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

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Martirosyan Vazgen Vartanovich

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

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

Disorders of motor functions can manifest themselves in the form of paralysis or paresis caused by damage to the central neuron - the corticospinal or pyramidal tract - or the peripheral one - the spino-muscular tract. Motor functions are very necessary for the body. I.M. Sechenov said that all external manifestations of brain activity are reduced to motor acts, that any cause of human action (the principle of determinism) is an external influence and that voluntary movements are reflex in the strict sense.

A dialectical understanding of the essence of the nervous processes occurring in the motor analyzer (in the peripheral and central sections), in conjunction with other analyzers, allows us to understand the pattern of physiological and pathological manifestations of motor activity. The evolutionary approach to the assessment of motor acts is essential.

The motor functions of a newborn child are carried out under the influence of the pallidal system as a higher subcortical center, and with the development of the pyramidal system, new functions appear - standing, walking, etc. Thus, structure and function are inextricably interconnected.

The motor analyzer is complex system. The cortical section of the motor analyzer is the anterior central gyrus, precentral and paracentral lobules, from which the corticospinal, or pyramidal, tract begins. The latest data on the structure of the cortex have shown that in the anterior central gyrus, i.e. in field 4, fields are distinguished: 4a, 4y, 4S. Field 4S belongs to the extrapyramidal system and is associated with the reticular formation of the brain stem. In the cerebral cortex there are zones of “suppression of motor activity” - 4S, 8S, 2S, 19S. In addition to fields 4 and 6, which belong to the main motor areas, there are additional motor areas - fields 9, 22, 24, 7, 8, etc. Motor functions are also associated with the posterior central gyrus, which belongs to the cortical section of the kinesthetic analyzer, which receives afferent impulses from receptors of the skin, muscles, tendons, ligaments, etc. I.M. Sechenov wrote that muscle feeling is the sum of sensations accompaniedaffecting any movement and change in position of the limbs and torso. There is a relationship between proprioceptive impulses going to the cerebral cortex and efferent impulses going from the cerebral cortex to the muscles to perform a motor act.

The cytoarchitecture of the cerebral cortex is variable in different areas. This is due to the functional characteristics of the corresponding cortical section of the analyzer. There are 6 layers in the cortex: I - zonal (lamina zonalis), II - external granular (lamina granularis externa), III - pyramidal (lamina pyramidalis), IV - internal granular (lamina granularis interna), V - ganglion (lamina ganglionaris). ), VI - multiform (lamina multiformis). In the anterior central gyrus, layers III and V are developed, in which pyramidal cells are located, and in layer V - giant cells (Betz cells). In Fig. Figure 1 (see color insert p. 96-97) shows the cyto- and myeloarchitecture of fields 4 and 6. From the Betz cells there is a pyramidal tract, the fibers of which end in the cells of the anterior horn spinal cord. Betz cells have a long axon and a large number of collaterals. The Betz cell is connected to several cells of the spinal cord, which ensures multisynaptic transmission of impulses. The interneurons that are part of the pyramidal tract “work out” impulses. The pyramidal fasciculus in the anterior horns of the spinal cord is more developed on the right side, most of its fibers ending in the lower cervical and upper thoracic segments. There are sometimes additional bundles at the level from Ci to Cs. The development of the anterior pyramidal fasciculus appears to be associated with the complex differentiated motor functions of the human hand. By recording responses in single fibers of the pyramidal tract during stimulation of the motor cortex, Adrian and Moruzzi noted that contraction of the muscle to which the impulses arrive is accompanied by rhythmic discharges in the fibers of the pyramidal tract. When stimulating the pyramidal tract and recording an antidromic response in the cerebral cortex, it was found that some neurons are excited after a long latent period, which is preceded by the appearance of a synaptic potential (S. Oke). There is a partial bilateral representation in the cerebral cortex, providing motor functions. When there is a lesion in the cortical part of the motor analyzer, degeneration of the fibers of the pyramidal tract is observed not only in the affected hemisphere, but partially also in the coptralateral one. Additional zones of the motor analyzer in the cerebral cortex determine the performance of complex motor acts and cooperative movements. Axons of pyramidal cells from area 4y go in a descending and partially ascending direction to area 4a (Fig. 2). In phylogenesis, the appearance of a larger number of depdrites of cells from which the pyramidal tract begins is noted, which indicates an increase in afferent connections of motor cells. The pyramidal tract contains myelinated and unmyelinated fibers. The axon initially does not have myelin, its diameter is reduced, but then a zone of myelination of the axon appears. This distribution of myelin is important for the conduction of impulses. The presence of spines on the dendrites provides the possibility of the development of refractoriness after excitation. The pyramidal tract is connected with the extrapyramidal system, which through the rings " feedback“affects the activity of the motor analyzer. Thanks to the “feedback” system, impulses coming from the cortex enter the optic thalamus, striopallidal system, reticular formation of the brain stem, cerebellum, red nucleus and then back to the cortex, controlling movement. From field 4S there is an inhibitory influence through the bulbar region reticular formation to interneurons and cells of the spinal cord.

