Eye movement coordination disorder from the word plane. Strabismus. Paramedian midbrain infarction

Strabismus Strabismus is usually called the incorrect position of the eyes, when the visual axis of one eye is deviated from the point fixed by the other eye. Strabismus has two varieties: concomitant and paralytic. Paralytic strabismus occurs due to

Strabismus

Strabismus Previously, strabismus was treated only with surgery, but now doctors prescribe surgery only as a last resort. It has been proven that strabismus is a purely functional vision disorder. If you relax the tight, tense muscles of the eyes,

squint / small: kosina, kosinka (colloquial)) Dictionary of synonyms of the Russian language. Practical guide. M.: Russian language. Z. E. Alexandrova ... Dictionary of synonyms

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

STRABISM - STRABISM, strabismus, pl. no, cf. Uneven direction of the eye pupils. Ushakov's explanatory dictionary. D.N. Ushakov. ... Ushakov’s Explanatory Dictionary

Squint - Squint, I, cf. Eye movement coordination disorder - unequal direction of the pupils. Divergent eye (with the eye deviating away from the nose). Converging to. (towards the nose). Ozhegov's explanatory dictionary. S.I. Ozhegov, N.Yu. Shvedova. ... Ozhegov's Explanatory Dictionary

strabismus - STRABISM1, decomposed. kosina, colloquial braid unraveled OBLIQUE, slanting, unraveled. mowing, collapsing reduction cross-eyed STRABISM2, decomposed. kosina, colloquial braid, colloquial squint... Dictionary-thesaurus of synonyms of Russian speech

Strabismus - Main article: Eye diseases Strabismus With strabismus, the 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 point of fixation. There are paralytic and concomitant strabismus. Paralytic strabismus (Fig. 1) is caused by damage to the oculomotor, trochlear and abducens nerves, ... ... Medical encyclopedia

STRABISM - honey. Strabismus is a pathology of the oculomotor system, in which one eye deviates from the common point of fixation with the other eye. The disease affects mainly children (1.5 2.5% of children). Classification and characteristics of individual ... ... Directory of diseases

STRABISMUS - Alumina, 6, 12 and bvr, feeling of coldness in the eyes, dryness of the 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. Gelsemium, 3x, 3 and bvr dysfunction of the oculomotor ... Reference book on homeopathy

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

What is motor coordination

With the development of a motor skill, the coordination of movements changes, including the development of the inertia of moving organs. At first, control occurs due to 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 development, inertial movements are used. In an already established dynamically stable movement, balancing of all inertial movements occurs automatically, without producing additional correction impulses.

Coordination of movements is given to a person so that he can perform precise movements and control them. If there is a lack of coordination, this indicates changes occurring 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, the limbs, torso or other parts of the body begin to move. If the central nervous system does not work coherently, if deviations occur in it, the signal does not reach the target or is transmitted in a distorted form.

Causes of impaired coordination of movements

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

• physical exhaustion of the body;
• exposure to alcohol, narcotic and other toxic substances;
• brain injuries;
• sclerotic changes;
• muscle dystrophy;
• Parkinson's disease;
• ischemic stroke;
• catalepsy is a rare phenomenon in which the muscles weaken due to an explosion of emotions, say, anger or delight.

Lack of coordination is considered a dangerous deviation for a person, because in such a state it costs nothing to get injured. This often accompanies old age, as well as previous neurological diseases, a striking example of which in this case is stroke.

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

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

Signs of impaired coordination of movements

People with such ailments move uncertainly, their movements show laxity, too much amplitude, and inconsistency. Having tried 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 incoordination is to ask the patient to touch the tip of the nose, which also fails.

Looking at the patient’s handwriting, you will also be convinced that his muscle control is not all right, since letters and lines creep on top of each other, becoming uneven and sloppy.

Symptoms of impaired coordination of movements

The following symptoms of impaired coordination of movements exist:

Shaky movements

this symptom occurs when the muscles of the body, especially the limbs, weaken. The patient's movements become uncoordinated. When walking, he sways a lot, his steps become abrupt and have different lengths.

Tremor

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

Ataxia

Ataxia is caused by damage to the frontal parts of the brain, cerebellum, and nerve fibers transmitting signals 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; with dynamic ataxia, it is difficult for him to move in a balanced manner.

Motor coordination tests

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

Test No. 1

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

Test No. 2

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

Test No. 3

Try placing your hand on your stomach and stroking it clockwise while tapping your head with the other hand. 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 good coordination. But if you were not able to immediately perfectly perform all of the above, do not despair!

Exercises to develop motor coordination

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

You can develop coordination of movements with the help of special exercises and training, thanks to Pilates, breaking exercises, as well as with the help of other sports that involve various objects (fitball, dumbbells, jump ropes, medicine balls, sticks, etc.)

Coordination exercises can be done anywhere, for example:

In transport

Do not look for free space, but rather stand and do the exercise. Place your feet shoulder-width apart and try not to hold on to the car's handrails while driving. Perform the exercise carefully so that when you stop abruptly, you do not roll to the floor. Well, let the surprised passengers look at you, but soon you will have excellent coordination!

On a stepladder

Holding the ladder with your hands, go up and down. Once you have rehearsed a few ascents and descents, try doing the same exercise, but without using your hands.

Standing on the floor

You will need an apple in each hand. Imagine that you are in a circus ring and juggling. Your task is to throw apples up and at the same time catch them again. You can make the task more difficult 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 a more complicated version of the exercise. Perform the same movement, but catch the apple with the other hand, placing your hands crosswise.

