Complementary system. Proteins of the complement system: properties and biological activity

7.1. STRUCTURE, CONNECTIONS AND FUNCTIONS OF THE CEREBELLUM

The cerebellum is located beneath the dura mater known as tentorium cerebellum(tentorium cerebelli), which divides the cranial cavity into two unequal spaces - supratentorial and subtentorial. IN subtentorial space, the bottom of which is the posterior cranial fossa, in addition to the cerebellum, there is a brain stem. The volume of the cerebellum is on average 162 cm3. Its weight varies between 136-169 g.

The cerebellum is located above the pons and medulla oblongata. Together with the superior and inferior medullary velum, it forms the roof of the fourth ventricle of the brain, the bottom of which is the so-called rhomboid fossa (see Chapter 9). Above the cerebellum are the occipital lobes of the cerebrum, separated from it by the tentorium cerebellum.

In the cerebellum there are two hemispheres(hemispherum cerebelli). Between them in the sagittal plane above the IV ventricle of the brain is located the phylogenetically most ancient part of the cerebellum - its worm(vermis cerebelli). The vermis and cerebellar hemispheres are fragmented into lobules by deep transverse grooves.

The cerebellum consists of gray and white matter. The gray matter forms the cerebellar cortex and the paired nuclei cerebelli located in its depth (Fig. 7.1). The largest of them are dentate cores(nucleus dentatus) - located in the hemispheres. In the central part of the worm there are tent cores(nuclei

Rice. 7.1. Cerebellar nuclei.

1 - dentate core; 2 - corky core; 3 - tent core; 4 - spherical nucleus.

Rice. 7.2.Sagittal section of the cerebellum and brainstem.

1 - cerebellum; 2 - “tree of life”; 3 - anterior cerebral sail; 4 - quadrigeminal plate; 5 - cerebral aqueduct; 6 - cerebral peduncle; 7 - bridge; 8 - IV ventricle, its choroid plexus and tent; 9 - medulla oblongata.

fastigii), between them and the dentate nuclei there are spherical And corky nuclei(nuctei. globosus et emboliformis).

Due to the fact that the cortex covers the entire surface of the cerebellum and penetrates into the depths of its grooves, on a sagittal section of the cerebellum its tissue has a leaf pattern, the veins of which are formed by white matter (Fig. 7.2), which makes up the so-called tree of life of the cerebellum (arbor vitae cerebelli). At the base of the tree of life there is a wedge-shaped notch, which is the upper part of the cavity of the IV ventricle; the edges of this recess form his tent. The roof of the tent is the cerebellar vermis, and its anterior and posterior walls are made up of thin cerebral plates, known as the anterior and posterior plates. brain sails(vella medullare anterior et posterior).

Some information about architectonics of the cerebellum, giving grounds for judgment about the function of its components. U cerebellar cortex There are two cellular layers: the inner - granular, consisting of small granular cells, and the outer - molecular. Between them there is a row of large pear-shaped cells, bearing the name of the Czech scientist I. Purkinje (1787-1869) who described them.

Impulses enter the cerebellar cortex via mossy and creeping fibers penetrating into it from the white matter, constituting the afferent pathways of the cerebellum. Mossy fibers carry impulses from the spinal cord

vestibular nuclei and pontine nuclei are transmitted to the cells of the granular layer of the cortex. The axons of these cells, together with creeping fibers passing through the granular layer in transit and carrying impulses from the inferior olives to the cerebellum, reach the superficial, molecular layer of the cerebellum. Here, the axons of the cells of the granular layer and the creeping fibers divide in a T-shape, and in the molecular layer their branches take a direction longitudinal to the surface of the cerebellum. Impulses that reach the molecular layer of the cortex, passing through synaptic contacts, fall on the branches of the dendrites of Purkinje cells located here. They then follow the dendrites of Purkinje cells to their bodies, located at the border of the molecular and granular layers. Then, along the axons of the same cells crossing the granular layer, they penetrate into the depths of the white matter. The axons of Purkinje cells end in the cerebellar nuclei. Mainly in the dentate nucleus. Efferent impulses coming from the cerebellum along the axons of the cells that make up its nuclei and take part in the formation of the cerebellar peduncles leave the cerebellum.

The cerebellum has three pairs of legs: lower, middle and upper. The lower leg connects it with the medulla oblongata, the middle one with the pons, and the upper one with the midbrain. The cerebral peduncles make up the pathways that carry impulses to and from the cerebellum.

The cerebellar vermis ensures stabilization of the center of gravity of the body, its balance, stability, regulation of the tone of reciprocal muscle groups, mainly the neck and torso, and the emergence of physiological cerebellar synergies that stabilize the balance of the body.

To successfully maintain body balance, the cerebellum constantly receives information passing through the spinocerebellar pathways from the proprioceptors of various parts of the body, as well as from the vestibular nuclei, inferior olives, reticular formation and other formations involved in controlling the position of body parts in space. Most of the afferent pathways going to the cerebellum pass through the inferior cerebellar peduncle, some of them are located in the superior cerebellar peduncle.

Impulses of proprioceptive sensitivity, going to the cerebellum, like other sensory impulses, following the dendrites of the first sensory neurons, reach their bodies located in the spinal ganglia. Subsequently, impulses traveling to the cerebellum along the axons of the same neurons are directed to the bodies of second neurons, which are located in the internal sections of the base of the dorsal horns, forming the so-called Clark's pillars. Their axons enter the lateral sections of the lateral cords of the spinal cord, where they form spinocerebellar pathways, in this case, part of the axons enters the lateral column of the same side and forms there Flexig's posterior spinocerebellar tract (tractus spinocerebellaris posterior). The other part of the axons of the dorsal horn cells passes to the other side of the spinal cord and enters the opposite lateral cord, forming in it anterior spinocerebellar tract of Gowers (tractus spinocerebellaris anterior). The spinocerebellar tracts, increasing in volume at the level of each spinal segment, ascend to the medulla oblongata.

In the medulla oblongata, the posterior spinocerebellar tract deviates in the lateral direction and, passing through the inferior cerebellar peduncle, penetrates the cerebellum. The anterior spinocerebellar tract transits through the medulla oblongata, the pons and reaches the midbrain, at the level of which it makes its second crossing in the anterior medullary velum and passes into the cerebellum through the superior cerebellar peduncle.

Thus, of the two spinal tracts, one never crosses (uncrossed Flexig's tract), and the other crosses to the opposite side twice (twice-crossed Gowers' tract). As a result, both conduct impulses from each half of the body, predominantly to the homolateral half of the cerebellum.

In addition to the spinocerebellar tracts of Flexig, impulses to the cerebellum pass through the inferior cerebellar peduncle along vestibulocerebellar tract (tractus vestibulocerebellaris), starting mainly in the superior vestibular nucleus of Bechterew, and along olivocerebellar tract (tractus olivocerebellaris), coming from the lower olive. Part of the axons of the cells of the thin and wedge-shaped nuclei, not participating in the formation of the bulbothalamic tract, in the form of external arcuate fibers (fibre arcuatae externae) also enters the cerebellum through the inferior cerebellar peduncle.

Through its middle peduncles, the cerebellum receives impulses from the cerebral cortex. These impulses travel through cortical-pontine-cerebellar pathways, consisting of two neurons. The bodies of the first neurons are located in the cerebral cortex, mainly in the cortex of the posterior parts of the frontal lobes. Their axons pass as part of the corona radiata, the anterior leg internal capsule and end in the pons cores. The axons of the cells of the second neurons, the bodies of which are located in the own nuclei of the bridge, pass to its opposite side and form the middle cerebellar peduncle after the decussation,

ending in the opposite hemisphere of the cerebellum.

Some of the impulses originating in the cerebral cortex reach the opposite hemisphere of the cerebellum, bringing information not about the performed, but only about the active movement planned for execution. Having received such information, the cerebellum instantly sends impulses that correct voluntary movements, mainly, by extinguishing inertia and the most rational regulation of reciprocal muscle tone - agonist and antagonist muscles. As a result, a kind of eimetry, making voluntary movements clear, sharpened, devoid of inappropriate components.

The pathways emerging from the cerebellum are composed of axons of cells whose bodies form its nuclei. Most efferent pathways, including those coming from the dentate nuclei, leave the cerebellum through its superior peduncle. At the level of the inferior colliculus, the efferent cerebellar pathways cross over (crossing of the superior cerebellar peduncles of Wernecking). After the cross, each of them reaches the red nuclei of the opposite side of the midbrain. In the red nuclei, cerebellar impulses switch to the next neuron and then move along the axons of cells whose bodies are located in the red nuclei. These axons are formed in red nuclear spinal tract (tracti rubro spinalis), Monakov's paths, which shortly after the exits from the red kernels undergo crossover (tire crossover or Trout crossover), after which they descend into the spinal cord. In the spinal cord, the red nucleus spinal tracts are located in the lateral cords; their constituent fibers end at the cells of the anterior horns of the spinal cord.

The entire efferent pathway from the cerebellum to the cells of the anterior horns of the spinal cord can be called cerebellar-rednuclear-spinal (tractus cerebello-rubrospinalis). He crosses himself twice (crossing of the superior cerebellar peduncles and decussation of the tegmentum) and ultimately connects each cerebellar hemisphere with peripheral motor neurons located in the anterior horns of the homolateral half of the spinal cord.

From the nuclei of the cerebellar vermis, efferent pathways go mainly through the inferior cerebellar peduncle to the reticular formation of the brainstem and the vestibular nuclei. From here, along the reticulospinal and vestibulospinal tracts passing along the anterior cords of the spinal cord, they also reach the cells of the anterior horns. Part of the impulses coming from the cerebellum, passing through the vestibular nuclei, enters the medial longitudinal fasciculus, reaches the nuclei of the III, IV and VI cranial nerves, which ensure the movements of the eyeballs, and affects their function.

To summarize, the following must be emphasized:

1. Each half of the cerebellum receives impulses mainly a) from the homolateral half of the body, b) from the opposite hemisphere of the brain, which has corticospinal connections with the same half of the body.

2. From each half of the cerebellum, efferent impulses are sent to the cells of the anterior horns of the homolateral half of the spinal cord and to the nuclei of the cranial nerves that provide movements of the eyeballs.

This nature of cerebellar connections makes it possible to understand why, when one half of the cerebellum is damaged, cerebellar disorders arise predominantly in the same half, i.e. homolateral half of the body. This is especially clearly manifested in cases of damage to the cerebellar hemispheres.

7.2. STUDY OF CEREBELLA FUNCTIONS

AND CLINICAL MANIFESTATIONS OF ITS DEFEAT

When the cerebellum is damaged, disorders of statics and coordination of movements, muscle hypotonia and nystagmus are characteristic.

Cerebellar damage first of all his worm leads to violations of statics - the ability to maintain a stable position of the center of gravity of the human body, balance, stability. When this function is disrupted, static ataxia (from the Greek ataxia - disorder, instability). The patient is noted to be unstable. Therefore, in a standing position, he spreads his legs wide and balances with his hands. Static ataxia is especially clearly detected when the area of ​​support is artificially reduced, in particular in the Romberg pose. The patient is asked to stand with his feet tightly together and his head slightly raised. In the presence of cerebellar disorders, the patient is unstable in this position, his body sways, sometimes he is “pulled” in a certain direction, and if the patient is not supported, he may fall. In cases of damage to the cerebellar vermis, the patient usually sways from side to side and often falls backward. With pathology of the cerebellar hemisphere, there is a tendency to fall predominantly towards the pathological focus. If the static disorder is moderately expressed, it is easier to identify it in the so-called complicated or sensitized Romberg position. The patient is asked to place his feet in one line so that the toe of one foot rests on the heel of the other. The stability assessment is the same as in the usual Romberg position.

Normally, when a person stands, the muscles of his legs are tense (ground reaction), if there is a threat of falling to the side, his leg on this side moves in the same direction, and the other leg comes off the floor (jump reaction). If the cerebellum (mainly the vermis) is damaged, the patient’s reactions are impaired

support and jump. Impaired support response is manifested by the patient's instability in a standing position, especially in the Romberg position. A violation of the jump reaction leads to the fact that if the doctor, standing behind the patient and securing him, pushes the patient in one direction or another, then the patient falls with a slight push (symptom of pushing).

When the cerebellum is damaged, the patient's gait is usually changed due to the development statolocomotor ataxia. Cerebellar gait In many ways, it resembles the gait of a drunk person, which is why it is sometimes called the “drunken gait.” Due to instability, the patient walks unsteadily, spreading his legs wide, while being “thrown” from side to side. And when the cerebellar hemisphere is damaged, it deviates when walking from a given direction towards the pathological focus. The instability is especially noticeable when turning. If ataxia turns out to be pronounced, then patients completely lose the ability to control their body and cannot not only stand and walk, but even sit.

Predominant damage to the cerebellar hemispheres leads to a disorder of its anti-inertial influences, in particular to the emergence kinetic ataxia. It is manifested by awkwardness of movements and is especially pronounced during movements that require precision. To identify kinetic ataxia, tests for coordination of movements are performed. The following is a description of some of them.

Test for diadochokinesis (from Greek diadochos - sequence). The patient is asked to close his eyes, stretch his arms forward and quickly, rhythmically supinate and pronate his hands. In case of damage to the cerebellar hemisphere, the movements of the hand on the side of the pathological process turn out to be more sweeping (a consequence of dysmetria, or more precisely, hypermetry), as a result of which the hand begins to lag. This indicates the presence of adiadochokinesis.

