fig. 68). These include: the palmar-chin reflex (when stroke irritation of the palm causes contraction of the muscles of the chin), labial (when lightly tapping with a finger or a hammer on the upper lip, protrusion of the lips occurs), sucking (stroke irritation of the lips causes a sucking movement), nasolabial (with slight by tapping on the bridge of the nose, the lips are extended with a “proboscis”), distansoral (when the hammer approaches the face, the lips protrude with the proboscis). Patients with pseudobulbar palsy also experience attacks of violent crying or laughter.

Rice. 68. Study of oral automatism reflexes:

a - palmomental; b - labial; V- nasolabial; G - distal In speech therapy practice, the differential diagnosis of bulbar and pseudobulbar dysarthria is important.

Syndromes involving the extrapyramidal system

Cerebellar lesion syndrome

Cerebellar lesion syndrome is expressed in disturbances of balance, coordination of movements and muscle tone.

Balance imbalances appear static ataxia. If statics are disturbed, the patient in the Romberg position deviates towards the affected cerebellar hemisphere. In severe cases, the static disorder is so pronounced that the patient cannot sit or stand even with his legs spread wide apart.

Impairment of balance and coordination during movements is called dynamic ataxia. Dynamic ataxia is detected when walking ( ataxic gait). It can also be detected using finger-nose and knee-heel tests. This reveals intentional tremors. In case of damage to the cerebellum, there is hypermetry- disproportionality of movements. Hypermetry is detected using a pronator test. The patient is asked to quickly move his outstretched hands from a palms up position (supination) to a palms down position (pronation). On the side of cerebellar disorders, the movement is performed with excessive rotation of the hand.

It is also revealed adiadochokinesis- impaired alternation of opposite movements. Adiadochokinesis is detected when trying to quickly alternately supinate and pronate the hand. The patient makes awkward, imprecise movements.

When the cerebellum is damaged, speech becomes slow, broken into syllables, and scanned (cerebellar dysarthria).

When the eyeballs move, nystagmus is detected - twitching of the eyeballs.

Due to tremors and impaired coordination of movement, patients' handwriting changes. It becomes uneven. The lines of the letters take on a zigzag character. The letters themselves are too large.

Damage to the cerebellum also leads to muscle hypotonia.

Pallidal system lesion syndrome

The symptom complex of damage to the pallidal system is called parkinsonism . The main symptoms of parkinsonism are impaired motor activity and muscle hypertension. The patient's movements become poor and inexpressive ( oligokinesia) and slow ( bradykinesia). Patients are inactive, inert, constrained, and when moving from a position of rest to movement, they often freeze in an uncomfortable position (the position of a wax doll or mannequin). The usual posture also changes: the back is bent, the head is tilted to the chest, the arms are bent at the elbows and wrists, and the legs are bent at the knee joints (Fig. 69). The gait of patients is slow, it is difficult for them to start moving (Parkinsonian stamping on the spot), but later the patient can “disperse” and move faster. But it is difficult for him to stop quickly. If it is necessary to stop, it continues to “pull” forward. Moves with difficulty, in small, frequent steps; At the same time, there are no physiological synkinesis (hands are motionless when walking).

Rice. 69. Characteristic posture of a patient with parkinsonism syndrome

Facial expressions are poor, the face is inexpressive, mask-like (hypomimia), speech is quiet and monotonous. Muscle tone is increased, and the resistance experienced during the study of tone remains uniform at the beginning and end of the movement (plastic, or extrapyramidal, muscle hypertension, or muscle rigidity).

With parkinsonism, tremor is noted in the fingers and (sometimes) in the lower jaw. Tremor occurs at rest and is characterized by rhythm, small amplitude and low frequency. Since the main symptoms of damage to the pallidal system are hypokinesia and muscle hypertension, this symptom complex is also called hypokinetic-hypertensive .

Striatal system lesion syndrome

In case of defeat striatal part of the extrapyramidal system is notedhyperkinetic-hypotonic symptom complex.

The main symptoms are muscle hypotonia and excessive involuntary movements - hyperkinesis. The latter arise involuntarily, disappear during sleep, and intensify with movement. When studying hyperkinesis, attention is paid to their shape, symmetry, side and localization of manifestation (in the upper, or proximal, parts of the extremities or in the lower - distal). Hyperkinesis has different forms of manifestation.

Choreic hyperkinesis manifest themselves in the form of rapid contractions of various muscle groups of the face, trunk and limbs; most often they are observed in the proximal parts of the limbs and on the face. They are irregular and uncoordinated. An acute change in localization is typical for them; either the muscles of the arms, legs, face, or simultaneously the muscles of different groups twitch. Involuntary frowning of the eyebrows and forehead, protruding tongue, and jerky, erratic movements of the limbs are noted. Hyperkinesis can be expressed in only one half of the body (hemichorrhea).

Athetosis observed in the lower extremities in the form of slow, worm-like, elaborate movements in the hands, fingers and feet (Fig. 70). Athetoid movements can also be observed in the facial muscles (protrusion of the lips, twisting of the mouth, grimacing).

Rice. 70. Consecutive phases of athetoid hyperkinesis in the arm (a, b, c) and athetosis in the leg (d)

Torsion spasm manifests itself in the form of tonic curvature of the spine in the lumbar and cervical regions. It is characterized by corkscrew-like movements of the body that occur when walking (Fig. 71).

Spasmodic torticollis- convulsive contractions of the neck muscles. At the same time, the head turns to the side and leans toward the shoulder (Fig. 72).

Hemiballism- large, sweeping throwing movements of the limbs performed with great force (Fig. 73).

Rice. 71. Torsion spasm

Rice. 72. Child with spasmodic torticollis

Rice. 73. Hemiballic hyperkinesis

Rice. 74. Facial hemispasm

Facial hemispasm- periodically repeated contractions of the muscles of half the face (Fig. 74).

Tremor- trembling of outstretched arms of the body, head.

Tiki They are forced, monotonous movements that give the impression of being deliberate. They are manifested by rapid wrinkling of the forehead, raising of the eyebrows, blinking, and sticking out the tongue.

Hyperkinesis, as a rule, is accompanied by muscle hypotonia. They are often observed in children; arise as a result of organic lesions of the striatal part of the extrapyramidal system due to the lack of the inhibitory influence of the striatum on the underlying motor centers. However, children often experience functional (neurotic) hyperkinesis, which is in the nature of obsessive movements. They occur after fear, overwork, previous illnesses, traumatic brain injuries, and experiences that are traumatic to the child’s psyche.

