Nystagmus (horizontal and vertical) - causes and treatment, features in children

Nystagmus is the name given to rapid, repetitive eye movements that occur regardless of a person’s conscious commands. A similar condition sometimes occurs normally if a person has to watch a rapidly moving object, cold water gets into his ear, or his body rotates in space (for example, on a carousel). Some diseases of the nervous system, eye or inner ear can also lead to the appearance of this symptom. The pathology is very easy to diagnose, but it is difficult to treat.

The mechanism for the development of nystagmus is a violation of a peripheral organ (eyeball, nerves of the extraocular muscles, labyrinth in the peripheral part of the vestibular apparatus and the nerve coming from it), or the brain.

The long-term existence of nystagmus, even when it appears as a result of damage to the central nervous system and vestibular apparatus, leads to an inevitable decrease in visual acuity, since the brain does not receive normal images of objects from the eyes.

Causes

Nystagmus is usually divided into congenital and acquired:

Congenital pathology is quite rare. It is inherited or occurs as a result of birth injuries and intrauterine infections, giving impetus to the development of incomplete atrophy of the optic nerve, strabismus, retinal dystrophy, farsightedness, astigmatism, and myopia.

Acquired nystagmus can develop due to:

Multiple sclerosis.
Tumors in the brain.
Brain contusion.
Inflammation of the inner ear.
Encephalitis.
Temporal bone cracks.
Stroke.
Tumors of the nerve that carries information from the vestibular and auditory analyzers (vestibular-cochlear).
Exposure to drugs and certain toxins.
Taking a number of medications (lithium compounds, carbamazepine, barbiturates).
Some ophthalmological diseases.

Pendulum-like eye movements often cause damage to the brain, namely: the cerebellum, brain stem, pons, midbrain, sella turcica, pituitary gland, rhomboid fossa, medulla oblongata.

At the same time, the direction of involuntary eye movement may indicate the localization of the lesion:

With horizontal movements, as a rule, the inner ear or middle sections in the rhombencephalon are affected.
With vertical or diagonal movements, the problem lies in the area of the upper sections in the diamond-shaped fossa.
During rotational movements, the lower parts of the rhombencephalon are often affected.
With converging movements, we are talking about pathologies of the midbrain.

When diagnosing, to more accurately determine the level of damage, the neurologist must also evaluate the speed of eyeball movements and their amplitude.

Diagnostics

When diagnosing the disease, an integrated approach is used , during which the following indicators and characteristics are checked:

visual potential;
state of the optical media of the eye;
visual acuity (if the patient wears corrective optics, vision will be checked first without it, and then with it);
condition of the optic nerve;
condition of the retina and fundus of the eye;
electroretinogram readings.

Additionally, examination methods such as MRI of the brain, echo-encephalography and electroencephalogram may be prescribed .

Types of nystagmus

According to the direction of oscillatory eye movements, the disease is divided into:

Vertical nystagmus, if the eye moves up and down (vertically);
Horizontal nystagmus, when movements occur along a horizontal axis;
Rotatory nystagmus, with rotational movements around the sagittal axis;
Convergent nystagmus, in which there is rapid movement of the eyes towards each other;
Diagonal nystagmus - movement along a diagonal.

The direction in which the nystagmus is directed must be judged by its rapid phase.

If the eye movements are of the same type, the nystagmus is called associated, if different - dissociated.

Nystagmus is also distinguished by the location of the lesion:

1. Vestibular. Its causes are due to pathologies of the part of the brain that receives information from the vestibular apparatus, as well as a disease of the labyrinth itself (peripheral vestibular apparatus). Such nystagmus can be caused by rotation of the body, as well as a caloric test (pour cold or warm water of a certain temperature into the ear). It can also occur spontaneously, accompanied by nausea and dizziness. 2. Central. Such nystagmus develops with traumatic, dystrophic, tumor or inflammatory lesions of the cerebellum, structures in the posterior cranial fossa, subcortical and cortical centers for the regulation of eye movements.

There are also other classifications.

Pathogenesis

Nystagmus is not just a cosmetic defect, but a severe form of oculomotor disorder, which leads to impaired visual acuity due to problems with eye fixation or improper focusing of the image in the retina (for example, myopia ) . It can also occur due to prolonged systematic eye strain and awkward posture (occupational nystagmus).