Finger test. Patient with eyes closed should move your hand away, and then, slowly, touch the tip of your nose with your index finger. In the case of cerebellar pathology, the hand on the side of the pathological focus makes excessive movement (hypermetry), As a result, the patient misses. A finger-nose test reveals a pattern characteristic of cerebellar pathology. cerebellar (intention) tremor, the amplitude of which increases as the finger approaches the target. This test also allows us to detect the so-called bradytelekinesia (symptom of bridle): not far from the target, the movement of the finger slows down, sometimes even pauses, and then resumes again.

Finger-finger test. The patient with his eyes closed is asked to spread his arms wide and then bring his index fingers together, trying to get the finger into the finger, in this case, as with the finger-to-nose test, intentional tremors and a bridle symptom are detected.

Heel-knee test (Fig. 7.3). The patient, lying on his back with his eyes closed, is asked to raise one leg high and then hit the knee of the other leg with his heel. With cerebellar pathology, the patient cannot or finds it difficult to hit the knee of the other leg with his heel, especially when performing the test with the leg homolateral to the affected cerebellar hemisphere. If, nevertheless, the heel reaches the knee, then it is proposed to move it, lightly touching the front surface of the shin, down to the ankle joint, while in the case of cerebellar pathology, the heel always slides off the shin in one direction or the other.

Rice. 7.3.Heel-knee test.

Index test: The patient is asked to use his index finger several times to hit the rubber tip of the hammer, which is in the hand of the examiner. In the case of cerebellar pathology, in the patient’s hand on the side of the affected cerebellar hemisphere there is a miss due to dysmetria.

Thomas-Jumenty's sign: If the patient picks up an object, such as a glass, he will spread his fingers excessively.

Cerebellar nystagmus. Twitching of the eyeballs when looking to the side (horizontal nystagmus) is considered as a consequence of intentional trembling of the eyeballs (see Chapter 30).

Speech disorder: Speech loses fluency, becomes explosive, fragmented, scanned like cerebellar dysarthria (see Chapter 25).

Changing handwriting: Due to a disorder in the coordination of hand movements, the handwriting becomes uneven, the letters are deformed, and excessively large (megalography).

Pronator phenomenon: The patient is asked to keep his arms extended forward in a supination position, while spontaneous pronation soon occurs on the side of the affected cerebellar hemisphere.

Hoff-Schilder sign: If the patient holds his arms extended forward, then on the side of the affected hemisphere the arm is soon retracted outward.

Imitation phenomenon. The patient, with his eyes closed, must quickly give his hand a position similar to that which the examiner had previously given to his other hand. When the cerebellar hemisphere is damaged, the hand homolateral to it makes a movement that is excessive in amplitude.

The Doinikov phenomenon. Finger phenomenon. The sitting patient is asked to place supinated hands with fingers apart on his hips and close his eyes. In case of damage to the cerebellum on the side of the pathological focus, spontaneous flexion of the fingers and pronation of the hand and forearm soon occur.

Stewart-Holmes sign. The examiner asks the patient sitting on a chair to bend his supinated forearms and at the same time, holding his hands by the wrists, resists him. If you unexpectedly release the patient’s hands, the hand on the affected side, bending by inertia, will forcefully hit him in the chest.

Muscle hypotension. Damage to the cerebellar vermis usually leads to diffuse muscle hypotonia. When the cerebellar hemisphere is damaged, passive movements reveal a decrease in muscle tone on the side of the pathological process. Muscle hypotonia leads to the possibility of hyperextension of the forearm and lower leg (Olshansky's symptom) with passive movements, to the appearance symptoms of a dangling hand or foot when they are passively shaken.

Pathological cerebellar asynergies. Violations of physiological synergies during complex motor acts are revealed, in particular, during the following tests (Fig. 7.4).

1. Asynergia according to Babinsky in a standing position. If a patient standing with his legs together tries to bend back, throwing his head back, then normally the knee joints bend. With cerebellar pathology, due to asynergia, this conjugal movement is absent, and the patient, losing balance, falls backward.

Rice. 7.4.Cerebellar asynergia.

1 - gait of a patient with severe cerebellar ataxia; 2 - normal back tilt of the body; 3 - with damage to the cerebellum, the patient, bending backwards, cannot maintain balance; 4 - performing a test for cerebellar asynergia according to Babinsky by a healthy person; 5 - performing the same test in patients with cerebellar damage.

2. Asynergia according to Babinsky in the supine position. The patient, lying on a hard surface with his legs extended and shoulder width apart, is asked to cross his arms over his chest and then sit down. In the presence of cerebellar pathology, due to the lack of concomitant contraction of the gluteal muscles (manifestation of asynergia), the patient cannot fix the legs and pelvis on the support area; as a result, the legs rise and he cannot sit down. The significance of this symptom should not be overestimated in elderly patients or people with a flabby or obese abdominal wall.

Summarizing the above, it is necessary to emphasize the variety and importance of the functions performed by the cerebellum. As part of a comprehensive regulatory mechanism with feedback, the cerebellum acts as a coordination center, ensuring body balance and maintaining muscle tone. As P. Duus (1995) notes, the cerebellum provides the ability to perform discrete and precise movements, however, the author reasonably believes that the cerebellum works like a computer, tracking and coordinating sensory input and modeling motor signals as output.

7.3. MULTISYSTEM DEGENERATIONS

WITH SIGNS OF CEREBELLAR PATHOLOGY

Multisystem degenerations are a group of neurodegenerative diseases common feature which is the multifocal nature of the lesion with the involvement of various functional and neurotransmitter systems of the brain in the pathological process and, in connection with this, the polysystemic nature of clinical manifestations.

7.3.1. Spinocerebellar ataxias

Spinocerebellar ataxias include progressive hereditary degenerative diseases, in which the structures of the cerebellum, brain stem and spinal cord pathways, related mainly to the extrapyramidal system, are mainly affected.

7.3.1.1. Hereditary Friedreich's ataxia

A hereditary disease described in 1861 by the German neurologist N. Friedreich (Friedreich N., 1825-1882). It is inherited in an autosomal recessive manner or (less commonly) in an autosomal dominant manner with incomplete penetrance and variable gene expression. Sporadic cases of the disease are also possible.

Pathogenesisdiseases not specified. In particular, there is no idea about the primary biochemical defect that forms its basis.

Pathomorphology.Pathoanatomical studies reveal pronounced thinning of the spinal cord, caused by atrophic processes in its posterior and lateral cords. As a rule, the wedge-shaped (Burdacha) and gentle (Gaull) pathways and the spinocerebellar pathways of Gowers and Flexig, as well as the crossed pyramidal tract containing

many fibers belonging to the extrapyramidal system. Degenerative processes are also expressed in the cerebellum, in its white matter and nuclear apparatus.

Clinical manifestations. The disease manifests itself in children or young people under the age of 25. S.N. Davidenkov (1880-1961) noted that more often clinical signs of the disease occur in children 6-10 years of age. The first sign of the disease is usually ataxia. Patients experience uncertainty, staggering when walking, and their gait changes (the legs are spread wide apart when walking). The gait in Friedreich's disease can be called tabetic-cerebellar, since its changes are caused by a combination of sensitive and cerebellar ataxia, as well as a usually pronounced decrease in muscle tone. Static disorders, incoordination in the hands, intention tremor, and dysarthria are also characteristic. Possible nystagmus, decreased hearing, elements of scanned speech, signs of pyramidal insufficiency (tendon hyperreflexia, pathological foot reflexes, sometimes a slight increase in muscle tone), imperative urge to urinate, decreased sexual potency. Sometimes hyperkinesis of an athetoid nature appears.

Early onset deep sensitivity disorder leads to a progressive decrease in tendon reflexes: first in the legs and then in the arms. Over time, muscle wasting in the distal legs develops. Characterized by the presence of skeletal developmental anomalies. First of all, this is manifested by the presence Friedreich's feet: the foot is shortened, “hollow”, with a very high arch. The main phalanges of her fingers are straightened, the rest are bent (Fig. 7.5). Possible deformation of the spine and chest. There are often manifestations of cardiopathy. The disease progresses slowly, but steadily leads to disability of patients who eventually become bedridden.

Treatment. Pathogenetic treatment has not been developed. Prescribed drugs that improve metabolism in the structures of the nervous system, general strengthening agents. For severe foot deformities, orthopedic shoes are indicated.

Rice. 7.5.Friedreich's foot.

7.3.1.2. Hereditary cerebellar ataxia (Pierre Marie disease)

This is a chronic progressive hereditary disease, manifesting itself at the age of 30-45 years, with slowly increasing cerebellar disorders in combination with signs of pyramidal insufficiency, characterized by static and dynamic cerebellar ataxia, intention tremor, scanned speech, tendon hyperreflexia. Possible clonus, pathological pyramidal reflexes, strabismus, decreased vision, narrowing of visual fields due to primary atrophy of the optic nerves and pigmentary degeneration of the retina. The course of the disease is slowly progressive. There is a decrease in the size of the cerebellum, cell degeneration

Purkinje, inferior olive, spinocerebellar tracts. Inherited in an autosomal dominant manner. The disease was described in 1893 by the French neurologist R. Marie (1853-1940).

Currently, there is no consensus in the understanding of the term “Pierre Marie disease”, and the question of the possibility of isolating it into an independent nosological form is debatable.

No treatment has been developed. Typically, metabolically active and restorative, as well as symptomatic agents are used.

7.3.2. Olivopontocerebellar dystrophy (Dejerine-Thomas disease)

This is a group of chronic progressive hereditary diseases, in which dystrophic changes develop mainly in the cerebellum, inferior olives, in the pons own nuclei and in the brain structures associated with them.

When the disease develops at a young age, about half of the cases are inherited in a dominant or recessive manner, the rest are sporadic. In sporadic cases of the disease, manifestations of akinetic-rigid syndrome and progressive autonomic failure are more common. The average age of the patient when the hereditary form of the disease manifests itself in the phenotype is 28 years, and when the disease is sporadic - 49 years, the average life expectancy is 14.9 and 6.3 years, respectively. In the sporadic form, in addition to atrophy of the olives, pons and cerebellum, damage to the lateral cords of the spinal cord, the substantia nigra and striatum, and the locus coeruleus in the rhomboid fossa of the fourth ventricle of the brain is more often detected.

Symptoms of increasing cerebellar syndrome are characteristic. Possible sensitivity disorders, elements of bulbar and akinetic-rigid syndromes, hyperkinesis, in particular myorhythmias in the uvula and soft palate, ophthalmoparesis, decreased visual acuity, intellectual disorders. The disease was described in 1900 by French neurologists J. Dejerine and A. Thomas.

The disease often debuts with disturbances when walking - instability, incoordination, unexpected falls are possible. These disorders may be the only manifestation of the disease for 1-2 years. Subsequently, coordination disorders in the hands arise and increase: manipulation of small objects is difficult, handwriting is impaired, and intention tremor occurs. Speech becomes intermittent, blurred, with a nasal tint and a breathing rhythm that does not correspond to the structure of speech (the patient speaks as if he is being strangled). At this stage of the disease, manifestations of progressive autonomic failure are added, and signs of akinetic-rigid syndrome appear. Sometimes the dominant symptoms for the patient are dysphagia and attacks of night suffocation. They develop in connection with mixed paresis of the bulbar muscles and can be life-threatening.

In 1970, German neurologists B.W. Konigsmark and L.P. Weiner singled out 5 main types olivopontocerebellar dystrophy, differing either in clinical and morphological manifestations or type of inheritance.

I type (Menzel type). At the age of 14-70 (usually 30-40) years it manifests itself with ataxia, dysarthria, dysphonia, muscle hypotonia, in the late stage - rough tremor of the head, torso, arms, muscles, signs of akinetic-rigid syndrome. Pathological pyramidal signs, gaze paresis, external and internal ophthalmoplegia, sensitivity disorders, and dementia are possible. Inherited in an autosomal dominant manner. It was identified as an independent form in 1891 by P. Menzel.

II type (Fickler-Winkler type) . At the age of 20-80 years, it manifests itself as ataxia, decreased muscle tone and tendon reflexes. Inherited in an autosomal recessive manner. Sporadic cases are possible.

III type with retinal degeneration. Manifests itself in childhood or young age (up to 35 years) with ataxia, tremor of the head and limbs, dysarthria, signs of pyramidal insufficiency, progressive decrease in vision resulting in blindness; nystagmus, ophthalmoplegia, and sometimes dissociated sensitivity disorders are possible. Inherited in an autosomal dominant manner.

IV type (Jester-Heimaker type). At the age of 17-30 years, it debuts with cerebellar ataxia or signs of lower spastic paraparesis; in both cases, already at an early stage of the disease, a combination of these manifestations is formed, which are subsequently joined by elements of bulbar syndrome, paresis of facial muscles, and deep sensitivity disorders. Inherited in a dominant manner.

V type. It manifests itself at the age of 7-45 years with ataxia, dysarthria, signs of akinetic-rigid syndrome and other extrapyramidal disorders, progressive ophthalmoplegia and dementia are possible. Inherited in a dominant manner.

7.3.3. Olivorubrocerebellar degeneration (Lejonne-Lhermitte syndrome, Lhermitte disease)

The disease is characterized by progressive atrophy of the cerebellum, mainly its cortex, dentate nuclei and superior cerebellar peduncles, inferior olives, and red nuclei. It manifests itself primarily as static and dynamic ataxia; in the future, other signs of cerebellar syndrome and damage to the brain stem are possible. The disease was described by French neurologists J. Lhermitte J.J., 1877-1959 and J. Lejonne J., born in 1894.