Obsessive movements differ from hyperkinesis in that the child can voluntarily delay them. They disappear if the child's attention is distracted. Obsessive movements intensify with anxiety, physical and mental fatigue.

Myoclonus- fast, lightning-fast twitching of separate muscle groups or single muscles.

Central paralysis occurs as a result of damage to the central motor neuron in any part of it. Since the arrangement of cells and fibers of the pyramidal bundles is quite close, central paralysis is usually diffuse, spreading to an entire limb or half of the body. Peripheral paralysis may be limited to damage to certain muscle groups or even individual muscles. There may, however, be exceptions to this rule. Thus, a small lesion in the cerebral cortex can cause the occurrence of isolated central paralysis of the foot, face, etc.; conversely, multiple diffuse lesions of the nerves or anterior horns of the spinal cord sometimes cause widespread paralysis of the peripheral type.

Minor diffuse muscle atrophy can sometimes be observed with central paralysis, but it never reaches such a significant degree as with peripheral paralysis, and is not accompanied by the degeneration reaction typical of the latter. This atrophy may result from lack of muscle activity, but sometimes it develops early after the lesion; in this case, it can be explained as a trophic disorder resulting from damage to the cortex (according to some data, more often than the parietal lobe). In cases of acute central paralysis (trauma, hemorrhage), muscle hypotonia and loss of reflexes are initially possible. At I.P. Pavlov, we find an indication that with thrombosis and hemorrhages in the cerebral hemispheres, accompanied by paralysis, and not “catalepsy” (i.e., not hypertension. - Author), there is even an absence of spinal reflexes.

The main features of central paralysis are muscle hypertonia, increased tendon reflexes, so-called accompanying movements, or synkinesis, and pathological reflexes.

Hypertension, or muscle spasticity, determines another name for central paralysis - spastic. The muscles are tense, dense to the touch; During passive movements, a clear resistance is felt, which is sometimes difficult to overcome. This spasticity is the result of increased reflex tone and is usually unevenly distributed, leading to typical contractures. With central paralysis, the upper limb is usually brought to the body and bent at the elbow joint: the hand and fingers are also in a flexed position. The lower limb is extended at the hip and knee joints, the foot is bent and the sole is turned inward (the leg is straightened and “elongated”). The gait in these cases is of a “circumducing” nature: due to the “lengthening” of the leg, the patient has to “circle” the affected leg (in order not to touch the floor with the toe).

Increased tendon reflexes (hyperreflexia) are also a manifestation of increased, disinhibited, automatic activity of the spinal cord. Reflexes from the tendons and periosteum are extremely intense and are easily evoked as a result of even minor irritations: the reflexogenic zone expands significantly, i.e. the reflex can be evoked not only from the optimal area, but also from neighboring areas. An extreme degree of increase in reflexes leads to the appearance of clonus (see above).

In contrast to tendon reflexes, skin reflexes (abdominal, plantar, cremasteric) do not increase with central paralysis, but disappear or decrease.

Concomitant movements, or synkinesis, observed with central paralysis, can occur in the affected limbs reflexively, in particular when healthy muscles are tense. Their occurrence is based on the tendency to irradiate excitation in the spinal cord to a number of neighboring segments of its own and opposite sides, which is normally moderated and limited by cortical influences. When the segmental apparatus is disinhibited, this tendency to spread excitation is revealed with particular force and causes the appearance of “additional” reflex contractions in the paralyzed muscles.

There are a number of synkinesis characteristic of central paralysis. Here are some of them:

• 1) if the patient, according to the instructions, resists with his healthy hand the extension in the elbow joint produced by the examiner, or strongly shakes his hand with his healthy hand, then a concomitant reflex flexion occurs in the paralyzed arm;
• 2) the same flexion of the affected arm occurs when coughing, sneezing, or yawning;
• 3) under the mentioned conditions, involuntary extension is observed in the paralyzed leg (if the patient is sitting with his legs hanging over the edge of the couch or table);
• 4) the patient lying on his back with his legs extended is asked to adduct and abduct his healthy leg, in which he is resisted. In this case, an involuntary corresponding adduction or abduction is observed in the paralyzed leg;
• 5) the most constant of the accompanying movements with central paralysis is the symptom of combined flexion of the hip and trunk. When the patient tries to move from a horizontal position to a sitting position (the patient lies on his back with his arms crossed on his chest and straightened legs apart), the paralyzed or paretic leg is raised (sometimes adducted).

Pathological reflexes are a group of very important and constant symptoms of central paralysis. Of particular importance are pathological reflexes on the foot, which are observed, of course, in cases where the lower limb is affected. The most sensitive symptoms are Babinski (perverted plantar reflex), Rossolimo and Bekhterev. The remaining pathological reflexes on the foot (see above) are less constant. Pathological reflexes in the hands are usually weakly expressed and have not acquired much significance in the practice of clinical research. Pathological reflexes on the face (mainly a group of “oral” reflexes) are characteristic of central paralysis or paresis of muscles innervated by cranial nerves, and indicate bilateral supranuclear lesions of the tractus cortico-bulbaris in the cortical, subcortical or brainstem regions.

The methodology for studying movements consists of

• 1) studying the general appearance, facial expressions, speech, posture and gait of the patient,
• 2) determining the volume and strength of active movements,
• 3) studies of passive movements and muscle tone,
• 4) studies of movement coordination
• 5) checking the electrical excitability of nerves and muscles

Just one external examination of the patient can reveal a lot of significant information and direct the investigator’s attention to one or another defect in the state of muscles and motor function.

Thus, muscle atrophy and limb contractures can be immediately detected. Sometimes the patient’s posture, low or, conversely, excessive mobility attracts attention. In a conversation with a patient, paresis of facial muscles, speech disorders, and phonation disorders may be noticed. Trembling, convulsive twitching, etc. are noticeable. Be sure to examine the patient's gait, which may be disordered. In particular, with hemiparesis of the central type, a “hemiplegic, circumducing” gait, Wernicke-Mann posture, is noted, as mentioned above. With spastic lower paraparesis, a “spastic” or “spastic-paretic” gait is observed, when the patient walks with straightened legs, without lifting the soles from the floor; When you move your legs, the tension in them is noticeable. With flaccid paraparesis, the feet usually hang down, and the patient, in order not to touch the floor with his toe, is forced to raise his leg high (the so-called “cock” or peroneal gait).

Active movements are examined in order from top to bottom; usually the volume of only some basic movements is determined.

