Oculomotor nerve (n. Oculomotorius, III pair of FMN)

Strabismus It is commonly called strabismus when the visual axis of one eye is deviated from the point fixed by the other eye. Strabismus has two varieties: friendly and paralytic. Paralytic strabismus occurs as a result of

Strabismus

Strabismus In the past, strabismus was treated only with surgery, but now doctors prescribe surgery only as a last resort. It is proved that strabismus is a purely functional visual disturbance. If you relax the tight, tense muscles of the eyes,

Strabismus

STRABISMUS -I am; wed Disorder of vision, consisting in a violation of the coordination of eye movement - unequal orientation of the pupils. Strabismus. His K. completely imperceptibly. Diverging to. (away from the nose). Converging to. (towards the nose).

(strabismus), disorder of coordinated eye movement: when one eye is directed at an observed object, the other deviates toward the temple (divergent strabismus) or nose (convergent strabismus). It develops more often at the age of 3-4 years.

CLOSTER-eye (strabismus), disorder of coordinated eye movement: when one eye is directed at the object being examined, the other deviates toward the temple (divergent strabismus) or nose (convergent strabismus). It develops more often at the age of 3-4 years.

encyclopedic Dictionary. 2009 .

See what strabismus is in other dictionaries:

Strabismus ... Spelling Dictionary

Strabismus, kosin, kosink, strabism Dictionary of Russian synonyms. strabismus / slight: kosina, kosinka (dec.)) Dictionary of synonyms of the Russian language. A practical guide. M .: Russian language. Z. E. Alexandrova ... Synonym dictionary

- (strabismus) disorder of the coordinated movement of the eyes: when one eye is directed at the observed object, the other deviates towards the temple (divergent strabismus) or nose (convergent strabismus). It develops more often at the age of 3 to 4 years ... Big Encyclopedic Dictionary

CONCOVERY, strabismus, pl. no, cf. The unequal direction of the eye pupils. Explanatory Dictionary Ushakov. D.N. Ushakov. 1935 1940 ... Explanatory Dictionary of Ushakov

CLOSED-eye, I, cf. Disorder in the coordination of eye movement uneven direction of the pupils. Divergent to. (With deviation of the eye to the side of the nose). Converging to. (Towards the nose). Explanatory Dictionary Ozhegova. S.I. Ozhegov, N.Yu. Shvedova. 1949 1992 ... Explanatory Dictionary Ozhegova

strabismus - COSOGLAZIE1, decomp. Kosin, decomp. kosink razg. Scythe, slanting, razg. mowing decline cross-eyed COSOGLAZIE2, decomp. Kosin, decomp. kosink, decomp. squint ... Dictionary-thesaurus of synonyms of Russian speech

Main article: Eye diseases Strabismus In strabismus, the eyes cannot be directed to the same point in space ... Wikipedia

I (strabismus) deviation of the visual axis of one of the eyes from the joint fixation point. There are paralytic and friendly strabismus. Paralytic strabismus (Fig. 1) is caused by damage to the oculomotor, block, and abducent nerves, ... ... Medical Encyclopedia

STRABISMUS - honey. Strabismus is a pathology of the oculomotor apparatus, in which one eye deviates from a common fixation point with the other eye. The disease affects mainly children (1.5 to 2.5% of children). Classification and characterization of individual ... ... Disease Reference

STRABISMUS - Aluminum, 6, 12 and bvr feeling cold in the eyes, dry eyelids, burning in them. Ptosis of the eyelids. Strabismus. Dry mucous membranes and skin, muscle paresis. Strabismus due to loss of strength of the internal rectus muscle. Helzemium, 3x, 3 and bvr dysfunction of the oculomotor ... Handbook of Homeopathy

Books

• Children without glasses. Vision correction without drugs and a scalpel, Ilyinskaya MV. Before you - a unique guide to help solve vision problems that are most common in children. With the birth of a child joy comes to the house, especially if the baby ...

Ataxia is a violation of coordination of movements, not associated with muscle weakness. This applies to coordination of movements of the arms and legs, as well as gait (sometimes elements of ataxia are distinguished in breathing and speech). It is not an independent disease, it develops a second time, against the background of other diseases of the nervous system (traumatic brain injuries, cerebrovascular accident, intoxication (poisoning)), that is, it is a symptom (sign).

Kinds

Depending on the main location of the lesion of the central nervous system and the characteristics of ataxia, the cerebellar form of the disease associated with damage to the cerebellum is isolated. In turn, it is divided into three forms:

static — coordination is mainly disturbed when standing, which is expressed in instability, swinging from side to side — this makes a person stand with legs spread wide and balancing with his hands. There is a tendency to fall to the side or back;

static locomotor, which is expressed in the unsteadiness of the gait, swinging while walking;

kinetic, which manifests itself in a violation of coordination when performing precise actions with limbs (for example, touching a nose with a finger causes a strong waving of the hand when approaching the nose);

sensitive, which is associated with damage to the conduction pathways, providing the conduct of sensitive nerve impulses. Manifestations of ataxia (shakiness, impaired coordination of movements) are most pronounced with eyes closed (when there is no visual control over the execution of movements);

vestibular, associated with the defeat of the vestibular apparatus, providing balance and making peculiar adjustments when performing movements. It is manifested by impaired gait and coordination of movements, as well as dizziness with nausea, vomiting. Often in such patients, nystagmus can be detected (involuntary twitching eyeballs) and hearing impairment;

cortical, associated with damage to the cerebral cortex, which is responsible for voluntary movements. Most often, the frontal lobe is affected, and therefore this ataxia is also called frontal lobe. With frontal ataxia, a “drunken gait” is observed: a person goes “braiding” his legs, while the body deviates in the opposite direction from the lesion. This type of ataxia can be combined with other signs of damage to the cerebral cortex, such as a change in the psyche, impaired smell, auditory and olfactory hallucinations, memory impairment for current events.

The reasons

Brain diseases:

acute disturbance of cerebral circulation (in the vertebrobasilar pool, which provides blood to the brain stem, in which vital centers are located - vasomotor, respiratory);

brain tumors (especially in the brainstem) or cerebellum;

head injuries;

malformations of the skull and brain: for example, with Arnold-Chiari anomaly (dropping part of the cerebellum into the large opening of the skull, leading to compression of the brain stem);

hydrocephalus - excessive accumulation of cerebrospinal fluid in the ventricular system of the brain (cerebrospinal fluid, which provides nutrition and metabolism in the brain);

demyelinating diseases (accompanied by the breakdown of myelin (a protein that provides quick conduction of nerve impulses along the fibers): for example, multiple sclerosis (a disease in which many small foci of demyelination form in the brain and cerebellum), disseminated encephalomyelitis (a disease of presumably infectious nature, in which many foci of demyelination are formed in the brain and cerebellum).

Diseases of the vestibular apparatus (responsible for maintaining balance, as well as helping to carry out precise movements) or vestibular cranial nerves:

labyrinthitis - inflammation inner earaccompanied by severe dizziness, hearing loss, nausea, as well as general infections (fever, chills, headache);

vestibular neuronitis - inflammation of the vestibular nerves, manifested by a decrease in hearing and nystagmus;

vestibular nerve neuroma - a tumor of the membranes of the vestibular nerve, manifested by a decrease in hearing, nystagmus.

Poisoning: sleeping pills and potent drugs (benzodiazepines, barbiturates).

Vitamin B12 deficiency.

Hereditary diseases: for example, Louis Bar's ataxia-telangiectasia (manifested by ataxia, expansion of capillaries on the skin (telangiectasia) and a decrease in immunity), Friedreich ataxia (manifested by heart defects, weakness in the legs, ataxia and deformity of the foot in the form of an increase in its height).

Symptoms

Shakiness in a standing position: a person sways from side to side until falling to the side or back.

Violation of the gait (it becomes uncertain, shaky, as if a person "brings side to side") with a tendency to fall while walking to the side or back.

Impaired coordination of voluntary movements: when you try to perform an exact movement (for example, bring a mug of tea to your lips), a pronounced trembling of the limb (intentional tremor) occurs, which leads to inaccurate execution of actions.

Violation of the rhythm of speech: speech becomes abrupt, “chanting”.