Magun and Rainis established that inhibition of motor activity of the spinal cord occurred when the reticular formation of the medulla oblongata was irritated. Using the method of transecting various sections of the spinal cord, it was shown that the paths along which impulses from the bulbar inhibitory area propagate to the spinal cord pass in the anterior and partly lateral (in its ventral part) columns of the spinal cord. After braking, a noticeable facilitation of motor reactions occurs. Detailed Study showed that the hypothalamus and a number of structures located in the reticular formation of the brain stem (in the gray matter of the midbrain tegmentum, pontine tegmentum and medulla oblongata) have a facilitating effect on the spinal cord. The reticular formation may influence directly the motor neurons of the spinal cord orthrough intermediate neurons. It has been established (Granite) that the reticular formation
brainstem affects the activity of not only alpha motor neurons,conducting impulses to contractile muscle fibers, and this happenssame strengthening or, conversely, suppression of the activity of gamma motor neurons, axonswhich go to the intrafusal fibers of the muscle spindles. Change functionthe national state of intrafusal fibers affects the conduction of afferentsstrong impulses from muscle proprioceptors to the central nervous system, whichaffects the activity of alpha and gamma motor neurons. Regulation of activities

Rice. 2. Structure of the anterior central gyrus with identification of fields

4a, 4u and 4S.

gamma efferent systems are carried out by the reticular formation of the midbrain tegmentum. Reticulospinal influences are transmitted along two pathways - fast and slow conducting. The first provides regulation of fast movements, the second regulates slow, tonic reactions. The activity of reticulospinal mechanisms is supported by humoral and nervous factors. The activity of the reticulospinal systems is supported by influences from the vestibular apparatus, cerebellum, and cerebral cortex. One of the ways through which the reticular formation influences the cerebral cortex is the medial group of thalamic nuclei, which makes up the nonspecific projection thalamo-cortical system.

Morison and Dempel (1942) described the electrophysiological phenomenon of the entrainment reaction that occurs in the cerebral cortex when the nuclei of the thalamus are irritated in a rhythm of 6-12 seconds. The nonspecific thalamo-cortical projection system affects the cerebral cortex and subcortical nodes. The entrainment reaction is a phenomenon of oscillatory nature, resulting from the circulation of impulses along closed circuits of neurons. Excitation that reaches the first group of cells spreads to subsequent ones until the impulse returns to the first element of the chain. Entrainment potentials in the motor cortex are accompanied by discharges in the pyramidal tract. They appear in parallel with the entrainment reaction in the cerebral cortex and are absent in the case of a single irritation of the nonspecific nuclei of the thalamus. Nonspecific thalamic afferent fibers ending in the motor cortex not only have a modulatory effect on the excitability of pyramidal neurons, but are capable of activating these neurons themselves. There is a correspondence between individual components

Rice. 3. A. Somatotopic arrangement of centers in the anterior
central gyrus.

entrainment potential pentami and depolarization cell membrane cortical neurons. The entrainment reaction is accompanied by a decrease in spontaneous discharges of cortical cells, while the activation reaction with high-frequency stimulation of the same structures causes an increase in the number of spontaneous discharges. The nonspecific thalamo-cortical system can be considered as a subcortical relay for transmitting a special type of influence on the cerebral cortex. The ascending part of the reticular formation of the brainstem and the diencephalic structures are the system through which the cerebellum influences cortical functions.

With electrical stimulation of the reticular formation, the electrical activity of the brain changes and increases energy metabolism in the brain, the release of chemical mediators increases - acetylcholine, which plays a role in the synaptic transmission of impulses through motor neurons.

Thus, there are two afferent systems - specific and nonspecific. Specific afferent fibers end in the fourth layer of the cortex, nonspecific - in all layers of the cortex. The interaction of both of these systems determines the final response of cortical neurons. The cerebral cortex, subcortical ganglia, cerebellum and brain stem act in close functional unity.

The representation of motor functions in the anterior central gyrus and paracentral lobule has a somatotopic principle (Fig. 3 A). Superior part of the anterior central gyrusand the paracentral lobule are connected to the leg muscles. Below is the zone from which the cortical innervation of the torso and arms comes, and in the lower section there are cells from which fibers go to the nuclei of the cranial nerves for the muscles of the face, tongue, larynx, and pharynx. The more developed the function, the more complex the structure in the anterior central gyrus is represented. Thus, the zone of cortical innervation of the hand and fingers occupies a larger area than the zone of innervation of the foot, which is explained by the special functional significance of the hand in humans.

Central paralysis occurs when the pyramidal tract is damaged, which, starting in the anterior central gyrus, passes through the corona radiata and, converging, enters the internal capsule, occupying the anterior two-thirds of the posterior thigh (Fig. 3 B). Next, the pyramidal and corticonuclear tracts pass through the cerebral peduncle, pons and medulla oblongata, occupying their ventral section (Fig. 4, A). In the lower part of the medulla oblongata, an incomplete crossing of the pyramidal fibers occurs, as a result of which the crossed fibers go in the lateral columns of the spinal cord, where there is a somatotopic distribution (Fig. 4, B), and the uncrossed fibers make up the uncrossed pyramidal tract, which occupies the medial part of the anterior column. Uncrossed fibers partially end in the cells of the anterior hornscollaterally, partially contralaterally, passing through the anterior white commissure of the spinal cord to the opposite side. The corticonuclear pathway conducts impulses from lower section anterior central gyrus to the motor nuclei of the cranial nerves. This path passes through the knee of the internal capsule and in the middle part of the base of the cerebral peduncle. Stimulation of field 4 causes contralateral movements of the corresponding muscles. When field 6 is stimulated, movements appear, the implementation of which occurs with the participation of a larger number of coordinating mechanisms. Integration of motor activity is noted: when performing movements of one finger, excitation and inhibition occur in the combined zones of innervation of other fingers, which indicates the relationship between the structure and functions of motor formations. In Fig. Figure 5 (see color insert p. 96-97) shows a diagram of reciprocal innervation.