On the face, we examine the wrinkling of the forehead upward, the closing of the eyelids, the movements of the eyeballs, the opening of the mouth and the pulling of the corners of the mouth outward, and the protrusion of the tongue.

The volume of head rotation to the sides is determined. The subject is asked to make a shoulder-raising movement (“shrug”). The arms are raised to the horizontal and higher; flexion and extension in the elbow, wrist and finger joints; pronation and supination of the hands; bringing and spreading fingers; To determine a mild degree of paresis and disorder of fine movements, it is advisable to ask the subject to make quick flexion and extension movements with his fingers, moving them in the air with his arms extended forward.

Flexion and extension are performed in the joints of the hip, knee, ankle, and toes, walking on the heels and on the toes.

In necessary cases, it is necessary to check more subtle and isolated movements relating to individual muscles during the study.

The presence of a full range of active movements does not always exclude the possibility of mild paresis, which in such cases may be limited by a weakening of muscle strength. Therefore, the study of the range of active movements of the limbs is usually accompanied by a simultaneous study of muscle strength, for which the subject provides a certain counteraction to the movement being performed. The grip force of the hand is determined, which can be measured with a dynamometer.

Passive movements, of course, will not be limited if there is a full range of active movements. Their study is necessary when establishing the absence or limitation of active movements in a particular muscle group. It may turn out that movements are limited not because of paresis, but because of damage to the joints, due to pain, etc. The study of passive movements is also carried out to determine muscle tone.

Tone is determined primarily by feeling the muscle at rest. With atony or hypotension, the muscles feel flabby and sluggish; with hypertension - dense, tense. With passive movements in the case of atony, excursions in the joints are completely free, even excessive; joints are “loose.” As tone increases, passive movements encounter significant resistance, which requires a certain amount of tension to overcome. With spasticity of the muscles that accompanies central paralysis, a phenomenon is observed that is called the “jackknife symptom”: if we make a fast passive movement, then the resistance provided by the rigid muscles is not the same throughout the entire movement; it is especially felt at the beginning and decreases later.

Coordination of movements is impaired as a result of damage to the cerebellar system and the loss of the “sense of position and movement” (articular-muscular sense).