On a narrow curb

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

There are a number of coordination exercises that can be done daily:

• do somersaults forward and backward;
• running, jumping and various relay races with a skipping rope;
• combining several exercises into one, for example, somersaulting and catching a 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 a partner in different directions (in this exercise it is necessary not only to throw the ball, but also to catch it in the same unpredictable directions).

Which doctors should you contact if there is a lack of coordination of movements:

Questions and answers on the topic “Coordination of movements”

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

Question: Good afternoon. I can't figure out what it is. Sometimes coordination suddenly disappears, then it appears and everything is fine. I'm not falling. I am physically strong, I go in for sports.

Question: Hello! I have problems with coordination of movements. I constantly hit door frames, I just can’t “fit” into the door (it’s like I’m skidding). It’s difficult to stand on public transport, I’m constantly dangling like a rag in the wind, falling over every bump. Could this be a consequence of osteochondrosis (I have had it for 4 years, in the cervical spine), or is it just a bad vestibular system and inattention?

Question: Hello. I have been sick for about 2 years (I am 25 years old). Loss of coordination of movement, dizziness when walking. Sitting, lying down, turning my head, I don’t feel dizzy. There was a strange sensation in my head, a spasm of blood vessels, at such moments it seemed to me that I might lose consciousness. There was a feeling of fear. Please answer me, what causes dizziness and how to treat it? Are there enough grounds to say that the cause is osteochondrosis of the cervical spine.

Question: Good afternoon What tests are there for motor coordination?

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

EQUILIBRIUM DISORDERS

Balance is the ability to maintain the orientation of the body and its parts in relation to the surrounding space. It depends on a 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, the cerebellum, or the sensory pathways that provide proprioception.

Such disorders usually present with at least one of two clinical symptoms: dizziness or ataxia.

DIZZINESS

Dizziness (vertigo) sensation of movement of the body or the surrounding space. It can be combined with other symptoms, such as impulsivity (a feeling of the body shifting in space under the influence of an external force), oscillopsia (visual illusion of oscillating movement), nausea, vomiting, and gait ataxia.

Differences between dizziness and other symptoms

Dizziness (vertigo) should be differentiated from non-vestibular symptoms that resemble dizziness, but unlike it are not accompanied by the illusion of movement (for example, lightheadedness, a feeling of “fog in the head”, etc.). Such sensations are usually associated with a disruption in the supply of blood, oxygen or glucose to the brain - due to hyperactivation of the vagus nerve, orthostatic hypotension, cardiac arrhythmia, myocardial ischemia, hypoxia or hypoglycemia. The culmination of these phenomena may be loss of consciousness (fainting).

Having diagnosed dizziness, you should first decide whether it is caused by damage to the peripheral or central vestibular structures.

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

Clinical manifestations

1. Peripheral dizziness is usually intermittent and short-lived, but more intense than central dizziness. Peripheral vertigo is almost always accompanied by nystagmus (rhythmic twitching of the eyeballs), which in this case is usually unidirectional and never vertical (see below). Damage to the peripheral vestibular structures often causes additional symptoms associated with pathology of the inner ear or auditory nerve, that is, hearing loss and tinnitus.
2. Central vertigo is not always accompanied by nystagmus. If it occurs, it can be vertical, unidirectional or multidirectional, as well as asymmetrical - different in nature in both eyes. (Vertical nystagmus - twitching of the eyeballs in a vertical plane). Central lesions may present with brainstem or cerebellar symptoms such as paresis, hypoesthesia, brisk reflexes, abnormal foot signs, dysarthria, or limb ataxia.

Peripheral and central vestibular structures. The vestibular portion of the VIII nerve ends in the vestibular nuclei of the brainstem and the median structures of the cerebellum, which, in turn, also project to the vestibular nuclei. From them, fibers in the medial longitudinal fasciculus ascend to the nuclei of the abducens and oculomotor nerves on both sides, and also follow down to the spinal cord.

ATAXIA

Ataxia is a lack 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 (proprioception). Ataxia can impair eye movements, speech (causing dysarthria), movement of individual limbs, trunk, balance, and walking.

Vestibular ataxia

Vestibular ataxia is caused by the same peripheral or central lesions as vertigo. Patients often exhibit nystagmus; it is usually unilateral and more pronounced when looking in the direction opposite to the lesion. There is no dysarthria. Vestibular ataxia depends on the position of the body in the gravitational field: coordination disorders are absent when the patient is lying down, but appear as soon as he tries to stand 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 cerebellar peduncles, red nucleus, pons, or spinal cord. There are crossed connections between the frontal cortex and the cerebellum, so unilateral pathology of the frontal cortex can mimic 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 hypotonia

Cerebellar ataxia is usually accompanied by muscle hypotonia, which results in impaired ability to maintain posture. When testing strength, the patient's resistance is overcome with a relatively small effort, and when shaking the limb makes movements with increased amplitude. The range of arm movements when walking may also increase. Tendon reflexes become pendulum-like: after inducing the reflex, 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 resistance, which is then removed, then the tensed muscles do not have time to relax, and the antagonist muscles do not have time to engage, which leads to excessive rebound movement (a symptom of the absence of a reverse push).

B. Impaired coordination of movements

In addition to muscle hypotonia, cerebellar ataxia is characterized by impaired coordination of voluntary movements. Simple movements are made with a delay, their acceleration and braking occur at the wrong time. The speed, rhythm, amplitude and strength of movements are characterized by inconsistency, as a result of which their smoothness is disrupted. Because movement disproportionality is greatest during the initiation and termination of movement, the most noticeable clinical manifestations of ataxia are terminal dysmetria (overshooting) during goal-directed movement and intention tremor that appears as the limb approaches the target. More complex movements are not performed as a single motor act, but are divided into a number of successive individual movements (decomposition of movements). Movements that require simultaneous contraction of several muscle groups (asynergia) are impaired. The most physiologically complex movements, such as walking, and movements involving rapid changes of direction, are most affected.

