Inflammation of the cerebellum symptoms. Diagnosis of cerebellar disorders. The triad of symptoms of cerebellar damage includes

The cerebellum is a component of the brain that is located in the posterior cranial fossa. Above it rises the medulla oblongata and the pons. The cerebellum is separated from the occipital lobes of the brain by the tentorium, or in other words, by the tent. The tentorium is represented by a process of the dura mater of the brain. Connect with the brain stem - the part that is responsible for everything vital functions body, such as breathing and heartbeat, the cerebellum can thanks to the 3 legs that connect it to the trunk.

At birth, the mass of the cerebellum is approximately 5% of the total body mass, about 20 g. But with age, the volume of the cerebellum increases, and by 5 months the mass increases 3 times, and by 9 months it is approximately 4 times the original. In humans, by the age of 15, the cerebellum stops increasing in size and weighs approximately 150 g. The cerebellum has a similar structure to the cerebral hemispheres. It is even called the “little brain.” There are two surfaces in it:

• Upper;
• Bottom.

And also two edges:

• Front;
• Rear.

The cerebellum has 3 sections:

• Ancient – ​​hook;
• The old one is the vermis, which is located in the midline of the cerebellum;
• New - hemispheres, which are 2 in number, are located on the sides of the worm and imitate the hemispheres of the cerebrum. In evolutionary terms, this is the most developed structure of the cerebellum. Each hemisphere is divided into 3 lobes by grooves, with each lobe corresponding to a specific section of the worm.

Like the brain, the cerebellum has gray and white matter. Gray makes up the cortex, and white makes up the fibers, with the cerebellar nuclei located inside - globular, dentate, tegmental. These nuclei play an important role in the conduction of nerve pathways that do not cross in their path, or cross twice, which leads to the localization of signs of the disorder on the affected side. The nerve impulse traveling through the cerebellar nuclei is necessary for the cerebellum to perform its functions:

• Coordination of movements, their proportionality and smoothness;
• Maintaining body balance;
• Regulation of muscle tone, its redistribution and maintenance, which ensures adequate performance of the functions assigned to the muscles;
• Providing a center of gravity;
• Synchronization of movements;
• Anti-gravity.

Each of these functions plays a big role in a person’s life. When these functions are lost or impaired, characteristic symptoms appear that unite general term"cerebellar syndrome". This syndrome is characterized by disorders of a vegetative nature, motor sphere, muscle tone, which cannot but affect the patient’s quality of life. One of the components of the syndrome is ataxia.

Cerebellar ataxia

Ataxia is a disorder of coordination and motor function. This manifests itself in the form of disturbances in movement, gait and balance. Ataxia is accompanied by another group of symptoms specific to it. If they appear in a stationary position, then we're talking about about static ataxia, if during movement, then about dynamic. Ataxia has many forms and occurs in a wide variety of diseases. Separately, there is cerebellar ataxia, which is associated with pathological processes in the cerebellum.

IN neurological practice It is customary to divide cerebellar ataxia into the following types, depending on the nature of the process:

• Acute onset;
• Subacute onset (from 7 days to several weeks);
• Chronic progressive (developing over several months or years) and episodic (paroxysmal).

Cerebellar lesions that lead to the development of ataxia can be either congenital, genetically programmed, or acquired. The main causative factors of this disease are:

• Ischemic stroke caused by blockage of an artery with an atherosclerotic plaque, embolus or any other foreign body;
• Hemorrhagic stroke;
• Trauma as a consequence of traumatic brain injury;
• Intracerebral hematoma, which led to compression of intracerebellar structures;
• Multiple sclerosis;
• Guillain's syndrome;
• Inflammatory diseases of the brain – encephalitis;
• Obstructive hydrocephalus is dropsy of the brain caused by blockage of brain structures;
• Acute intoxications of various origins;
• Metabolic disorders.