7.3.4. Multiple system atrophy

In recent decades, a sporadic, progressive neurodegenerative disease called multiple system atrophy has been identified as an independent form. It is characterized by combined damage to the basal ganglia, cerebellum, brain stem, and spinal cord. Main clinical manifestations: parkinsonism, cerebellar ataxia, signs of pyramidal and autonomic failure (Levin O.S., 2002). Depending on the predominance of certain features of the clinical picture, three types of multisystem atrophy are distinguished.

1) olivopontocerebellar type, characterized by a predominance of signs of cerebellar attack;

2) strionigral type, in which signs of parkinsonism dominate;

3) Shy-Drager syndrome, characterized by a predominance in the clinical picture of signs of progressive autonomic failure with symptoms of orthostatic arterial hypotension.

Multiple system atrophy is based on selective degeneration of certain areas of predominantly gray matter of the brain with damage to neurons and glial elements. The causes of degenerative manifestations in brain tissue remain unknown today. Manifestations of multisystem atrophy of the olivopontocerebellar type are associated with damage to Purkinje cells in the cerebellar cortex, as well as neurons of the inferior olives, pontine nuclei, demyelination and degeneration of mainly pontocerebellar pathways.

Cerebellar disorders are usually represented by static and dynamic ataxia with impaired locomotor movements. Characterized by instability in the Romberg position, ataxia when walking, dysmetria, adiadochokinesis, intention tremor, there may be nystagmus (horizontal vertical, beating downwards), intermittency and slowness of tracking movements of the gaze, impaired convergence of the eyes, scanned speech.

Multiple system atrophy usually begins in adulthood and progresses rapidly. Diagnosis is based on clinical data and is characterized by a combination of signs of parkinsonism, cerebellar insufficiency and autonomic disorders. Treatment for the disease has not been developed. The duration of the disease is within 10 years and ends in death.

7.4. OTHER DISEASES ACCOMPANIED BY SIGNS OF CEREBELLA DAMAGE

If a patient shows signs of damage to the cerebellum, then in most cases, first of all we need to think about the possibility cerebellar tumors(astrocytoma, angioblastoma, medulloblastoma, metastatic tumors) or multiple sclerosis. At cerebellar tumors Signs of intracranial hypertension appear early. In multiple sclerosis, it is usually possible to identify, in addition to cerebellar pathology, clinical manifestations of damage to other structures of the central nervous system, primarily the visual and pyramidal systems. In classical neurology, characteristic features of multiple sclerosis Charcot's triad: nystagmus, intention tremor and scanned speech, as well as Nonne's syndrome: motor coordination disorder, dysmetria, scanned speech and cerebellar asynergies.

Cerebellar disorders are the main ones in post-traumatic Mann syndrome, which is characterized by ataxia, discoordination, asynergia, nystagmus. Trauma or infectious lesions can cause cerebellar Goldstein-Reichmann syndrome: disorders of statics and coordination of movements, asynergia, intentional trembling, decreased muscle tone, hypermetry, megalography, impaired perception of the mass (weight) of an object in the hands.

Disorders of cerebellar function can also be congenital, manifesting themselves, in particular, Zeeman's syndrome: ataxia, delayed speech development, and subsequently cerebellar dysarthria.

Congenital cerebellar ataxia manifested by a delay in the development of the child’s motor functions (at the age of 6 months he cannot sit, he begins to walk late, and the gait is ataxic), as well as speech delay, long-term persistence of dysarthria, sometimes mental retardation, and manifestations of microcrania are not uncommon. On CT, the cerebellar hemispheres are reduced. Compensation usually occurs around age 10 brain functions, which, however, can be disrupted under the influence of harmful exogenous influences. Progressive forms of the disease are also possible.

A manifestation of congenital cerebellar hypoplasia is Fanconi-Turner syndrome. It is characterized by disturbances in statics and coordination of movements, nystagmus, which are usually accompanied by mental retardation.

Congenital also includes inherited autosomal recessive type, which is rare Betten's disease: It is characterized by congenital cerebellar ataxia, manifested in the first year of life by disturbances in statics and coordination of movements, nystagmus, gaze coordination disorder, and moderate muscle hypotonia. Dysplastic signs are possible. The child begins to hold his head up late, sometimes only at 2-3 years of age, and even later - to stand, walk, and talk. His speech is altered according to the type of cerebellar dysarthria. Autonomic-visceral disorders and manifestations of immunosuppression are possible. After a few years, the clinical picture usually stabilizes, and the patient, to some extent, adapts to the existing defects.

Spastic ataxia according to the proposal of A. Bell and E. Carmichel (1939), cerebellar ataxia, inherited in an autosomal dominant manner, is called, which is characterized by the onset of the disease at 3-4 years of age and is manifested by a combination of cerebellar ataxia with dysarthria, tendon hyperreflexia and increased muscle tone in spastic type, while atrophy of the optic nerves, retinal degeneration, nystagmus, and oculomotor disorders are possible (but are not obligate signs of the disease).

Inherited in an autosomal dominant manner Feldman syndrome(described German doctor H. Feldmann, b. in 1919): cerebellar ataxia, intention tremor and early graying of hair. It appears in the second decade of life and then slowly progresses, leading to disability after 20-30 years.

Late cerebellar atrophy, or Tom syndrome, described in 1906 by the French neurologist A. Thomas (1867-1963), usually manifests itself in people over 50 years of age with progressive atrophy of the cerebellar cortex. The phenotype shows signs of cerebellar syndrome, primarily cerebellar static and locomotor ataxia, scanned speech, and changes in handwriting. In an advanced stage, manifestations of pyramidal insufficiency are possible.

The combination of cerebellar disorders with myoclonus is characterized by myoclonic cerebellar dyssynergia of Hunt, or myoclonus-ataxia, with this symptom complex, the clinical picture includes intention tremor, myoclonus that occurs in the hands and later becomes generalized, ataxia and dyssynergia, nystagmus, scanned speech, and decreased muscle tone. It is a consequence of degeneration of the cerebellar nuclei, red nuclei and their connections, as well as cortical-subcortical structures.

In an advanced stage of the disease, epileptic seizures and dementia are possible. The prognosis is bad. Refers to rare forms of progressive hereditary ataxias. Inherited in an autosomal recessive manner. It usually appears at a young age. The nosological independence of the symptom complex is disputed. The disease was described in 1921 by the American neurologist R. Hunt (1872-1937).

Among degenerative processes, it occupies a certain place Holmes cerebellar degeneration or familial cerebellar olivary atrophy, or progressive atrophy of the cerebellar system, mainly the dentate nuclei, as well as the red nuclei, with manifestations of demyelination in the superior cerebellar peduncle. Characterized by static and dynamic ataxia, asynergia, nystagmus, dysarthria, decreased muscle tone, muscle dystonia, head tremor, myoclonus. Epileptic seizures appear almost simultaneously. Intelligence is usually preserved. The EEG shows paroxysmal dysrhythmia. The disease is recognized as hereditary, but the type of its inheritance is not specified. The disease was described in 1907 by the English neuropathologist G. Holmes

(1876-1965).

Alcoholic cerebellar degeneration - a consequence of chronic alcohol intoxication. Damage occurs predominantly to the cerebellar vermis, with cerebellar ataxia and impaired coordination of leg movements primarily manifested, while arm movements, oculomotor and speech functions are disrupted to a much lesser extent. Usually this disease is accompanied by a pronounced decrease in memory in combination with polyneuropathy.

manifested by cerebellar ataxia, which can sometimes be the only clinical symptom caused by a malignant tumor, without local signs indicating the place of its origin. Paraneoplastic cerebellar degeneration may, in particular, be a secondary manifestation of breast or ovarian cancer.

Barraquer-Bordas-Ruiz-Lara syndrome manifested by cerebellar disorders arising in connection with rapidly progressive cerebellar atrophy. The syndrome in patients with bronchial cancer, accompanied by general intoxication, was described by the modern Spanish doctor L. Barraquer-Bordas (born in 1923).

Rarely found recessive X-chromosomal ataxia- a hereditary disease that manifests itself almost only in men with slowly progressive cerebellar insufficiency. It is transmitted in a recessive, sex-linked manner.

Worthy of attention and familial paroxysmal ataxia, or periodic ataxia. It often debuts in childhood, but can appear later - up to 60 years. Clinical picture comes down to paroxysmal manifestations of nystagmus, dysarthria and ataxia, decreased muscle tone, dizziness, nausea, vomiting, headache, lasting from several minutes to 4 weeks.

Attacks of familial paroxysmal ataxia can be provoked by emotional stress, physical fatigue, fever, alcohol intake, while between attacks focal neurological symptoms are not detected in most cases, but sometimes nystagmus and mild cerebellar symptoms are possible.

The morphological substrate of the disease is considered to be an atrophic process mainly in the anterior part of the cerebellar vermis. The disease was first described in 1946 by M. Parker. Inherited in an autosomal dominant manner. In 1987, with familial paroxysmal ataxia, a decrease in the activity of pyruvate dehydrogenase of blood leukocytes to 50-60% of the normal level was discovered. In 1977, R. Lafrance et al. drew attention to the high preventive effect of diacarb; later, flunarizine was proposed for the treatment of familial paroxysmal ataxia.

Acute cerebellar ataxia, or Leiden-Westphal syndrome, is a well-defined symptom complex that is a parainfectious complication. It occurs more often in children 1-2 weeks after a general infection (influenza, typhus, salmonellosis, etc.). Characterized by severe static and dynamic ataxia, intention tremor, hypermetry, asynergia, nystagmus, scanned speech, decreased muscle tone. Lymphocytic pleocytosis and a moderate increase in protein are detected in the cerebrospinal fluid. At the onset of the disease, dizziness, disturbances of consciousness, and convulsions are possible. No pathology is detected on CT and MRI. The course is benign. In most cases, after a few weeks or months - full recovery, sometimes - residual disorders in the form of mild cerebellar insufficiency.

Marie-Foy-Alajouanine disease - late symmetrical cortical atrophy of the cerebellum with predominant damage to piriform neurons (Purkinje cells) and the granular layer of the cortex, as well as the oral part of the cerebellar vermis and degeneration of the olives. It manifests itself in people aged 40-75 years with balance disorders, ataxia, gait disturbances, coordination disorders and decreased muscle tone, mainly in the legs; Intentional trembling in the hands is insignificantly expressed. Speech disturbances are possible, but are not obligatory signs of the disease. The disease was described in 1922 by French neurologists P. Marie, Ch. Foix and Th. Alajouanine. The disease is sporadic. The etiology of the disease is not clear. There are opinions about the provoking role of intoxication, primarily alcohol abuse, as well as hypoxia, and hereditary burden. The clinical picture is confirmed by head CT data, which reveals a pronounced decrease in the volume of the cerebellum against the background of diffuse atrophic processes in the brain. In addition, a high level of aminotransferases in the blood plasma is recognized as characteristic (Ponomareva E.N. et al., 1997).

With damage to any part of the cerebellum, three main cerebellar symptoms are always pronounced clinically: atony, ataxia and asynergia. But the degree of their manifestation depends on the location and size of the lesion.

Atony or hypotension. Decreased muscle tone is one of the constant symptoms of cerebellar damage. When the powerful flow of cerebellar impulses into the anterior horns of the spinal cord ceases, especially if these impulses are interrupted more or less acutely, a decrease in muscle tone always occurs. With a slow and gradual shutdown of the cerebellar function, the decrease in tone will be insignificant due to compensation of the impaired function due to cortical activity or the preserved parts of the cerebellum. It is natural, therefore, that when both hemispheres of the cerebellum are damaged, there is almost no compensation for the lost function and hypotension is always grossly expressed, regardless of the degree of development of the pathological process. The atony of all muscles is especially intense when the cerebellar vermis is damaged, since the latter is equally connected to both halves of the body.

It should be emphasized that cerebellar hypotonia spreads evenly throughout the entire body musculature and is expressed to the same extent in both the arm and leg muscles, both in agonists and antagonists. When one hemisphere of the cerebellum is affected, hypotonia predominates on the side of the same name.

Ataxia. Dysfunction of the cerebellum is manifested by a group of symptoms united under common name- ataxia, which means disorder, lack of coordination of movements.

There are static and kinetic ataxia.

Static ataxia there is an expression of imbalance of the body - a violation of the stabilization of the center of gravity. The most severe imbalance manifests itself when the cerebellar vermis is damaged and to a lesser extent when its hemispheres are damaged. Instability of the body is detected when standing and is expressed in a rough sway of the body in all directions. In order not to fall, the patient spreads his legs wide, balances with his arms and, swaying from side to side, maintains balance only due to the function of the vestibular apparatus. The gait becomes uncertain (“drunk gait”). When one hemisphere of the cerebellum is affected, staggering occurs towards the lesion and is especially pronounced when turning the body. If ataxia is very severe, patients are unable not only to stand and walk, but even to sit. The function of stabilizing the body's center of gravity is completely eliminated.

Kinetic, or locomotor, ataxia. Dysmetria is the basis of kinetic ataxia. All movements become disproportionate, uncoordinated, and their volume is excessive (hypermetry). The accuracy and smoothness of movements are sharply impaired, especially with subtle movements of the hands. The patient spreads his fingers disproportionately wide when trying to grasp any small object. For example, he pushes a glass and splashes water from it, and if he grabs it in his hand, he can crush it. The patient is unable to smoothly lower the object onto the table and places it with a jerk. He cannot draw a line of a given size: due to the inertia of movement, he certainly continues it further than necessary. For the same reason, he cannot draw a circle. Due to dysmetria, handwriting changes dramatically, the letters turn out to be disproportionate, uneven, and all the lines are broken. Ataxia of the speech muscles is manifested by a speech disorder of the dysarthria type.