central paralysis muscle atrophy

Central paralysis is a consequence of damage to both the motor zone of the cerebral cortex and any part of the nervous system connecting it with peripheral motor neurons. Along with damage to the motor cortex of the cerebral hemispheres, the cause of central paralysis may be a dysfunction of the corticonuclear, mono- and polysynaptic corticospinal tracts at the level of the corona radiata, knee and two anterior thirds of the posterior femur of the internal capsule, cerebral peduncle, and trunk brain, spinal cord. In most cases, the pathological focus does not damage all structures of the motor zone of the cortex and corticospinal tracts; moreover, some of these tracts do not cross. Therefore, on the side of the body opposite to the pathological focus, all muscles are never affected. More often, the function of the muscles of the hand and shoulder is more impaired, then the lower leg. With central paralysis, peripheral motor neurons are preserved and also disinhibited, so with it, as a rule, tendon reflexes are excessively high, pathological reflexes and synkinesis appear. Thus, central paralysis is the impossibility of voluntary movements while maintaining and even increasing the intensity of elementary reflex motor acts. The following symptoms are characteristic of central, or spastic, paralysis. 1. Increased muscle tone of the contractile type, or muscle spasticity, caused by the cessation of the restraining effects of central neurons on peripheral motor neurons. 2. Increased tendon and periosteal reflexes, also associated with a violation of the restraining influences of central neurons on peripheral motor neurons. 3. The appearance of clonus, which can be considered as a result of pronounced tendon hyperreflexia, while a single stimulation of the reflexogenic zone leads to multiple rhythmic repetition of a stereotypical motor response. 4. Pathological reflexes, many of which are evoked in young children and then disappear. With the disinhibition of peripheral neurons due to the weakening of the restraining influence of cerebral structures, these innate reflexes appear again and are already considered pathological. 5. The appearance of protective reflexes and pathological synkinesis (accompanying movements). 6. Unlike peripheral paralysis, with central paralysis there is no reaction of degeneration (or degeneration) of muscles and nerves. Muscle spasticity. Spastic muscle tension, in which muscle tone unevenly increases during movements and jackknife and recoil symptoms are possible, is a characteristic sign of damage to the structures connecting central motor neurons with peripheral ones. In acute damage, spastic tone usually does not develop immediately; paralyzed muscles may be flaccid for some time, but tendon reflexes are increased, and the Babinski foot pathological reflex may appear early. Spastic tone is associated with excessive activity of peripheral motor neurons, freed from the inhibitory effects of the structures of the reticular formation of the brain stem. Mainly in the arms, the tone in the flexor muscles increases, in the legs - in the extensors. Patients with central hemiparesis usually develop Wernicke-Mann posture and gait over time. Clonus. As already noted, central paresis or paralysis is characterized not only by an increase in tendon myotatic reflexes, which are also evoked normally, but often by the appearance of multiple motor reactions to their induction (clonus). In practice, the following forms of clonus are most often caused. Foot clonus is caused as follows: the patient lies on his back, the examiner bends his leg at the knee and hip joints and, holding his lower leg with one hand, sharply extends (dorsiflexes) the foot with the other hand, while it is desirable that the patient slightly sits down. rubbed the plantar surface of the foot against the palm of the examiner. The response is a rhythmic alternation of flexion and extension of the foot throughout the entire period while the examiner stretches the heel (Achilles) tendon. With central paresis, especially in cases of damage to the pyramidal tracts of the spinal cord, foot clonus sometimes occurs spontaneously if the patient rests the front of the foot on the floor or on the headboard (Fig. 4.8a). Patellar clonus is caused by the patient lying on his back with his legs straight. The examiner grabs the upper pole of the patella with his thumb and forefinger and then sharply shifts it towards the lower leg and holds it in this position. The quadriceps femoris muscle is stretched and its rhythmic clonic contraction occurs, which does not stop until the stretching of the muscle tendon stops (Fig. 4.86). Much less often than the described forms of clonus, it is possible to detect clonus of the lower jaw, clonus of the hand, and clonus of the gluteal muscle. Pathological reflexes. Depending on the location of invocation and the nature of the motor response, pathological reflexes can be divided into foot and hand reflexes, as well as extension (extensor) and flexion (flexor). Rice. 4.8. Detection of clonus of the foot (a) and patella (b). With all pathological foot extensor reflexes, especially common in central paresis and paralysis, the response is extension of the big toe, sometimes in combination with a fan-shaped divergence of the remaining toes. Extensor pathological reflexes include the following. Babinsky reflex - caused by line irritation of the skin of the outer edge of the plantar surface of the foot, directed from the heels to the toes (Fig. 4.9a, b). It is most constant in central paralysis and paresis, but it must be borne in mind that in children under 2 years of age it is usually caused and is normal. Rice. 4.9. Babinski's pathological reflex (a) and its diagram (b). Rice. 4.10. Oppenheim's pathological reflex. Oppenheim reflex - caused by running the thumb and index finger along the crest of the tibia with some pressure from top to bottom towards the ankle joint (Fig. 4.10). Gordon reflex - caused by compression of the triceps surae muscle (Fig. 4.11). Schaeffer reflex - caused by compression of the heel tendon (Fig. 4.12). With all pathological flexion foot reflexes, the motor response is reduced to rapid nodding plantar flexion of the toes. Pathological foot flexion reflexes include the following. Rossolimo reflex - is caused by short light blows with the fingers of the examiner’s hand on the plantar surface of the terminal phalanges of the II-V toes of the patient’s foot (Fig. 4.13). Rice. 4.11. Gordon's pathological reflex. Rice. 4.12. Pathological reflex of Schaefer. Rice. 4.13. Pathological Rossolimo reflex. Bekhterev-Mendelian reflex - is caused by tapping with a hammer on the back of the foot above the III-IV metatarsal bones. The Zhukovsky-Kornilov reflex is caused by tapping on the central part of the sole (Fig. 4.14). When the pyramidal tracts are damaged above the level of the cervical enlargement of the spinal cord, pathological carpal reflexes can also be caused, which can generally be considered as analogues of the foot reflexes. Rice. 4.14. Pathological reflex Zhukovsky-Kornilov. Protective reflexes. Like pathological reflexes, protective reflexes, or reflexes of spinal automatism, arise due to the isolation of reflex arcs from the higher parts of the brain that close at the level of the spinal segments. They are involuntary movements of paralyzed parts of the body in response to their irritation. Irritants for jtom can be injections, pinch-like compression of the skin, irritation with ether, etc. (Fig. 4.15a). Protective reflexes can also be obtained in response to rapid passive movement in any joint of the paralyzed limb - Fig. 4.15. Protective reflexes. a - ether method, b - ankylosing spondylitis-Marie-Foy method. ty due to the resulting irritation of proprioceptors. Thus, with passive plantar flexion of the toes of a paralyzed leg (Fig. 4.15a, b), a pull-up of the leg occurs due to its spontaneous flexion in the hip and knee joints (Bekhterev-Marie-Foy reflex). With the Remak protective femoral reflex, in response to streak irritation of the skin of the anterior surface of the thigh, plantar flexion of the foot and fingers occurs. Protective reflexes can also arise from random irritations of the body: touching a sheet, air movement, etc. In cases where the stimulus goes unnoticed, such reflexes are often called “spontaneous” protective reflexes. Protective reflexes, as a rule, occur with combined damage to the corticospinal tracts and extrapyramidal-spinal polysynaptic connections, and are especially pronounced when the pyramidal and extrapyramidal tracts are damaged at the spinal level. The level below which tissue irritation leads to the emergence of protective reflexes can help identify the lower pole of the pathological focus in the spinal cord. Pathological synkinesis. Synkinesis, or conjugate movements, are called involuntary movements that join voluntary ones. Synkinesias can be physiological and are observed in healthy people. Thus, clenching the hand into a fist is usually accompanied by extension in the wrist joint; when walking, accompanying arm movements occur (cheirokinesis), etc. With central paresis and paralysis, due to the weakening of the inhibitory effect on the reflex arcs that close at the spinal level, prerequisites arise for the development of pathological synkinesis, which can be global, or spastic, coordination and imitation. Global, or spastic, syncynesias are observed in spastic hemiplegia. Attempts to actively move the affected limbs or sudden tension in the muscles of the healthy side of the body causes involuntary flexion in the paralyzed arm and extension in the leg. Global synkinesias in the paralyzed part of the body can occur with general emotional reactions, as well as with yawning, coughing, and sneezing. Coordination synkinesis are movements that the patient cannot perform in isolation, but during a complex motor act they arise as additional ones and then cannot be voluntarily delayed. An example of coordination synkinesis can be the Raymist symptom, which consists of Fig. 4.16. The Wernicke-Mann position with central hemiparesis is blind. involuntary abduction and adduction of the paralyzed leg when the examiner attempts to adduct or abduct the healthy leg of the patient lying on his back and offering resistance to the examiner. Another example of coordination synkinesis - the tibial Strümpel phenomenon - is that in a patient who could not straighten the foot due to central paresis of the leg, when trying to bend the affected leg at the knee, overcoming the resistance of the examiner, involuntary extension occurs foot, and sometimes the big toe. Imitative synkinesias are rarely observed, usually in cases of massive damage to the pyramidal and extrapyramidal tracts. With them, involuntary movements occur in the paralyzed limb, identical to those that are voluntarily performed in a symmetrical healthy limb, for example, flexion and extension of the fingers, pronation and supination of the forearm, etc.

The development of paralysis due to organic factors is known: due to physical damage, severe poisoning, metabolic or nutritional disorders, vascular pathology, cancer, infections, hereditary or congenital pathologies.

Central paralysis syndrome occurs after infections that have developed in the brain or spinal cord - syphilis, tuberculosis, viral encephalitis, meningitis, polio.

Paralysis due to intoxication means poisoning with heavy metal derivatives, alcoholic neuritis, lack of vitamin B1, and lack of nicotinic acid.

Multiple sclerosis, the nature of which has not been identified, causes dysfunction of movements of varying degrees. Wounds and fractures are fraught with similar consequences if motor centers or pathways are damaged.

Paralysis can occur even under the influence of psychogenic factors.

Central paralysis more often affects older people, but now there is a clear trend towards its “rejuvenation”. According to statistics, more than half of cases of paralysis are a consequence of a stroke. A thrombus, like hemorrhages, can lead to disruption of blood supply by blocking blood vessels in the area of ​​the brain responsible for movement or pathways. Infantile paralysis usually occurs as a result of birth injuries or as a result of inherited spastic paraplegia.

Pathogenesis

The most common pathological conditions of the nervous system are destruction, degenerative, inflammatory processes, sclerotic changes, demyelination. Paralysis occurs due to pathological conditions of the brain or due to damage to peripheral nerves.