First, the patient begins to notice changes in the quality of vision - twitching, blurriness. Most often, to focus on an object, you need to change the tilt of your head. In the future, headaches, nausea and dizziness .

Symptoms of nystagmus

Nystagmus is characterized by movements of the eyeball that occur spontaneously or after some provocation. Movements are pendulum-like (back and forth) and last the same amount of time in the horizontal and vertical planes or diagonally. If the eye moves faster in one direction than in the other, then such nystagmus is defined as jerky.

There is also a mixed type, in which when a person looks forward, pendulum-like movements occur, but when looking in any direction, jerky movements occur.

Classification

Types of vertical nystagmus:

Infantile. Most often develops between 2 and 3 months of age. Associated with other conditions such as albinism, congenital absence of the iris (the colored part of the eye), underdeveloped optic nerves, and congenital cataracts.
Drooping. Usually occurs between 6 months and 3 years. Children with this form of nystagmus often nod and tilt their heads. Their eyes can move in any direction. This type of nystagmus usually does not require treatment.
Acquired. Develops later in childhood or adulthood. The cause is often unknown, but it may be due to central nervous system and metabolic disorders, alcohol toxicity, drug toxicity.

Based on the type of shocks, a distinction is made between pendulum-like and jerk-like. The first is characterized by sinusoidal oscillations, the second - by alternating a slow phase and a corrective fast one.

There is another classification for neurological patients. There are labyrinthine-vestibular, periodically alternating and dissociated VN.

Nystagmus in children

Nystagmus in children has its significant differences:

1. The likelihood of a child having the disease exists if the baby does not fix his gaze by the 4th week of life. This type of pathology is congenital in nature and is caused by the influence of unfavorable factors on the child’s brain during the prenatal period of development or a genetic disorder of the innervation of the extraocular muscles. This condition has the following characteristics:

Appears by 2-3 months, persisting for life;
Not visible during sleep;
It has a jerky character and a horizontal orientation;
There is a direction of gaze in which nystagmus does not appear.

2. Early acquired nystagmus is caused by pathology of both eyes, which reduces central vision. In terms of symptoms, it is similar to congenital, but appears a little later. In this case, the child notices eye twitching and this greatly bothers him. 3. Nodule spasm is a pathological condition that accompanies nystagmus, which develops by 3-18 months. It may be of unknown nature (and disappears by the age of 3 years), and is often caused by some pathology (including tumors) of the brain or cranial nerves. In this case, nystagmus has a small amplitude, high frequency and develops in the horizontal plane (sometimes with vertical components), accompanied by nodding of the head. 4. Hidden, latent nystagmus, develops due to infantile strabismus, occurs without paresis of upward or downward gaze. Such nystagmus is absent with open eyes, but appears when the intensity of illumination of one eye decreases and has a horizontal direction. 5. Infantile nystagmus is often observed with albinism, a genetic disease characterized by the absence of pigment in the iris. Involuntary eye movements in children can also be caused by post-traumatic encephalopathy or be the first signs of Meniere's disease.

Strabismus

Strabismus is a deviation of the eye from the general point of fixation, which is accompanied by a violation of visual (monocular, binocular) functions.

There are two types of strabismus:

Friendly . Eye mobility is not impaired, the primary and secondary angles of strabismus (deviation) are equal, the same in all directions of gaze).

Unfriendly . The main symptom of this strabismus is a more or less severe limitation of eye mobility. In non-conjugate strabismus, the primary and secondary angles of strabismus are not equal and are different in one or more directions of gaze.

Paralytic (complete lack of eye mobility in the direction of the paralyzed extraocular muscle) and paretic (weakening of eye mobility in the direction of the paretic extraocular muscle) strabismus require, first of all, examination and treatment by a neurologist.

Patients planning surgery for strabismus need to understand that surgical intervention allows for a good cosmetic effect. That is, achieving a symmetrical or close to it eye position. But it does not allow, in most patients, to achieve a functional result. That is, to form binocular or stereoscopic vision.