Violation of the rhythm of breathing: breathing has the wrong rhythm, the intervals between breaths are constantly changing.

Symptoms associated with damage to adjacent parts of the brain, but not specifically related to ataxia, can also occur:

dizziness;

nausea and vomiting;

headache.

Diagnostics

Analysis of complaints and medical history:

How long have the first complaints of shaky gait, a lack of coordination of movements;

Did anyone have such complaints in the family;

Did the person take any medications (benzodiazepines, barbiturates).

Neurological examination: assessment of gait, coordination of movements with the help of special tests (finger-bearing and knee-calcaneal), assessment of muscle tone, strength in the limbs, the presence of nystagmus (oscillating rhythmic movements of the eyes from side to side).

Otolaryngologist examination: balance examination, ear examination, hearing assessment.

Toxicological analysis: search for signs of poisoning (residues of toxic substances).

Blood test: it is possible to detect signs of inflammation in the blood (increase in the sedimentation rate of red blood cells (red blood cells), the number of leukocytes (white blood cells)).

The concentration of vitamin B12 in the blood.

EEG (electroencephalography): the method evaluates the electrical activity of different parts of the brain, which changes with various diseases.

CT ( cT scan) and MRI (magnetic resonance imaging) of the head and spinal cord allow a layer-by-layer study of the structure of the brain, to reveal a violation of the structure of its tissue, as well as to determine the presence of ulcers, hemorrhages, tumors, foci of decay of the nervous tissue.

MRA (magnetic resonance angiography): the method allows to assess the patency and integrity of the arteries in the cranial cavity, as well as detect brain tumors.

Consultation of a neurosurgeon is also possible.

Treatment

Treatment should be directed to the cause of the ataxia.

Surgical treatment of the brain or cerebellum:

Tumor removal;

Hemorrhage removal;

Removal of an abscess, antibacterial therapy;

Decreased pressure in the posterior cranial fossa with Arnold-Chiari anomaly (dropping part of the cerebellum into the large opening of the skull, leading to compression of the brain stem);

Creating an outflow for cerebrospinal fluid (cerebrospinal fluid, providing nutrition and metabolism of the brain) with hydrocephalus (excessive accumulation of cerebrospinal fluid in the ventricular system).

Normalization of arterial (blood) pressure and drugs that improve cerebral blood flow and metabolism (angioprotectors, nootropics), in cases of cerebrovascular accident.

Antibiotic therapy for infectious lesions of the brain or inner ear.

Hormonal drugs (steroids) and plasmapheresis (removal of blood plasma with the preservation of blood cells) in demyelinating diseases (associated with the breakdown of myelin - the main protein of the membranes of nerve fibers).

Treatment of poisoning (the introduction of solutions, vitamins of groups B, C, A).

The introduction of vitamin B12 with its deficiency.

The consequences of non-interference and complications

Preservation of a neurological defect (unsteady gait, lack of coordination of movements).

Violation of social and labor adaptation.

Motoneurons of the oculomotor nerves (n. Oculomotorius, III pair of FMN) are located on both sides of the midline in the rostral part of the midbrain. The five external muscles of the eyeball innervate these nuclei of the oculomotor nerve, including the muscle that raises the upper eyelid. The nuclei of the oculomotor nerve also contain parasympathetic neurons (the Edinger-Westphal nucleus), which are involved in the processes of pupil narrowing and accommodation.

There is a division of supranuclear groups of motor neurons for each individual eye muscle. The fibers of the oculomotor nerve, innervating the medial straight, lower oblique and lower rectus muscles of the eye, are located on the same side. The suboconus of the oculomotor nerve for the superior rectus muscle is located on the contralateral side. The muscle that lifts the upper eyelid is innervated by the central group of cells of the oculomotor nerve.

Block nerve (n. Trochlearis, IV pair of FMN)

Motor neurons of the block nerve (n. Trochlearis, IV pair of FMN) are closely adjacent to the main part of the complex of nuclei of the oculomotor nerve. The left core of the block nerve innervates the right upper oblique muscle of the eye, the right core - the left upper oblique muscle of the eye.

Abducent nerve (n. Abducens, VI pair of FMN)

Motoneurons of the abduction nerve (n. Abducens, VI pair of FMN), innervating the lateral (external) rectus muscle of the eye on the same side, are located in the nucleus of the abduction nerve in the caudal part of the bridge. All three oculomotor nerves, leaving the brain stem, pass through the cavernous sinus and enter the orbit through the superior orbital fissure.

Clear binocular vision is provided precisely by the joint activity of individual eye muscles (oculomotor muscles). The friendly movements of the eyeballs are controlled by the supranuclear centers of the gaze and their connections. Functionally, there are five different supranuclear systems. These systems provide different kinds eyeball movements. Among them there are centers that control:

• saccadic (fast) eye movements
• targeted eye movements
• converging eye movements
• holding the gaze in a certain position
• vestibular centers

Saccadic (fast) eye movements

Saccadic (fast) movements of the eyeball arise as a command in the opposite visual field of the cortex of the frontal region of the brain (field 8). An exception is the fast (saccadic) movements that occur when the central fossa of the retina is irritated, which comes from the occipital-parietal region of the brain. These frontal and occipital control centers in the brain have projections on both sides of the supranuclear stem centers. The activity of these supranuclear stem centers of vision is also affected by the cerebellum and the complex of vestibular nuclei. The paracentral sections of the reticular formation of the bridge are the stem center, providing friendly fast (saccadic) eyeball movements. The simultaneous innervation of the internal (medial) direct and opposite external (lateral) rectus muscles during the horizontal movement of the eyeballs is provided by the medial longitudinal bundle. This medial longitudinal bundle connects the nucleus of the abduction nerve with the subnucleus of the complex of oculomotor nuclei, which are responsible for the innervation of the opposite internal (medial) rectus muscle of the eye. To begin vertical fast (saccadic) eye movements, bilateral stimulation of the paracentral sections of the reticular bridge formation from the cortical structures of the brain is required. The paracentral sections of the reticular formation of the bridge transmit signals from the brain stem to the supranuclear centers, which control the vertical movements of the eyeballs. Such a supranuclear center of eye movement includes the rostral interstitial nucleus of the medial longitudinal bundle located in the midbrain.

Targeted eye movements

The cortical center for smooth targeted or tracking movements of the eyeballs is located in the occipital-parietal region of the brain. Control is carried out on the same side, that is, the right occipital-parietal region of the brain controls smooth targeted movements of the eyes to the right.

Converging eye movements

The mechanisms for controlling converging movements are less understood, however, as you know, the neurons responsible for converging eye movements are located in the reticular formation of the midbrain surrounding the complex of nuclei of the oculomotor nerve. They give projections into the motor neurons of the internal (medial) rectus muscle of the eye.

Holding the gaze in a certain position

Stem centers of eye movement called neuronal integrators. They are responsible for keeping the gaze in a certain position. These centers change the incoming signals about the speed of movement of the eyeballs into information about their position. Neurons with this property are located in the bridge below (caudal) the nucleus of the abducent nerve.

Eye movement with a change in gravity and acceleration

The coordination of the movements of the eyeballs in response to changes in gravity and acceleration is carried out by the vestibular system (vestibuloocular reflex). In case of violation of the coordination of movements of both eyes, double vision develops, since images are projected onto disparate (inappropriate) parts of the retina. With congenital strabismus, or strabismus, an imbalance in the muscles leading to the incorrect positioning of the eyeballs (non-paralytic strabismus) can help the brain suppress one of the images. Such a decrease in visual acuity in a nonfixing eye is called amblyopia without anopsy. With paralytic strabism, double vision occurs as a result of paralysis of the muscles of the eyeball, usually due to damage to the oculomotor (III), block (IV) or abduction (VI) cranial nerves.

Muscles of the eyeball and eye paralysis

There are three types of paralysis of the external muscles of the eyeball:

Paralysis of individual muscles of the eye

Characteristic clinical manifestations occur with isolated damage to the oculomotor (III), block (IV) or abduction (VI) nerve.