There are two types of central palsy: cerebral (brain) and spinal. The nature of spinal paralysis is pathological changes in the neurons responsible for movement. Cerebral palsy implies a capsular, bulbar, cortical or subcortical nature.

Two types of neurons are responsible for movement. They differ in functional load and their structure. Therefore, if pathological changes have occurred in them, two different types of signs are distinguished: the affected nerve cells responsible for movement cause spastic paralysis, while the peripheral nerve cells cause flaccid paralysis.

There are no internal causes for paralysis of a psychogenic nature, so it masquerades as any of the types, exhibits general signs of central and peripheral paralysis, or any combination of them.

Central paralysis may combine symptoms of peripheral paralysis, or may exhibit exclusively pure symptoms; it is often accompanied by disturbances in vascular tone, sensitivity, and digestion. A common manifestation of peripheral paralysis is sensory disturbances.

In a body with paralysis, motor function often suffers entirely and does not selectively affect muscles. Paralyzed muscle tissue is in permanent tension and does not atrophy (this is possible solely due to complete inactivity). In immobilized limbs, deep tendon reflexes are maintained or exacerbated, and clonus (fast convulsive contractions) are often detected. On the side affected by paralysis, abdominal reflexes weaken or disappear completely.

Symptoms of central paralysis

We list the first signs of central paralysis:

• muscle hypertonicity;
• expanding the scope of reflective reactions;
• increased reflective reactions;
• rapid convulsive contractions of the muscles of the knees or feet (clonus).

With hypertonicity, the muscles are too dense. High muscle resistance is noted. A high degree of muscle tension is fraught with the appearance of contractures. Therefore, movements are limited partially or entirely. Contracture is characterized by an unnatural frozen position of the limb.

The most noticeable visible signs of paralysis are provoked by an expansion of the area of ​​​​action of reflex reactions. Convulsive rhythmic contractions of the muscles of the knees or feet appear due to stretching of the tendons. Typically, such contractions appear due to the intensification of tendon reflex reactions. The contraction of the feet is the result of accelerated dorsiflexion. Reflexive twitching of the leg is a response to such an impact. Patella clonus is noticeable during rapid abduction of the limb. Pathological reflexes in the feet or hands are a visible symptom of pyramidal tract pathology. The most typical are the reflex reactions of Oppenheim, Rossolimo, Zhukovsky, Babinsky Gordon and Schaeffer.

Protective reflexes, manifested by trembling of the affected limb, reacting to mechanical irritation, are also a manifestation of central paralysis syndrome.

Sykinensia is another symptom of paralysis. Synchronizations are reflexive simultaneous movements in the affected limb with conscious active movements. Like, say, swinging your arms while walking, flexion - extension of the limbs simultaneously with directed movements on the half of the body that is not subject to paralysis. There are many types of synkinesia that indicate the development of paralysis.

Muscle spasms due to hypertonicity are often distributed unequally. More often, the left or right part of the body as a whole is affected; the arm is usually pressed down, the hand and fingers are twisted, the leg is straightened, and the foot is bent and turned inward.

With central paralysis, reflexive reactions in the tendons are more pronounced, and abdominal, muscular and plantar reactions disappear completely or become noticeably weakened.

The most obvious symptoms of central paralysis:

• Unnatural body position;
• Weakened or increased mobility;
• Weakening of facial muscles;
• Articulation and speech disorders;
• Convulsive contractions and trembling of muscles;
• Unnatural gait;
• Accidental opening of the mouth;
• Closing the eyes;
• Undirected shoulder movements;
• Random flexion and extension of the joints of the arms or legs;
• Muscular hypertonicity.

The symptoms accompanying central paralysis help to accurately separate it from other types of motor dysfunction and even identify the area of ​​the pyramidal tract susceptible to pathological processes.

Central facial palsy occurs due to disturbances in cortical processes or pathology of the nerve pathways leading to the facial nerve. Facial paralysis appears opposite the affected area and is usually located in the lower region.

Facial muscles contract randomly due to the connection of the nerve with the extrapyramidal system. It looks like a tic or spasm. This type of paralysis may be accompanied by epileptic seizures.

The development of central paralysis of the limbs occurs due to pathological changes in the descending system of nerve fibers. A noticeable manifestation of pathology is reflex reactions in the tendons, muscle hypertonicity, and manifestations of pathological reflex reactions. Such symptoms may appear in conjunction with other signs of organic paralysis.

With paralysis of functional etiology, the reflex reactions of the tendons do not undergo changes and normal muscle tone is maintained.

Central spastic paralysis indicates that the area of ​​the brain in the hemisphere opposite to the affected limb is damaged.

Combined pathologies of the limbs are characteristic of disorders in the brain stem.

Cross paralysis refers to disturbances at the junction of the medulla oblongata and the spinal cord.

When the limbs are paralyzed only on the left or right, and the nerves of the skull have not been injured, this indicates a failure of the descending system of the nervous tissues of the cervical region.

Central paralysis of the legs means pathologies either along the path of the lateral cord of the spinal cord, in the convolutions of the brain, or in the corona radiata.

Infantile central palsy

Infantile central paralysis unites a whole group of diseases characterized by damage to the central nervous system, motor dysfunction, and delayed mental development. Infantile central palsy does not develop. This may indicate perinatal paralysis of the central nervous system or brain damage during childbirth, when lack of oxygen, birth trauma, or stroke causes the development of encephalopathy. Paralysis is often associated with impaired oxygen supply to brain cells. Complications of hypoxia are insufficient development of areas of the brain responsible for balance, coordination and ensuring the functioning of reflexes. This is why asymmetric muscle tone develops and pathological motor reactions appear.

Diagnosis of central paralysis

Instrumental diagnosis of central paralysis includes: neuroimaging (CT and MRI), radiography of the bones of the spine and skull, electromyography, puncture of the spinal cord fluid, histology and histochemistry of a biopsy of the affected muscles.

Differential diagnosis

Differential diagnosis includes assessment of the volume and severity of paralysis. A map of the affected muscles can indicate the area of ​​pathological processes in the central nervous system.

In case of paralysis of the limbs, it is necessary to assess its volume: immobility of four limbs means damage to the spinal cord in the area in the neck; paralysis of the limbs on one side is characteristic of the pathology of the internal capsule; paralysis of the legs - for spinal cord disorders in the chest or lower back; The cause of paralysis of one limb lies in peripheral nerve disorders.