In cerebellar ataxia, the phenomenon of intention tremor occupies a special place. The accuracy of any movement is possible only if the timing of the main movement and the counter-movement are exactly matched. In other words, for coordinated movement, it is necessary for an additional cerebellar impulse to hit the anterior horns in a timely manner following the pyramidal impulse. When the cerebellar impulse is delayed along the way, the regulatory counter-movement is delayed and the main movement is produced in large volume. Consequently, there is a separation in time of two phases of movement - the main and additional ones, which normally occur together. The stronger the main movement, the stronger the delayed regulatory counter-movement will be. Under this condition, all movements will occur with constant intermittent recoils: delayed counter-movements will all the time “pull back” the moving part of the body. This kind of movement with constant feedback is called intention tremor. Intention tremor is especially pronounced when trying to hit a certain point with a finger. It can also be observed during eye movements and is known as cerebellar nystagmus (as opposed to vestibular nystagmus). The appearance of intention tremor in speech motor skills causes a peculiar speech disorder, reminiscent of the chanting of ancient Greek poetry. All three of these symptoms (intention tremor, nystagmus and scanned speech) were first described by Charcot when localizing foci of multiple sclerosis in the pons, which is why the whole syndrome is called Charcot’s triad.

To identify dynamic ataxia, there are a number of tests (coordination tests), for example, finger-nose, index, heel-knee, etc.

The test by quickly alternating directly opposite movements of the hands deserves special attention. The disorder of rapid alternating movements in the hands is called adiadochokinesis. To identify this symptom, the patient is asked to quickly supinate and pronate the outstretched hands. When the cerebellar hemisphere is damaged, the influence of inertia of movement is manifested by the inability to quickly change the direction of movement to the opposite and by excessive movement due to inertia (hypermetry). Therefore, when trying to quickly rotate the hand, hypersupination and hyperpronation are detected with a slow and awkward transition from one type of movement to another on the side of the same name as the lesion of the cerebellum.

Asynergy. In cerebellar disorders, asynergia is a consequence of the exclusion of additional cerebellar components in a complex motor act. It is expressed in the inability to perform complex movements simultaneously, synergistically (essentially the same phenomena of cerebellar ataxia are observed).

While walking, the torso lags behind the movement of the legs and the patient falls backward, as the center of gravity of the torso moves too far back. Similar phenomena are observed if the patient is forced to quickly and strongly bend backward while standing. This reveals a lack of synergistic flexion in the ankle and knee joints, the center of gravity moves posteriorly and the patient falls. He also fails to simultaneously flex his thigh and lower leg when trying to place his knee on the seat of a chair: first he bends his leg at the hip joint, then at the knee joint and forcefully lowers his knee down.

Asynergy is especially pronounced if a patient lying on his back is asked to sit up without using his hands. A healthy person fixes the legs and pelvis at the same time as bending the torso. With asynergia, this is impossible: instead of the body, the legs or one leg rises in case of unilateral damage to the cerebellum.

Additional cerebellar symptoms. In addition to the main symptoms of cerebellar damage described above (atony, ataxia, asynergia), there are additional signs disorders of cerebellar functions.

The complex sense of weight is the result of a combination of indications from multiple proprioceptors and tactile sensitivity, which is perceived by the cerebral cortex as a result of preliminary cerebellar activity. Therefore, patients with cerebellar lesions incorrectly estimate weight. On the affected side, the weight will seem significantly less to the patient.

When the anterior legs and dentate nuclei of the cerebellum are damaged, choreic hyperkinesis develops.

The absence or reduction of counter-movement, regulated by the cerebellum, is detected through a test with passive extension of the bent forearm. If the doctor suddenly stops extension, the patient will not be able to immediately turn on the antagonists and stop flexion, as a result of which he will hit himself in the chest with his hand.

In the absence of cerebellar impulses, the limbs become inert, obeying the laws of moving mass. If a patient passively raises and lowers his arm, it will swing much longer than a healthy one. A similar pendulum-like movement is also observed when receiving a knee-jerk reflex: after a single blow to the quadriceps tendon, the lower leg makes several fading pendulum-like swings.

Missing symptom. To the subject with with open eyes They suggest touching the researcher’s finger with their index finger several times. Then the subject must repeat this movement, but with his eyes closed. On the side of the cerebellar focus, the hand misses, more often passing outward from the target, and this is noted both with closed and open eyes.

Pronation symptom. When the arms are extended forward in a pronated position in a patient with his eyes closed, the arm on the side of the cerebellar lesion pronates more strongly.
A symptom of bradytelekinesia is that in patients with cerebellar damage, during the finger-nose test, the movement of the finger near the target seems to slow down, then resumes again, and the finger reaches the tip of the nose. It is interesting that a peculiar slowing of the target’s movement is detected even in the presence of intentional tremor. This symptom is observed on the side of the lesion in the cerebellum.

Cerebellar imitation phenomenon. With the patient's eyes closed, one leg is slightly bent at the knee joint and he is asked to give the other leg the same position. In this case, the patient bends it much more.

Dizziness varying degrees observed in all patients with cerebellar disease. Such dizziness is characterized by the absence of hearing impairment.

Associated symptoms. The special topographical position of the cerebellum in the cranial cavity causes the occurrence of a number of accompanying symptoms when it is damaged.

With processes in the cerebellum that change the brain space in the posterior cranial fossa (tumors, abscesses, cysts, etc.), general brain symptoms appear early as a result of increased intracranial pressure. Increasing headaches, dizziness, and vomiting often act as initial symptoms of the development of a tumor process in the cerebellum. Early development of common brain symptoms is explained by the indicated position of the cerebellum in the cranium and the possibility of very early development of venous stagnation and cerebral edema.

When the tumor is localized in the cerebellar vermis, an acute development of increased intracranial pressure may occur. A severe headache occurs suddenly, sometimes with loss of consciousness, impaired breathing and cardiac function (Bruns syndrome). In severe cases, the development of this syndrome can result in death from respiratory or cardiac paralysis.

Tumor-like processes in the cerebellar hemisphere can compress the brain stem and cause a number of associated symptoms: damage to the cranial nerves (usually V, VI and VII), dysfunction of the pyramidal system and sensory conductors. In this case, alternating syndrome type disorders often appear. In some cases, the opposite ratio may be observed as a result of compression of the opposite half of the trunk by the tumor.

Topical diagnosis of lesions of the vermis and cerebellar hemispheres. Such a diagnosis is very limited and is generally possible only within the limits of the difference between the lesions of the vermis and the cerebellar hemispheres.

Worm damage is characterized by severe imbalance accompanied by diffuse muscle hypotonia. A particularly pronounced violation of the stabilization of the center of gravity is caused by the involvement in the process of the posterior lobe of the vermis - nodulus and the adjacent lobe of the hemisphere - floculus. In this case, the patient can not only stand, but even sit.

Atony and ataxia are diffusely expressed. To identify a slight imbalance, the patient is placed in the Romberg position, and a uniform swaying of the body in all directions is noted. With more severe impairment, patients fall back and forth. Unlike spinal ataxia, turning off vision has almost no effect on the worsening of cerebellar ataxia.

Damage to the cerebellar hemispheres most strongly affects the movements of the limbs, i.e., dynamic ataxia occurs. Ataxic phenomena and hypotonia are found on the side of the cerebellar lesion, in the limbs of the same side, and the patient staggers towards the affected side. When a tumor develops in the cerebellopontine angle, cerebellar symptoms appear on the side of the lesion. The clinical picture of a tumor of the VIII pair sometimes coincides with that of a tumor of the cerebellar hemispheres. The correct diagnosis depends on identifying the early, initial symptoms of the disease. With a tumor of the VIII pair, the first phenomena to occur are from this nerve, and with a tumor of the cerebellar hemisphere, cerebellar symptoms occur.

During processes in the frontal lobe, phenomena of ataxia similar to cerebellar ataxia are also sometimes expressed. Balance, standing and walking are impaired; coordination of movements is less impaired. These symptoms are sometimes incorrectly regarded as cerebellar, which leads to an erroneous diagnosis. For a correct diagnosis, it is necessary to take into account a number of other accompanying symptoms characteristic of damage to the frontal lobes, as well as the fact that when the frontal lobe is damaged, ataxia is present on the side opposite to the lesion.

Typically, cerebellar ataxia is accompanied by scanned speech, intention tremor, postural tremor of the head and torso, and muscle hypotonia. Diagnosis is carried out using MRI, CT, MSCT, MAG of the brain, Dopplerography, cerebrospinal fluid analysis; if necessary, genetic research. Treatment and prognosis depend on the causative disease that caused the development of cerebellar symptoms.

Cerebellar ataxia

Cerebellar ataxia is a symptom complex that includes specific disorders of static and dynamic human motor skills and is pathognomonic for any diseases of the cerebellum. The same type of movement coordination disorders occur both with congenital defects of the cerebellum and with a wide variety of pathological processes in the cerebellum: tumors, multiple sclerosis, strokes, inflammatory and degenerative changes, toxic or metabolic damage, external compression, etc. The degree of their severity varies significantly depending on on the location and size of the affected area of ​​the cerebellum.

The nature of the disease can be judged by the symptoms accompanying ataxia, as well as the characteristics of the occurrence and course of pathological changes. The latter was the basis for the classification that many specialists in the field of neurology use in their practice. According to it, cerebellar ataxia is distinguished with an acute onset, with a subacute onset (from 7 days to several weeks), chronically progressive (developing over several months or years) and episodic (paroxysmal).

Causes of cerebellar ataxia

The most common cause of acute cerebellar ataxia is ischemic stroke caused by embolism or atherosclerotic occlusion of the cerebral arteries, which also supply the cerebellar tissue. A hemorrhagic stroke, traumatic damage to the cerebellum as a result of a head injury, or its compression by a formed intracerebral hematoma is also possible. Acute cerebellar ataxia can develop with multiple sclerosis, Guillain's syndrome, post-infectious cerebellitis and encephalitis, obstructive hydrocephalus, various acute intoxications and metabolic disorders.

Subacute cerebellar ataxia most often occurs as a symptom of an intracerebral tumor (astrocytoma, hemangioblastoma, medulloblastoma, ependymoma) located in the cerebellum, or meningioma of the cerebellopontine angle. Its cause may be normal pressure hydrocephalus due to subarachnoid hemorrhage, previous meningitis, or brain surgery. Cerebellar ataxia with subacute onset is possible with an overdose of anticonvulsants, vitamin deficiency, endocrine disorders (hyperparathyroidism, hypothyroidism). It can also act as a paraneoplastic syndrome in malignant tumor processes of extracerebral localization (for example, lung cancer, ovarian cancer, non-Hodgkin's lymphoma, etc.).

Chronically progressive cerebellar ataxia is often a consequence of alcoholism and other chronic intoxications (including substance abuse and polydrug abuse), slowly growing cerebellar tumors, genetically determined cerebral degenerative and atrophic processes with damage to the cerebellar tissue or its pathways, and a severe form of Chiari anomaly. Among the genetically determined progressive ataxias of the cerebellar type, the most famous are Friedreich's ataxia, non-Friedreichian spinocerebellar ataxia, Pierre-Marie ataxia, Holmes cerebellar atrophy, and olivopontocerebellar degeneration (OPCD).

Cerebellar ataxia with a paroxysmal course can be hereditary or acquired. Among the causes of the latter are TIA, multiple sclerosis, intermittent obstruction of the cerebrospinal fluid pathways, and transient compression in the foramen magnum.

Symptoms of cerebellar ataxia

Cerebellar ataxia is manifested by sweeping, uncertain, asynergic movements and a characteristic unsteady gait, during which the patient places his legs wide apart for greater stability. When trying to walk along one line, there is a significant swaying to the sides. Ataxic disorders increase with sudden change directions of movement or quickly starting to walk after getting up from a chair. Sweeping movements are a consequence of a violation of their proportionality (dysmetria). It is possible to have both an involuntary stop of a motor act before its goal is achieved (hypometry) and an excessive range of movements (hypermetry). Dysdiadochokinesis is observed - the patient’s inability to quickly perform opposite motor acts (for example, supination and pronation). Due to impaired coordination and dysmetria, a change in handwriting that is pathognomonic for cerebellar ataxia occurs: macrography, unevenness and sweep.

Static ataxia is most obvious when the patient tries to get into the Romberg position. For pathology of the cerebellar hemisphere, a deviation, and even a fall, in the direction of the lesion is typical, with changes in its midline structures(worm) falling is possible in any direction or backward. Carrying out a finger-nose test reveals not only missingness, but also the intention tremor accompanying ataxia - trembling of the fingertip, which intensifies as it approaches the nose. Testing a patient in the Romberg position with eyes open and closed shows that visual control does not particularly affect the test results. This feature of cerebellar ataxia helps to differentiate it from sensitive and vestibular ataxia, in which the lack of visual control leads to a significant worsening of coordination impairment.

As a rule, cerebellar ataxia is accompanied by nystagmus and dysarthria. Speech has a specific “cerebellar” character: it loses its smoothness, slows down and becomes intermittent, stress is placed on each syllable, making speech resemble a chant. Often, cerebellar ataxia is observed against the background of muscle hypotonia and decreased deep reflexes. When tendon reflexes are evoked, pendulum-like movements of the limb are possible. In some cases, titubation occurs - low-frequency postural tremor of the torso and head.