Damage to the pyramidal tract is characterized bymaking voluntary movements. Thanks to the decussation of the pyramidal tract at the border of the medulla oblongata and the spinal cord, motordisorders due to brain damage occur eventuallyon the side opposite to the hearth. Symptoms of centralparalysis or paresis: 1) absence or limitation of the volume of movementmarriages and loss of strength; 2) increase muscle tone(hypermuscle tone) according to the spastic type: in the hand the tone increases inadductor muscles of the shoulder, flexors and pronators of the forearm,flexors of the hand and fingers. In leg 1, the tone is increased in the extensorsthighs and lower legs, adductor muscles of the thigh and plantar flexionbodies of the feet. Due to uneven distribution of tonemuscles, the Wernicke-Mann position arises (the arm is bent at the elbow

Rice. 4. Diagrams of pathways. Course of the corticospinal and corticonuclear tract (A); somatotopic arrangement of pyramidal tract fibers in the lateral columns of the spinal cord (B).

joint, adducted and pronated, the leg is extended at the knee joint and abducted); 3) increased tendon reflexes: on the arm with the biceps and triceps muscles, periosteal (metacarpal radial), on the leg knee and Achilles reflexes. With hyperreflexia, the amplitude of movements increases and the reflexogenic zone expands. With an increase in the knee reflex, clonus of the patella is detected, and with an increase in the Achilles reflex, clonus of the foot. With increased tendon and periosteal reflexes in the hand, hand clonus. Skin (abdominal) reflexes on the side of paralysis are reduced. The joint reflexes of Lehry and Mayer are absent in central paralysis; 4) pathological reflexes: on the lower extremities reflexes of the extensor type (Babinsky, Oppenheim, Redlich, Gordon, Schaeffer, Grossman) and flexion type (Rossolimo, Bekhterev-Mendel, Bekhterev II, Zhukovsky), on the upper extremities pathological reflexes Rossolimo, Bekhterev-Jacobson - Lyask, Zhukovsky, Tremner, Venderovich (“ulnar motor defect”).

Pathological reflexes on the face appear with bilateral damage to the corticonuclear cells coming from the cortex

anterior central gyrus to the nuclei of the cranial nerves. Pseudobulbar reflexes (reflexes of jural automatism) include: Palmar-mental reflex Marinesko Radovici, Toulouse-Wurp labial reflex, Oppenheim sucking reflex, Bekhterev mental reflex, Astvatsaturov naso-labial reflex, buccal reflex, proboscis reflex, “bulldog reflex”, buccal reflex rotational reflex, oralHenneberg reflex, labio-mental reflex, paso-mental reflex, naso-oral reflex, buccal-rotational and distance-mental Babkin reflex, distance-oral reflex Karchikyan-Rastvorova. We have described the buccal-oral reflex (contraction of the muscles of the mouth when the cheek is irritated with strokes), the distance-oral reflex (the reflex opening of the mouth when the hammer is re-approached to the lips) and the distance-ocular reflex (the reflex raising of the upper eyelids and the widening of the palpebral fissures when the hammer is re-approached to the lips). face). Pseudobulbar reflexes also include violent crying and laughter. Pseudobulbar syndrome develops with a multifocal process in both hemispheres: in the cortex, subcortex, internal capsule and other parts of the brain; 5) adductor periosteal reflexes: adduction of the thigh: a) with percussion along the ilium, b) with percussion of the tibia (P. Marie reflex), c) with tapping along the inner edge of the knee; 6) protective reflexes on the lower extremities in response to nociceptive irritations (injection, irritation with ether, etc.) of the sole, lower leg and thigh (flexion at the hip, knee and ankle joints and dorsiflexion of the thumb, less often extension of the hip, lower leg and flexion of the foot) . Protective reflexes in the upper extremities (in response to an injection or pinch in the upper chest) in the form of flexion or extension of the arm with pronation of the forearm; 7) clonus of the foot, kneecap, buttock, hand and fingers, arising from jerky proprioceptive irritation of the corresponding muscles; 8) friendly movements - global, coordinating, imitation synkinesis. Global synkinesis is a friendly contraction of paretic limbs (with hemiplegia in the restitution stage) with forced contractions of the muscles of healthy limbs. Coordination synkinesis in paretic muscle groups when performing voluntary movements. These include: Strumpel’s platysmal synkinesis (tension of the platysma on the paresis side when baring the mouth); Logra synkinesis (friendly extension of the thumb with forced flexion of the shin), tibial synkinesis of Strumpel (dorsal flexion of the foot with forced flexion of the shin and thigh with resistance); friendly movements in the form of pressure of the paretic leg on the bed with active lifting of the healthy leg and involuntary flexion in hip joint paretic leg with active pressure of the heel of the healthy leg on the bed; adductor synkinesis of Raymist (involuntary adduction of a paretic lower limb when trying to actively adduct the healthy leg, overcoming an obstacle provided to the researcher); abductor synkinesis of Raymist (friendly abduction of a paretic lower limb when trying to produce, overcoming the resistance provided by the researcher’s hand, an identical movement with the “healthy” limb); Hoover's synkinesis (inability to hold the healthy and paretic lower limbs raised at the same time in a supine position: raised paretic lower limb unpronouncedfalls freely onto the bed and cannot be restrained at the moment when the healthy leg rises); friendly plantar flexion of the paretic foot during extension (dorsal flexion) of the foot of the opposite limb; friendly extension movement of the paretic foot with active plantar flexion of the foot of the healthy leg; friendly flexion of the trunk and lower leg of the paretic limb when the patient tries to sit down; friendly flexion of the trunk and hip (Babinski synkinesis); flexion of the leg at the hip joint when the patient tries to actively change the lying position to a sitting one; friendly movements of the torso and fingers: when moving from supine position in a sitting position, conducive to trunk flexion, the fingers of the paretic lower limb are separated; Neri synkinesis (friendly flexion of a paretic limb at the knee joint when the torso is tilted forward); friendly tension of the anterior pectoral muscle on the side of the paresis with active adduction of the healthy upper limb; brachio-brachial synkinesia (comfortable flexion and pronation of the forearm of a paretic upper limb when counteracted by a healthy upper limb); synkinesis Bitch (friendly extension of the fingers when raising the shoulder of the paretic arm); friendly pronation when flexing the forearm, as a result of which the hand, turned by the back of the hand, approaches the shoulder, involuntary pronation of the paretic hand from a position of extreme supination (Babinsky) or supination of both upper limbs lowered down; friendly supination when a lying patient raises an outstretched arm with a pronated hand; Balducci synkinesis - adduction of the foot during percussion on the contralateral heel. Synkinesias on the face (described by N. K. Bogolepov): a) oculolingual (movement of the tongue in the direction of abduction of the eyes), b) oral-platysmal (tension of the platysma when puffing out the cheeks or opening the mouth), c) respiratory-manual (spreading the fingers at deep breath or cough) and d) symptoms of foot rotation: 1) outward rotation of the foot (during the period of diaschisis with damage to the pyramidal tract), 2) inward rotation of the foot (during the restorative period central paresis or with damage to the premotor zone in the cerebral cortex). Imitative synkinesis occurs simultaneously in a paralyzed limb during voluntary contractions.