The occurrence of a subacute form of ataxia is most often associated with an intracerebral tumor - astrocytoma, hemangioblastoma, medulloblastoma ependymoma. Moreover, the tumor is located in the cerebellum, compressing and destroying its structures. But not only tumors cause the subacute form of cerebellar ataxia. The reasons listed above can also cause it to occur.

The chronic form of ataxia is often the result of many years of alcoholism and chronic intoxication - substance abuse or drug addiction. Hereditary forms of ataxia are most often associated with genetic diseases:

• Friedreich's ataxia, manifested by disturbances in walking, speech, handwriting, and hearing. The disease is characterized by progressive muscle atrophy with involvement of the optic nerve in the degenerative process, which leads to blindness. Over a long period of time, intelligence decreases and dementia occurs;
• Hereditary cerebellar ataxia of Pierre-Marie, which has a high tendency to progression, consists of cerebellar hypoplasia, that is, its underdevelopment. This manifests itself as disturbances in gait, speech and facial expressions, involuntary muscle twitches, decreased strength in the limbs, twitching eyeballs. These symptoms are combined with depression and decreased intelligence. The disease usually makes itself felt around the age of 35;
• Holmes cerebellar atrophy;
• Tardive cerebellar ataxia or cortical cerebellar atrophy of Marie-Foy-Alajouanine;
• Olivopontocerebellar degeneration (OPCD).

Cerebellar ataxia and symptoms

The symptoms of ataxia are quite specific. It immediately catches your eye. It is very difficult to miss the occurrence of a disorder. The main characteristic symptoms for cerebellar ataxia are:

• Sweeping, uncertain, uncoordinated movements, as a result of which a person may fall;
• Unsteady gait that prevents you from walking in a straight line. Moreover, patients are so unsteady on their feet that they prefer to spread their legs wide for greater stability and balance with their hands;
• Involuntary stops of motor activity earlier than planned;
• Increased motor amplitude;
• Inability to stand upright;
• Involuntary swaying from side to side;
• Intention tremor, which is characterized by the absence of tremors at rest and intense tremor when moving;
• Nystagmus, which consists of involuntary twitching of the eyeballs;
• Adiadochokinesis, which is manifested by the patient’s inability to quickly perform alternating opposite motor acts. Such people cannot quickly perform the “unscrewing a light bulb” movement. Their hands will not move in concert;
• Impaired handwriting, which becomes uneven, sweeping and large;
• Dysarthria is a speech disorder in which speech loses its smoothness, slows down, and increased pauses appear between words. Speech is intermittent, chanted - the emphasis is on each syllable;
• Muscular hypotonia, that is, weakness with decreased deep reflexes.

In this case, the phenomena of ataxia increase significantly with a sudden change in the direction of movement, with standing up abruptly, when moving quickly. Depending on the nature of the manifestation, two types of ataxia are distinguished:

• Static, which manifests itself at rest. Patients find it difficult to maintain an upright posture;
• Dynamic, which is characterized by signs of disorder during movement.

Diagnostic tests for ataxia

Diagnosis of cerebellar ataxia is not difficult. For the study they carry out functional tests, which allow you to separate static ataxia from dynamic. Static ataxia is more clearly identified with the following tests:

• Romberg, in which the patient is asked to stand up straight, eyes closed and arms extended. There is instability and staggering. It is difficult for a person to maintain coordination. If you ask him to stand on one leg, it will be impossible without losing his balance;
• Walking along a conventional straight line is impossible. A person will deviate to the right or left, back or forward, but will not be able to walk straight along the line;
• Walking with a side step is impossible. Patients seem to dance while performing this movement, and the torso inevitably lags behind the limbs;
• “Stars”, which consists of sequentially taking 3 steps in a straight line, followed by 3 steps back along the same line. The test is carried out with open eyes, and then with closed ones;
• It is impossible to sit with your arms crossed on your chest when leaving a lying position. Normal cerebellar function ensures synchronous contraction of the trunk muscles, as well as posterior muscles hips. Static ataxia deprives the cerebellum of this ability, as a result of which a person is unable to sit down without helping himself with his hands; he falls back, while at the same time his leg rises. This symptom complex bears the name of the author, Babinsky.