Complete damage to the oculomotor (III) nerve leads to ptosis. Ptosis is manifested in the form of weakening (paresis) of the muscle that raises the upper eyelid and impaired voluntary movements of the eyeball up, down and inside, as well as divergent strabismus due to the preservation of the functions of the lateral (lateral) rectus muscle. In case of damage to the oculomotor (III) nerve, pupil dilation and its lack of response to light (iridoplegia) and accommodation paralysis (cycloplegia) also occur. Isolated paralysis of the muscles of the iris and ciliary body is called internal ophthalmoplegia.

Damage to the block (IV) nerve causes paralysis of the superior oblique muscle of the eye. Similar damage to the block (IV) nerve leads to the deviation of the eyeball outside and the difficulty of movement (paresis) of the gaze down. Paresis of the gaze down most clearly manifests itself when the eyes are turned inwards. Diplopia (double vision) disappears when the head is tilted to the opposite shoulder, in which there is a compensatory deviation of the intact eyeball inside.

Damage to the abduction (VI) nerve leads to paralysis of the muscles that divert the eyeball to the side. When the abduction (VI) nerve is damaged, a convergent strabismus develops due to the predominance of the influence of the tone of the normally working internal (medial) rectus muscle of the eye. In case of incomplete paralysis of the abduction (VI) nerve, the patient can turn his head towards the affected abduction muscle of the eye in order to eliminate his double vision by compensating for the weakened lateral (lateral) rectus muscle of the eye.

The severity of the above symptoms in case of damage to the oculomotor (III), block (IV) or abduction (VI) nerve will depend on the severity of the lesion and its location in the patient.

Friendly paralysis

The friendly gaze is the simultaneous movement of both eyes in one direction. An acute lesion of one of the frontal lobes, for example, with a cerebral infarction (ischemic stroke), can lead to transient paralysis of voluntary friendly eyeball movements in the horizontal direction. At the same time, independent eye movements in all directions will be completely preserved. Paralysis of voluntary friendly movements of the eyeballs in the horizontal direction is detected using the doll’s eye phenomenon with passive rotation of the head of a horizontally lying person or with the help of caloric stimulation (pouring cold water into the external auditory canal).

Unilateral damage to the paracentral section of the reticular formation of the bridge located downward at the level of the nucleus of the abduction nerve causes persistent paralysis of the gaze towards the lesion and loss of the oculocephalic reflex. The oculocephalic reflex is a motor reaction of the eyes to irritation of the vestibular apparatus, as in the case of the doll’s head and eyes or caloric stimulation of the walls of the external auditory canal with cold water.

Damage to the rostral interstitial nucleus of the medial longitudinal bundle in the anterior part of the midbrain and / or damage to the posterior commissure cause supranuclear paralysis of the gaze upward. To this focal neurological symptom, the dissociated reaction of the patient's pupils to the light is added:

• sluggish reaction of the pupils to the light
• rapid reaction of pupils to accommodation (changing the focal length of the eye) and looking at closely located objects

In some cases, the patient also develops convergence paralysis (eye movement towards each other, in which the gaze will focus on the bridge of the nose). This symptom complex is called Parino syndrome. Parino's syndrome occurs with tumors in the area pineal gland, in some cases with cerebral infarction (ischemic stroke), multiple sclerosis and hydrocephalus.

Isolated gaze palsy is rare in patients. When this happens, the cause is most often a blockage of the lumen (occlusion) of the penetrating arteries of the midline and bilateral heart attacks (ischemic strokes) of the midbrain. Some hereditary extrapyramidal diseases (Huntington's chorea, progressive supranuclear palsy) can cause restrictions on the movements of the eyeballs in all directions, especially up.

Mixed paralysis of the gaze and individual muscles of the eyeball

The simultaneous combination in a patient of paralysis of the gaze and paralysis of the individual muscles moving the eyeball is usually a sign of damage to the midbrain or brain bridge. Damage to the lower parts of the brain bridge with the destruction of the nuclei of the abduction nerve located there can lead to paralysis of the fast (saccadic) horizontal movements of the eyeballs and paralysis of the lateral (external) rectus muscle of the eye (abduction nerve, VI) on the affected side.

With lesions of the medial longitudinal beam, various disorders of the gaze arise in the horizontal direction (internuclear ophthalmoplegia).

Unilateral damage to the medial longitudinal bundle caused by a heart attack (ischemic stroke) or demyelination leads to impaired adduction of the eyeball inside (to the nose). This can be clinically manifested in the form of complete paralysis with the inability to move the eyeball inward from the midline, or in the form of moderate paresis, which manifests itself in the form of a decrease in the speed of leading fast (saccadic) eye movements to the bridge of the nose (leading (adduction) delay). On the side opposite to the defeat of the medial longitudinal bundle, as a rule, abduction (abduction) nystagmus is observed: nystagmus that occurs when the eyeballs are pulled outwards with a slow phase directed towards the midline and with fast horizontal saccadic movements. The asymmetric arrangement of the eyeballs relative to the vertical line often develops with unilateral internuclear ophthalmoplegia. On the affected side of the eye will be located higher (hypertropy).

Bilateral internuclear ophthalmoplegia occurs with demyelinating processes, tumors, heart attacks or arteriovenous malformations. Bilateral internuclear ophthalmoplegia leads to a more complete disorder of the movements of the eyeballs, which are manifested by bilateral paresis of the muscles leading the eyeball to the nose, impaired vertical movements, tracking targeted movements and movements due to the influence of the vestibular system. Violation of the gaze in a vertical line, nystagmus up when looking up and nystagmus down when looking down are noted. Lesions of the medial longitudinal bundle in the overlying (rostral) parts of the midbrain are accompanied by a violation of convergence (converging eye movement towards each other, towards the nose).

strabismus / slight: kosina, kosinka (dec.)) Dictionary of synonyms of the Russian language. A practical guide. M .: Russian language. Z. E. Alexandrova ... Dictionary of synonyms

CLOSE-eyed - (strabismus) disorder of coordinated eye movement: when one eye is pointing at a surveyed object, the other deviates toward the temple (divergent strabismus) or nose (convergent strabismus). Develops more often at the age of 3 4 years ... Big Encyclopedic Dictionary

CLOSE-EYE - CLOSE-EYE, squint, pl. no, cf. The unequal direction of the eye pupils. Explanatory Dictionary Ushakov. D.N. Ushakov. ... Explanatory dictionary of Ushakov

COGLOGUE - COGLOGUE, I, cf. Disorder in the coordination of eye movement uneven direction of the pupils. Divergent to. (With deviation of the eye to the side of the nose). Converging to. (Towards the nose). Explanatory Dictionary Ozhegova. S.I. Ozhegov, N.Yu. Shvedova. ... Explanatory Dictionary Ozhegova

strabismus - COSOGLAISE1, dis. Kosin, decomp. kosink razg. Scythe, slanting, razg. mowing decline cross-eyed COSOGLAZIE2, decomp. Kosin, decomp. kosink, decomp. squint ... Dictionary-thesaurus of synonyms of Russian speech

Strabismus - Main article: Eye diseases Strabismus In strabismus, eyes cannot be directed to the same point in space ... Wikipedia

Strabismus - I (strabismus) deviation of the visual axis of one of the eyes from the joint fixation point. There are paralytic and friendly strabismus. Paralytic strabismus (Fig. 1) is caused by damage to the oculomotor, block and abducent nerves, ... ... Medical Encyclopedia

CONCOVERY - honey. Strabismus is a pathology of the oculomotor apparatus, in which one eye deviates from a common fixation point with the other eye. The disease affects mainly children (1.5 to 2.5% of children). Classification and characterization of individual ... ... Handbook of Diseases

CONCOVERY - Alumina, 6, 12 and bvr feeling cold in the eyes, dry eyelids, burning in them. Ptosis of the eyelids. Strabismus. Dry mucous membranes and skin, muscle paresis. Strabismus due to loss of strength of the internal rectus muscle. Helzemium, 3x, 3 and bvr dysfunction of the oculomotor ... Homeopathy Reference

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Coordination of movements - causes and symptoms of impaired coordination of movements, as well as exercises for its development

What is coordination of movements

With the development of motor skill, coordination of movements is modified, including the development of the inertia of moving organs. Initially, control occurs due to the active static fixation of these organs, then - due to short-term physical impulses directed at a certain moment to the desired muscle.

At the final stages of coordination, inertial movements are used. In the already established dynamically stable movement, the balancing of all inertial movements occurs automatically, without producing additional correction pulses.