With prolonged paralysis of the limbs, their atrophy develops as a result of the loss of trophic influences on the muscles, which, unlike peripheral paralysis is not accompanied by degenerative changes in the study of electrical excitability and electromyography. Sometimes in paralyzed limbs in patients with hemiplegia, edema of the upper limb develops as a result of impaired trophism and increased capillary permeability.

Differential diagnostic signs of central and peripheral paresis: with central paresis, the pyramidal tract is affected at various levels from the cerebral cortexto the cells of the anterior horns of the spinal cord; muscle tone (spastic paresis) and tendon reflexes increase and their reflexogenic zone expands, skin reflexes are absent or decreased, pathological Babinsky and Rossolimo reflexes (and their analogues) appear, adductor periosteal reflexes, clonus of the foot, patella, buttocks, hands, protective reflexes on the lower limb, less often on the upper limb, synkinesis (global, coordination); there is no muscle atrophy (or mildly expressed) and fibrillary twitching, vasomotor phenomena are weak or absent, the electromyogram shows a decrease in the amplitude of oscillations in the paretic muscles. With peripheral paresis, the nuclei of the cranial nerves or the cells of the anterior horns of the spinal cord and the axons of the cranial nerves or the anterior roots of the spinal cord coming from them are affected; muscle tone (flaccid paresis) and tendon reflexes decrease; skin reflexes are preserved; there are no pathological reflexes, adductor periosteal reflexes, clonus, protective reflexes and synkinesis; degenerative muscle atrophy and fibrillary twitching are determined (with a chronic process affecting the cells of the anterior horn); vasomotor and trophic disorders are expressed; Low-voltage potentials, fibrillations and monophasic positive denervation potentials appear on the electromyogram.

Central paralysis varies depending on: 1) the degree of impairment of motor functions (paresis or paralysis); 2) on the prevalence of paralysis (monoplegia, paraplegia, hemiplegia, triplegia, tetraplegia); 3) from muscle tone (spastic paralysis with increased muscle tone, usually in the flexors and adductors of the arm and extensors of the leg, or atonic - diaschisal paralysis); 4) from predominant damage to the proximal or distal part of the paralyzed limbs (if the internal capsule is damaged, the distal part of the extremities is more affected and the function of the proximal part of the extremities is more likely to be restored). If the lower part of the anterior central gyrus is affected (the vascularization zone of the middle cerebral artery) the hand suffers more clearly, and when damaged upper section the anterior central gyrus and paracentral lobule have greater impairment of leg function; 5) from the period that has passed since the development of paralysis, or the stage of the pathological process (diaschisal, restorative, residual); 6) from etiology (traumatic, dyscirculatory, demyelinating processes); 7) from the pathogenesis of paralysis (conduction disturbances due to damage to the pyramidal tract, reflex paralysis, etc.); 8) on the level of damage to the central motor neuron (cortical, capsular, alternating paralysis with damage to the brain stem, spinal paralysis).