Diagnosis of cerebellar ataxia

Since cerebellar pathology can have a wide variety of etiologies, specialists are involved in its diagnosis various directions: traumatologists, neurosurgeons, oncologists, geneticists, endocrinologists. A thorough examination of the neurological status by a neurologist makes it possible to determine not only the cerebellar nature of the ataxia, but also the approximate area of ​​the lesion. Thus, pathology in the cerebellar hemisphere is indicated by hemiataxia, the unilateral nature of coordination disorders and decreased muscle tone; about the pathological process in the cerebellar vermis - the predominance of walking and balance disorders, their combination with cerebellar dysarthria and nystagmus.

In order to exclude vestibular disorders, a vestibular analyzer is examined: stabilography, vestibulometry, electronystagmography. If an infectious lesion of the brain is suspected, a blood test is performed for sterility and PCR tests are performed. Lumbar puncture with examination of the obtained cerebrospinal fluid can reveal signs of hemorrhage, intracranial hypertension, inflammatory or tumor processes.

The main methods for diagnosing diseases underlying cerebellar pathology are neuroimaging methods: CT, MSCT and MRI of the brain. They make it possible to detect cerebellar tumors, post-traumatic hematomas, congenital anomalies and degenerative changes in the cerebellum, its prolapse into the foramen magnum and compression when neighboring anatomical structures are displaced. In the diagnosis of ataxia of a vascular nature, MRA and Dopplerography of cerebral vessels are used.

Hereditary cerebellar ataxia is established based on the results of DNA diagnostics and genetic analysis. The risk of having a child with pathology in a family where cases have been reported can also be calculated. of this disease.

Treatment of cerebellar ataxia

Treatment of the causative disease is fundamental. If cerebellar ataxia has an infectious-inflammatory origin, it is necessary to prescribe antibacterial or antiviral therapy. If the cause lies in vascular disorders, then measures are taken to normalize blood circulation or stop cerebral bleeding. For this purpose, angioprotectors, thrombolytics, antiplatelet agents, vasodilators, and anticoagulants are used in accordance with indications. For ataxia of toxic origin, detoxification is performed: intensive infusion therapy in combination with the prescription of diuretics; in severe cases - hemosorption.

Ataxia of a hereditary nature does not yet have a radical treatment. Metabolic therapy is mainly carried out: vitamins B12, B6 and B1, ATP, meldonium, ginko biloba preparations, piracetam, etc. To improve metabolism in skeletal muscles, increase its tone and strength, massage is recommended for patients.

Tumors of the cerebellum and posterior cranial fossa often require surgical treatment. Removal of the tumor should be as radical as possible. If the malignant nature of the tumor is established, a course of chemotherapy or radiotherapy treatment is additionally prescribed. For cerebellar ataxia caused by cerebrospinal fluid duct occlusion and hydrocephalus, shunt operations are used.

Prognosis and prevention

The prognosis depends entirely on the cause of cerebellar ataxia. Acute and subacute ataxia caused by vascular disorders, intoxication, inflammatory processes, with timely elimination of the causative factor (vascular occlusion, toxic effects, infection) and adequate treatment, can completely regress or partially persist as residual effects. Chronically progressive, hereditary ataxias are characterized by an increasing aggravation of symptoms, leading to disability of the patient. The most unfavorable prognosis is for ataxia associated with tumor processes.

The prevention of injuries, the development of vascular disorders (atherosclerosis, hypertension) and infection is of a preventive nature; compensation of endocrine and metabolic disorders; genetic counseling when planning pregnancy; timely treatment of pathology of the cerebrospinal fluid system, chronic cerebral ischemia, Chiari syndrome, processes of the posterior cranial fossa.

Cerebellar ataxia - treatment in Moscow

Directory of diseases

Nervous diseases

Last news

• © 2018 “Beauty and Medicine”

for informational purposes only

and does not replace qualified medical care.

Cerebellar damage due to stroke

Cerebellar stroke, risks if untreated, examination for pathology

Cerebellar stroke in medicine is the most dangerous defeat among other types of damage. The cerebellum is a section in the brain that is responsible for proper coordination and balance of the body. A stroke in this part occurs when blood flow in it is disrupted.

Sometimes this pathology can be confused with the brainstem form of stroke, since both organs are located nearby in the central nervous system, but during a brainstem stroke the bundle of nerves directly in the brainstem is damaged.

In appearance, the cerebellum resembles a round-shaped process located on the back of the head close to the spine. Its work is very important for the functioning of the whole organism:

• Coordination of movements.
• Functioning of the optic nerve.
• The work of the vestibular apparatus, balance, coordination and orientation in space.

What can cause an attack?

The pathology is formed when the supply of oxygen to the brain is interrupted or due to internal hemorrhage in the brain.

Stroke in the cerebellum is classified into two main types - hemorrhagic and ischemic. The ischemic type is much more common - in 75% of all cases of the disease, and is triggered by an unexpected deterioration in blood flow to the brain, which causes the formation of necrosis in the tissues. This process can be triggered by the following factors:

• A large blood clot that forms in another part of the body interferes with blood flow in the vessels that supply the brain.
• A blood clot that has formed in the artery that carries blood towards the brain.
• A rupture of a blood vessel that is responsible for the flow of blood to one or another part of the brain.
• Sudden changes in blood pressure.

It is important! The causes of hemorrhagic stroke are ruptures in blood vessels, causing hemorrhages in the brain.

Symptoms indicating a stroke in the cerebellum

Symptoms of a cerebellar stroke develop unexpectedly and include the following:

• Loss of coordination in the movements of the arms, legs and the whole body.
• Difficulty while walking, imbalance of the body in space.
• Abnormal reflex disorders.
• Trembling of limbs.
• Nausea with vomiting.
• Dizziness.
• Intense headaches.
• Speech disturbances and difficulty swallowing.
• Disturbances in the sensations of pain and body temperature.
• Hearing impairment.
• Visual impairment - rapid eye movements that are difficult to control by the person himself.
• Problems with eye function, for example, drooping eyelids.
• Loss of consciousness.

If a person develops at least one of the listed signs, then it is better to immediately contact a specialist, since it is the brain tissue that is characterized by a rapid rate of death.

What is needed for effective diagnosis of the disease?

The consequences of a cerebellar stroke can be disastrous if a diagnostic examination of the patient’s body is not carried out in a timely manner. Due to the fact that a cerebellar stroke becomes an unexpected unpleasant surprise, the doctor must make the correct diagnosis as soon as possible. Tests include:

1. Computed tomography is a type of x-ray examination that uses a computer to obtain images.
2. Angiography is a type of computed tomography that allows you to study the condition of blood vessels in the neck and brain.
3. An MRI is a test that uses magnetic radiation to take pictures of the brain.
4. Tests to determine the normal functioning of the heart.
5. A form of Doppler ultrasound, sound waves are used to determine the condition of blood vessels.
6. Blood tests.
7. Kidney function test.
8. A test to check your ability to swallow normally.

Organizing a suitable treatment process

If each of the listed symptoms of a cerebellar stroke is subject to abnormal influences, then doctors, in order to save the patient’s life, prescribe him treatment in a hospital setting. Treatment of cerebellar stroke involves eliminating embolism, blood clots, blood clots and scarring of blood vessels in the cerebellar area. For this purpose, appropriate medications are used to help thin the blood, control blood pressure, and treat abnormalities of fibrillation in the heart.

It is important! In almost half of all cases of the disease, the doctor prescribes surgery. For ischemic strokes, doctors redirect blood flow to the blocked vessel, remove the clot, and then carry out the complex process of removing fat deposits in the carotid artery. In addition, stenting and angioplasty are often performed as operations to widen the lumen of the arteries.

With the development of a hemorrhagic form of stroke, surgical intervention may involve craniotomy and removal of part of it to reduce intracranial pressure. In addition, a special plug is placed in the aneurysm and heavy bleeding is stopped.

The consequences of a cerebellar stroke are that, as a rule, after the development of a severe form of the disease, it is almost impossible to completely return to a person the functions he has lost. The main assistant in treatment is an optimistic attitude and caring for the patient. Thus, every year, the patient must go to a sanatorium-resort treatment, subject to the obligatory completion of a whole course of rehabilitation procedures - physical therapy, massages, reflexology, etc.

The prognosis of the disease already in the first minutes of the attack will depend on the location of the lesion, on the size and number of existing lesions, as well as on the timing of the attack. healing process. When a large number of lacunar foci are formed, a cerebellar infarction and a hemorrhagic form of stroke are transformed.

Unfavorable factors in the manifestation of a stroke are the patient’s advanced age, a persistent rise in body temperature, that is, damage to the thermoregulatory center in the brain, cardiac arrhythmia, somatic diseases with their decompensation, depression of the patient’s consciousness, pronounced cognitive impairment, advanced angina.

Cerebellar stroke

Cerebellar stroke, early recognition of which can save the patient’s life.

Cerebellar infarction is a consequence of thrombosis or embolism of the cerebellar arteries arising from the vertebral or basilar artery. It is manifested by hemiataxia and muscle hypotonia on the affected side, headache, dizziness, nystagmus, dysarthria and signs of concomitant damage to the trunk - limited mobility of the eyeballs, weakness of the facial muscles or impaired facial sensitivity on the affected side, sometimes hemiparesis or hemihypesthesia on the affected side. opposite side.

As a result of rapidly growing edema, compression of the trunk with the development of coma and herniation of the cerebellar tonsils into the foramen magnum are possible, with a fatal outcome that can only be prevented by surgical intervention. It should be taken into account that cerebellar hemiataxia may be a manifestation of a more favorably developing infarction of the medulla oblongata, which also causes Horner's syndrome (miosis, drooping of the upper eyelid), decreased sensitivity on the face, paresmuscles of the larynx and pharynx on the affected side and impaired pain and temperature sensitivity according to the hemitype on the opposite side (Wallenberg-Zakharchenko syndrome).

Hemorrhage into the cerebellum is often caused by arterial hypertension and is manifested by sudden intense headache, vomiting, dizziness, and ataxia. Rigidity of the neck muscles, nystagmus, and sometimes limited movement of the eyeballs towards the affected side, inhibition of the corneal reflex and paresis of the facial muscles on the affected side appear. Depression of consciousness rapidly increases with the development of coma. As a result of compression of the trunk, increased tone in the legs and pathological foot signs occur. In some cases, death can only be prevented by surgical intervention (hematoma evacuation).

Emergency care boils down to pain relief. For this purpose, analgesics and non-steroidal anti-inflammatory drugs, sometimes corticosteroids, are administered parenterally. In the acute period, immobilization of the limb is necessary. Subsequently, therapeutic exercises and physiotherapeutic procedures are important to prevent the development of a “frozen” shoulder.

Acute impairment of motor coordination may be caused by damage to the cerebellum or its connections in the trunk (cerebellar ataxia), nerve fibers carrying deep sensitivity(sensitive ataxia), vestibular system (vestibular ataxia), frontal lobes and associated subcortical structures (frontal ataxia). It can also be a manifestation of hysteria.

Acute cerebellar ataxia is manifested by impaired balance, walking and coordination of movements in the limbs. Damage to the midline structures of the cerebellum is accompanied by nystagmus and dysarthria [. ]

Differential diagnosis is made with cervical radiculopathy, which is not characterized by gross muscle atrophy, but is characterized by increased pain when moving the neck and straining, and pain radiating to the root. It is important to exclude diabetes mellitus, which can manifest as brachial plexopathy and vasculitis. Herpes zoster sometimes begins in a similar way, but the appearance of a characteristic rash after a few days resolves diagnostic difficulties. A slightly different localization of pain is observed with [. ]

Acute lumbodynia can be triggered by injury, lifting an excessive load, unprepared movement, prolonged stay in a non-physiological position, or hypothermia. Most often it occurs against the background of an ongoing degenerative process in the spine (spinal osteochondrosis). The intervertebral disc gradually loses water, shrinks, loses its shock-absorbing function and becomes more sensitive to mechanical stress.

Cerebellum and motor coordination disorders

The cerebellum is a part of the brain that is responsible for the coordination of movements, as well as the ability to ensure body balance and regulate muscle tone.

Basic functions and disorders of the cerebellum

The structure of the cerebellum itself is similar to the structure of the cerebral hemispheres. The cerebellum has a cortex and white matter underneath, which consists of fibers with cerebellar nuclei.

The cerebellum itself is closely connected with all parts of the brain, as well as with the spinal cord. The cerebellum is primarily responsible for the tone of the extensor muscles. When the function of the cerebellum is impaired, characteristic changes appear, which are commonly called “cerebellar syndrome.” On at this stage The development of medicine has revealed that the cerebellum is related to the impact on many important functions of the body.

When the cerebellum is damaged, various disorders can develop motor activity, autonomic disorders appear, and muscle tone is also disturbed. This occurs due to the close connection of the cerebellum with the brain stem. Therefore, the cerebellum is the center of coordination of movements.

Main symptoms of cerebellar damage

When the cerebellum is damaged, muscle function is disrupted, making it difficult for the patient to keep the body in balance. Today, there are main signs of cerebellar motor coordination disorders:

• intention tremor
• voluntary movements and slow speech
• the smoothness of movements of the arms and legs is lost
• handwriting changes
• speech becomes chanted, the placement of stress in words is more rhythmic than semantic

Cerebellar disorders of motor coordination are expressed in gait disturbances and dizziness - ataxia. Difficulties may also arise when trying to rise from supine position. The combination of simple movements and complex motor acts is disrupted, since the cerebellar system is affected. Cerebellar ataxia causes the patient to have an unsteady gait, which is characterized by staggering from side to side. Also, when looking away extreme position Rhythmic twitching of the eyeballs may be observed, which indicates a violation of the movement of the oculomotor muscles.