The coordination of movements is given to a person so that he can perform clear movements and control them. If a lack of coordination occurs, this indicates changes in the central nervous system.

Our central nervous system is a complex, interconnected formation of nerve cells located in the spinal cord and brain.

When we want to make any movement, the brain sends a signal, and in response to it, limbs, trunk or other parts of the body begin to move. If the central nervous system works unsteadily, if deviations occur in it, the signal does not reach the target or is transmitted in a distorted form.

Causes of impaired coordination

There are many reasons for the violation of coordination of movement. These include the following factors:

• physical exhaustion of the body;
• exposure to alcohol-containing, narcotic and other toxic substances;
• brain injuries;
• sclerotic changes;
• muscular dystrophy;
• parkinson's disease;
• ischemic stroke;
• catalepsy is a rare occurrence in which the muscle weakens due to an explosion of emotions, say, anger or rapture.

Violation of coordination is considered a deviation dangerous for a person, because in this state nothing costs to get injured. Often this is accompanied by old age, as well as past neurological diseases, a striking example of which in this case is stroke.

Impaired coordination of movements also occurs with diseases of the musculoskeletal system (with poor coordination of muscles, weakness in the muscles of the lower extremities, etc.) If you look at such a patient, it becomes noticeable that it is difficult to maintain an upright position, to walk.

In addition, impaired coordination of movements can be a symptom of the following diseases:

Signs of impaired coordination

People with similar ailments move insecurely, slowness, too large amplitude, inconsistency are visible in the movements. Trying to outline an imaginary circle in the air, a person is faced with a problem - instead of a circle, he gets a broken line, a zigzag.

Another test for impaired coordination is that the patient is asked to touch the tip of the nose, and he also fails.

By looking at the patient’s handwriting, you will also see that his muscle control is not all right, as letters and lines creep into each other, become uneven, inaccurate.

Symptoms of impaired coordination of movements

The following symptoms of impaired motor coordination are:

Shaky movements

this symptom manifests itself when the muscles of the body are weakened, especially the limbs. Patient movements become inconsistent. When walking, he sways a lot, the steps become sharp, have different lengths.

Tremor

Tremor - trembling hands or head. There is a strong and almost imperceptible tremor. In some patients, it begins only in the process of movement, in others - only when they are motionless. With severe anxiety, tremor increases; shaky, uneven movements. When the muscles of the body are weakened, the limbs do not receive a sufficient basis during movements. The patient steps unevenly, intermittently, the steps have different lengths, he sways.

Ataxia

Ataxia - caused by damage to the frontal parts of the brain, cerebellum, nerve fibers that transmit a signal through the channels of the spinal cord and brain. Doctors distinguish between static and dynamic ataxia. With static ataxia, a person cannot maintain balance in a standing position, while with dynamic ataxia it is difficult for him to move balanced.

Coordination tests

Unfortunately, many people have poor coordination. If you want to test yourself, we offer you a very simple test.

Test number 1

To do this, you need to perform an exercise while standing. Try pushing your socks and heels together while your eyes are closed.

Test number 2

Another option to check your coordination of movements is to sit on a chair and raise your right leg up. Rotate the foot clockwise, and at the same time draw the letter “b” with your right hand, imitating its silhouette in the air, starting to perform with the “tail” of the letter.

Test number 3

Try putting your hand on your stomach and stroking it clockwise, and with your other hand, tap yourself on the head. If as a result of the test you completed all the tasks the first time - this is an excellent result. We congratulate you! You have a good coordination. But if you were unable to immediately perfectly perform all of the above, do not despair!

Exercises for the development of coordination of movements

The greatest effect can be achieved if coordination is developed from 6-10 years. During this period, the child develops, learns agility, speed, accuracy, coordinating his movements in games and exercises.

You can develop coordination of movements with the help of special exercises and trainings, thanks to Pilates, break exercises, and also with the help of other sports that involve various objects (fitball, dumbbells, jump ropes, medical balls, sticks, etc.)

Coordination exercises can be performed anywhere, for example:

In transport

Do not look for free space, but rather stand still and do the exercise. Spread your feet shoulder-width apart and try not to hold onto the handrails of the car during the journey. Perform the exercise carefully so that when you stop abruptly, you will not roll to the floor. Well, let surprised passengers look at you, but soon you will have excellent coordination!

On the stepladder

Holding hands on a stepladder, climb up and go down. As soon as you have rehearsed several ascents and descents, try the same exercise, but without the help of your hands.

Standing on the floor

You will need an apple in each hand. Imagine you are in a circus arena and juggling. Your task is to throw the apples up and at the same time catch them again. You can complicate the task by throwing both apples at the same time. As soon as you get the hang of throwing both apples and catching them with the hand that made the throw, proceed to the complicated version of the exercise. Follow the same movement, but you should catch the apple with the other hand, with your arms crossed.

On a narrow curb

On a narrow curb, you can perform a series of exercises that coordinate your movements. Find a narrow curb and walk on it daily until your gait becomes like a cat - graceful, smooth and beautiful.

There are a number of coordination exercises that you can perform daily:

• do somersaults forward, backward;
• running, jumping and various relay races with a skipping rope;
• combining several exercises into one, for example, somersault and catching the ball;
• hitting the target with the ball.

Using the ball: hitting the wall and catching it, hitting the ball on the floor, throwing the ball from the chest to the partner in different directions (in this exercise you need to not only throw the ball, but also catch it in the same unpredictable directions).

Which doctors should I contact if there is a violation of coordination of movements:

Questions and answers on the topic "Coordination of movements"

Question: Tell me, if I remove my meningioma, will coordination be adjusted? Or is it a cervical affair, where I also have a problem with hernias?

Question: Good day. I can’t understand what it is. Coordination abruptly disappears, then it appears and everything is fine. I do not fall. Physically fit, doing sports.

Question: Hello! I have a problem with coordination of movements. I constantly hit the doorposts, I just can’t “fit in” the door (it seems to bring me in). In public transport it’s difficult to stand, constantly hanging out like a rag in the wind, falling on every bump. Could this be a consequence of osteochondrosis (I have it for 4 years, the cervical spine), or is it just a bad vestibular apparatus and inattention?

Question: Hello. I am sick for about 2 years (I'm 25 years old). Lack of coordination of movement, dizziness when walking. Sitting, lying, with head turns I do not feel dizzy. There was a strange sensation in my head, spasm of blood vessels, at such moments it seemed to me I could lose consciousness. There was a feeling of fear. Please answer me, what makes you dizzy and how to treat? Is there enough evidence to say that the cause is osteochondrosis of the cervical spine.

Question: Good day! What are the coordination tests?

Question: Hello! How to improve coordination of movements? Thank.

EQUILIBRIUM DISORDERS

Balance - the ability to maintain the orientation of the body and its parts in relation to the surrounding space. It depends on the continuous flow of visual, vestibular and somatosensory (proprioceptive) impulses and its integration at the level of the brain stem and cerebellum.

Balance disorders occur due to damage to the central or peripheral vestibular structures, cerebellum, or sensory pathways providing proprioception.

Such disorders are usually manifested by at least one of two clinical symptoms: dizziness or ataxia.

DIZZINESS

Dizziness (vertigo) A sensation of movement of the body or surrounding space. It can be combined with other symptoms, such as an impulse (a sensation of a displacement of the body in space due to external forces), oscillosis ( visual illusion vibrational movement), nausea, vomiting, ataxia of walking.

Differences between dizziness and other symptoms

Dizziness (vertigo) should be differentiated with bribery symptoms resembling dizziness, but unlike it, not accompanied by the illusion of movement (for example, fainting states, a feeling of “fog in the head”, etc.). Such sensations are usually associated with a violation of the supply of the brain with blood, oxygen or glucose - due to hyperactivation vagus nerveorthostatic hypotension, cardiac arrhythmias, myocardial ischemia, hypoxia or hypoglycemia. The culmination of these phenomena can be loss of consciousness (fainting).

Having diagnosed dizziness, it is first of all necessary to decide whether it is caused by damage to peripheral or central vestibular structures.