Treatment of nystagmus

Treatment for the condition depends on the type of pathology detected:

Inflammation of the labyrinth or eye requires conservative treatment of these diseases;
For albinism, wearing sunglasses or pierced glasses and tinted contact lenses is prescribed;
In some cases, vision correction by surgical methods is required;
Surgical removal of a brain tumor;
Medications are prescribed to improve the nutrition of the retina and other structures of the organ of vision (vitamin complexes, vasodilators, drugs that reduce blood viscosity).

In the medical department, everyone can undergo examination using the most modern diagnostic equipment, and based on the results, receive advice from a highly qualified specialist. The clinic is open seven days a week and operates daily from 9 a.m. to 9 p.m. Our specialists will help identify the cause of vision loss and provide competent treatment for identified pathologies.

You can find out the cost of a particular procedure or make an appointment at the Moscow Eye Clinic by calling 8 8 (499) 322-36-36 (daily from 9:00 to 21:00) or using the online registration form.

(from the book Neurology. G.D. Weiss. Edited by M. Samuels. Translated from English - M., Praktika, 1997. -640 p.)

Dizziness is one of the most common and at the same time one of the most “disliked” complaints by doctors. The fact is that dizziness can be a symptom of a wide variety of neurological and mental diseases, diseases of the cardiovascular system, eyes and ears.

I. Definition. Since patients can call a variety of sensations “dizziness,” during the interview it is necessary first of all to clarify the nature of these sensations. They can usually be classified into one of four categories.

A. Vestibular dizziness (true dizziness, vertigo) is usually caused by damage to the peripheral or central part of the vestibular system. It manifests itself as the illusion of movement of one’s own body or surrounding objects. In this case, sensations of rotation, falling, tilting or swaying occur. Acute dizziness is often accompanied by autonomic symptoms (nausea, vomiting, increased sweating), anxiety, imbalance and nystagmus (the latter sometimes leading to blurred vision).

B. Fainting and pre-syncope. These terms refer to temporary loss of consciousness or the feeling of impending loss of consciousness. In a pre-fainting state, increased sweating, nausea, a feeling of fear and darkening of the eyes are often observed. The immediate cause of fainting is a drop in cerebral blood flow below the level necessary to supply the brain with glucose and oxygen. Fainting and presyncope usually develop against the background of arterial hypotension, heart disease or due to autonomic reactions, and the tactics for these conditions are completely different than for vestibular vertigo.

B. Impaired balance is characterized by instability, a wobbly (“drunk”) gait, but not true dizziness. The cause of this condition is damage to various parts of the nervous system that provide spatial coordination. However, patients with cerebellar, visual, extrapyramidal and proprioceptive disorders often define the feeling of unsteadiness as “dizziness.”

D. Vague sensations , often described as dizziness, occur with emotional disorders, such as hyperventilation syndrome, hypochondriacal or hysterical neurosis, depression. Patients usually complain of “brain fog,” feeling slightly intoxicated, lightheaded, or fear of falling. These sensations are quite clearly different from the sensations associated with vestibular dizziness, fainting and balance disorders. Since any dizziness, regardless of its cause, can cause anxiety, it cannot serve as evidence of the psychogenic nature of the disease.

D. Some patients with complaints of dizziness find it difficult to describe their sensations. In this case, it is advisable to conduct provocative tests.

1. The standard set of provocative tests for dizziness includes:

A. Orthostatic test. b. Forced hyperventilation for 3 minutes. V. Sharp turns while walking or spinning in a circle while standing. d. Nilen-Barany test for positional vertigo. d. Valsalva maneuver, which increases dizziness caused by craniovertebral anomalies (for example, Arnold-Chiari syndrome) or perilymphatic fistula, and also causes lightheadedness in patients with cardiovascular diseases.

2. After each test, it is necessary to ask whether the resulting dizziness resembles the sensation that worries the patient. For orthostatic hypotension, hyperventilation syndrome, positional vertigo and many vestibular disorders, test results are well reproducible, which provides important diagnostic information.