Ataxia happens different types, however, they are all similar in one main feature, namely movement disorders. The patient has statistical violations; even if he is pushed, he will fall without noticing that he is falling.

Cerebellar ataxia is observed in many diseases: hemorrhages of various origins, tumors, hereditary defects, poisoning.

Cerebellar congenital and acquired diseases

Diseases associated with the cerebellum can be congenital or acquired. Marie's hereditary cerebellar ataxia is a congenital genetic disease of the dominant type. The disease begins its manifestation with a lack of coordination of movements. This is due to hypoplasia of the cerebellum and its connections with the periphery. Often this disease is accompanied by a gradual manifestation of a decrease in intelligence, and memory is impaired.

During treatment, the type of inheritance of the disease is taken into account, at what age the first symptoms, changes, and deformities of the skeleton and feet appeared. There are also several other variants of chronic atrophy of the cerebellar system.

Typically, doctors prescribe conservative treatment to a patient with this diagnosis. This treatment can significantly reduce the severity of symptoms. During treatment, the nutrition of nerve cells can be significantly increased, as well as blood supply improved.

Acquired cerebellar disease can result from traumatic brain injury when a traumatic hematoma occurs. Having established this diagnosis, doctors perform surgery to remove the hematoma. Also, damage to the cerebellum can be caused by malignant tumors, the most common of which are medulloblastomas and sarcomas. Stroke-infarction of the cerebellum can also cause hemorrhage, which occurs with atherosclerosis of blood vessels or a hypertensive crisis. With such diagnoses, surgical treatment of the cerebellum is usually prescribed.

Currently, transplantation of individual parts of the brain is not possible. This is due to ethical considerations, since the death of a person is determined by the fact of brain death; therefore, when the owner of the brain is still alive, he cannot be an organ donor.

Cerebellar stroke: causes and treatment

A cerebellar stroke occurs when the blood supply to a given area of ​​the brain is interrupted. Brain tissue that does not receive oxygen and nutrients from the blood quickly dies and this leads to the loss of some body functions. Therefore, a stroke is a life-threatening condition and requires emergency medical care.

There are two types of cerebellar stroke:

The most common form is ischemic cerebellar stroke, which occurs due to a sharp decrease in blood flow to the brain area. In turn, this condition can cause:

• a clot that blocks the flow of blood into a blood vessel
• a clot (thrombus) that has formed in an artery that carries blood to the brain
• when a blood vessel ruptures and a cerebral hemorrhage occurs

The consequences of a cerebellar stroke are: excessive sweating, uneven breathing, excessive pallor, rapid heartbeat, unstable pulse, redness of the face. To dissolve the blood clot that caused the ischemic stroke, emergency treatment is performed. Medical attention is also necessary to stop bleeding during a hemorrhagic stroke.

During the treatment of ischemic cerebellar stroke, it is prescribed medications, which help dissolve blood clots and prevent their formation, prescribe medications that thin the blood, control blood pressure, and treat irregular heart rhythms. To treat ischemic cerebellar stroke, your doctor may perform surgery. It is strictly forbidden to self-medicate, because the wrong approach to the problem can cause the condition to worsen.

Cerebellum

Pathology

In diseases of the cerebellum, three groups of symptoms appear: 1) depending on damage to the tissue of the cerebellum itself; 2) from involvement in the process of formations located near the cerebellum within the posterior fossa (stem syndrome and dysfunction of the cranial nerves); 3) from the involvement of supratentorially located parts of the central nervous system in the process. When the neocerebellar parts are damaged, cerebellar symptoms develop, and when the so-called vestibular parts are damaged, cerebellar-vestibular symptoms develop. With the progression of a local lesion (tumor), cerebellar-vestibular symptoms are a consequence of damage to the cerebellar tissue only in the initial stages of the disease; in the future they will to a greater extent arise due to the involvement in the process of central vestibular formations located in the brain stem.

Cerebellar symptoms include cerebellar hypotonia, impaired coordination of limb movements, cerebellar cutting (asthenia, adynamia), hyperkinesis (tremor and myoclonus), speech disorders of cerebellar origin; to the cerebellar-vestibular - disturbances in statics and gait, Babinsky asynergia.

Cerebellar hypotonia. The severity of muscle hypotonia increases according to an increase in damage to the cerebellar cortex and, possibly, with the involvement of the dentate nucleus in the process. An increase in tone and its complex irregular distribution, sometimes observed with damage to the cerebellum, is largely associated with the involvement of stem formations in the process.

Impaired coordination of limb movements. The term cerebellar ataxia (in relation to specialized movements of the limbs) combines a number of symptoms indicating a violation of the regulation of motor acts and their coordination. These symptoms include: violation of the scope of the motor act (dysmetria, hypermetry, hypometry), errors in its direction, disturbance of tempo (slowness). Loss of motor coordination is one of the components of hemispheric cerebellar syndrome. At the same time, it is more clearly detected in the upper extremities, which is associated with special development in humans, fine specialized asymmetrical movements of the upper limbs.

Cerebellar paresis (asthenia, adynamia). With damage to the cerebellum during acute and chronic forms disease, a decrease in muscle strength is observed homolateral to the lesion and is a consequence of impaired tone.

Hyperkinesis. With lesions of the cerebellum, the following types of hyperkinesis occur: 1) ataxic, or dynamic, tremor, which appears during active movements in the limbs; it includes the so-called intention tremor, which intensifies when a goal is achieved; 2) myoclonus - rapid twitching of individual muscle groups or muscles, observed in humans in the limbs, neck and swallowing muscles. Choreic-athetotic movements in the limbs with lesions of the cerebellum are rarely observed; they are associated with the involvement of the dentate nucleus systems in the process. Twitching in the neck muscles and myoclonus of the soft palate and pharyngeal walls also rarely occur. Myoclonus occurs when stem formations are involved in the process.

Speech disorders in diseases of the cerebellum are observed in three forms: cerebellar bradyllia and scanned speech, bulbar, mixed. With bulbar disorders, expressed even to a mild degree, it is difficult to decide whether there are in this case In addition to them, speech disorders are also of cerebellar origin. Only in rare cases, with mild symptoms of damage to the IX and X pairs of cranial nerves, can one assume its cerebellar origin based on the severity of scanned speech. In chanted speech, the stresses are not placed according to meaning, but are separated by even intervals.

Static and gait disturbances that occur in patients with cerebellar disease may be a consequence of damage to the cerebellar-vestibular formations located in the cerebellum, as well as vestibular formations located in the brainstem. In this case, statokinetic disorders can be of varying intensity - from barely noticeable staggering when standing or walking (with slight separation of the legs) to pronounced forms of trunk ataxia, when the patient is unable to stand or sit and falls back or to the side without support. Severe gait disturbances include a staggering gait with legs widely spaced, zigzag evasion or deviation in a certain direction from a given direction; this often creates the impression of a “drunken gait.”

Asynergy (or dissynergy) - the impossibility of simultaneous joint, or synergistic, execution complex movement. If healthy person lay him on his back with crossed arms and invite him to take a sitting position, he will do this without difficulty, since simultaneously with the bending of the torso, the legs and pelvis are fixed to the plane of support. A patient with asynergia cannot do this, since due to the lack of synergy of muscle groups that flex the torso and fix the pelvis and lower limbs, instead of the torso, both legs, or one leg on the affected side, rise.

Contents [Show]

Cerebellar ataxia is a syndrome that occurs when a special structure of the brain called the cerebellum or its connections to other parts of the nervous system are damaged. Cerebellar ataxia is very common and can be the result of a wide variety of diseases. Its main manifestations are a disorder of coordination of movements, their smoothness and proportionality, disturbance of balance and maintenance of body posture. Some signs of cerebellar ataxia are visible to the naked eye even to a person without medical education, while others are detected using special tests. Treatment of cerebellar ataxia largely depends on the cause of its occurrence, on the disease from which it is a consequence. You will learn about what can cause cerebellar ataxia, what symptoms it manifests and how to deal with it by reading this article.

The cerebellum is a part of the brain located in the posterior cranial fossa below and behind the main part of the brain. The cerebellum consists of two hemispheres and the vermis, the middle part that connects the hemispheres with each other. The average weight of the cerebellum is 135 g, and its size is 9-10 cm × 3-4 cm × 5-6 cm, but despite such small parameters, its functions are very important. None of us thinks about what muscles need to be tensed in order, for example, to simply sit down or stand up, or take a spoon in our hand. It seems to happen automatically, you just have to want it. However, in fact, to perform such simple motor acts, the coordinated and simultaneous work of many muscles is necessary, which is only possible with the active functioning of the cerebellum.

The main functions of the cerebellum are:

• maintaining and redistributing muscle tone to keep the body in balance;
• coordination of movements in the form of their accuracy, smoothness and proportionality;
• maintenance and redistribution of muscle tone in synergist muscles (performing the same movement) and antagonist muscles (performing multidirectional movements). For example, to bend a leg, you must simultaneously tense the flexors and relax the extensors;
• economical use of energy in the form of minimal muscle contractions necessary to perform a specific type of work;
• participation in processes motor learning(for example, the formation of professional skills related to the contraction of certain muscles).

If the cerebellum is healthy, then all these functions are carried out unnoticed by us, without requiring any thought processes. If any part of the cerebellum or its connections with other structures is affected, then the performance of these functions becomes difficult and sometimes simply impossible. This is when the so-called cerebellar ataxia occurs.

The spectrum of neurological pathology occurring with signs of cerebellar ataxia is very diverse. The causes of cerebellar ataxia can be:

• violations cerebral circulation in the vertebrobasilar region (ischemic and hemorrhagic stroke, transient ischemic attacks, discirculatory encephalopathy);
• multiple sclerosis;
• tumors of the cerebellum and cerebellopontine angle;
• traumatic brain injury with damage to the cerebellum and its connections;
• meningitis, meningoencephalitis;
• degenerative diseases and anomalies of the nervous system with damage to the cerebellum and its connections (Friedreich's ataxia, Arnold-Chiari anomaly and others);
• intoxication and metabolic damage (for example, alcohol and drug use, lead intoxication, diabetes mellitus, and so on);
• overdose of anticonvulsants;
• vitamin B12 deficiency;
• obstructive hydrocephalus.

Symptoms of cerebellar ataxia

It is customary to distinguish two types of cerebellar ataxia: static (static-locomotor) and dynamic. Static cerebellar ataxia develops with damage to the cerebellar vermis, and dynamic ataxia develops with pathology of the cerebellar hemispheres and its connections. Each type of ataxia has its own characteristics. Cerebellar ataxia of any type is characterized by a decrease in muscle tone.

Static-locomotor ataxia

This type of cerebellar ataxia is characterized by a violation of the antigravity function of the cerebellum. As a result, standing and walking become too much of a strain on the body. Symptoms of static-locomotor ataxia may include:

• inability to stand straight in the “heels and toes together” position;
• falling forward, backward or swaying to the sides;
• the patient can stand only by spreading his legs wide apart and balancing with his hands;
• unsteady gait (like a drunk);
• when turning, the patient “slides” to the side, and he may fall.

To identify static-locomotor ataxia, several simple tests are used. Here are some of them:

• standing in the Romberg pose. The pose is as follows: toes and heels pushed together, arms extended forward to a horizontal level, palms facing down with fingers spread wide. First, the patient is asked to stand with his eyes open, and then with his eyes closed. With static-locomotor ataxia, the patient is unstable both with his eyes open and with his eyes closed. If no deviations are detected in the Romberg position, then the patient is asked to stand in a complicated Romberg position, when one leg must be placed in front of the other so that the heel touches the toe (maintaining such a stable position is possible only in the absence of pathology on the part of the cerebellum);
• the patient is asked to walk along a conventional straight line. With static-locomotor ataxia, this is impossible; the patient will inevitably deviate in one direction or another, spread his legs wide apart, and may even fall. They are also asked to stop abruptly and turn 90° to the left or right (with ataxia the person will fall);
• The patient is asked to walk with a side step. Such a gait with static-locomotor ataxia becomes as if dancing, the torso lags behind the limbs;
• "star" or Panov test. This test allows you to identify disorders in mildly expressed static-locomotor ataxia. The technique is as follows: the patient needs to successively take three steps forward in a straight line, and then three steps back, also in a straight line. First, the test is carried out with open eyes, and then with closed ones. If with open eyes the patient is even more or less able to perform this test, then with closed eyes he inevitably turns around (a straight line does not come out).

In addition to impaired standing and walking, static-locomotor ataxia manifests itself as a violation of coordinated muscle contraction when performing various movements. This is called in medicine cerebellar asynergies. Several tests are also used to identify them:

• the patient is asked to sit up sharply from a lying position with his arms crossed over his chest. Normally, the muscles of the trunk and the posterior group of thigh muscles contract synchronously, and the person is able to sit down. With static-locomotor ataxia, synchronous contraction of both muscle groups becomes impossible, as a result of which it is impossible to sit without the help of hands, the patient falls back and one leg rises at the same time. This is the so-called Babinski asynergy in the supine position;
• Babinsky's synergy in a standing position is as follows: in a standing position, the patient is asked to bend back, throwing back his head. Normally, for this, a person will have to involuntarily bend his knees slightly and straighten his hip joints. With static-locomotor ataxia, neither flexion nor extension occurs in the corresponding joints, and an attempt to bend ends in a fall;
• Orzechowski's test. The doctor extends his hands, palms up, and invites the standing or sitting patient to rest his palms on them. Then the doctor suddenly moves his hands down. Normally, the patient's lightning-fast, involuntary muscle contractions cause him to either lean back or remain motionless. This will not work for a patient with static-locomotor ataxia - he will fall forward;
• phenomenon of absence of reverse shock (positive Stewart-Holmes test). The patient is asked to forcefully bend his arm at the elbow joint, and the doctor counteracts this, and then suddenly stops the opposition. With static-locomotor ataxia, the patient's hand is thrown back with force and hits the patient's chest.