When assessing the symptoms of central paralysis, the stage of the pathological process is important. In the initial period of acute lesions of the pyramidal tract in stroke,diaschisis (nervous shock), in which pyramidal paralysis syndrome is characterized by muscle atony, decreased tendon reflexes, and the presence of the Babinski reflex, in contrast to the period of restitution of impaired motor functions, characterized by restoration of movements, muscle tone, increased reflexes and the presence of the pathological Rossolimo reflex and its analogues.

Functional dysfunction can manifest itself differently depending on the nature of the pathological process in the cortex of the motor analyzer. When the cortex of the anterior central gyrus is irritated, a local epileptic seizure with convulsions of the limbs opposite to the focus is observed. Such attacks of Jacksonian epilepsy occur during extracerebral processes: with a tumor, traumatic cyst, subarachnoid hemorrhage, etc. With loss of motor functions as a result of damage to the cortical part of the motor analyzer, monoplegia of the opposite limb develops, and with a large lesion - hemiplegia.

The symptoms of central paralysis vary with different levels of damage. When the focus is localized in the cortical part of the motor analyzer, there are various syndromes: with damage to the anterior central gyrus (motor zone) and premotor zone, they differ in the dynamics of restoration of impaired motor functions during the period of restitution. When the motor zone is damaged, the hemiplegia of the opposite limbs is significantly expressed and restitution is slow; when the premotor zone is damaged, motor functions are less impaired and the restoration of movements is faster. When the motor zone is damaged in the initial period of hemiplegia, atony occurs and muscle tone is restored slowly, the increase in tendon reflexes occurs gradually in combination with the development of spastic muscle hypertension, extensor type reflexes predominate (Babinsky and its analogues), there are no cervical tonic reflexes and grasping reflex of the hand, foot rotated outward, coordinating and global synkinesis are determined. When the premotor zone is damaged, spastic hypertension of the leg extensor muscles develops early, tendon reflexes with an expanded reflexogenic zone are sharply increased, clonus of the foot and kneecap appears early, flexion type reflexes predominate (Rossolimo, etc.), cervical tonic reflexes are observed, a tendency to grasping movements and flexion synergies of the fingers, the foot is rotated inward with its adductor position, global synkinesis of the flexion type, coordinating synkinesis in the paretic arm and leg are determined.

When the frontal lobes are damaged (for example, when blood circulation is impaired in both anterior cerebral arteries), scapulocrural diplegia occurs (paralysis of the shoulder girdle and lower extremities), which is differentiated with akinetic mutism and “hypothalamic stupor,” in which there is no paralysis, but impaired ability for voluntary movement.

Pontine (pontine) alternating syndromes: 1. Millar-Gubler syndrome occurs when the lower part of the pons is affected. It is characterized by peripheral paralysis of the facial nerve on the affected side, central paralysis of the opposite limbs (Fig. 6, c). 2. Brissot-Sicart syndrome is detected by irritation of the cells of the nucleus of the facial nerve in the form of contraction of the facial muscles on the side of the lesion and spastic hemiparesis or hemiplegia of the opposite limbs. 3. Foville syndrome is characterized by paralysis of the facial and abducens nerves (in combination with gaze paralysis) on the side of the lesion and hemiplegia, and sometimes hemianesthesia (due to damage to the medial lemniscus) of the opposite limbs (Fig. 6, d). 4. Raymond-Sestap syndrome is characterized by the absence of combined movements of the eyeballs, ataxia on the affected side, choreoathetoid movements, hemianesthesia and hemiparesis of the limbs of the opposite side.

Bulbar alternating syndromes: 1. Jackson syndrome is characterized by peripheral paralysis of the hypoglossal nerve on the affected side and hemiplegia or hemiparesis of the limbs of the opposite side (Fig. 6, e). 2. Avellis syndrome includes damage to the glossopharyngeal and vagus nerves (paralysis of the soft palate and vocal cord on the side of the lesion with choking when eating, getting liquid food into the nose, dysarthria and dysphopia) and hemiplegia on the opposite side. 3. Babinski-Nageotte syndrome is manifested by cerebellar symptoms in the form of hemiataxia, hemiasynergia, lateropulsin (as a result of damage to the inferior cerebellar peduncle, olivo-cerebellar fibers), miosis or Claude Bernard-Horner syndrome on the side of the lesion and hemiplegia and hemianesthesia of the opposite limbs

2. Schmidt syndrome includes paralysis of the vocal cords, soft palate and trapezius and sternocleidomastoid muscles on the affected side (IX, X and XI nerves), hemiparesis of the opposite limbs. 5. Wallenberg-Zakharchenko syndrome is characterized by symptoms on the side of the lesion: paralysis of the soft palate and vocal cord, anesthesia of the pharynx and larynx, sensitivity disorder on the face, Horner's syndrome, hemiataxia with damage to the cerebellar tract and respiratory distress (with an extensive lesion in the medulla oblongata) and on contralateral side: hemiplegia, analgesia and thermoanesthesia. There are 5 types of Wallepberg-Zakharchenko syndrome: 1) alternating hemianalgesia (on the face on the side of the lesion, on the trunk and limbs on the opposite side);

false side), paralysis of the soft palate, vocal cord, Horner's syndrome and ataxia on the side of the lesion (Fig. 6, e); 2) alternating hemianalgesia, paralysis of the soft palate and vocal cord, Horner's syndrome, ataxia on the side of the lesion, paresis of the VI and VII nerves (on the side of the lesion); 3) alternating hemianalgesia, paralysis of the soft palate, vocal cord, Horner's syndrome, ataxia on the side of the lesion, triplegia or cross hemiplegia; 4) hemianesthesia on the side opposite to the lesion, paralysis of the soft palate, vocal cord, Horner's syndrome, ataxia on the side of the lesion; 5) paralysis of the soft palate, vocal cord, Horner's syndrome and ataxia on the side of the lesion, sensitivity disorder on the face on both sides and on the trunk and limbs on the opposite side.