Peripheral dizziness may be associated with damage to the labyrinth of the inner ear or the vestibular portion of the cochleovestibular (VIII) nerve. Central dizziness is caused by damage to the vestibular nuclei of the brain stem or their connections. Dizziness is occasionally of cortical origin, arising as a manifestation of a complex partial seizure.

Clinical manifestations

1. Peripheral dizziness is usually intermittent in nature and is short-lived, but more intense than central dizziness. Peripheral dizziness is almost always accompanied by nystagmus (rhythmic twitching of the eyeballs), which in this case usually has a unidirectional character and is never vertical (see below). Damage to peripheral vestibular structures often causes additional symptoms associated with pathology of the inner ear or auditory nerve, that is, hearing loss and noise in the ear.
2. Central dizziness is not always accompanied by nystagmus. If it occurs, it can be vertical, unidirectional or multidirectional, as well as asymmetric - differing in character in both eyes. (Vertical nystagmus - twitching of the eyeballs in a vertical plane). Central lesions can be manifested by symptoms of damage to the brain stem or cerebellum, for example, paresis, hypesthesia, revitalization of reflexes, pathological stop signs, dysarthria or ataxia of the extremities.

Peripheral and central vestibular structures. The vestibular portion of the VIII nerve terminates in the vestibular nuclei of the brain stem and the median structures of the cerebellum, which, in turn, also project onto the vestibular nuclei. From them, the fibers in the medial longitudinal bundle ascend to the nuclei of the abducent and oculomotor nerves on both sides, and also follow down to the spinal cord.

ATAXIA

Ataxia is a violation of coordination of movements, not associated with muscle weakness. It can be caused by pathology of the vestibular structures, the cerebellum or a violation of deep sensitivity (proprioreception). Ataxia can disrupt eye movements, speech (causing dysarthria), movements of individual limbs, torso, the function of maintaining balance and walking.

Vestibular ataxia

Vestibular ataxia is caused by the same peripheral or central lesions as dizziness. Nystagmus is often detected in patients, it usually has a one-sided character and is more pronounced when looking in the direction opposite to the lesion. Dysarthria is absent. Vestibular ataxia depends on the position of the body in the gravitational field: coordination disorders are absent when the patient is lying, but appear as soon as he tries to get up or start walking.

Cerebellar ataxia

Cerebellar ataxia is caused by damage to the cerebellum, as well as its efferent or afferent connections in the cerebellum legs, red nucleus, bridge, or spinal cord. There are crossed connections between the frontal cortex and cerebellum, therefore, the unilateral pathology of the frontal cortex can mimic the symptoms of damage to the opposite hemisphere of the cerebellum. Cerebellar ataxia is manifested by a violation of the proportionality of speed, rhythm, amplitude and strength of voluntary movements.

A. Muscular hypotension

Cerebellar ataxia is usually accompanied by muscle hypotension, which results in impaired ability to maintain a posture. When checking the strength, the patient's resistance is overcome by a relatively small effort, and when shaking, the limb makes movements with increased amplitude. The range of hand movements when walking can also increase. Tendon reflexes become pendulum-like: after the reflex is invoked, the limb makes several oscillatory movements, although the strength and speed of the reflex movement do not increase. If the patient tries to make a movement against the resistance, which is then removed, then the tensed muscles do not have time to relax, and the antagonist muscles turn on, which leads to excessive ricocheting movement (a symptom of the absence of a backward push).

B. Lack of coordination of movements

In addition to muscle hypotension, cerebellar ataxia is characterized by impaired coordination of voluntary movements. Simple movements are delayed; their acceleration and braking do not occur on time. Speed, rhythm, amplitude and strength of movements are characterized by inconstancy, as a result of which their smoothness is disturbed. Since disproportionality of movements is most pronounced during the beginning and end of movement, the most noticeable clinical manifestations of ataxia are terminal dysmetria (miss) with targeted movement and intentional tremor, which appears as the limb approaches the target. More complex movements are not performed as a single motor act, but are split into a series of consecutive separate movements (decomposition of movements). Movements that require simultaneous contraction of several muscle groups (asynergy) are disrupted. The most physiologically complex movements, such as walking, as well as movements involving rapid changes in direction, suffer most.

B. Concomitant oculomotor disorders

The cerebellum plays a significant role in controlling the movement of the eyes, so when it is damaged, oculomotor disorders often occur. Most often, nystagmus and other oscillatory eye movements, paralysis of the gaze, violations of saccadic and tracking movements are noted.

G. The relationship of cerebellar symptoms with the localization of the lesion

Different anatomical areas of the cerebellum perform different functions, which corresponds to the somatotopic organization of their motor, sensory, visual and auditory connections.

1. Damage to the median structures of the cerebellum.

The middle region of the cerebellum - the worm, the flocculo-nodular lobe and the subcortical nuclei (tent nuclei) associated with them - is involved in the control of axial motor functions, including eye movements, position of the head and body, statics and walking. Therefore, with damage to the median structures, nystagmus and other oculomotor disorders, vibrational movements of the head and body (titubation), a violation of statics, and ataxia of walking occur. With selective damage to the upper part of the cerebellar worm (which, for example, is often observed with alcoholic cerebellar degeneration), walking ataxia is the dominant or only clinical manifestation, as follows from the somatotopic map of the cerebellum.

2. Damage to the cerebellar hemispheres.

The cerebellar hemispheres are involved in coordinating movements and maintaining muscle tone in the ipsilateral limbs. In addition, they provide regulation of the gaze in the ipsilateral direction. Lesions of the cerebellar hemisphere cause ipsilateral hemataxia and hypotension of the ipsilateral limbs, nystagmus and transient paresis of the gaze in the ipsilateral direction. With paramedian lesions of the left cerebellar hemisphere, dysarthria may occur.

3. Diffuse lesion of the cerebellum.

Many diseases, usually of metabolic or degenerative origin, as well as intoxication, are characterized by diffuse damage to the cerebellum. In such cases clinical picture consists of the symptoms characteristic of damage to the median structures and both cerebellar hemispheres.

SENSITIVE ATAXIA

Pathways of deep (proprioceptive) sensitivity

Sensitive ataxia develops as a result of damage to fibers carrying proprioceptive impulses, consisting of peripheral nerves, posterior roots, posterior columns of the spinal cord, and medial loop. Rare causes of sensitive hemataxia are lesions of the thalamus and parietal lobe on the contralateral side. The articular-muscular feeling is provided by the receptor apparatus represented by Pacini bodies, unencapsulated nerve endings in the capsules of the joints, ligaments, muscles and periosteum. Impulses from receptors follow thick myelinated type A fibers, which are processes of sensory neurons of the first order. These fibers enter the posterior horn of the spinal cord and, without crossing, ascend as part of the posterior pillars. Proprioceptive information from the lower extremities is carried out along the medially located thin bundle, and from the upper extremities - along the more laterally located wedge-shaped bundle. The fibers traveling in these pathways form synapses with second-order sensory neurons that form the nuclei of the thin and wedge-shaped bundles in the lower part of the medulla oblongata. The processes of the 2nd order neurons cross and then rise as part of the contralateral medial loop to the ventral posterior nucleus of the thalamus, where the 3rd order sensory neurons are located, connected with the cortex of the parietal lobe.

Sensitive ataxia with polyneuropathies or damage to the posterior pillars usually causes a symmetrical disturbance in walking and lower limb movements; upper limb movements usually suffer less or remain normal. On examination, a violation of the joint-muscle feeling and vibration sensitivity is detected. Characteristic is the absence of dizziness, nystagmus and dysarthria.

PERIPHERAL VESTIBULAR DISORDERS

POSITIVE POSITIVE HEADING

Benign positional dizziness (benign positional vesiculopathy) occurs with a certain position of the head. Usually positional dizziness is characteristic of damage to peripheral vestibular structures, but it can also have a central origin, arising from damage to the brain stem and cerebellum.

Benign positional dizziness is the most common cause of peripheral dizziness, which accounts for about 30% of its cases. Of the established causes, the most common is traumatic brain injury, but in most cases benign positional dizziness occurs in the absence of any obvious cause. The pathophysiological basis of the disease is considered to be canalolithiasis - the presence in the endolymph of one of the semicircular canals of particles, which at a certain position of the head irritate its receptors.