B. Associated oculomotor disorders

The cerebellum plays a significant role in controlling eye movements, so when it is damaged, oculomotor disorders often occur. Most often, nystagmus and other oscillatory eye movements, gaze paralysis, and disturbances in saccadic and pursuit movements are observed.

G. Relationship between cerebellar symptoms and location of the lesion

Different anatomical regions 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 median region of the cerebellum - the vermis, the flocculonodular lobe and the associated subcortical nuclei (tent nuclei) - is involved in the control of axial motor functions, including eye movements, head and torso position, static behavior and walking. Therefore, when the median structures are damaged, nystagmus and other oculomotor disorders, oscillatory movements of the head and torso (titubation), static disturbances, and gait ataxia occur. With selective damage to the upper part of the cerebellar vermis (which, for example, is often observed in alcoholic cerebellar degeneration), walking ataxia is the dominant or only clinical manifestation, as follows from the somatotopic map of the cerebellum.

2. Lesions of 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 gaze to the ipsilateral side. Lesions of the cerebellar hemisphere cause ipsilateral hemiataxia and hypotonia of the ipsilateral limbs, nystagmus and transient gaze paresis to the ipsilateral side. With paramedian lesions of the left hemisphere of the cerebellum, dysarthria may occur.

3. Diffuse damage to 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, the clinical picture consists of symptoms characteristic of damage to the median structures and both hemispheres of the cerebellum.

SENSITIVE ATAXIA

Conducting pathways of deep (proprioceptive) sensitivity

Sensitive ataxia develops as a result of damage to fibers carrying proprioceptive impulses in the peripheral nerves, dorsal roots, dorsal columns of the spinal cord, and medial lemniscus. Rare causes of sensitive hemiataxia are lesions of the thalamus and parietal lobe on the contralateral side. Joint-muscular sensation is provided by the receptor apparatus, represented by Pacinian corpuscles, non-encapsulated nerve endings in joint capsules, ligaments, muscles and periosteum. From the receptors, impulses follow thick myelinated type A fibers, which are processes of 1st order sensory neurons. These fibers enter the posterior horn of the spinal cord and, without crossing, ascend as part of the posterior columns. Proprioceptive information from the lower extremities is carried out through the medially located gracilis fasciculus, and from the upper extremities through the more laterally located cuneate fasciculus. The fibers running as part of these pathways form synapses with second-order sensory neurons, forming the nuclei of the thin and cuneate fasciculi in the lower part of the medulla oblongata. The processes of 2nd order neurons cross and then rise as part of the contralateral medial loop to the ventral posterior nucleus of the thalamus, where 3rd order sensory neurons associated with the parietal lobe cortex are located.

Sensitive ataxia due to polyneuropathy or damage to the dorsal columns usually causes symmetrical impairment of walking and movements of the lower extremities; movements of the upper extremities are usually less affected or remain normal. Upon examination, a violation of the joint-muscular sense and vibration sensitivity is revealed. Characterized by the absence of dizziness, nystagmus and dysarthria.

PERIPHERAL VESTIBULAR DISORDERS

BENIGN POSITIONAL VERTIGO

Benign positional vertigo (benign positional vestibulopathy) occurs when the head is positioned in a certain position. Typically, positional vertigo is characteristic of lesions of peripheral vestibular structures, but it can also be of central origin, occurring with lesions of the brainstem and cerebellum.

Benign positional vertigo is the most common cause of peripheral vertigo, accounting for about 30% of cases. Of the established causes, the most common is traumatic brain injury, but in most cases, benign positional vertigo 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 that, 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 head position, but are usually most pronounced when the patient turns on his side and lies on the affected ear. Episodes of dizziness usually occur over a period of several weeks, followed by spontaneous remission. In some cases, dizziness recurs. Hearing loss is not typical.

Peripheral and central positional vertigo are differentiated using the Neelen-Barany (Dix-Hallpike) test. With benign positional vertigo, positional nystagmus is almost always observed, which is usually unidirectional, has a rotatory component and occurs with a delay of several seconds after the head occupies that position that provokes dizziness. If the position of the head does not change, then dizziness and nystagmus disappear after a few seconds or minutes. When the test is repeated, the severity of the symptoms decreases. In contrast, central positional vertigo is usually less pronounced and may not be accompanied by positional nystagmus. When cent In general positional vertigo, there is no delay in the onset of nystagmus, there is no exhaustion of symptoms while maintaining the posture, and there is no addiction when the test is repeated.

In most cases of benign peripheral positional vertigo (canalolithiasis), the therapeutic effect can be achieved using repositioning techniques, the purpose of which is to, under the influence of gravity, remove particles suspended in the endolymph from the bulbar canal, moving them to the vestibule, where they can be reabsorbed . One of these techniques is that the patient’s head is turned 45° towards the affected ear (the side is determined clinically - according to the signs described above), after which the patient is placed on his back so that the head (while remaining turned 45°) hangs from the ear. edges of the couch. Then the thrown back head is turned 90°, as a result of which it is turned in the other direction at an angle of 45°. After this, the patient is turned onto his side, with the affected ear on top, and the head remains thrown back and turned 45° towards the healthy ear. Finally, the patient turns over onto his stomach and sits up.

Reposition therapy scheme

In the acute period, vestibulolytic agents can be effective. Recovery is accelerated using vestibular rehabilitation techniques, which provide compensation for impaired vestibular function through other sensory modalities. According to some studies, recovery is also accelerated by betahistine dihydrochloride, which helps normalize the functional state of histaminergic vestibular neurons.