II. Clinical examination of patients with vestibular vertigo. In order to evaluate the results of research, it is necessary to have a good knowledge of the relationships of the vestibular system with the oculomotor, auditory and spinocerebellar systems. There are two main types of vestibular reflexes. Thanks to the vestibulo-ocular reflexes, gaze fixation on the objects under consideration is maintained, that is, the constancy of the image on the retina. Vestibulospinal reflexes provide the positioning of the head and torso necessary for coordinated movements and maintaining an upright posture.

A. Nystagmus in patients with dizziness is the most important sign of vestibular disorders. Knowing a few simple physiological principles can help you avoid common mistakes in interpreting nystagmus.

1. Canal-ocular reflexes. Each horizontal semicircular canal is connected through the neurons of the brain stem with the oculomotor muscles in such a way that a decrease in impulses from it causes the eyes to deviate towards this canal, and an increase causes movement in the opposite direction. Normally, the impulses constantly flowing into the brain stem from the right and left semicircular canals and otolith organs are equal in intensity. A sudden imbalance of vestibular afferentation causes a slow eye deviation that is interrupted by rapid cortical activation-induced corrective eye movements in the opposite direction (nystagmus).

2. Lesions of the labyrinth usually cause a decrease in impulses from one or more semicircular canals. In this regard, with acute unilateral lesions of the labyrinth, unidirectional nystagmus occurs, the slow phase of which is directed towards the affected ear, and the fast phase - in the opposite direction. Nystagmus can be rotatory or horizontal. It intensifies when the eyes are moved towards its fast phase (that is, towards the healthy ear). With acute vestibular dysfunction, surrounding objects usually “rotate” in the direction of the fast phase of nystagmus, and the body in the direction of the slow phase. Patients sometimes better determine the direction of rotation with their eyes closed. In a standing position, patients deviate and fall predominantly towards the slow phase of nystagmus (that is, the affected ear).

3. Central nystagmus. Alternating nystagmus, which changes its direction depending on the direction of gaze, is more often observed with drug intoxication, lesions of the brain stem, or pathological processes in the posterior cranial fossa. Vertical nystagmus almost always indicates damage to the brainstem or midline cerebellar structures.

B. Cold test. Normal physiological stimuli simultaneously affect both labyrinths. The value of the cold test is that it allows you to study the function of each labyrinth separately. The study is carried out with the patient lying down; the head is raised at an angle of 30°. The external auditory canal is washed with cold water, thereby simulating unilateral vestibular hypofunction (observed, for example, with vestibular neuronitis or labyrinthitis). Cold water causes movement of the endolymph, as a result of which the impulse from the horizontal semicircular canal decreases. Normally, this leads to nausea, dizziness and horizontal nystagmus, the slow phase of which is directed in the direction being examined, and the fast phase in the opposite direction. Monitor the direction, duration and amplitude of nystagmus. A decrease in response on one side indicates damage to the labyrinth, vestibulocochlear nerve, or vestibular nuclei on that side. The study is contraindicated if the eardrum is damaged.

B. Electronystagmography. The retina is negatively charged in relation to the cornea, so when the eyes move, the electric field changes and an electric current occurs. Recording this current (and therefore eye movements) using electrodes placed around the eyes is called electronystagmography. This method allows you to quantify the direction, speed and duration of nystagmus. Electronystagmography is used in functional vestibular tests to record spontaneous, positional, cold and rotational nystagmus. Electronystagmography can be used to record nystagmus with eyes closed. This provides important additional information since nystagmus is often suppressed during gaze fixation.

D. Hearing loss and tinnitus can occur with diseases of the peripheral vestibular system (inner ear or vestibulocochlear nerve), if the hearing aid is involved in the process. When the central nervous system is damaged, hearing is rarely impaired. For vestibular vertigo, audiological testing often helps establish the diagnosis.

1. In pure-tone audiometry, the threshold for the perception of sounds of different frequencies is measured. For differential diagnosis of sensorineural and conductive hearing loss, the auditory threshold for air and bone conduction of sound is compared.

2. For a more accurate audiological assessment, speech perception and intelligibility, the phenomenon of accelerated increase in sound volume and tone decay are additionally examined.

D. Stabilography - the study of balance using a moving platform - allows you to quantify involuntary postural reflexes that prevent falls, as well as the role of information from various senses in maintaining balance.