It can paralyze other muscles. For example, dysfunction of the eye muscles is a pathology of the cranial nerves; immobility of facial muscles - pathology of the facial nerve or central motor neuron of the opposite hemisphere; laxity of the sternocleidomastoid and trapezius muscles means disturbances in the accessory nerve; lethargy of the tongue muscles - the hypoglossal nerve is damaged.

For diagnosis, it is necessary to clarify the circumstances of the appearance of paralysis: how it began, whether it was accompanied by injuries, impaired consciousness, fainting, high temperature, signs of an infectious disease. It is important to analyze whether other neurological symptoms have appeared: sensory disorders, ataxia, vision problems, disturbances in bladder emptying, bowel cleansing.

For the differential diagnosis of central and peripheral paralysis, electromyography is effective, which notes pathologies inherent in damaged neurons of the anterior horn of the spinal cord and resulting neuropathies. These disorders are not characteristic of central paralysis. With central paralysis, the H-reflex changes. It manifests itself in all affected muscles, when normally it is detected exclusively in the lower leg.

Treatment of central paralysis

Patients are treated for the main disease with treatment of the paralysis itself at the same time. If the vessels are affected, the immobilized limb is given a position that does not interfere with the normal blood supply.

In parallel with the prevention of contractures, they are treated with medications. The therapy intensifies metabolism in the nerves, circulation in small vessels, and improves nerve and synaptic conduction.

Conservative treatment brings results when the morphological substrate has survived, allowing the regeneration of muscle functions. If it remains possible to resume muscle function, the goal of conservative treatment is to avoid contractures and deformities and accelerate the resumption of muscle function.

Physiotherapeutic treatment, balneotherapy, physical therapy, and reflexology are widely used.

Physiotherapy for central paralysis is prescribed after some time. The timing of physical therapy depends on the factors causing the paralysis: inflammation, injury or stroke.

Electrophoresis of medications helps restore blood circulation to the affected area of ​​the brain. For inflammation, UHF and microwave treatment is used. Electrical stimulation in the area of ​​the immobilized limb is carried out at the motor points of the antagonist muscles. This helps relieve hypertonicity and reduce the reflex response of paralyzed muscles. Electrical stimulation is combined with taking muscle relaxing drugs and acupuncture. To reduce the risk of contractures, therapy is carried out with warm ozokerite or paraffin. Positive dynamics are possible when using cold, especially with spastic infantile central palsy.

Physical rehabilitation for central paralysis begins with massage, and after a week or a week and a half, physical therapy begins.

The first exercises involve working on maintaining the occupied position of the limb. When working on the development of conscious movements, they use special equipment: frames with blocks and various ropes attached to the bed, balls, expanders.

When the patient can already sit independently, the next stage of therapeutic exercises is learning to walk. First, the methodologist helps, and then the patient tries to move independently, using crutches and sticks. Then they begin to master more subtle movements: buttoning clothes, lacing shoes, controlling equipment using a remote control or keyboard.

Drug treatment for paralysis

The main drugs are benzodiazepines, baclofen, dantrolene. How these medications work has not been reliably established. Medicines are prescribed if disturbances in normal muscle activity occur every day. Medication therapy will give excellent results if you use two or more medications and combine them with other methods of therapy.

• Baclofen has an inhibitory effect, affecting gamma-aminobutyric acid receptors that are not susceptible to bicuculline. The dose is prescribed individually in each case in order to identify the minimum effective dosage that is not associated with side effects. Results are usually obtained with dosages ranging from 30 to 75 mg daily.

For the first 3 days, half a tablet is prescribed 3 times a day (if the dosage of the tablet is 10 mg); 4-6 days – a whole tablet; Days 7–9, 1.5 tablets 3 times a day; Days 10–12 - 2 tablets. A gradual increase in dosage ensures good tolerability of the drug. Abruptly stopping taking baclofen is fraught with hallucinations and exacerbation of signs of paralysis.

• Benzodiazepines enhance the postsynaptic effects of GABA by promoting presynaptic inhibition. Medicines also affect processes in the brain stem. The drug diazepam is very often used. Dosage – within 2–8 mg 2 times a day. A course of diazepam involves complete restriction of alcohol. Adverse reactions include liver dysfunction and blood disorders. Extreme care should be taken when administering diazepam and when discontinuing it for patients taking blood thinning medications.

Diazepam can cause drowsiness, dizziness, slow down the reaction, provoke allergies, nausea, and vomiting.

• Dantrolene inhibits the release of calcium in the muscles by dividing electromechanical coordination. That is, it reduces tone, increasing muscle weakness. For hypertonicity, the drug gives noticeable results, but it is usually prescribed to patients with plegia. For administration, it is prescribed in a dosage of 4-8 mg per day in 3 or 4 doses. Dantrolene is excreted through metabolism in the liver, and is therefore limited for use in patients with unhealthy livers. Special care is also needed when prescribing dantrolene to people with problems with the lungs or heart.
• Sirdalud acts on the polysynaptic pathways of the spinal cord, reducing the production of excitatory signals to alpha motor neurons. The drug's effectiveness on muscle hypertonicity is similar to baclofen, but sirdalud has better tolerability. Sirdalud is prescribed to adults, starting with a dosage of 1 to 2 mg per day (in 2-3 doses) with a gradual increase in dosage to 12-14 mg, distributed over 3 or 4 doses. May cause a reaction in the form of weakness, dry mouth, and sleep disturbances.

Anticholinesterase drugs are also used to treat central palsy. Anticholinesterase drugs quickly enter the central nervous system, intensify the transmission of signals to the muscles from the nerves and reduce signs of central nervous system dysfunction.

Surgical treatment of paralysis

Before the operation, the functional capabilities of the muscles are identified, measures are taken to strengthen them, and measures to eliminate contractures that have arisen. After the operation, measures are developed to promote the growth and strengthening of the function of the implanted muscles, and then training of movements that are difficult from the point of view of coordination. Surgical intervention is more often performed for flaccid paralysis or cerebral palsy, when conservative therapy has not improved the situation.

Surgery is advisable for neurogenic deformity, when the muscles of the limb are partially affected, changes in the mechanical axis, shape, and size are noticeable, for example, with complete paralysis of the muscular portion of the limb. Then surgical treatment is a preparatory stage before subsequent prosthetics.

Surgery for cerebral palsy seeks to remove deformation of the limb, distorting statics. Such intervention is advisable when conservative treatment methods have failed. It is also effective if areas with fixed deformation are found, which are caused by disorders of the tendon-muscular system and ligaments of the system. Sometimes operations are aimed at eliminating reflective contractures.