MENIERE'S DISEASE

Meniere's disease is characterized by recurrent episodes of dizziness lasting from a few minutes to several days, accompanied by tinnitus and progressive sensorineural hearing loss. Most cases are sporadic, but family cases have also been described, which are characterized by the phenomenon of anticipation - with each generation, the age of manifestation of the disease decreases. Some familial cases are associated with a mutation of the cochlin gene on chromosome 14 (locus 14 ql 2-ql 3). Approximately at 15% In cases, the disease manifests itself between the ages of 20 and 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 endolymph in the labyrinth (endolymphatic hydrops), but the pathogenetic mechanisms remain unclear.

Even before the first attack, patients may notice a gradual increase in noise and a feeling of congestion in the ear, decreased hearing. The attack is manifested by dizziness, nausea, and vomiting. The intervals between attacks vary from several weeks to several years. Hearing deteriorates step by step. In 10-70% of patients, a bilateral process is observed. As hearing decreases, the severity of dizziness decreases.

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

Treatment is with diuretics, such as hydrochlorothiazide or triamterene. It is possible to use betagestin dihydrochloride, which, by enhancing histaminergic transmission in the vestibular system and improving blood supply to the labyrinth, according to some data, reduces the severity of dizziness. In severe cases resistant to drug therapy, surgical treatment is resorted to: endolymphatic shunting, 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 that self-regress and are not accompanied by hearing loss or signs of central nervous system dysfunction. This group includes disorders referred to as acute labyrinthitis or vestibular neuronitis - these terms reflect insufficiently substantiated assumptions about the location of the disease or its nature. However, sometimes vestibulopathy occurs after a recent cold with fever.

Acute peripheral vestibulopathy is characterized by acute onset of dizziness, nausea and vomiting, which usually lasts up to 2 weeks. Sometimes the tomato symptom 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 upward and tries not to move his head. Nystagmus is always detected, the fast phase of which is directed in the direction opposite to the affected ear. The caloric test reveals changes on one or both sides with approximately the same frequency. Hearing is not affected.

Acute peripheral vestibulopathy should be differentiated from central disorders that cause acute dizziness, for example, circulatory disorders in 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, and dysarthria. Treatment includes the use of glucocorticoids, as well as betahistine dihydrochloride and other agents.

OTOSCLEROSIS

Otosclerosis is characterized by impaired mobility of the stapes, a small bone in the ear that transmits vibration from the eardrum to other structures in the inner ear. The main manifestation of the disease is conductive hearing loss, but sensorineural hearing loss and dizziness are also possible. Tinnitus is uncommon. Hearing often begins to decline before age 30. A family history is often noted.

Vestibular dysfunction is most often manifested by repeated episodes of dizziness, sometimes of a positional nature, as well as a feeling of instability when changing posture. Over time, symptoms may become more persistent and the frequency and severity of attacks may increase. Upon examination, manifestations of vestibular dysfunction may be detected, such as spontaneous or positional peripheral nystagmus, decreased response in the caloric test, which are usually unilateral.

Audiometry always detects hearing loss, usually of a mixed nature with elements of conductive and sensorineural hearing loss, and in approximately 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 characterized by a family history, the onset of symptoms at an earlier age, the presence of a conductive component of hearing loss, and bilateral symmetrical hearing loss. Imaging techniques help make the diagnosis.

A combination of sodium fluoride, calcium gluconate and vitamin D can have a therapeutic effect. In resistant cases, surgical treatment (stapedectomy) is possible.

CRANIO BRAIN INJURY

Traumatic brain injury is the most common identified cause of benign positional vertigo. Typically, the cause of post-traumatic vertigo is damage to the labyrinth. However, a petrous fracture with damage to the vestibular nerve can also lead to dizziness and hearing loss. Signs of such a fracture may include hemotympanitis or leakage of CSF from the ear.

TUMORS OF THE PONTOCEREBELLAR ANGLE

The cerebellopontine angle is a triangular region in the posterior cranial fossa, bounded by the cerebellum, the lateral part of the pons, and the bony crest. The most common tumor in this area is a histologically benign acoustic neuroma (also called neurilemmoma, neuroma, or schwannoma). The tumor grows from the membrane (neurilemma) of the vestibular portion of the auditory nerves of the internal auditory canal. Less commonly, meningioma and primary epidermoid cyst are localized in this area. Symptoms are caused by compression or displacement of the cranial nerves, brain stem and cerebellum, as well as disruption of CSF flow. The trigeminal (V) and facial (VII) nerves are often affected due to their anatomical proximity to the auditory nerve.

Tumor of the cerebellopontine angle, dorsal view (the brain has been removed to expose the cranial nerves and base of the skull). The tumor, a neuroma of the auditory (VIII) nerve, can compress neighboring structures, including the trigeminal (V) and facial (VII) nerves, the brain stem and the cerebellum.

Acoustic neuroma most often occurs as a solitary lesion in patients, but can also be a manifestation of neurofibromatosis. Neurofibromatosis type 1 (Recklinghausen disease) is a common autosomal dominant disease associated with a mutation in the neurofibromin gene on chromosome 17 (17 qll .2). In addition to unilateral acoustic neuroma, neurofibromatosis type 1 is characterized by the presence of pigment spots on the skin of a light coffee color (cafe-au-lait), cutaneous neurofibromas, small pigment spots (“freckles”) in the axillary or groin area, optic nerve gliomas, hamartoma of the iris, osteodysplasia. Neurofibromatosis type 2 is a rare autosomal dominant disease resulting from a mutation in the neurofibromin 2 gene on chromosome 22 (22 ql 1.1-13.1). Its main manifestation is considered to be bilateral acoustic neuroma, 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 decrease in hearing. Less commonly, patients experience headache, dizziness, gait ataxia, facial pain, noise and a feeling of fullness in the ear, and weakness of facial muscles. True dizziness (ver tigo) develops only in 20-30% of patients - a nonspecific feeling of instability is much more common. Unlike Meniere's disease, mild vestibular symptoms persist between attacks. Symptoms of the disease may remain stable or progress slowly over many months or years. Upon examination, unilateral hearing loss of the sensorineural type is most often detected. Ipsilateral weakness of the facial muscles, decrease or loss of the corneal reflex, and decreased sensitivity on the face are also often noted. Less commonly observed are ataxia, spontaneous nystagmus, lesions of other cranial nerves, and signs of increased intracranial pressure. A caloric test reveals signs of unilateral vestibular dysfunction.