E. Functional vestibular tests, electronystagmography and stabilography are complex and labor-intensive procedures. They cannot replace a thorough clinical examination, and for non-vestibular vertigo they are not necessary.

III. Diagnosis and treatment of diseases accompanied by vestibular vertigo. The two most common causes of vestibular vertigo are vestibular neuronitis and benign positional vertigo.

A. Vestibular neuronitis (acute peripheral vestibulopathy, vestibular neuritis).

1. General information. Vestibular neuronitis is characterized by a sudden, prolonged attack of dizziness, often accompanied by nausea, vomiting, loss of balance, and a feeling of fear. Symptoms worsen with head movements or changes in body position. Patients tolerate this condition extremely hard and often do not get out of bed. Spontaneous nystagmus is characteristic, the slow phase of which is directed towards the affected ear. On the same side, the reaction to a cold test decreases. Positional nystagmus is often noted. Sometimes there is noise and a feeling of fullness in the ear. Hearing does not decrease, and the results of audiological examination remain normal. There are no focal symptoms indicating damage to the brain stem (paresis, diplopia, dysarthria, sensory disturbances). The disease occurs in adults of any age. Acute dizziness usually resolves spontaneously within a few hours, but may recur over the next few days or weeks. Subsequently, residual vestibular dysfunction may persist, manifested by imbalance, especially pronounced when walking. In almost half of cases, attacks of dizziness recur after several months or years. The cause of vestibular neuronitis is unknown. A viral etiology has been suggested (as with Bell's palsy), but there is no evidence of this. Vestibular neuronitis is more of a syndrome than a separate nosological form. Neurological and otoneurological examinations help establish the peripheral nature of vestibular dysfunction and exclude lesions of the central nervous system, which usually have a less favorable prognosis.

2. Therapeutic measures. A few simple techniques can significantly reduce dizziness.

1) Since head movements and external stimuli increase dizziness, the patient is recommended to lie in a darkened room for 1-2 days.

2) Gaze fixation reduces nystagmus and dizziness in peripheral vestibular disorders. Often the condition improves - and even to a greater extent than when lying with eyes closed - if patients fix their gaze on some nearby object (for example, on a picture or a raised finger).

3) Since mental stress increases dizziness, it is advisable to combine gaze fixation with mental relaxation methods.

4) In case of persistent vomiting, intravenous fluid administration is indicated to prevent dehydration.

5) Measures for persistent dizziness. With vestibular neuronitis, the condition does not improve significantly in the first 1-2 days. The person feels seriously ill and is afraid of repeated attacks of dizziness. In such a situation, it is important to reassure the patient, convincing him that vestibular neuronitis and most other acute vestibular disorders are not dangerous and pass quickly. It should also be explained that within a few days the nervous system will adapt to the imbalance between both vestibular organs (even if one of them is irreversibly damaged) and the dizziness will stop.

6) Vestibular gymnastics, which stimulates central compensatory processes, begins a few days after the acute manifestations subside.

B. Benign positional vertigo

1. General information. Benign positional vertigo is probably the most common vestibular disorder. Dizziness in this case appears only when moving or changing the position of the head, especially when tilting it back and forth. This condition often occurs when the patient turns over from his back to his side and suddenly, at a certain position of the head, feels that “the room has moved.” Dizziness usually lasts a few seconds. Often patients know in what position of the head it occurs. Changes in head position can worsen vertigo in vestibular neuronitis and many other peripheral or central vestibular disorders, but in benign positional vertigo, symptoms occur only with certain movements and are absent at other times.

2. Differences from positional vertigo of central origin. Positional vertigo can also occur with many other diseases, including lesions of the brain stem (multiple sclerosis, stroke or tumor). In order to distinguish benign positional vertigo from more dangerous diseases of the central nervous system, the Nilen-Barany test is performed. The seated patient is tilted with his head at an angle of 45°, after which he is lowered onto his back. Then the test is repeated, after first turning the thrown back head first to the right, then to the left. The result is assessed by the appearance of nystagmus and dizziness. The latent period, duration, direction and exhaustibility of nystagmus are of important diagnostic importance. In benign positional vertigo, the latent period of nystagmus and dizziness is several seconds, the nystagmus is rotatory, and its fast phase is usually directed towards the affected ear. Nystagmus and dizziness are usually short-lived (less than 30 s) and decrease with repetition of the test (depletion of nystagmus). The Nilen-Barany test can confirm the diagnosis of benign positional vertigo. However, a negative result does not exclude this disease, since its symptoms are transient and are not always triggered by head movement.