Operations are divided into three different types:

• operations on tendons and muscles;
• ligament surgeries;
• operations on bones and joints.

It happens that operations combine elements of all types.

The success of the operation and recovery time depend on a set of conservative therapy measures.

Folk recipes

Traditional medicine advises patients to drink the juice of fresh celery, nettle or plantain.

If the cause of paralysis lies in pathologies of blood circulation in the brain, feijoa will help. A noticeable improvement comes from taking the juice and the fruits themselves.

For paralysis, drink a tincture of cleft wolfberry. For 5 grams of bark or roots you need to take 0.5 liters of vodka or alcohol. Take a two-week course of 1 – 2 drops three times a day. The ointment with the tincture is rubbed in externally. To prepare, pour 20 ml of tincture into 50 grams of heated lanolin, and, without stopping stirring, gradually pour in 50 grams of Vaseline. The ointment is applied along the entire path of the nerve, and the treated area is wrapped in woolen cloth.

Baths can also help recovery from paralysis. To prepare a bath with a decoction of rosehip roots, take 4-6 teaspoons of crushed roots, add a liter of boiling water, and boil for 20-30 minutes. Then the broth is poured into the bath. For a bathroom, the water temperature should be moderate - 38 degrees is enough. You can also prepare a juniper decoction for the bath: 4 - 6 teaspoons of juniper branches or fruits, pour a liter of water, boil for 20-30 minutes. For baths, one plant is used up to 10 times, and then it must be replaced with some other one.

Brew 1 teaspoon of roots with a liter of boiling water, and after an hour strain through a sieve or cheesecloth. Take an infusion of peony roots, 1 tablespoon 3 times before meals. The roots infused with alcohol are drunk in a dosage of 30-40 drops 3 times a day.

• A decoction of sumac leaves.

1 tbsp. A spoonful of tinting sumac or tanning sumac is brewed in 0.5 liters of boiling water and left for an hour. Take 1 tablespoon of decoction 3-4 times a day.

• Tincture of pine cones

10-15 ripe pine cones are prepared for the tincture. The cones are filled with vodka (0.5-0.6 liters) and infused for a month. Drink 1 teaspoon of tincture 3 times a day.

Homeopathy

It is optimal to combine homeopathic medicines with classical medicine medications. Homeopathy does not replace primary treatment, but can complement a set of measures that stimulate the body to recover.

• The homeopathic drug Konium relieves seizures. Its basis is an extract from spotted hemlock, an extremely poisonous plant. Conium is indicated for paralysis accompanied by paresthesia, and the patient feels weak, suffers from insomnia, and often freezes. Dissolve 8 granules 5 times a day. Conium is taken for up to 2 months.
• Fibiaron is a complex drug. Acts as a prevention of paralysis, in addition, it is indicated for treatment. Belladonna, white mistletoe, and ambergris in Fibiaron harmonize the excitation-inhibition mechanism and protect the central nervous system. Dosage - 5-7 granules 3 to 5 times a day. Fibirion is taken for 6 to 8 months.
• Barium aceticum is available in granules and drops. Prescribed for paralysis rising from the limb to the center. The drug is prescribed for absent-mindedness, hesitation before making decisions, a feeling of “pins and needles”, a feeling of cobwebs on the face, tingling and pain spreading along the left leg. Barium aceticum acts almost like Barita acetica.
• Bothrops is made from the venom of a spearhead snake and is produced in the form of granules or drops. Bothrops is prescribed for paralysis with signs of speech impairment, signs of paralysis on the right side of the body.
• CAUSTICUM (Caustic) is effective for paralysis caused by lead intoxication.

Rehabilitation after central paralysis may take months or perhaps years, the most important thing is to follow the recommendations, regular independent exercise, efforts to expand motor functions, and gradually move on to sports activities: swimming pool exercises, jogging, jumping.

Central paralysis is one of the most dangerous diseases affecting the human nervous system. When it appears, the quality of life decreases significantly, and in order to return to the previous rhythm, it is necessary to take all possible measures as soon as possible. Such a disease can be cured only by using an integrated approach, which includes taking medications, physiotherapy, homeopathy, surgery, etc.

Description of the disease

Central paralysis is called a disruption of the activity of certain parts of the brain, resulting in a disorder of the muscles and tendons. This disease indicates that a person has a break in the neural connection, which makes it difficult to transmit information from the brain to the endings in the body.

In the initial stages of the disease, it is very important to be able to distinguish between central and:

1. In the first case, there is a malfunction in the functioning of the pyramidal system; an interesting feature is the fact that disruption in the functioning of human muscles very often occurs on the opposite side of the place where the problem areas of the nerves are located.
2. In the second case, a malfunction occurs in completely different parts of the brain, and the symptoms detected will be completely opposite to central paralysis, for example, instead of an increase in muscle tone, there is a decrease in muscle tone.

Central and peripheral facial palsy differ in the same characteristics. An experienced specialist can easily distinguish the two types of this disease from each other.

The main causes of the disease

For more effective treatment of paralysis of the central nervous system, it is necessary to correctly determine the cause of the malfunction in the motor centers of the brain. There are a huge number of different factors that can trigger the onset of the disease. Here are some of them:

• heredity and predisposition of the body;
• congenital and acquired pathologies;
• the presence of infectious diseases that affect the nervous system and develop in the spinal cord or brain. These include syphilis, tuberculosis, meningitis, etc.;
• eating large amounts of unhealthy and fatty foods, not following a diet;
• metabolic disease;
• poisoning with various toxic substances, including alcohol;
• the formation of malignant tumors that affect the functioning of the human brain and nervous system;
• destruction of neural connections can occur when problems arise in the functioning of the circulatory system, such as bleeding, blood clot formation or vascular stenosis;
• In most cases, central palsy is a complication after a stroke.

The reasons why this disease can develop are very diverse. Therefore, you need to carefully monitor your health and, at the slightest suspicion, seek help from a specialist. Recently, central paralysis has become much younger. If previously older people suffered more from it, now similar disorders can occur at a younger age.

It is worth noting that in people burdened with a hereditary factor, central paralysis can develop in the first years of life. For example, in the presence of a birth injury or under the influence of internal factors.