To identify dynamic ataxia, the following tests are used:

• Finger-nasal, which is characterized by missing the mark when trying to hit the nose with a finger;
• Hitting the hammer is also difficult. The doctor asks the patient to hit the moving hammer with his finger;
• Heel-knee, the meaning of which is to suggest that the patient, lying on his back, hit the knee of the opposite leg with his heel and lower the heel with sliding movements to the foot of the other leg. Ataxia does not allow you to hit the knee and lower the heel smoothly evenly;
• “Twisting out the light bulb” is a characteristic hand movement that imitates this action. Patients wave their arms unevenly, wildly and roughly;
• To check the redundancy and disproportion of movements, ask the patient to extend his arms to a horizontal level, palms forward. The doctor's command to change the position of the palms down will not be successful. A clear 180° turn is simply impossible. In this case, one hand may rotate excessively, while the other lags behind;
• Finger Doynikova, which consists in the inability to bend the fingers and rotate the hand from a sitting position, when the hand is relaxed and lies on the knees, palms up;
• Finger-digital, in which the patient is asked to close his eyes and is asked to hit the ends index fingers, which are somewhat spaced and set aside. Missing and tremor are observed;

An examination by a neurologist reveals decreased muscle tone, nystagmus, dysarthria and tremor. In addition to the doctor's assessment, they use instrumental methods research. They are aimed at identifying changes in the cerebellum, in its structure - tumor nature, post-traumatic hematomas, congenital anomalies or degenerative changes in cerebellar tissue, compression and displacement of adjacent anatomical structures. Among these methods, the following are of great importance:

• Stabilography;
• Vestibulometry;
• Electronystagmography;
• Computed tomography (CT);
• Magnetic resonance imaging (MRI);
• Magnetic resonance angiography (MRA);
• Dopplerography of cerebral vessels.

Laboratory tests are used to identify infectious brain lesions:

• Blood analysis;
• PCR research;
• Lumbar puncture to examine the cerebrospinal fluid for infection or hemorrhage.

In addition, a DNA study is performed to determine the hereditary nature of ataxia. This diagnostic method allows us to identify the risk of having a baby with this pathology in a family where cases of cerebellar ataxia have been recorded.

Treatment of cerebellar ataxia

Treatment of any disease is aimed, first of all, at eliminating the cause of the disease. If ataxia is not genetic character, fundamental therapy should be directed against causative factor, be it a brain tumor, an infectious disease, a circulatory disorder. Depending on the cause, treatment will vary. However symptomatic therapy It has common features. The main drugs to eliminate signs of the disease include:

• Betahistine group drugs (Betaserc, Vestibo, Westinorm);
• Nootropic and antioxidants (Piracetam, Phenotropil, Picamilon, Phenibut, Cytoflavin, Cerebrolysin, Actovegin, Mexidol);
• Medicines that improve blood circulation (Cavinton, Pentoxifylline, Sermion);
• Vitamin B complexes, as well as their complexes (Milgamma, Neurobeks);
• Drugs that affect muscle tone (Mydocalm, Baclofen, Sirdalud);
• Anticonvulsants (Carbamazepine, Pregabalin).

Thus, in case of infectious-inflammatory genesis of the disease, antibacterial or antiviral therapy is prescribed. At vascular disorders drugs are prescribed that stabilize blood circulation - angioprotective agents, thrombolytics, antiplatelet agents and vasodilators, as well as anticoagulants. Ataxia, which is caused by intoxication, requires detoxification measures with intensive infusion therapy, diuretics and hemosorbic acid.

For ataxias with a hereditary nature of the lesion radical treatment does not exist. In these cases, metabolic therapy is prescribed:

• IN itamins B12, B6 or B1;
• Meldonium;
• Ginko biloba or piracetam preparations.