CEREBELLAR AND CENTRAL VESTIBULAR DISORDERS

Many pathological conditions cause acute or chronic cerebellar dysfunction. Some of these conditions are also accompanied by central vestibular dysfunction, most notably Wernicke encephalopathy, circulatory disorders in the vertebrobasilar region, multiple sclerosis and tumors of the posterior cranial fossa.

ACUTE DISORDERS

WERNICKE'S ENCEPHALOPATHY

Wernicke encephalopathy is an acutely occurring 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 can be a consequence of nutritional disorders of any origin. The pathological process mainly affects the medial nuclei of the thalamus, mammillary bodies, periaqueductal and periventricular nuclei of the brain stem (especially the nuclei of the oculomotor, abducens and pre-cochlear nerves), as well as the upper part of the cerebellar vermis. The development of ataxia is caused by both damage to the cerebellum and vestibular dysfunction.

Ataxia occurs predominantly or exclusively when walking. Impaired coordination of the lower extremities is observed only in a fifth of patients, and impaired coordination of the upper extremities is observed in only one tenth of them. Dysarthria is rare. Other classic manifestations include amnestic syndrome, confusion, horizontal or combined horizontal-vertical nystagmus, bilateral external rectus muscle weakness, and loss of the Achilles reflex. A caloric test reveals bilateral or unilateral vestibular dysfunction. Possible gaze paresis, disturbances of pupillary innervation, hypothermia.

The diagnosis is confirmed by a positive reaction to thiamine, which is usually initially administered intravenously at a dose of 100 mg. Improvement primarily concerns oculomotor functions and usually appears within a few hours after the start of treatment. The reverse development of ataxia, nystagmus, and confusion begins after a few days. Movements of the eyeballs are usually restored completely, sometimes only horizontal nystagmus remains.

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

ISCHEMIA IN THE VERTEBROBASILAR BASIS

Transient ischemic attacks or ischemic stroke in the vertebrobasilar region are often accompanied by dizziness and ataxia.

OCCLUSION OF THE INTERNAL AUDITORY ARTERY

The combination of central vertigo with unilateral hearing loss may occur due to occlusion of the internal auditory artery, which supplies the auditory nerve. This vessel can arise from the basilar or anterior inferior cerebellar arteries. Dizziness is accompanied by nystagmus, the fast phase of which is directed to the side contralateral to the lesion. Hearing loss is unilateral and belongs to the sensorineural type.

Main arteries of the posterior cranial fossa

LATERAL INFARCTION OF THE MEDULENA

Lateral medulla oblongata infarction is clinically manifested by Wallenberg syndrome and is most often a consequence of proximal occlusion of the vertebral artery. Symptoms are variable and depend on the extent of the infarction. Characterized by the presence of dizziness, nausea, vomiting, dysphagia, hoarseness and nystagmus in combination with Horner's syndrome, hemiataxia, disturbance of 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 hemiataxia is explained by involvement of the inferior cerebellar peduncle.

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

CEREBELLA INFARCTION

The cerebellum is supplied by three pairs of arteries: the superior cerebellar, anterior inferior cerebellar and posterior inferior 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 superior, middle, and inferior cerebellar peduncles are supplied by the superior, anterior inferior, and posterior inferior cerebellar arteries, respectively.

Cerebellar infarction occurs as a result of occlusion of one of the cerebellar arteries. The clinical manifestations that develop in this case can be distinguished only by the accompanying brainstem disorders. In all cases, cerebellar signs are represented by ataxia and muscle hypotonia in the ipsilateral limbs. Other symptoms may include headache, nausea, vomiting, dizziness, nystagmus, dysarthria, paralysis of gaze and external eye muscles, decreased sensitivity in the face, weakness of facial muscles, hemiparesis and hemihypesthesia in the contralateral limbs. Brainstem infarction or compression due to cerebellar edema can lead to coma and death. Diagnosis of cerebellar infarction is carried out using CT and MRI, which make it possible to differentiate between infarction and hemorrhage and, accordingly, should be performed as quickly as possible. When the brain stem is compressed, the only option to save the patient's life is surgical decompression and resection of necrotic tissue.

PARAMEDIAN MIDDLE BRAIN INFARCTION

Paramedian midbrain infarction is caused by occlusion of the paramedian penetrating branches of the basilar artery and is characterized by damage to the oculomotor nerve root and red nucleus. The resulting clinical picture (Benedict's syndrome) consists of paralysis of the ipsilateral medial rectus muscle with a dilated pupil that is not responsive to light and contralateral ataxia, usually involving only the arm. Cerebellar signs are caused by a lesion of the red nucleus, which receives crossed projection fibers coming from the cerebellum as part of its superior peduncle.