Main symptoms

Recognizing the appearance of central paralysis syndrome is very simple. After all, most of the signs of this disease are visible to the naked eye. Let's list them:

• weakening of facial muscles;
• the mouth becomes slightly open;
• involuntary opening and closing of the eyes;
• there is a violation of speech functions;
• gait is distorted;
• hypertonicity of the muscles makes them denser and static, which makes movement significantly more difficult and the limbs take an unnatural position;
• due to stretching of the tendons, you can notice convulsive, rhythmic contractions of the muscles of the knees or feet;
• as a protective reaction to mechanical irritation, noticeable tremor of the limbs appears;
• anomalies of mobility appear, it becomes weakened or, conversely, strengthened;
• unnatural and random movements of the shoulders, flexion and extension of the joints of the arms or legs;
• Abdominal reflexes also weaken or disappear completely.

With central facial palsy, most of the symptoms described above are localized on the person’s face. Usually the disease is expressed in unnatural facial expressions and involuntary muscle contractions.

This disease is very dangerous because it can lead to disruption of brain activity, and the number of cells that cannot be restored is growing every day. Therefore, the earlier therapy was started, the greater the chances of getting a positive result.

Diagnosis of the disease

Signs of central palsy can be identified during a visual examination. But to make an accurate diagnosis, experts resort to the following methods:

1. Computed tomography and magnetic resonance imaging, which can be used to see neural connections.
2. X-ray of joints and bones of the limbs, spine and skull.
3. Electromyography.
4. Analysis of the histology of painful muscles.
5. Spinal cord fluid puncture.

A neurologist treats central paralysis. It is he who should be contacted when the first symptoms of the disease are detected.

Differential diagnosis

During differential diagnosis, the specialist determines the volume and severity of symptoms of central paralysis. At this stage, all information about the disease is collected and analyzed in order to prescribe effective and safe therapy. Using external signs, you can find out the root of the problem and determine where the damage occurred:

1. If all limbs are immobilized, this indicates that damage to the spinal cord has occurred in the neck area.
2. If the functioning of the right or left side of the body is disrupted, we can conclude that the internal capsule is damaged.
3. Paralysis of the legs indicates predominantly in the chest or lower back.
4. Impaired functioning of one limb indicates the presence of peripheral paralysis.
5. Failure in the functioning of the eye muscles indicates a pathology of the cranial nerves.
6. Facial paralysis is characterized by unnatural facial expressions.
7. When observing a sluggish tongue, the root of the problem will be a malfunction

Another task facing the specialist will be to find out the cause of central paralysis. It is also very important to determine whether any other neurological changes have occurred. And if they are present, you need to start complex therapy. The duration of the course is determined by the doctor.

Drug treatment

People suffering from central nervous paralysis are prescribed complex therapy. During it, the main disease that caused the dysfunction of the muscles and the paralysis itself are treated. Conservative treatment methods will give the desired results only if the morphological substrate with which the affected muscles are regenerated has survived.

Most often, patients with a similar illness are prescribed the following drugs:

1. "Baclofen" - this drug has a strong effect on the transmission of nerve impulses to the muscles. It also helps cope with depression and improve well-being.
2. "Diazepam" - the drug affects the activation of processes in the brain stem, helps to cope with seizures, has a sedative and central muscle relaxant effect. Side effects include drowsiness, lethargy, nausea, vomiting, allergies, etc.
3. "Dantrolene" - this medication reduces muscle tone. Use with caution for people suffering from lung or heart disease.
4. Their effectiveness lies in the fact that they very quickly enter the nervous system and improve the quality of signal transmission to the muscles, thereby weakening the main signs of the disease.

The dosage is selected individually for each person, taking into account all the structural features of the body.

Physiotherapy

The goal of physical therapy is to return muscles to their previous condition and prevent their deformation. The introduction of these methods into basic therapy does not occur immediately. More specific deadlines are set by the attending physician, taking into account all the features of the course of the disease. The specific procedure is selected depending on the cause of central paralysis and the degree of damage to the body.

The most commonly used methods in this practice are:

1. Electrophoresis.
2. UHF and microwave treatment.
3. Electrical stimulation of immobilized limbs is carried out in conjunction with acupuncture.
4. Treatment with warm paraffin.

Physical rehabilitation of the patient begins with a restorative massage. Then he is gradually re-taught to use his body, that is, to perform conscious actions. As soon as a person can sit independently, they begin to teach him to walk. The last step will be to help with fine motor skills and various complex tasks such as fastening buttons, zippers, etc.

Surgery for central palsy

Surgery is usually used for flaccid paralysis or cerebral palsy, when conservative therapy has failed and neurogenic deformation has occurred, that is, the muscles of the limbs have been partially damaged and cannot be restored. In case of cerebral palsy, the purpose of this intervention will be to correct the functioning of the limbs that distort statics.

In practice, there are three types of such operations:

• normalization of tendons and muscles;
• ligament surgeries;
• restoration of bone and joint functions.

It is worth noting that the key to successful surgical intervention will be a properly selected set of other therapeutic measures to allow recovery after surgery.

Homeopathy

Homeopathic medicines are very good at promoting recovery from central paralysis, but they should not replace traditional medicine. Using these drugs together gives a better chance of restoring muscle activity and neural connections. We offer a small list:

1. "Conium" - helps get rid of seizures and tremors, side effects include weakness, chills and insomnia.
2. "Fibiaron" - this drug is more actively used for prevention, but it can also help recover from paralysis, harmonizing the functioning of the central nervous system.
3. "Botrops" - such a homeopathic remedy is a good assistant in restoring speech.
4. "Caustic" - the drug helps to recover from lead intoxication.

Baths for central paralysis

Another aid to recovery would be taking baths with various herbal infusions:

1. Two or three tablespoons of finely chopped rosehip roots are poured into a liter of boiling water and boiled for half an hour. The resulting decoction is added to the bath. It is worth noting that the water temperature should be 37-39 degrees.
2. You can also use juniper decoction to fill the bath, which is prepared according to the same recipe as the previous one.

For best effectiveness, after every 10 doses it is recommended to change the composition of the decoction poured into the bath.

Traditional medicine recipes for oral administration

1. Daily consumption of celery, nettle, plantain or feijoa juice will help you recover from central paralysis.
2. 20-30 grams are poured into a liter of hot water and left for 1 hour, after which they are thoroughly filtered. Take this remedy one tablespoon three times a day.
3. 10-15 pine cones are poured with half a liter of vodka for 30 days. After the tincture is ready, take 30-50 drops 3 times a day before meals.

Central paralysis is a disease that severely damages the human nervous system. In order to achieve a positive result in the treatment of the disease, you need to use complex therapy and apply all kinds of methods (home procedures, folk recipes).