We present the following observations to illustrate the development of central paralysis during various localizations pathological process.

Patient T., 42 years old, received a tangential wound to the skull, as a result of which paresis of the lower extremities developed. 4 years after the injury, the following are noted: spastic paresis of the legs, increased muscle tone in the extensors of the leg, increased knee reflexes, pyramidal reflexes of Babinsky and Rossolimo on both sides. Sensitivity is not upset. Disturbed urination. Paresis of both legs developed as a result of traumatic brain injury in the parasagittal region.

Patient S., 26 years old, gradually began to notice weakness in his left leg. After 5 months, the paresis increased, and there was radicular pain in the Dn-Div area on the left. The examination revealed central paralysis of the left leg with spastic muscle hypertension, a symptom of an outwardly rotated left foot. Anesthesia of pain and temperature sensitivity at the Du-Div level on the left, hypoesthesia of pain and temperature sensitivity on the right leg and half of the torso from the Div level. Deep sensitivity disorder in the left leg. Increased knee and Achilles reflexes with expansion of their reflexogenic zone on the left lower limb, a sharp decline abdominal reflexes on the left. Pathological reflexes of Babinsky, Oppenheim, Rossolimo on the left. The combination of central paralysis with a disorder of deep sensitivity on the affected side and a disorder of superficial sensitivity on the opposite side is characteristic of Brown-Séquard syndrome, which is observed when half of the spinal cord is affected. Symptoms indicate a lesion in the left half of the spinal cord at the level of the Dn-Div segments.

Determining the symptoms of central paresis is of great importance in medical practice. To identify paresis, Barre's techniques are used: 1) to determine paresis of the arm, the patient is asked to stretch his arms forward at a horizontal level and hold them in this position for some time with his eyes closed; at the same time, the paretic arm slowly lowers and the hand pronates; 2) to identify leg paresis, the patient is asked to lie on his stomach with his legs bent at the knee joints at an angle of 90°; if there is paresis, the leg slowly lowers. Panchenko's technique allows you to identify paresis of the hand: the patient is asked to raise his hands above his head, palms up, touching each other with the ends of his fingers; on the side of the paresis, the tendency of the hand to pronate is determined.

In the process of restoring impaired motor functions, the interaction of the cerebral cortex and subcortex changes, new functional relationships and new connections are formed.zi motor cortex with other analyzers and subcortical nodes. I. P. Pavlov established that when the diffuse diffuse inhibition formed after damage gradually dissipates and disappears and the relationships between the processes of excitation and inhibition in the cerebral cortex are restored, then functions that were temporarily obscured and, as it were, washed away by neurodynamic changes, are restored. When the motor zone of the cortex is damaged, muscle hypotonia first occurs, which is replaced by spasticity, and then, if the course is favorable, recovery. The duration of dysfunction depends on the depth of damage to the cortex of the motor analyzer: when the upper layers of the cerebral cortex are destroyed, paresis is mild and short-lived. When all layers of the cortex are destroyed, it is more pronounced and the restoration of impaired functions occurs more slowly. If afferent innervation is disrupted in combination with impaired motor functions, restoration of movements becomes significantly more difficult. The preservation of reticulocortical influences, cerebellar, thalamic and other supraspinal regulations is essential for the restoration of motor functions. motor functions, carried out with the participation of feedback rings.

To restore impaired motor functions, the nature of the pathological process, the ability to quickly restore collateral circulation in the event of a disruption in the blood supply to the brain, the size and location of the lesion, the primacy or recurrence of the stroke, are important. therapeutic measures, promoting the development of compensatory and adaptive mechanisms for movement disorders.

At acute development In the process, paralysis of the limbs first occurs with muscle atony, decreased tendon reflexes, the appearance of the Babinski reflex and sometimes protective reflexes. This variant of motor disorders can be called a flaccid form of hemiplegia, caused by deep transcendental inhibition, spreading to the cortex and to the underlying subcortical and brainstem apparatus. Important signs that make it possible to identify paralysis of the limbs in a state of diaschisis (deep transcendental inhibition) are the following symptoms described by us: a symptom of an outwardly rotated foot due to a decrease in the strength and tone of the muscles rotating the foot, a symptom of a “spread hip” (the thigh, due to loss of muscle tone, becomes flabby and wide), a symptom of eyelid hypotonia (in the patient both eyelids are passively raised, on the side of hemiplegia the eyelid drops slowly and does not completely cover the eyeball).

The symptoms of the acute, initial period of hemiplegia change if tonic spasms, excessive movements such as gesticulation, protective reflex movements, “early” hyperkinesis, “early” clonus, various “violent” changes in the position of the limbs, and contractures appear. These movements are especially pronounced in hormetonia.