Paramedian midbrain infarction (Benedict syndrome). The infarct area is highlighted

HEMORRHAGE INTO THE CEREBELLUM

Most cases of cerebellar hemorrhage are associated with hypertensive arteriopathy. Less common causes are the use of anticoagulants, arteriovenous malformations, blood diseases, tumors and traumatic brain injury. Hypertensive cerebellar hemorrhages are usually localized in the deep white matter and often break into the fourth 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. This is usually followed by gait ataxia and depression of consciousness within a few hours. By the time of hospitalization, the patient may be lucid, confused, or comatose. Patients with clear consciousness often experience nausea and vomiting. Blood pressure is usually elevated. Rigidity of the neck muscles may be detected. The pupils are often constricted and react sluggishly to light. Paralysis of horizontal gaze to the ipsilateral side often occurs (the patient’s eyes are turned in the direction opposite to the lesion) and ipsilateral paralysis of the facial muscles. Gaze paresis is not overcome by caloric stimulation. Nystagmus and weakening of the corneal reflex on the affected side may be detected. In patients with clear consciousness, ataxia is detected when standing and walking; ataxia of the limbs is detected less frequently. At the late stage of compression of the brain stem, spasticity of the lower extremities and pathological foot reflexes develop. The CSF is bloody, but if cerebellar hemorrhage is suspected, lumbar puncture should be avoided as it may lead to herniation. The method of choice for diagnosing cerebellar hemorrhage is CT. The patient's life can often be saved only by surgical intervention with evacuation of the hematoma.

CHRONIC DISORDERS

MULTIPLE SCLEROSIS

Multiple sclerosis can cause ataxia of the cerebellar, vestibular or sensory type. The occurrence of cerebellar signs is associated with the appearance of foci of demyelination (plaques) in the cerebellar white matter, cerebellar peduncles or 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 nature. Dizziness is a common symptom of the advanced stage of the disease, but is rarely its first manifestation.

When the cerebellum is involved, gait ataxia is the first manifestation in 10-15% of patients. At the first examination, cerebellar signs are detected in a third of patients; later they occur in two thirds of patients.

One of the most common symptoms found on examination is nystagmus, which may or may not be accompanied by other signs of cerebellar dysfunction. Dysarthria is often noted. Gait ataxia is more often cerebellar in nature than sensory. Limb ataxia is common and is usually bilateral, involving both legs or all four limbs.

Multiple sclerosis is supported by anamnestic indications of a relapsing-remitting course of the disease, the presence of signs of multifocal damage to the central nervous system and such manifestations as optic neuritis, internuclear ophthalmoplegia, pyramidal signs, as well as data from paraclinical research methods. The CSF reveals oligoclonal antibodies, increased levels of IgG and protein, and mild lymphocytic pleocytosis. The study of visual, auditory and somatosensory evoked potentials allows us to identify areas of subclinical damage. CT and MRI detect areas of demyelination. However, it should be noted that the data of no paraclinical method are specific for multiple sclerosis, and when making a diagnosis, one should rely primarily on medical history and the results of a neurological examination.

ALCOHOL DEGENERATION CEREBELLA

Patients with chronic alcoholism may develop a characteristic cerebellar syndrome, which is likely the result of nutritional deficiency. Such patients usually have a history of daily or binge drinking for 10 years or more and inadequate nutrition. Most patients have already had or have other complications of chronic alcoholism: liver cirrhosis, delirium tremens, Wernicke encephalopathy, polyneuropathy. Alcoholic cerebellar degeneration occurs more often in men and usually appears between the ages of 40 and 60.

Degenerative changes are usually limited to the superior part of the cerebellar vermis. Since this area is also affected in Wernicke encephalopathy, both conditions appear to be considered part of a single clinical spectrum.

Alcoholic degeneration of the cerebellum begins imperceptibly, progresses steadily and, reaching a certain level, stabilizes. Progression usually takes several weeks or months, but occasionally continues for years. In some cases, ataxia appears suddenly or is mild and does not progress from the very beginning.

Walking ataxia is a universal symptom, which is almost always the main problem of patients, forcing them to seek medical help. During the knee-heel test, discoordination in the lower extremities is detected in 80% of patients. Frequent associated 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). Less commonly observed are upper limb ataxia, nystagmus, dysarthria, muscle hypotonia, and trunk ataxia.

FRIEDREICH'S ATAXIA

Among idiopathic degenerative diseases that cause cerebellar ataxia, Friedreich's ataxia occupies a special place due to the fact that it is more common than others and is characterized by unique clinical and pathomorphological manifestations. Unlike the autosomal dominant spinocerebellar ataxias of late age, which were discussed above, Friedreich's ataxia begins in childhood. It is transmitted according to an autosomal recessive mode of inheritance and is associated with an increase in the number of repeats of the GAA trinucleotide 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 mostly to the spinal cord. They are represented by degeneration of the spinocerebellar tracts, dorsal columns and dorsal roots, and a decrease in the number of neurons in Clark’s columns, from which the dorsal spinocerebellar tract originates. Thick myelinated axons of peripheral nerves and the bodies of 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 manifests itself. The initial symptom is usually progressive gait ataxia, which is followed by ataxia of all limbs over the next two years. Already at an early stage, knee and Achilles reflexes are lost and cerebellar dysarthria appears. Tendon reflexes in the upper extremities and sometimes knee reflexes may be preserved. In the lower extremities, joint-muscular sensation and vibration sensitivity are impaired, as a result of which gait ataxia is supplemented by a sensitive component. Disorders of tactile, pain and temperature sensitivity occur less frequently. Weakness of the lower and, less commonly, upper extremities develops later and may result from 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 - a foot with a high arch and deformation of the toes, 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). Severe progressive kyphoscoliosis aggravates functional disorders and can lead to the development of chronic restrictive respiratory failure. Myocardiopathy, sometimes detected only by echocardiography or vectorcardiography, can lead to heart failure and is one of the main causes of disability and death.