Cerebellar ataxia of a tumor nature often requires surgical resolution. Chemotherapy or radiation treatment depending on the type of neoplasm. Any treatment of ataxia is complemented by physiotherapy and massage. This helps prevent muscle atrophy and contractures. Classes are aimed at improving coordination and gait, as well as maintaining muscle tone.

In addition, a gymnastic complex is prescribed physical therapy, the purpose of which is to reduce incoordination of movements and strengthen muscle groups limbs. Severe clinical symptoms of the disease not only significantly reduce the patient’s quality of life, cerebellar ataxia is fraught with life-threatening consequences. Its complications include:

• Frequent repeated infectious processes;
• Chronic heart failure;
• Respiratory failure.

The prognosis of cerebellar ataxia syndrome depends entirely on the cause of its occurrence. Timely treatment of acute and subacute forms of ataxia caused by vascular pathology, intoxication, inflammation, leads to complete or partial restoration cerebellar functions. Often, it is not possible to completely cure ataxia. It has a poor prognosis due to the fact that the disease tends to progress.

The disease reduces the patient’s quality of life, causes multiple disorders other organs and systems. The first warning symptoms require a visit to a doctor. A timely diagnosis and initiation of treatment provide a much higher chance of restoring damaged functions or slowing down the process with a more favorable outcome than in the case of late treatment.

The most severe course is hereditary ataxia. They are characterized by chronic progression with an increase and aggravation of symptoms, which ends in the inevitable disability of the patient. There is no specific prophylaxis against ataxia. The development of the disease can be prevented by preventing injuries, vascular imbalances, intoxications, and infections. And when they appear - timely treatment.

Hereditary pathology can be avoided only through genetic consultation with a specialist about planning the birth of a child. To do this, collect the maximum amount of information about hereditary diseases in the family. They analyze possible risks and may take samples for DNA testing. All this allows us to preliminarily assess the possibility of having a child with genetic disease. Planning pregnancy is a prevention for many diseases.

Video

Coordination motor disorder caused by cerebellar pathology. Its main manifestations include gait disorder, disproportionality and asynergy of movements, dysdiadochokinesis, and changes in handwriting such as sweeping macrography. 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.

General information

Chronically progressive cerebellar ataxia is often a consequence of alcoholism and other chronic intoxications (including substance abuse and polydrug addiction), 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 malformation. Among the genetically determined progressive ataxias of the cerebellar type, the most famous are Friedreich's ataxia, non-Friedreich's spinocerebellar ataxia, Pierre-Marie's 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 a sharp change in the direction of movement or a rapid start of walking 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 median structures (the vermis), a fall 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 the patient in the Romberg position with open and eyes closed, shows that visual control does not particularly affect the test results. This feature of cerebellar ataxia helps differentiate it from sensory and vestibular ataxia, in which the lack of visual control leads to a significant worsening of coordination problems.

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 called tendon reflexes 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 from various fields are involved in its diagnosis: 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 can detect cerebellar tumors, post-traumatic hematomas, congenital anomalies and degenerative changes cerebellum, its prolapse into the foramen magnum and compression when adjacent 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 a pathology in a family where there have been cases of this disease can also be calculated.

Treatment of cerebellar ataxia

Treatment of the causative disease is fundamental. If cerebellar ataxia has an infectious-inflammatory genesis, it is necessary to prescribe an 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; V 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, patients are recommended to massage.

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 occlusion of the cerebrospinal fluid pathways 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 may completely regress or partially persist as residual effects. Chronically progressive, hereditary ataxias are characterized by an increasing worsening 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 pathologies of the cerebrospinal fluid system, chronic cerebral ischemia, Chiari syndrome, processes in the posterior cranial fossa.