The disease is characterized by short-term (from several seconds to several minutes) episodes of severe dizziness, which may be accompanied by nausea and vomiting. Symptoms can occur with any change in the position of the head, but are usually most pronounced when the patient, turning on his side, lies on the affected ear. Dizziness episodes usually occur within a few weeks, after which spontaneous remission occurs. In some cases, dizziness recurs. Hearing loss is not characteristic.

Peripheral and central positional dizziness are differentiated using the Nilen-Barani test (Dix-Holpike. With benign positional dizziness, positional nystagmus is almost always observed, which is usually unidirectional, has a rotator component and occurs with a delay of several seconds after the head takes the position that causes dizziness. If the head position does not change, then dizziness and nystagmus disappear after a few seconds or minutes. When the test is repeated, the severity of symptoms decreases. In contrast, central positional dizziness is usually less pronounced and may not be accompanied by positional nystagmus. There is no delay in the occurrence of nystagmus in the current positional dizziness; there is no depletion of symptoms while maintaining the posture and addiction when repeating the test.

In most cases, benign peripheral positional dizziness (canalolithiasis) therapeutic effect it is possible to achieve using repositional techniques, the purpose of which is to remove particles suspended in the endolymph from the semicircular canal under the action of gravity, moving them on the eve of where they can be reabsorbed. One of these methods is that the patient’s head is turned 45 ° towards the affected ear (the side is clinically determined according to the signs described above), after which the patient is laid on his back so that the head (remaining turned 45 °) hangs from the edge of the couch. Then the thrown back head is turned 90 °, as a result of which it turns out to be turned in the opposite direction at an angle of 45 °. After this, the patient is turned on his side, while the affected ear is on top, and the head remains thrown back and turned 45 ° towards the healthy ear. Finally, the patient rolls onto his stomach and sits down.

Reposition therapy regimen

In the acute period, vestibulolytic agents may be effective. Recovery is accelerated using vestibular rehabilitation techniques that compensate for impaired vestibular function due to other sensory modalities. According to some studies, recovery also accelerates betahistine dihydrochloride, which helps normalize functional state histaminergic vestibular neurons.

MENIER'S DISEASE

Meniere's disease is characterized by repeated episodes of dizziness lasting from several minutes to several days, accompanied by tinnitus and progressive sensorineural hearing loss. Most cases are sporadic, but family cases are also described, for which the phenomenon of anticipation is characteristic - with each generation, the age of the manifestation of the disease decreases. Some family cases are associated with a mutation of the cochlin gene on the 14th chromosome (locus 14 ql 2-ql 3). Approximately at 15% cases, the disease appears between the ages of 20 to 50 years. Men get sick more often than women. The cause of Meniere's disease is considered to be an increase in the volume of the endolymph in the labyrinth (endolymphatic dropsy), but the pathogenetic mechanisms remain unclear.

Even before the first attack, patients may notice a gradual increase in noise and a feeling of stuffiness in the ear, hearing loss. The attack is manifested by dizziness, nausea, and vomiting. The intervals between seizures vary from a few weeks to several years. Hearing deteriorates stepwise. 10-70% of patients have a bilateral process. As hearing loss decreases, the severity of dizziness decreases.

During an attack during examination, spontaneous horizontal or rotatory nystagmus is detected, the direction of which can change. Although in the interictal period, spontaneous nystagmus is usually absent, the caloric test reveals a violation of vestibular function. Hearing impairment may not be significant enough to be detected during a routine examination. However, audiometry usually reveals an increase in the threshold of perception of low-frequency tones, which can fluctuate, as well as a violation of word discrimination and increased sensitivity to loud sounds. As already noted, dizziness attacks usually subside as hearing loss builds up.

Treatment is with diuretics, for example, hydrochlorothiazide or triamteren. It is possible to use betagestin dihydrochloride, which, by enhancing histaminergic transmission in the vestibular system and improving the blood supply of the labyrinth, according to some reports, reduces the severity of dizziness. In severe cases that are resistant to drug therapy, they resort to surgical treatment: endolymphatic bypass, labyrinthectomy, or resection of the vestibular portion of the VIII nerve.

ACUTE PERIPHERAL VESTIBULOPATHY

The term is used to refer to spontaneous episodes of dizziness of unknown origin, independently regressing and not accompanied by hearing loss or signs of central nervous system dysfunction. This group includes disorders designated as acute labyrinthitis or vestibular neuronitis - these terms reflect inadequate assumptions about the localization of the disease or its nature. Nevertheless, sometimes vestibulopathy occurs after a recent illness with a febrile illness.

Acute peripheral vestibulopathy is characterized by acute onset of dizziness, nausea and vomiting, which usually lasts up to 2 weeks. Sometimes the sim tomato recurs. After regression of the main symptoms, persistent moderate vestibular dysfunction may persist.

In the acute phase, the patient usually lies on his side with the affected ear facing up and tries not to move his head. Nystagmus is always determined, the fast phase of which is directed to the side opposite to the affected ear. A caloric test reveals changes on one or both sides with approximately the same frequency. Hearing does not suffer.

Acute peripheral vestibulopathy should be differentiated from central disorders causing acute dizziness, for example, circulatory disorders in the pool of the posterior cerebral artery. The central genesis of the disease can be judged by the presence of vertical nystagmus, impaired consciousness, motor functions or sensitivity, dysarthria. Treatment includes the use of glucocorticoids, as well as betahistine dihydrochloride and other drugs.

OTOSCLEROSIS

Otosclerosis is characterized by impaired mobility of the stapes, a small bone in the ear that transmits vibration of the eardrum to other structures of the inner ear. The main manifestation of the disease is conductive hearing loss, however, sensorineural hearing loss and dizziness are also possible. Tinnitus is infrequent. Hearing often begins to decline to 30 years. Often there is a family history.

Vestibular dysfunction is most often manifested by repeated episodes of dizziness, sometimes having a positional character, as well as a sense of instability when changing posture. Over time, symptoms may become more permanent, and the frequency and severity of seizures may increase. On examination, manifestations of vestibular dysfunction, such as spontaneous or positional peripheral nystagmus, a decrease in the reaction in a caloric test, which usually have a one-sided character, can be detected.

With audiometry, a decrease in hearing is always determined, usually of a mixed nature with elements of conductive and sensorineural hearing loss, in about two thirds of cases it is bilateral. In the presence of episodes of dizziness, progressive hearing loss and tinnitus, the disease should be differentiated from Meniere's disease. Otosclerosis is more characteristic of a burdened family history, the onset of symptoms at an earlier age, the presence of a conductive component of hearing loss, bilateral symmetrical hearing loss. Diagnosis is facilitated by imaging techniques.

The combination of sodium fluoride, calcium gluconate and vitamin D may have a therapeutic effect. In resistant cases it is possible surgery (stapedectomy).

CRANIOCRAIN INJURY

Traumatic brain injury is the most common established cause of benign positional dizziness. Typically, the cause of post-traumatic dizziness is damage to the maze. However, a fracture of the pyramid of the temporal bone with damage to the vestibular nerve can also lead to dizziness and hearing loss. Signs of such a fracture may be hemotympanitis or the expiration of CSF from the ear.

Tumors of the Bridge of the Coronary Angle

The cerebellar angle is a triangular region in the posterior cranial fossa, limited by the cerebellum, the lateral part of the bridge and the bone crest. The most common tumor in this area is the histologically benign auditory nerve neurinoma (also called neurilemma, neuroma, or schwannoma). The tumor grows from the membrane (neurilemma) of the vestibular portion of the auditory nerves of the inner auditory canal. Less often, in this zone, a meningioma and a primary epidermoid cyst are localized. Symptoms are caused by compression or displacement of the cranial nerves, brain stem and cerebellum, as well as a violation of CSF current. Often affected trigeminal (V) and facial (VII) nerves - due to the anatomical proximity to the auditory nerve.

Tumor of the cerebellar angle, top view (the brain is removed so that the cranial nerves and the base of the skull are visible). A tumor is a neuroma of the auditory (VIII) nerve, which can compress neighboring structures, including trigeminal (V) and facial (VII) nerves, brain stem and cerebellum.