LITERATURE

General

• Brandt T: Management of vestibular disorders. J Neurol 2000;247:.
• Fetter M: Assessing vestibular function: which tests, when? J Neurol 2000;247:.
• Fife T D, Baloh RW: Disequilibrium of unknown cause in older people. Ann Neurol 1993;34:.
• Furman JM, Jacob RG: Psychiatric dizziness. Neurology 1997;48:.
• Hotson JR, Baloh RW: Acute vestibular syndrome. N Engl J Med 1998;339:.
• Nadol FB: Hearing loss. N Engl J Med 1993;329:.

Benign positional vertigo

• Epiey JM: The canalith repositioning procedure: for treatment of benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg 1992;107:.
• Furman JM, Cass SP: Benign paroxysmal position al vertigo. N Engl J Med 1999;341:.

Meniere's disease

• Slattery WH, 3rd, Fayad JN: Medical treatment of Meniere’s disease. Otolaryngol Clin North Am 1997;30:.
• Weber PC, Adkins WY, Jr: The differential diagnosis of Meniere’s disease. Otolaryngol Clin North Am 1997;30:.

Traumatic brain injury

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

Tumors of the cerebellopontine angle

• Gutmann DH et al: The diagnostic evaluation and multidisciplinary management of neurofibromatosis 1 and neurofibromatosis 2. JAMA 1997;278:51-57.
• Zamani AA: Cerebellopontine angle tumors: role of magnetic resonance imaging. Top Magn Reson Imaging 2000;11:98-107.

Wernicke's 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:.

Friedreich's ataxia

• 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 the process of meaningful perception of the internal and external world, the ability to analyze, remember, transform and reproduce information. Disorders of consciousness are divided into: Conditions with an altered LEVEL of consciousness, impairment of maintaining the level of wakefulness and reaction to external stimuli - for example: ACUTE CONFUSION, SUPPORT, COMA. Conditions with altered CONTENT of consciousness, with a normal level of consciousness - impairment of cognitive functions, for example: DEMENTIA, AMNESIA, APHASIA. ...

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Motor neurons of the oculomotor nerves (n. oculomotorius, III pair of cranial nerves) are located on both sides of the midline in the rostral part of the midbrain. These nuclei of the oculomotor nerve innervate the five extrinsic muscles of the eyeball, including the levator palpebral muscle. The nuclei of the oculomotor nerve also contain parasympathetic neurons (Edinger-Westphal nucleus), which are involved in the processes of pupil constriction 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 rectus, inferior oblique and inferior rectus muscles of the eye are located on the side of the same name. The subnucleus of the oculomotor nerve for the superior rectus muscle is located on the contralateral side. The levator palpebrae superioris muscle is innervated by the central group of cells of the oculomotor nerve.

Trochlear nerve (n. trochlearis, IV pair of cranial nerves)

The motor neurons of the trochlear nerve (n. trochlearis, IV pair of cranial nerves) are closely adjacent to the main part of the complex of nuclei of the oculomotor nerve. The left nucleus of the trochlear nerve innervates the right superior oblique muscle of the eye, the right nucleus innervates the left superior oblique muscle of the eye.

Abducens nerve (n. abducens, VI pair of cranial nerves)

Motor neurons of the abducens nerve (n. abducens, VI pair of cranial nerves), innervating the lateral (external) rectus muscle of the eye on the side of the same name, are located in the nucleus of the abducens nerve in the caudal part of the pons. 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 ensured precisely by the joint activity of individual muscles of the eye (oculomotor muscles). Conjugate movements of the eyeballs are controlled by the supranuclear gaze centers and their connections. Functionally, there are five different supranuclear systems. These systems provide various types of movements of the eyeballs. Among them there are centers that control:

• saccadic (rapid) eye movements
• purposeful eye movements
• convergent eye movements
• holding the gaze in a certain position
• vestibular centers

Saccadic (rapid) eye movements

Saccadic (fast) movements of the eyeball occur as a command in the opposite visual field of the cortex of the frontal region of the brain (field 8). The exception is fast (saccadic) movements that occur when the central fovea of ​​the retina is irritated, which originate from the occipital-parietal region of the brain. These frontal and occipital control centers in the brain have projections on both sides in the supranuclear brainstem centers. The activity of these supranuclear brain stem centers of vision is also influenced by the cerebellum and the vestibular nuclei complex. The paracentral sections of the reticular formation of the bridge are the stem center, providing friendly rapid (saccadic) movements of the eyeballs. Simultaneous innervation of the internal (medial) rectus and opposite external (lateral) rectus muscles when moving the eyeballs horizontally is provided by the medial longitudinal fasciculus. This medial longitudinal fasciculus connects the nucleus of the abducens nerve with the subnucleus of the complex of oculomotor nuclei, which are responsible for innervation of the opposite internal (medial) rectus muscle of the eye. To initiate vertical rapid (saccadic) eye movements, bilateral stimulation of the paracentral sections of the pontine reticular formation is required from the cortical structures of the brain. The paracentral sections of the pontine reticular formation transmit signals from the brain stem to the supranuclear centers that control the vertical movements of the eyeballs. This supranuclear eye movement center includes the rostral interstitial nucleus of the medial longitudinal fasciculus, located in the midbrain.

Purposeful 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 from the side of the same name, i.e. the right occipital-parietal region of the brain controls smooth, targeted eye movements to the right.

Convergent eye movements

The mechanisms of control of convergent movements are less understood, however, as is known, the neurons responsible for convergent eye movements are located in the reticular formation of the midbrain, surrounding the complex of oculomotor nerve nuclei. They give projections to the motor neurons of the internal (medial) rectus muscle of the eye.