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 top part cavity of the fourth 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 going to the cerebellum along the axons of the same neurons are sent to the bodies of second neurons, which are located in the internal sections of the base posterior 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 cortico-pontocerebellar ways, 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 of the internal capsule and end in the nuclei of the bridge. 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. Some of the impulses coming from the cerebellum, passing through the vestibular nuclei, enter the medial longitudinal fasciculus and reach nuclei III, IV and VI cranial nerves, providing movement 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. The patient with his eyes closed should move his hand away, and then, slowly, index finger touch the tip of your nose. 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, towards 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) at 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 - the patient’s gait with pronounced 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 absence of concomitant contraction gluteal muscles(manifestation of asynergy) the patient cannot fix his legs and pelvis on the support area, as a result, his 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 complex feedback regulatory mechanism, the cerebellum serves as a focal point for maintaining 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, the common feature of 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 (Gaulle) pathways and the spinocerebellar pathways of Gowers and Flexig, as well as the crossed pyramid path 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, hearing loss, elements of scanned speech, signs 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. Prescribe drugs that improve metabolism in structures nervous system, restoratives. 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 optic nerves and retinal pigmentary degeneration. 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 are more common akinetic-rigid syndrome and progressive autonomic failure. 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 as ataxia, dysarthria, dysphonia, muscle hypotonia, in 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, to which elements are subsequently added bulbar syndrome, paresis of facial muscles, 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, sporadic, progressive neurodegenerative disease called multiple system atrophy. 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 of clinical picture 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 manifests itself as developmental delay motor functions child (at the age of 6 months he cannot sit, begins to walk late, and the gait is ataxic), as well as speech delay, long-term persistence of dysarthria, and sometimes lag mental development, manifestations of microcrania are not uncommon. On CT, the cerebellar hemispheres are reduced. By about 10 years of age, compensation of brain functions usually occurs, which, however, can be disrupted under the influence of harmful exogenous influences. Progressive forms of the disease are also possible.

Manifestation congenital hypoplasia the cerebellum is and 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 by the German physician H. Feldmann, born 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, it is possible epileptic seizures and dementia. The prognosis is bad. Refers to rare forms 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 impaired 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 due to malignant tumor, without local signs indicating the place of its origin. Paraneoplastic cerebellar degeneration may, in particular, be a secondary manifestation of cancer mammary gland or ovaries.

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. The clinical picture boils 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 a family paroxysmal ataxia a decrease in the activity of pyruvate dehydrogenase of blood leukocytes was found to 50-60% of the normal level. 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. Occurs more often in children 1-2 weeks after a general infection (flu, 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).

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 appear motor disorders, changes in a person’s speech, handwriting, gait, 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 genetic pathology, called Marie's ataxia.

Important! Damage to the cerebellum can result from strokes, injuries, cancer, 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.

Cerebellum, i.e. hemorrhage due to a violation of the integrity of the vessel is a common cause of movement, speech, and eye symptoms. Hemorrhages into the cerebellar substance occur when 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.

The key symptom of cerebellar damage is. 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. , one of the symptoms of cerebellar damage, manifests itself in sweeping movements and excessive amplitude at the end.
2. – trembling 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 – involuntary movement eye.
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. Lumbar puncture performed to determine infection in the cerebrospinal fluid, as well as markers of stroke or inflammation. The head is held. 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. When 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 and radiation therapy, or surgical treatment. 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.

cerebellum ensures muscle tone, body balance, coordination, accuracy and proportionality of movements. Consists of two hemispheres and a worm. The worm contains the muscles of the trunk, and the hemispheres contain the muscles of the limbs. The worm provides static coordination of movements (postures), and the hemisphere provides dynamic coordination (movements of the limbs, walking). The cerebellum is connected to the spinal cord, cortex and brain stem by three pairs of peduncles: inferior, middle and superior. Through the lower and middle peduncles, the cerebellum receives information about the position of the body in space, and through the upper peduncles it sends impulses to the spinal cord, extrapyramidal system and cerebral cortex. As a result, information from the body's proprioceptors is combined in the cerebellum with information from the cortex and extrapyramidal system, which ensures smooth and precise movements. Symptoms of cerebellar damage Damage to the cerebellum is manifested by impaired coordination of movements, balance and muscle tone due to inconsistency in the work of antagonist muscles. Damage to the cerebellum is characterized by: ataxia; “drunk” gait (shaky, with legs spread wide apart); nystagmus - rhythmic twitching of the eyeballs when fixing gaze; cerebellar dysarthria (scanned speech: slow, monotonous, syllable-by-syllable); intention tremor (tremor in the limbs when moving, especially when approaching a target); adiadochokinesis; megalography (large, uneven handwriting); dysmetria; dizziness; decreased muscle tone