We have established a certain dynamics of restoration of motor functions and noted that poor recovery, and sometimes gradual progression of motor disorders, occurs with a bilateral multifocal process in the cerebral cortex and subcortical nodes (pseudobulbar palsy with a progressive course). Symptoms due to a large lesion depend on general violations cortical-subcortical systems, causing a progressive course of the process (“protracted diaschisis”).

Restoration of motor functions can occur gradually, slowly (with damage to the cortical part of the motor analyzer and subcortex) and quickly (if the lesion is localized in the peripheral parts of the motor analyzer, premotor area), when the functions of the subcortex and internal bursa are impaired only as a result of neurodynamic changes. Recovery may initially be delayed for a long time, then a “breaking point” occurs and recovery gradually begins. In such cases, apparently, there is initially a deep inhibition in the cerebral cortex, caused by a large lesion or several lesions. In addition, deterioration of the condition may be associated with complications.

The speed of recovery of impaired motor functions depends on various conditions: 1) the farther this area is from the lesion, the sooner it is freed from inhibition, the faster its functions return to normal; 2) the degree of restoration of motor functions depends on whether the function of the motor analyzer is completely or partially impaired; 3) whether there is irreversible damage to the cerebral cortex and motor pathway; 4) on the duration and depth of transcendental inhibition, which causes inhibition of the entire motor system; 5) on the localization of the lesion (cortex, subcortical nodes or cortical-subcortical region). Motor functions in combination with sensory disorders are restored more slowly.

First, unconditioned reflexes are restored, then conditioned ones. First, reflexes and muscle tone are restored, then global and coordinating synkinesis and auxiliary movements appear, and finally voluntary movements are restored. The restoration of movements occurs sequentially, in a certain order: first, movements are restored in the proximal part of the limb, then in the distal part. The more specialized the movements, the more difficult they are to recover: global movements (walking, arm movements in shoulder joint) recover faster and better. More subtle, specialized coordinated movements performed by the hand are slower to recover. With varying degrees of damage to the cortical zones of the arms and legs and their corticospinal conductors, movements of the upper limb can be restored first, and then the lower. Restoring motor functions is difficult with extensive damage to the cerebral cortex, as well as with damage to the connections between both hemispheres (simultaneous damage to the corpus callosum).

Motor functions with left-sided hemiparesis are restored somewhat faster than with right-sided hemiparesis. Patients with right-sided paralysis become more helpless, as they lose specialized movements that are usually performed with the right hand. With right-sided hemiparesis, adaptation to work is also significantly difficult due to the slow and less perfect recovery of motor functions, often combined with a speech or writing disorder, which in turn significantly reduces the patient’s ability to engage in work. When combining right-sided hemiparesis with speech and writing impairment during the period of movement recovery right hand become difficult if the patient is forced to fix the tongue in the mouth between the teeth. The mechanism of friendly movement of the tongue during reading and writing is developed in childhood. It is known that children “help with their tongue” when writing and when performing difficult tasks. If a speaker who is accustomed to gesturing has his hand fixed and thus deprived of the ability to combine speech with gesture, his speech becomes emotionally less expressive. Thus, there is an inextricable connection between speech and writing, due to the synthesis of kinesthetic ideas in the cerebral cortex.

Sometimes during the recovery period, excessive effort to make a movement makes it difficult to implement the movement itself and, conversely, when attention is distracted, the movements are performed more smoothly. During the recovery period, it happens that movements are not performed voluntarily, but can be carried out by creating positions that facilitate the movement of the limbs, for example, the patient can bend his lower leg if he lies not on his back, but on his side; he performs movements with the fingers of the hand if the hand is fixed on the table. In performing movements, the visual analyzer is important (movements are performed more accurately with open eyes and worsen when vision control is turned off).

In the process of restoring motor functions, the state of muscle tone is important. Sometimes early hemitonia appears, differing from hemihormetonia by the absence of tonic spasms. Restoration of impaired motor functions with early developing muscle hypertension can proceed sequentially: withIn case of damage to the pyramidal tract, hypotension is replaced by spastic hypertension, and in case of damage to the subcortical nodes, muscle hypertension is replaced first by hypotension, then by hypertension, which ends with contracture, passing through the stage of conjugate movements. Rigidity can be observed in the initial period not in the paralyzed limbs, but homolaterally; it then gradually decreases, sometimes reappearing during the recovery period. Sometimes flexion contracture of the lower limb develops in the limbs on the side of the lesion - concomitant flexion of the non-paralyzed limb as the flexion joint progresses.Tractures of a paralyzed lower limb. Plastic hypertension in the extremities of the same name as the lesion occurs when a vascular lesion is localized in the frontoparietal region or the internal capsule, and muscle rigidity when the process is localized in the area of ​​the internal capsule is more pronounced than with a lesion in the cerebral cortex. With damage to the pyramidal tract and pallidal system, one would expect the appearance of plastic hypertension in the limbs opposite to the lesion. However, in acute period hemiplegia, depression of tone occurs, not plastic hypertension develops, but hypotension, and later, during the period of restoration of movements, spastic hypertension with selective distribution of tone develops. If the function of the globus pallidus is disrupted during the vascular process, then plastic muscle hypertension and postural reflexes are detected on the side of the lesion, which are not detected on the opposite side due to the presence of spastic muscle hypertension. With lesions localized in the cerebral cortex, the tone of the hand muscles first increases; with lesions in the area of ​​the internal bursa, the tone of the forearm flexor and shoulder adductor muscles increases.