3. Etiology. Benign positional vertigo can occur after traumatic brain injury, a viral disease, otitis media or stapedectomy, as well as with certain intoxications (for example, alcohol and barbiturates). Idiopathic cases of the disease, apparently, in most cases are associated with cupulolithiasis, a degenerative process with the formation of otoconial deposits in the cupula of the frontal semicircular canal, resulting in a sharp increase in the sensitivity of this canal to gravitational influences when the position of the head changes.

4. The course of the disease can be very different. In many cases, symptoms resolve on their own within a few weeks and then do not return until months or years later. Sometimes a short-term attack occurs only once in a lifetime. Only rarely does positional vertigo persist for a long time.

5. Treatment. For symptomatic therapy, the above remedies are used, but they are often ineffective. With careful repetition of movements that provoke dizziness, pathological reactions are gradually “exhausted.” Some believe that vestibular exercises, which include provocative head movements, speed up recovery. Patients are advised to hold their head in a position that usually causes dizziness for 30 seconds. This simple exercise, performed 5 times every few hours, in most cases brings improvement within a few weeks. If such vestibular gymnastics is accompanied by too unpleasant sensations, then a soft corset is used that immobilizes the neck and prevents the head from tilting in an unfavorable direction. As with vestibular neuronitis, it is important to convince the patient that, despite the extremely unpleasant sensations, the disease will soon pass and is not life-threatening. It is extremely rare for severe persistent positional vertigo to transect the ampullary nerve coming from the frontal semicircular canal on the affected side.

B. Post-traumatic dizziness. Despite the fact that the labyrinth is protected by a bone sheath, its thin membranes are easily damaged by injury. Uncomplicated concussion is accompanied by dizziness in more than 20% of cases. With traumatic brain injury, transient autonomic disorders (palpitations, hot flashes, increased sweating), which are accompanied by non-vestibular dizziness, are also possible. Post-traumatic dizziness manifests itself in two main syndromes.

1. Acute post-traumatic dizziness. Vestibular dizziness, nausea and vomiting can occur immediately after injury due to the sudden shutdown of one of the labyrinths (labyrinth shock). Less commonly, dizziness is caused by transverse or longitudinal fractures of the temporal bone, which are accompanied, respectively, by hemorrhage in the middle ear or damage to the eardrum with bleeding from the external auditory canal.

Clinical picture. Dizziness is constant. Characterized by spontaneous nystagmus with a slow phase directed towards the lesion, and imbalance with a tendency to fall in the same direction. Symptoms intensify with sudden movements of the head and in a position where the damaged labyrinth is at the bottom.

2. Post-traumatic positional vertigo. Within a few days or weeks after the injury, repeated short-term attacks of vestibular dizziness and nausea may occur, which are provoked by head movement.

A. The clinical picture is the same as for benign positional vertigo.

b. Forecast. In most cases, spontaneous remission occurs within 2 months after injury, and within 2 years in almost all.

3. Perilymphatic fistula. The membranous labyrinth filled with endolymph is surrounded by the perilymphatic space. When a rupture occurs in the area of the oval or round opening, a perilymphatic fistula can form, through which changes in pressure in the middle ear cavity are directly transmitted to the inner ear. The cause of a perilymphatic fistula can be, in particular, barotrauma (from straining, sneezing, coughing, diving).

A. Clinical picture. Characterized by intermittent or positional vestibular vertigo and variable sensorineural hearing loss. Worsening often occurs with elevation (including rapid ascent in an elevator) and with physical exertion similar to the Valsalva maneuver (straining or lifting). Sometimes dizziness occurs with loud sounds (Tullio's symptom).

b. Diagnostics. A perilymphatic fistula should be suspected when vestibular or auditory disturbances appear after trauma. However, due to the variability of symptoms, it can be difficult to distinguish from other diseases (Meniere's syndrome, benign positional vertigo, craniovertebral anomalies). There are no pathognomonic signs in the study of pressor nystagmus, electronystagmography, or stabilography. Perilymphatic fistula is probably one of the common causes of vestibular vertigo of “unexplained etiology.”