6. Sensitivity, its types. The structure of sensitivity pathways.

Sensitivity is the body’s ability to respond to signals from the external environment, its own organs and tissues. Irritations are perceived by receptors. A receptor is a sensor located in the skin, mucous membranes, muscles, ligaments, internal organs and blood vessels. It reacts to stimuli and encodes them into nerve impulses. There are three types of receptors: 1 exteroceptors– perceive pain, temperature and tactile irritations of the skin and mucous membranes; 2. proprioceptors– provide information about the relative positions of body parts; located in the musculoskeletal system: muscles, tendons, ligaments, joints; 3 interoreceptors– respond to pressure and chemical composition of blood and contents gastrointestinal tract; located in internal organs and blood vessels. According to the types of receptors, the following types are distinguished: general sensitivity: § superficial (pain, temperature, tactile); § deep (muscular-articular, vibration, pressure, mass); § complex species sensitivity (two-dimensional spatial, discriminatory, stereognosis, kinesthesia, sense of localization); § interoceptive (sensitivity of blood vessels and internal organs). Except general sensitivity, there are special sensitivity, arising in response to irritation from the outside of special sensory organs. This sensitivity includes vision, hearing, smell, and taste. The structure of sensitivity pathways. Sensory impulses are carried out by peripheral nerves. These nerves, with the exception of the intercostal nerves, form plexuses in their proximal section: the cervicobrachial and lumbosacral. The cells of the first neurons of all types of sensitivity are located in the intervertebral node. Their dendrites, as part of peripheral nerves, follow to the receptors of the trunk and limbs. The axons of the first neurons go to the spinal cord as part of the dorsal root. Fibers in the spinal cord various types sensitivities diverge. Conductors of deep sensitivity included in posterior cord spinal cord on its side, rise to the medulla oblongata and end on the cells of the second neuron (Gaull and Burdach nuclei). The axon of the second neuron passes to the opposite side and rises to the thalamus, where the third neuron is located. Surface Sensitivity Conductors as part of the dorsal root they enter into posterior horn spinal cord, where the second neuron is located. The axon of the second neuron passes to the opposite side and rises in the lateral funiculus to the thalamus (third neuron). Starting from the thalamus, the pathways of deep and superficial sensitivity are common - the axon of their third neuron ends in the posterior central gyrus.

7.Syndromes of sensory disorders, their diagnostic significance.

Peripheral– with damage to peripheral nerves and nerve plexuses. Manifested by hypoesthesia or anesthesia of all types of sensitivity in the area of ​​innervation of the nerve or plexus. Multiple lesions of peripheral nerves (polyneuropathy) cause a symmetrical disorder of all types of sensitivity in the distal parts of the extremities, like “gloves” and “socks”. Segmental– with damage to the dorsal roots, dorsal horns or sensory nuclei of the cranial nerves. When the dorsal roots are damaged in the area of ​​their innervation, all types of sensitivity are impaired, and pain appears along the root. When the posterior horns are damaged, a dissociated type of sensitivity disorder occurs: superficial sensitivity is lost while deep sensitivity is preserved. Conductive– occurs below the lesion of the sensory pathways in the brain or spinal cord. In this case, deep sensitivity is impaired on the side of the same name as the pathological focus, and superficial sensitivity is impaired on the opposite side.