I. P. Pavlov noted that weeks and months pass and the movement disorder is so leveled out that the animal is not much different from normal, and explained this by the replacement of damaged analyzers.

With poor restitution and incomplete restoration of functions, contractures of the limbs develop: hyperpronator (Fig. 8, a), hypersupinator, paraflexor, triflexor (Fig. 8, b), quadriflexor. Changes in motor impairments in advanced cases of central paralysis with poor functional recovery are described in detail by us in the monograph “Motor dysfunctions in vascular lesions of the brain” (1953).

Treatment. To restore impaired functions in central paralysis, biostimulants, proserin, vitamins, therapeutic exercises, and massage are used.

It arises as a result of damage to the central motor neuron in any part of it and differs from the peripheral one in a number of ways: pronounced muscles are not characteristic here and there is no degeneration reaction, neither muscle atony nor loss of reflexes is observed.

Symptoms:

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. For central paralysis upper limb usually brought towards 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”). This position of the limbs with central hemiplegia creates a peculiar Wernicke-Mann position, the interpretation of the patterns of its occurrence from the point of view of the history of the development of the nervous system was given by M.I. Astvatsaturov.

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 horizontal position in 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 persistent symptoms 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 of great importance in practice clinical trial did not purchase. 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.

Symptoms such as increased tendon reflexes of the limbs, weakened abdominal reflexes and Babinski's symptom are very subtle and early signs of a violation of the integrity of the pyramidal system and can be observed when the lesion is not yet sufficient to cause paralysis or even paresis. Therefore, their diagnostic value is very great. E.L. Venderovich described a symptom of “ulnar motor defect”, indicating a very mild degree of pyramidal lesion: on the affected side, the patient’s resistance to forced abduction of the little finger as far as possible towards the fourth finger is weaker.

Causes:

Spastic paralysis occurs due to damage to the motor neuron. Since the arrangement of cells and fibers of the pyramidal fasciculi 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.
The most common causes of spasticity are stroke, traumatic brain and spinal injuries, perinatal (cerebral palsy), etc. Spasticity is caused by an imbalance in nerve impulses. Which are sent by the nervous system to the muscles. It leads to increased tone of the latter.
Other causes of spasticity:

      * Brain injuries
      * Spinal cord injury
      * Brain damage due to lack of oxygen (hypoxia)
      *
      * (inflammation of brain tissue)
      * (inflammation of the tissue of the meninges)
      * Adrenoleukodystrophy
      * Amyotrophic lateral sclerosis
      *

Treatment:

For treatment the following is prescribed:

There are several treatments for spasticity. They all pursue the following goals:

      * Relief of symptoms of spasticity
      * Reducing pain and muscle spasm
      * Improving gait, daily activity, hygiene and care
      * Facilitation of voluntary movements

Physiotherapeutic methods for treating spasticity:

Physiotherapy is performed to reduce muscle tone and improve movement, strength and muscle coordination.

Drug therapy for spasticity:

The use of drug therapy is indicated for daily disruption of normal muscle activity. Effective drug treatment involves the use of two or more drugs in combination with other treatment methods. Drugs used for spasticity include:

      * Baclofen
      * Benzodiazepines
      * Datrolene
      * Imidazoline
      * Gabaleptin

Botulinum toxin injections for spasticity:

Botulinum toxin, also known as Botox, is effective in very small quantities when injected into paralyzed muscles. When Botox is injected into a muscle, the action of the neurotransmitter acetylcholine, which helps transmit impulses in nerves, is blocked. This leads to muscle relaxation. The effect of the injection begins within a few days and lasts about 12 – 16 weeks.

Surgical treatment of spasticity:

Surgical treatments include intrathecal baclofen and selective dorsal rhizotomy.

Intrathecal administration of baclofen. At severe cases spasticity, baclofen is prescribed by injecting directly into cerebrospinal fluid. To do this, an ampoule with baclofen is implanted into the skin of the abdomen.

Selective dorsal rhizotomy. In this operation, the surgeon cuts certain nerve roots. This method is used to treat severe spasticity that interferes with normal walking. In this case, only the sensory nerve roots are crossed.

Central paralysis occurs when the central nutrient 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, and therefore 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. Clonus kneecap caused by its sudden abduction downwards.

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.

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 calf muscle(Gordon reflex), compression of 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 is an involuntary movement that occurs 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 more often leads to monoplegia on the opposite side. 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 - reflexes of oral automatism - are detected. 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.

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 general view, 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; for determining mild degree paresis and disorders 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 During the course of the study, it is necessary to check more subtle and isolated movements relating to individual muscles.

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, to overcome which a certain amount of tension is required. 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

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 paralysis occurs due to disturbances in cortical processes or pathology 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, 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 diagnostics central paralysis includes: neuroimaging (CT and MRI), radiography of the bones of the spine and skull, electromyography, puncture of 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 muscle can indicate the area pathological processes CNS.

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 eye muscles- this 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, heat, 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, reflexology.

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 therapeutic exercises- 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. Among adverse reactions– disorders of the liver, disorders in the composition of the blood. 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 surgery– This is the 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

For tincture, prepare 10-15 ripe pine cones. 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

Optimally 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 right side bodies.
• 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.