Dynamic cerebellar ataxia

In general, its essence lies in the disruption of smoothness and proportionality, accuracy and dexterity of movements. It can be bilateral (with damage to both hemispheres of the cerebellum) and unilateral (with pathology of one hemisphere of the cerebellum). Unilateral dynamic ataxia is much more common.

Some of the symptoms of dynamic cerebellar ataxia overlap with those of static-locomotor ataxia. For example, this concerns the presence of cerebellar asynergies (Babinski asynergia lying and standing, Orzechowski and Stewart-Holmes tests). There is only a slight difference: since dynamic cerebellar ataxia is associated with damage to the cerebellar hemispheres, these tests predominate on the affected side (for example, if the left hemisphere of the cerebellum is damaged, “problems” will occur with the left extremities and vice versa).

Dynamic cerebellar ataxia also manifests itself:

• intention tremor (tremor) in the limbs. This is the name for trembling that occurs or intensifies towards the end of the movement being performed. At rest, no trembling is observed. For example, if you ask the patient to take ballpoint pen from the table, then at first the movement will be normal, but by the time you actually take the pen, your fingers will begin to tremble;
• missing and missing. These phenomena are the result of disproportionate muscle contraction: for example, the flexors contract more than necessary to perform a particular movement, and the extensors do not relax properly. As a result, it becomes difficult to fulfill the most habitual actions: bring a spoon to your mouth, fasten buttons, lace your shoes, shave, and so on;
• handwriting disorder. Dynamic ataxia is characterized by large, uneven letters and a zigzag direction of the writing;
• chanted speech. This term refers to the intermittency and jerkiness of speech, the division of phrases into separate fragments. The patient’s speech looks as if he were speaking from the podium with some slogans;
• nystagmus. Nystagmus is involuntary shaking movements of the eyeballs. Essentially, this is the result of incoordination of contraction of the eye muscles. The eyes seem to twitch, this is especially pronounced when looking to the side;
• adiadochokinesis. Adiadochokinesis is a pathological movement disorder that occurs during quick repetition multidirectional movements. For example, if you ask a patient to quickly turn his palms against their axis (as if screwing in a light bulb), then with dynamic ataxia the affected hand will do this more slowly and awkwardly compared to the healthy one;
• pendulum-like nature of knee reflexes. Normally, a blow with a neurological hammer under the kneecap causes a single movement of the leg of varying degrees of severity. With dynamic cerebellar ataxia, the leg oscillates several times after one blow (that is, the leg swings like a pendulum).

To identify dynamic ataxia, it is customary to use a series of tests, since the degree of its severity does not always reach significant limits and is immediately noticeable. With minimal lesions of the cerebellum, it can only be detected by testing:

• finger-nose test. With the arm straightened and raised to a horizontal level with a slight abduction to the side, with eyes open and then with eyes closed, ask the patient to touch the nose with the tip of the index finger. If a person is healthy, he can do this without much difficulty. With dynamic cerebellar ataxia, the index finger misses, and when approaching the nose, an intention tremor appears;
• finger-finger test. With eyes closed, the patient is asked to touch each other with the tips of the index fingers of slightly spaced hands. Similar to the previous test, in the presence of dynamic ataxia, no hit occurs, trembling may be observed;
• finger hammer test. The doctor moves the neurological hammer in front of the patient’s eyes, and the patient must place his index finger exactly on the elastic band of the hammer;
• test with hammer A.G. Panova. The patient is given a neurological hammer in one hand and is asked to alternately and quickly squeeze the hammer with the fingers of the other hand, either by the narrow part (handle) or by the wide part (elastic band);
• heel-knee test. It is performed in a supine position. It is necessary to raise the straightened leg approximately 50-60°, hit the knee of the other leg with the heel and, as it were, “ride” the heel along the front surface of the shin to the foot. The test is carried out with eyes open and then with eyes closed;
• test for redundancy and disproportion of movements. The patient is asked to stretch his arms forward to a horizontal level with his palms up, and then, at the doctor’s command, turn his palms down, that is, make a precise 180° turn. In the presence of dynamic cerebellar ataxia, one of the arms rotates excessively, that is, more than 180°;
• test for diadochokinesis. The patient should bend his arms at the elbows and seem to take an apple in his hands, and then quickly make twisting movements with his hands;
• Doinikov finger phenomenon. In a sitting position, the patient places his relaxed hands on his knees, palms up. On the affected side, flexion of the fingers and rotation of the hand is possible due to an imbalance in the tone of the flexor and extensor muscles.

Such a large number of tests for dynamic ataxia is due to the fact that it is not always detected with only one test. It all depends on the extent of the damage to the cerebellar tissue. Therefore, for more in-depth analysis, several samples are usually carried out simultaneously.

Treatment of cerebellar ataxia

There is no single treatment strategy for cerebellar ataxia. This is due to a large number of possible reasons for its occurrence. Therefore, first of all, it is necessary to establish the pathological condition (for example, stroke or multiple sclerosis) that led to cerebellar ataxia, and then a treatment strategy is developed.

The symptomatic remedies most often used for cerebellar ataxia include:

• drugs of the Betagistine group (Betaserc, Vestibo, Westinorm and others);
• nootropics and antioxidants (Piracetam, Phenotropil, Picamilon, Phenibut, Cytoflavin, Cerebrolysin, Actovegin, Mexidol and others);
• drugs that improve blood flow (Cavinton, Pentoxifylline, Sermion and others);
• B vitamins and their complexes (Milgamma, Neurobeks and others);
• agents affecting muscle tone (Mydocalm, Baclofen, Sirdalud);
• anticonvulsants (Carbamazepine, Pregabalin).

Help in the fight against cerebellar ataxia is physical therapy and massage. Performing certain exercises allows you to normalize muscle tone, coordinate the contraction and relaxation of flexors and extensors, and also helps the patient adapt to new conditions of movement.

In the treatment of cerebellar ataxia, physiotherapeutic methods can be used, in particular electrical stimulation, hydrotherapy (baths), and magnetic therapy. Sessions with a speech therapist will help normalize speech disorders.

In order to facilitate the process of movement, a patient with severe manifestations of cerebellar ataxia is recommended to use additional means: canes, walkers and even wheelchairs.

In many ways, the prognosis for recovery is determined by the cause of cerebellar ataxia. Thus, in the presence of a benign cerebellar tumor, complete recovery is possible after its surgical removal. Cerebellar ataxia associated with mild circulatory disorders and traumatic brain injuries, meningitis, and meningoencephalitis are successfully treated. Degenerative diseases and multiple sclerosis are less responsive to therapy.

Thus, cerebellar ataxia is always a consequence of some kind of disease, and not always neurological. Its symptoms are not so numerous, and its presence can be detected using simple tests. It is very important to establish the true cause of cerebellar ataxia in order to cope with the symptoms as quickly and effectively as possible. Patient management tactics are determined in each specific case.

Neurologist M. M. Shperling talks about ataxia:

Impaired Coordination - Ataxia. Treatment of Ataxia (doctor's recommendations).

The cerebellum is a part of the central nervous system located under the cerebral hemispheres. It has the following formations: two hemispheres, legs and a worm. Responsible for coordination of movements and muscle function. With lesions of the cerebellum, symptoms manifest themselves as motor disturbances, changes in speech, handwriting, gait, and loss of muscle tone.

Causes of cerebellar diseases

The causes of cerebellar diseases can be injuries, congenital underdevelopment of this structure, as well as circulatory disorders, the consequences of drug addiction, substance abuse, neuroinfections, and intoxication. There is a congenital defect in the development of the cerebellum caused by a genetic pathology called Marie's ataxia.

Important! Damage to the cerebellum can result from strokes, injuries, cancer, infections of the nervous system, and intoxication.

Cerebellar injuries are observed with fractures of the base of the skull and injuries to the occipital part of the head. Impaired blood supply to the cerebellum occurs with atherosclerotic vascular damage, as well as with ischemic, hemorrhagic stroke of the cerebellum.

Atherosclerosis of the vessels directly supplying the cerebellum, as well as sclerotic lesions of the carotid arteries in combination with vasospasm can cause transient hypoxia (transient ischemic attacks). Ischemic stroke is usually caused by blockage of a vessel with a thrombus or emboli of various origins (air, cholesterol plaque). It also manifests itself as a dysfunction of the cerebellum.

Hemorrhagic stroke of the cerebellum, i.e. hemorrhage due to a violation of the integrity of the vessel is a common cause of impaired coordination of movements, speech, and eye symptoms. Hemorrhages in the cerebellar substance occur with high blood pressure and hypertensive crises.

In older people, the vessels are not elastic, are affected by atherosclerosis and are covered with calcified cholesterol plaques, so they cannot withstand high pressure and their wall is torn. The result of hemorrhage is ischemia of the tissues that received nutrition from the ruptured vessel, as well as the deposition of hemosiderin in the intercellular substance of the brain and the formation of a hematoma.

Oncological diseases associated directly with the cerebellum, or with metastases, also cause disorders of this structure. Sometimes cerebellar lesions are caused by impaired outflow of cerebral fluid.

Symptoms of cerebellar damage

The key symptom of cerebellar damage is cerebellar ataxia. It manifests itself in trembling of the head and the whole body at rest and during movement, incoordination of movements, and muscle weakness. Symptoms of cerebellar diseases can be asymmetrical if one of the hemispheres is damaged. The main manifestations of pathology in patients are identified:

1. Intention tremor, one of the symptoms of cerebellar damage, manifests itself in sweeping movements and excessive amplitude at the end.
2. Postural tremor is a shaking of the head and body at rest.
3. Dysdiadochokinesis manifests itself in the impossibility of rapid opposite muscle movements - flexion and extension, pronation and supination, adduction and abduction.
4. Hypometry is the stopping of a motor act without achieving its goal. Hypermetry is an increase in pendulum-like movements when approaching the achievement of the goal of the movement.
5. Nystagmus is an involuntary movement of the eyes.
6. Muscle hypotension. The patient's muscle strength decreases.
7. Hyporeflexia.
8. Dysarthria. Scanned speech, i.e. patients emphasize words rhythmically and not in accordance with the rules of orthoepy.
9. Gait disturbance. Shaky movements of the body do not allow the patient to walk in a straight line.
10. Handwriting disorders.

Diagnosis and treatment of cerebellar disorders

The neurologist examines and tests superficial and deep reflexes. Electronystagmography and vestibulometry are performed. Assign general analysis blood. A lumbar puncture is performed to detect infection in the cerebrospinal fluid, as well as markers of stroke or inflammation. Magnetic resonance imaging of the head is performed. The condition of the cerebellar vessels is determined using Dopplerography.

Treatment of cerebellar diseases in ischemic stroke is carried out using thrombus lysis. Fibrinolytics (streptokinase, alteplase, urokinase) are prescribed. To prevent the formation of new blood clots, antiplatelet agents (aspirin, clopidogrel) are used.

For ischemic and hemorrhagic strokes, metabolic drugs (Mexidol, Cerebrolysin, Cytoflavin) improve metabolism in brain tissue. To prevent recurrent strokes, drugs that lower blood cholesterol are prescribed, and in case of hemorrhagic hemorrhage, antihypertensive drugs are prescribed.

Neuroinfections (encephalitis, meningitis) require antibiotic therapy. Pathologies of the cerebellum caused by intoxications require detoxification therapy, depending on the nature of the poisons. Forced diuresis, peritoneal dialysis and hemodialysis are performed. In case of food poisoning - gastric lavage, administration of sorbents.

For oncological lesions of the cerebellum, treatment is carried out in accordance with the type of pathology. Chemotherapy, radiation therapy, or surgical treatment are prescribed. If the outflow of cerebrospinal fluid is disrupted, causing cerebellar syndrome, an operation is performed with craniotomy and shunting of the pathways for the outflow of cerebrospinal fluid.

Conclusion

Damage to the cerebellum, the consequence of which can be disability, the patient’s need for care, requires timely and thorough treatment, as well as care and rehabilitation of the patient. If there is a sudden disturbance in gait or speech disorder, it is necessary to visit a neurologist.

The cerebellum is a part of the brain that is responsible for the coordination of movements, as well as the ability to ensure body balance and regulate muscle tone.

Basic functions and disorders of the cerebellum

The structure of the cerebellum itself is similar to the structure of the cerebral hemispheres. The cerebellum has a cortex and white matter underneath, which consists of fibers with cerebellar nuclei.

The cerebellum itself is closely connected with all parts of the brain, as well as with the spinal cord. The cerebellum is primarily responsible for the tone of the extensor muscles. When the function of the cerebellum is impaired, characteristic changes appear, which are commonly called “cerebellar syndrome.” At this stage of development of medicine, it has been revealed that the cerebellum is related to the impact on many important functions of the body.

If the cerebellum is damaged, various motor activity disorders may develop, autonomic disorders may appear, and muscle tone may be impaired. This occurs due to the close connection of the cerebellum with the brain stem. Therefore, the cerebellum is the center of coordination of movements.