Keeping your gaze in a certain position

Brainstem centers of eye movement, called neuronal integrators. They are responsible for holding the gaze in a certain position. These centers change incoming signals about the speed of movement of the eyeballs into information about their position. Neurons with this property are located in the pons below (caudal) the abducens nucleus.

Eye movement with changes in gravity and acceleration

Coordination of the movements of the eyeballs in response to changes in gravity and acceleration is carried out by the vestibular system (vestibular-ocular reflex). When the coordination of movements of both eyes is disturbed, double vision develops, since images are projected onto disparate (inappropriate) areas of the retina. In congenital strabismus, or strabismus, a muscle imbalance that causes the eyeballs to be misaligned (nonparalytic strabismus) may cause the brain to suppress one of the images. This decrease in visual acuity in the non-fixing eye is called amblyopia without anopia. In paralytic strabismus, double vision occurs as a result of paralysis of the muscles of the eyeball, usually due to damage to the oculomotor (III), trochlear (IV) or abducens (VI) cranial nerves.

Eyeball muscles and gaze palsies

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

Paralysis of individual eye muscles

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

Complete damage to the oculomotor (III) nerve leads to ptosis. Ptosis manifests itself in the form of weakening (paresis) of the muscle that lifts the upper eyelid and disruption of voluntary movements of the eyeball upward, downward and inward, as well as divergent strabismus due to the preservation of the functions of the lateral (lateral) rectus muscle. When the oculomotor (III) nerve is damaged, pupil dilation and lack of reaction to light (iridoplegia) and paralysis of accommodation (cycloplegia) also occur. Isolated paralysis of the muscles of the iris and ciliary body is called internal ophthalmoplegia.

Injuries to the trochlear (IV) nerve cause paralysis of the superior oblique muscle of the eye. Such damage to the trochlear (IV) nerve leads to outward deviation of the eyeball and difficulty moving (paresis) downward gaze. Paresis of downward gaze is most clearly manifested when turning the eyes inwards. Diplopia (double vision) disappears when the head is tilted to the opposite shoulder, which causes a compensatory inward deviation of the intact eyeball.

Damage to the abducens (VI) nerve leads to paralysis of the muscles that abduct the eyeball to the side. When the abducens (VI) nerve is damaged, convergent strabismus develops due to the predominance of the influence of the tone of the normally working internal (medial) rectus muscle of the eye. With incomplete paralysis of the abducens (VI) nerve, the patient can turn his head towards the affected abductor muscle of the eye in order to eliminate the existing double vision using a compensatory effect on the weakened lateral rectus muscle of the eye.

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

Friendly gaze paralysis

Companionate gaze is the simultaneous movement of both eyes in the same direction. Acute damage to one of the frontal lobes, for example, during cerebral infarction (ischemic stroke), can lead to transient paralysis of voluntary conjugate movements of the eyeballs in the horizontal direction. At the same time, independent eye movements in all directions will be completely preserved. Paralysis of voluntary conjugate movements of the eyeballs in the horizontal direction is detected using the doll eye phenomenon when passively turning the head of a horizontally lying person or using caloric stimulation (infusion of cold water into the external auditory canal).

Unilateral damage to the inferiorly located paracentral section of the reticular formation of the pons at the level of the nucleus of the abducens nerve causes persistent paralysis of gaze in the direction of 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 with the phenomenon of the head and eyes of a doll or caloric stimulation of the walls of the external auditory canal with cold water.

Damage to the rostral interstitial nucleus of the medial longitudinal fasciculus in the anterior midbrain and/or damage to the posterior commissure causes supranuclear upward gaze palsy. Added to this focal neurological symptom is the dissociated reaction of the patient’s pupils to light:

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

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

Isolated downward gaze palsy is rare in patients. When this occurs, the cause is most often blockage (occlusion) of the penetrating arteries in the midline and bilateral infarctions (ischemic strokes) of the midbrain. Some hereditary extrapyramidal diseases (Huntington's chorea, progressive supranuclear palsy) can cause restrictions in the movement of the eyeballs in all directions, especially upward.

Mixed paralysis of gaze and individual muscles of the eyeball

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

With lesions of the medial longitudinal fasciculus, various gaze disturbances occur in the horizontal direction (internuclear ophthalmoplegia).

Unilateral damage to the medial longitudinal fasciculus caused by infarction (ischemic stroke) or demyelination leads to disruption of the inward adduction of the eyeball (to the bridge of the nose). This can manifest clinically as complete paralysis with the inability to move the eyeball inward from the midline, or as a moderate paresis, which will manifest itself as a decrease in the speed of adducting rapid (saccadic) eye movements to the bridge of the nose (adductive delay). On the side opposite to the lesion of the medial longitudinal fasciculus, as a rule, abduction nystagmus is observed: nystagmus that occurs when the eyeballs are abducted outward with a slow phase directed towards the midline and fast horizontal saccadic movements. An asymmetrical arrangement of the eyeballs relative to the vertical line often develops with unilateral internuclear ophthalmoplegia. On the affected side, the eye will be positioned higher (hypertropia).

Bilateral internuclear ophthalmoplegia occurs with demyelinating processes, tumors, infarction, or arteriovenous malformations. Bilateral internuclear ophthalmoplegia leads to a more complete syndrome of eyeball movement disorders, which are manifested by bilateral paresis of the muscles that lead the eyeball to the bridge of the nose, impaired vertical movements, purposeful tracking movements and movements caused by the influence of the vestibular system. There is a disturbance of gaze along a vertical line, upward nystagmus when looking up and downward nystagmus when looking down. Lesions of the medial longitudinal fasciculus in the overlying (rostral) parts of the midbrain are accompanied by a violation of convergence (convergent movement of the eyes towards each other, towards the bridge of the nose).