Auditory nerve neurinoma most often occurs as a single formation in a patient, but it can also be a manifestation of neurofibromatosis. Type 1 neurofibromatosis (Recklinghausen disease) is a common autosomal dominant disease associated with a mutation of the neurofibromin gene on chromosome 17 (17 qll .2). In addition to unilateral auditory nerve neuroma, type 1 neurofibromatosis is characterized by the presence of pigmented spots on the skin of light coffee color (cafe - au - lait), skin neurofibromas, small pigmented spots ("freckles") in the axillary or inguinal region, gliomas of the optic nerve, hamart of the iris, osteodysplasia. Type 2 neurofibromatosis is a rare autosomal dominant disease resulting from a mutation of the neurofibromin 2 gene on chromosome 22 (22 ql 1.1-13.1). Its main manifestation is bilateral auditory nerve neurinoma, which may be accompanied by other tumors of the central or peripheral nervous system, including neurofibromas, meningiomas, gliomas, and schwannomas.

Clinical picture

The initial manifestation is usually a gradual hearing loss. Less commonly, patients have headache, dizziness, walking ataxia, facial pain, noise and a feeling of stuffiness in the ear, weak facial muscles. True dizziness (ver tigo) develops only in 20-30% of patients - a nonspecific sensation of instability is much more often observed. Unlike Meniere's disease, mild vestibular symptoms persist between seizures. Symptoms may remain stable or progress slowly for many months or years. On examination, one-sided hearing loss of the neurosensory type is most often detected. Often there are also ipsilateral weakness of the facial muscles, a decrease or loss of the corneal reflex, and a decrease in sensitivity on the face. Ataxia, spontaneous nystagmus, lesions of other cranial nerves, signs of increased intracranial pressure are less common. With a caloric test, signs of unilateral vestibular dysfunction are detected.

CEREBRAL AND CENTRAL VESTIBULAR DISORDERS

Many pathological conditions cause acute or chronic cerebellar dysfunction. Some of these conditions are also accompanied by central vestibular dysfunction, especially Wernicke encephalopathy, circulatory disorders in the vertebro-basilar pool, multiple sclerosis and tumors of the posterior cranial fossa.

ACUTE DISORDERS

ENCEPHALOPATHY WERNIKE

Wernicke encephalopathy is an acute disease, manifested by a triad of clinical signs: ataxia, ophthalmoplegia and confusion. The immediate cause is thiamine deficiency . Wernicke encephalopathy most often occurs in patients with chronic alcoholism, although it may be a consequence of malnutrition of any genesis. The pathological process mainly affects the medial nuclei of the thalamus, the mammillary bodies, the periaqueductive and periventricular nuclei of the brain stem (especially the nuclei of the oculomotor, abducent, and suspected cochlear nerves), as well as the upper part of the cerebellar worm. The development of ataxia is caused by damage to the cerebellum as well as vestibular dysfunction.

Ataxia manifests itself mainly or exclusively when walking. Impaired coordination of the lower extremities is noted only in one fifth of patients, and impaired coordination of the upper extremities - only in one tenth of them. Dysarthria is rare. Other classic manifestations include amnestic syndrome, confusion, horizontal or combined horizontal-vertical nystagmus, bilateral weakness of the external rectus muscles of the eye, loss of the Achilles reflex. With a caloric test, bilateral or unilateral vestibular dysfunction is detected. Paresis of the gaze, impaired pupillary innervation, hypothermia are possible.

The diagnosis confirms a positive reaction to thiamine, which is usually initially administered intravenously at a dose of 100 mg. The improvement primarily relates to oculomotor functions and usually manifests itself within a few hours after the start of treatment. The reverse development of ataxia, nystagmus, confusion begins in a few days. The movements of the eyeballs are usually fully restored, sometimes only horizontal nystagmus persists.

Ataxia is completely reversible in only 40% of patients - in these cases, walking is completely normal in a few weeks or months.

ISCHEMIA IN THE VERTEBRO-BASILAR POOL

Transient ischemic attacks or ischemic stroke in the vertebro-basilar basin are often accompanied by dizziness and ataxia.

OCCLUSION OF THE INTERNAL HEARING ARTERY

A combination of central dizziness and unilateral hearing loss may occur due to occlusion of the internal auditory artery, which supplies the auditory nerve. This vessel may depart from the basilar or anterior inferior cerebellar arteries. Dizziness is accompanied by nystagmus, the rapid phase of which is directed to the side of the contralateral lesion. Hearing loss is one-sided and belongs to the sensorineural type.

The main arteries of the posterior cranial fossa

LATERAL LENGTH INFARCTION

Lateral infarction of the medulla oblongata is clinically manifested by Wallenberg syndrome and is most often the result of proximal vertebral artery occlusion. Symptoms are variable and depend on the extent of myocardial infarction. Characteristic is the presence of dizziness, nausea, vomiting, dysphagia, hoarseness of the voice and nystagmus in combination with Horner syndrome, hemataxia, impaired all types of sensitivity on the face, tactile and deep sensitivity in the limbs on the affected side, as well as pain and temperature sensitivity in the contralateral limbs. Dizziness develops due to damage to the vestibular nuclei, and hemataxia is due to involvement of the lower leg of the cerebellum.

Lateral infarction of the medulla oblongata (Wallenberg syndrome). A heart attack zone (highlighted) and damaged anatomical structures are shown.

Cerebellar infarction

The cerebellum supplies three pairs of arteries: the superior cerebellar, the anterior lower cerebellar and the posterior lower cerebellar arteries. The boundaries of the blood supply zones of each of them are extremely variable and differ not only in different people, but even in both hemispheres of the cerebellum in the same person. The upper, middle, and lower legs of the cerebellum are supplied with blood by the upper, anterior lower, and posterior lower cerebellar arteries, respectively.

Cerebellar infarction occurs as a result of occlusion of one of the cerebellar arteries. The clinical manifestations developing in this case can be distinguished only by concomitant stem disorders. In all cases, cerebellar signs are represented by ataxia and muscle hypotension in the ipsilateral limbs. Other symptoms may include headache, nausea, vomiting, dizziness, nystagmus, dysarthria, paralysis of the gaze and external muscles of the eyes, decreased sensitivity on the face, weak facial muscles, hemiparesis and hemigipesthesia in the contralateral limbs. A brain stem infarction or its compression in cerebellar edema can lead to the development of coma and death. Diagnosis of cerebellar infarction is carried out using CT and MRI, which allow to differentiate heart attack and hemorrhage and, accordingly, should be carried out as quickly as possible. With the compression of the brain stem, the only option to save the patient's life is surgical decompression and resection of necrotic tissue.

MIDDLE PARAMEDIC INFARCTION

Paramedial heart attack of the midbrain is caused by occlusion of the paramedian penetrating branches of the basilar artery and is characterized by damage to the root of the oculomotor nerve and red nucleus. The resulting clinical picture (Benedict's syndrome) is represented by paralysis of the ipsilateral medial rectus muscle of the eye with an enlarged pupil that does not respond to light and contralateral ataxia, which usually involves only the arm. Cerebellar signs are caused by damage to the red nucleus, which receives crossed projection fibers following from the cerebellum as part of its upper leg.

Paramedian heart attack of the midbrain (Benedict's syndrome). Heart attack area highlighted

HEMORRHEMIA IN THE CEREBELLUM

Most cases of cerebral hemorrhage are associated with hypertensive arteriopathy. Less commonly, the cause is the use of anticoagulants, arteriovenous malformations, blood diseases, swelling and traumatic brain injury. Hypertensive cerebellar hemorrhages are usually localized in the deep parts of the white matter and often break into the IV ventricle.

The classic clinical picture of hypertensive cerebellar hemorrhage is represented by a suddenly developing headache, which is often accompanied by nausea, vomiting, and dizziness. Following this, walking ataxia and depression of consciousness usually develop within a few hours. By the time of hospitalization, the patient may have a clear consciousness, confusion, or coma. In patients with clear consciousness, nausea and vomiting are often expressed. Blood pressure is usually elevated. Rigidity of the cervical muscles can be determined. The pupils are often narrowed and sluggishly react to light. Often there is paralysis of the horizontal gaze to the ipsilateral side (the patient’s eyes are turned in the direction opposite to the lesion) and ipsilateral paralysis of the facial muscles. Paresis of the gaze is not overcome by caloric stimulation. Nystagmus and weakening of the corneal reflex on the affected side can be detected. In patients with clear consciousness, ataxia is detected when standing and walking, ataxia of the extremities is detected less often. At a late stage of compression of the brain stem, spasticity of the lower extremities, pathological foot reflexes develop. CSF is bloody in nature, but if you suspect hemorrhage in the cerebellum, lumbar puncture should be avoided, as it can lead to wedging. The method of choice for the diagnosis of cerebral hemorrhage is CT. A patient’s life can often be saved only by surgery with the evacuation of a hematoma.