Main symptoms of cerebellar damage

When the cerebellum is damaged, muscle function is disrupted, making it difficult for the patient to keep the body in balance. Today, there are main signs of cerebellar motor coordination disorders:

• intention tremor
• voluntary movements and slow speech
• the smoothness of movements of the arms and legs is lost
• handwriting changes
• speech becomes chanted, the placement of stress in words is more rhythmic than semantic

Cerebellar disorders of motor coordination are expressed in gait disturbances and dizziness - ataxia. Difficulties may also arise when trying to rise from a lying position. The combination of simple movements and complex motor acts is disrupted, since the cerebellar system is affected. Cerebellar ataxia causes the patient to have an unsteady gait, which is characterized by staggering from side to side. Also, when looking away to the extreme position, rhythmic twitching of the eyeballs may be observed, which is how the movement of the oculomotor muscles is impaired.

There are different types of ataxia, but they are all similar in one main feature, namely movement disorder. The patient has statistical violations; even if he is pushed, he will fall without noticing that he is falling.
Cerebellar ataxia is observed in many diseases: hemorrhages of various origins, tumors, hereditary defects, poisoning.

Cerebellar congenital and acquired diseases

Diseases associated with the cerebellum can be congenital or acquired. Marie's hereditary cerebellar ataxia is a congenital genetic disease of the dominant type. The disease begins its manifestation with a lack of coordination of movements. This is due to hypoplasia of the cerebellum and its connections with the periphery. Often this disease is accompanied by a gradual manifestation of a decrease in intelligence, and memory is impaired.

During treatment, the type of inheritance of the disease is taken into account, at what age the first symptoms, changes, and deformities of the skeleton and feet appeared. There are also several other variants of chronic atrophy of the cerebellar system.

Typically, doctors prescribe conservative treatment to a patient with this diagnosis. This treatment can significantly reduce the severity of symptoms. During treatment, the nutrition of nerve cells can be significantly increased, as well as blood supply improved.

Acquired cerebellar disease can result from traumatic brain injury when a traumatic hematoma occurs. Having established this diagnosis, doctors perform surgery to remove the hematoma. Also, damage to the cerebellum can be caused by malignant tumors, the most common of which are medulloblastomas and sarcomas. Stroke-infarction of the cerebellum can also cause hemorrhage, which occurs with atherosclerosis of blood vessels or a hypertensive crisis. With such diagnoses, surgical treatment of the cerebellum is usually prescribed.

Currently, transplantation of individual parts of the brain is not possible. This is due to ethical considerations, since the death of a person is determined by the fact of brain death; therefore, when the owner of the brain is still alive, he cannot be an organ donor.

Cerebellar stroke: causes and treatment

A cerebellar stroke occurs when the blood supply to a given area of ​​the brain is interrupted. Brain tissue that does not receive oxygen and nutrients from the blood quickly dies and this leads to the loss of some body functions. Therefore, a stroke is a life-threatening condition and requires emergency medical care.

There are two types of cerebellar stroke:

• ischemic
• hemorrhagic

The most common form is ischemic cerebellar stroke, which occurs due to a sharp decrease in blood flow to the brain area. In turn, this condition can cause:

• a clot that blocks the flow of blood into a blood vessel
• a clot (thrombus) that has formed in an artery that carries blood to the brain
• when a blood vessel ruptures and a cerebral hemorrhage occurs

The consequences of a cerebellar stroke are: excessive sweating, uneven breathing, excessive pallor, rapid heartbeat, unstable pulse, redness of the face. To dissolve the blood clot that caused the ischemic stroke, emergency treatment is performed. Medical attention is also necessary to stop bleeding during a hemorrhagic stroke.

During the treatment of ischemic cerebellar stroke, medications are prescribed to help dissolve blood clots and prevent their formation, blood thinners are prescribed to control blood pressure, and to treat irregular heart rhythms. To treat ischemic cerebellar stroke, your doctor may perform surgery. It is strictly forbidden to self-medicate, because the wrong approach to the problem can cause the condition to worsen.

Coordination of movements is a natural and necessary quality of any living creature that has mobility, or the ability to arbitrarily change its position in space. This function must be performed by special nerve cells.

In the case of worms that move on a plane, there is no need to allocate a special organ for this. But already in primitive amphibians and fish, a separate structure appears, which is called the cerebellum. In mammals, this organ is improved due to the variety of movements, but greatest development he received it from birds, since the bird perfectly masters all degrees of freedom.

A person has a specific movement pattern that is associated with the use of hands as tools. As a result, coordination of movements turned out to be unthinkable without mastering fine motor skills of the hands and fingers. Besides, the only way human movement is upright walking. Therefore, coordination of the position of the human body in space is unthinkable without constantly maintaining balance.

It is these functions that distinguish the human cerebellum from a seemingly similar organ in other higher primates, and in a child it must still mature and learn proper regulation. But, like any individual organ or structure, the cerebellum can be affected various diseases. As a result, the above functions are disrupted and a condition called cerebellar ataxia develops.

How does a “normal” cerebellum work?

Before approaching the description of diseases of the cerebellum, it is necessary to briefly talk about how the cerebellum is structured and how it functions.

The cerebellum is located at the bottom of the brain, under the occipital lobes of the cerebral hemispheres.

It consists of a small middle section, the vermis, and hemispheres. The vermis is an ancient section, and its function is to ensure balance and statics, and the hemispheres developed along with the cerebral cortex, and provide complex motor acts, for example, the process of typing this article on a computer keyboard.

The cerebellum is closely connected to all the tendons and muscles of the body. They contain special receptors that “tell” the cerebellum what state the muscles are in. This sense is called proprioception. For example, each of us knows, without looking, in what position and where his leg or arm is, even in the dark and at rest. This sensation reaches the cerebellum via the spinocerebellar tracts that ascend in the spinal cord.

In addition, the cerebellum is connected with the system of semicircular canals, or the vestibular apparatus, as well as with the conductors of the joint-muscular sense.

The olivocerebellar pathway passes through the inferior cerebellar peduncles, which connects it with the extrapyramidal system of unconscious movements. The reverse, efferent pathway is the path from the cerebellum to the red nuclei.

It is this path that works brilliantly when, having slipped, a person “dances” on the ice. Without having time to figure out what is happening, and without having time to get scared, the person restores his balance. This triggered a “relay” that switched information from the vestibular apparatus about changes in body position immediately, through the cerebellar vermis to basal ganglia, and further, to the muscles. Since this happened “automatically”, without the participation of the cerebral cortex, the process of restoring balance occurs unconsciously.

The cerebellum is closely connected to the cerebral cortex, regulating conscious movements of the limbs. This regulation occurs in the cerebellar hemispheres

What is cerebellar ataxia?

Translated from Greek, taxis is movement, taxis. And the prefix “a” means negation. In the broadest sense of the word, ataxia is a disorder of voluntary movements. But this disorder can occur, for example, during a stroke. Therefore, an adjective is added to the definition. As a result, the term “cerebellar ataxia” refers to a set of symptoms that indicate a lack of coordination of movements, the cause of which is a dysfunction of the cerebellum.

It is important to know that in addition to ataxia, cerebellar syndrome is accompanied by asynergia, that is, a violation of the consistency of the movements performed relative to each other.

Some believe that cerebellar ataxia is a disease that affects adults and children. In fact, this is not a disease, but a syndrome that can have various causes and occur with tumors, injuries, multiple sclerosis and other diseases. How does this cerebellar lesion manifest itself? This disorder manifests itself as static ataxia and dynamic ataxia. What it is?

Static ataxia is a violation of coordination of movements at rest, and dynamic ataxia is a violation of their movement.. But doctors, when examining a patient who suffers from cerebellar ataxia, do not distinguish such forms. Much more important are the symptoms that indicate the location of the lesion.

Symptoms of cerebellar disorders

The function of this body is as follows:

• maintaining muscle tone using reflexes;
• maintaining balance;
• coordination of movements;
• their consistency, that is, synergy.

Therefore, all symptoms of cerebellar damage are, to one degree or another, a disorder of the above functions. Let us list and explain the most important of them.

Atactic gait

Everyone has seen cerebellar ataxia of alcoholic origin, when a heavily drunk person walks in front of you. The “cerebellar” gait looks the same. The legs are spread wide apart, the patient staggers, and “skids” when turning. Also, during gait, various deviations to the side and a fall are possible. And the deviation most often occurs on the affected side, since the cerebellar tracts pass ipsilaterally, without crossing, unlike the pyramidal tract.

Intention tremor

This symptom appears with movement, and is almost not observed at rest. Its meaning is the appearance and intensification of the amplitude of oscillations of the distal limbs when reaching a goal. If you ask a sick person to touch his own nose with his index finger, the closer the finger is to the nose, the more he will begin to tremble and describe various circles. Intention is possible not only in the arms, but also in the legs. This is detected during the heel-knee test, when the patient is asked to hit the knee of the other, extended leg with the heel of one leg.

Nystagmus

Nystagmus is an intention tremor that occurs in the muscles of the eyeballs. If the patient is asked to move his eyes to the side, a uniform, rhythmic twitching of the eyeballs occurs. Nystagmus can be horizontal, less often – vertical or rotatory (rotational).

Adiadochokinesis

This phenomenon can be verified as follows. Ask the seated patient to place their hands on their knees, palms up. Then you need to quickly turn them over with your palms down and up again. The result should be a series of “shaking” movements, synchronous in both hands. If the test is positive, the patient becomes confused and synchrony is disrupted.

Missing, or hypermetry

This symptom manifests itself if you ask the patient to quickly hit an object with the index finger (for example, a neurologist’s hammer), the position of which is constantly changing. The second option is to hit a static, motionless target, but first with your eyes open and then with your eyes closed.

Scanned Speech

Symptoms speech disorders is nothing more than an intention tremor of the vocal apparatus. As a result, speech acquires an explosive, explosive character and loses its softness and smoothness.

Diffuse muscle hypotonia

Since the cerebellum regulates muscle tone, the cause of its diffuse decrease may be signs of ataxia. In this case, the muscles become flabby and sluggish. The joints become “wobbly” because the muscles do not limit the range of motion, and habitual and chronic subluxations may occur.

In addition to these symptoms, which are easy to check, cerebellar disorders can be manifested by changes in handwriting and other signs.

Causes of the disease

It should be said that the cerebellum is not always to blame for the development of ataxia, and the doctor’s task is to figure out at what level the damage occurred. Here are the most characteristic causes of the development of both the cerebellar form and ataxia outside the cerebellum:

• Damage to the posterior cords of the spinal cord. This causes sensory ataxia. Sensitive ataxia is so named because the patient has impaired joint-muscular sensation in the legs and is unable to walk normally in the dark until he can see his own legs. This condition is characteristic of funicular myelosis, which develops in a disease associated with a lack of vitamin B12.

• Extracerebellar ataxia can develop in diseases of the labyrinth. Thus, vestibular disorders and Meniere's disease can cause dizziness and falling, although the cerebellum is not involved in the pathological process;

• The appearance of neuroma of the vestibulocochlear nerve. This benign tumor may present with unilateral cerebellar symptoms.

The actual cerebellar causes of ataxia in adults and children can occur due to brain injuries, vascular diseases, and also due to a cerebellar tumor. But these isolated lesions are rare. More often, ataxia is accompanied by other symptoms, for example, hemiparesis, dysfunction of the pelvic organs. This happens with multiple sclerosis. If the process of demyelination is successfully treated, then the symptoms of cerebellar damage will regress.

Hereditary forms

However, there is a whole group of hereditary diseases in which the motor coordination system is predominantly affected. Such diseases include:

• Friedreich's spinal ataxia;
• hereditary cerebellar ataxia of Pierre Marie.

Cerebellar ataxia of Pierre Marie was previously considered a single disease, but now there are several variants of its course. What are the signs of this disease? This ataxia begins late, at the age of 3 or 4, and not at all in a child, as many people think. Despite the late onset, the symptoms of cerebellar ataxia are accompanied by speech impairment such as dysarthria and increased tendon reflexes. Symptoms are accompanied by spasticity of skeletal muscles.

Typically, the disease begins with a disturbance in gait, and then nystagmus begins, coordination in the hands is impaired, deep reflexes revive, and an increase in muscle tone develops. Poor prognosis occurs with optic nerve atrophy.

This disease is characterized by a decrease in memory, intelligence, as well as impaired control of emotions and volition. The course is steadily progressive, the prognosis is unfavorable.

Sometimes this hereditary ataxia is difficult to differentiate from a tumor of the posterior cranial fossa. But the absence of fundus congestion and intracranial hypertension syndrome allows a correct diagnosis to be made.

About treatment

Treatment of cerebellar ataxia, as a secondary syndrome, almost always depends on success in treating the underlying disease. If the disease progresses, for example, like hereditary ataxia, then in the later stages of the disease the prognosis is disappointing.

If, for example, as a result of a brain contusion in the occipital region, severe coordination disorders occur, then treatment of cerebellar ataxia can be successful if there is no hemorrhage in the cerebellum and there is no cell necrosis.

Very an important component treatment is vestibular gymnastics, which must be performed regularly. The cerebellum, like other tissues, is capable of “learning” and restoring new associative connections. This means that it is necessary to train coordination of movements not only with damage to the cerebellum, but also with strokes, diseases of the inner ear, and other lesions.

There are no folk remedies for cerebellar ataxia, because ethnoscience I had no idea about the cerebellum. The maximum that can be found here is remedies for dizziness, nausea and vomiting, that is, purely symptomatic remedies.

Therefore, if you have problems with gait, tremor, fine motor skills, then you should not put off visiting a neurologist: the disease is easier to prevent than to treat.