CHRONIC DISORDERS

MULTIPLE SCLEROSIS

Multiple sclerosis can cause ataxia of the cerebellar, vestibular or sensitive type. The occurrence of cerebellar signs is associated with the appearance of foci of demyelination (plaques) in the white matter of the cerebellum, the legs of the cerebellum, or the brain stem. Like other manifestations of multiple sclerosis, these symptoms can regress and reappear.

Damage to the vestibular pathways in the brainstem causes dizziness, which often occurs acutely and sometimes has a positional character. Dizziness is a common symptom of the advanced stage of the disease, but rarely is its first manifestation.

With cerebellar involvement, walking ataxia is the first manifestation in 10-15% of patients. At the first examination, cerebellar signs are detected in one third of patients, later they occur in two thirds of patients.

One of the most common symptoms found during examination is nystagmus, which may be accompanied by other signs of cerebellar dysfunction or occur without them. Dysarthria is often noted. Ataxia of walking is more often cerebellar in nature than sensitive. Ataxia of the extremities is common, usually bilateral, involving both legs or all four limbs.

Multiple sclerosis is supported by anamnestic indications of a relapsing-relapsing course of the disease, signs of multifocal damage to the central nervous system and such manifestations as optic neuritis, internuclear ophthalmoplegia, pyramidal signs, and also data from paraclinical research methods. In CSF, oligoclonal antibodies, an increase in the level of IgG and protein, and mild lymphocytic pleocytosis are determined. The study of visual, auditory and somatosensory evoked potentials allows to identify areas of subclinical lesions. CT and MRI reveal foci of demyelination. However, it should be noted that the data of not a single paraclinical method are specific for multiple sclerosis, and when making a diagnosis, you should rely primarily on the history and results of a neurological examination.

ALCOHOLIC CEREBELLAL DEGENERATION

In patients with chronic alcoholism, a characteristic cerebellar syndrome may develop, which is probably the result of nutritional deficiency. A history of these patients usually has indications of daily or drunken alcohol consumption for 10 years or more and inadequate nutrition. Most patients already had or have other complications of chronic alcoholism: cirrhosis, delirium tremens, Wernicke encephalopathy, polyneuropathy. Alcoholic cerebellar degeneration often develops in men and usually manifests itself between the ages of 40 and 60.

Degenerative changes are usually limited to the upper part of the cerebellar worm. Since this area also suffers from Wernicke encephalopathy, both conditions, apparently, can be considered as parts of a single clinical spectrum.

Alcoholic degeneration of the cerebellum begins unnoticed, progresses steadily and, reaching a certain level, stabilizes. Progression usually takes several weeks or months, but rarely lasts for years. In some cases, ataxia appears suddenly or proceeds easily and does not progress from the very beginning.

Ataxia of walking is a universal symptom, which is almost always the main problem of patients, forcing them to resort to medical care. With a knee-heel test, discoordination in lower limbs detected in 80% of patients. Common concomitant manifestations include sensory disturbances in the feet and loss of Achilles reflexes due to polyneuropathy, signs of malnutrition (loss of subcutaneous fat, generalized muscle atrophy, glossitis). Ataxia of the upper extremities, nystagmus, dysarthria, muscle hypotension, trunk ataxia are less commonly observed.

ATAXIA Friedreich

Among idiopathic degenerative diseases that cause cerebellar ataxia, Friedreich's ataxia occupies a special place due to the fact that it occurs more often than others and is characterized by unique clinical and pathomorphological manifestations. In contrast to the autosomal dominant late-spinocerebellar ataxia, which were discussed above, Friedreich's ataxia begins in childhood. It is transmitted according to the autosomal recessive type of inheritance and is associated with an increase in the number of GAA trinucleotide repeats in the non-coding region of the frataxin gene on chromosome 9 (Table 3-10). The recessive nature of inheritance involves a mutation leading to loss of function. Most patients are homozygotes for the expansion of trinucleotide repeats in the frataxin gene, but some of them are heterozygotes and have a typical mutation in one allele and a point mutation in the other allele.

Pathomorphological changes are limited mainly by the spinal cord. They are represented by degeneration of the spinocerebellar tracts, posterior columns and posterior roots, a decrease in the number of neurons in the Clark columns, from which the dorsal spinocerebellar tract originates. The thick myelinated axons of the peripheral nerves and the body of the primary sensory neurons of the spinal ganglia are also affected.

CLINICAL PICTURE

Clinical manifestations almost always occur after the age of four, but before the end of puberty, and the higher the number of trinucleotide repeats in a given patient, the earlier the disease appears. The initial symptom is usually progressive walking ataxia, to which ataxia of all limbs joins over the next two years. At an early stage, knee and Achilles reflexes are lost and cerebellar dysarthria appears. Tendon reflexes in the upper limbs, and sometimes knee reflexes, can be preserved. On the lower extremities, the articular-muscular feeling and vibrational sensitivity are disturbed, as a result of walking ataxia is supplemented by a sensitive component. Violations of tactile, pain, and temperature sensitivity occur less frequently. Weakness of the lower and less often upper limbs develops later and may be the result of dysfunction of central and (or) peripheral motor neurons.

Pathological foot reflexes appear, as a rule, during the first five years of the disease. A well-known diagnostic sign of the disease is the "hollow foot" (pes cavus - foot with a high arch and deformation of the fingers, developing as a result of weakness and atrophy of the internal muscles of the foot). It can also occur in healthy family members of the patient, as well as in other neurological diseases, especially some hereditary polyneuropathies (for example, Charcot-Marie-Tooth disease). Rough progressive kyphoscoliosis exacerbates functional disorders and can lead to the development of chronic restrictive respiratory failure. Myocardiopathy, sometimes detected only by echocardiography or vector cardiography, can lead to heart failure and is one of the main causes of disability and death.

LITERATURE

Total

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Benign Positional Dizziness

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Meniere's disease

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Head injury

• Healy GB: Hearing loss and vertigo secondary to head injury. N Engl J Med 1982; 306 :.

Cerebellar Angle Tumors

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• Zamani AA: Cerebellopontine angle tumors: role of magnetic resonance imaging. Top Magn Reson Imaging 2000; 11: 98-107.

Wernicke Encephalopathy

Multiple sclerosis

• Noseworthy JH et al: Multiple sclerosis. N Engl J Med 2000; 343 :.
• Rudick RA et al: Management of multiple sclerosis. N Engl J Med 1997; 337 :.

Alcoholic cerebellar degeneration

• Charness ME, Simon RP, Greenberg DA: Ethanol and the nervous system. N Engl J Med 1989; 321 :.

Ataxia Friedreich

• Campuzano V et al: Friedreich’s ataxia: autosomal Science 1996; 271 :.
• Diirr A et al: Clinical and genetic abnormalities is patients with Friedreich’s ataxia. N Engl J Med 1996; 335:

Consciousness is a process of meaningful perception of the inner and outer world, the ability to analyze, remember, transform and reproduce information. Consciousness disorders are divided into: Conditions with a changed LEVEL of consciousness, impaired maintenance of the level of wakefulness and reaction to external stimuli - for example: ACUTE CONFUSION OF CONSCIOUSNESS, SOPOR, COMA. States with altered CONTENTS of consciousness, at a normal level of consciousness - impaired cognitive functions, for example: DEMENTIA, AMNESIA, APHASIA. ...

Clinic of rehabilitation treatment

The main specialization of the Seasons Clinic is a comprehensive rehabilitation treatment (neurorehabilitation) for children and adults who have suffered various brain and spinal cord injuries ...

How we treat

The basis of our approach to rehabilitation treatment is an individual complex of physical rehabilitation, based on evidence-based medicine, using advanced foreign technologies and our own developments ...