V. Treatment. The perilymphatic fistula usually closes spontaneously, which is accompanied by the disappearance of symptoms. In persistent cases, if a perilymphatic fistula is suspected, surgical intervention is indicated (tympanotomy with restoration of the integrity of the oval or round foramen). After surgery, vestibular symptoms usually improve, but hearing is rarely restored.

G. Meniere's syndrome

1. General information. Meniere's syndrome usually begins between 20 and 40 years of age. It is characterized by sudden attacks of severe vestibular vertigo, lasting from a few minutes to several hours. Before an attack, and sometimes after it, there is a feeling of stuffiness and fullness, or noise in the ear, transient hearing loss. After an attack, imbalance may persist for a long time, especially noticeable when walking.

2. The course is characterized by remissions and exacerbations. At the onset of the disease, sensorineural hearing loss (mainly for low sounds) is episodic. As a result of repeated attacks, hearing progressively decreases, but periods of improvement are possible.

3. Pathogenesis. The main morphological changes in Meniere's syndrome are stretching of the walls and an increase in the volume of the endolymphatic space (endolymphatic hydrops). The cause may be impaired absorption of fluid in the endolymphatic sac or obstruction of the endolymphatic duct.

4. Treatment. During an attack, bed rest and vestibulolytic drugs are prescribed. The rational choice of drugs for the prevention of attacks and the assessment of their effectiveness are difficult due to insufficient knowledge about the pathogenesis of the disease and the unpredictability of its course (including the possibility of long-term spontaneous remissions). According to recent studies, any of the existing treatment regimens (including placebo) causes temporary improvement in approximately 70% of patients.

A low-sodium diet in combination with diuretics (thiazides or acetazolamide) has been recommended for the treatment of Meniere's syndrome; it has been suggested that this may reduce fluid accumulation in the endolymphatic space. However, the pathophysiological feasibility of this therapy has not been proven, and in recent years it has been used less frequently.

5. In a small proportion of cases, for frequent, severe, treatment-resistant attacks, surgical treatment is indicated. There is no ideal surgery for Meniere's syndrome. Shunting of the endolymphatic sac reduces dizziness in 70% of patients, but in 45%, hearing continues to decline after surgery. Destructive operations (selective transtemporal transection of the vestibular part of the vestibulocochlear nerve, labyrinthectomy or translabyrinthine vestibulectomy) are indicated for persistent severe dizziness and severe unilateral hearing loss.

6. Differential diagnosis

A. In all cases, it is necessary to exclude a tumor of the cerebellopontine angle (including schwannoma of the vestibular-cochlear nerve. Tumors of this location cause noise in the ear, hearing loss, imbalance, but only rarely - attacks of dizziness.

b. The cause of attacks of dizziness and hearing loss can also be infectious labyrinthitis, perilymphatic fistula, Cogan's syndrome, and hyperviscosity syndrome.

V. Congenital syphilis. Symptoms of labyrinthine lesions in congenital syphilis often appear only in middle age and can mimic Meniere's syndrome. Treponema pallidum persisting in the temporal bone causes chronic inflammation leading to endolymphatic hydrops and labyrinthine degeneration. The course is progressive. As a result, both ears are affected. All patients with bilateral Meniere-like symptoms should be examined for latent syphilis using treponemal reactions (primarily RIF-ABS), since non-treponemal reactions (including the reagin rapid test and the VDRL reaction) in syphilitic labyrinthitis can give negative results.

D. Labyrinthitis

1. Bacterial labyrinthitis. When there is a bacterial infection of the middle ear or mastoid process (such as chronic otitis media), bacterial toxins can cause inflammation of the structures of the inner ear (serous labyrinthitis). Symptoms may be minimal at first, but they gradually worsen without treatment. Direct infection of the labyrinth (purulent labyrinthitis) is possible with bacterial meningitis or disruption of the integrity of the membranes separating the inner ear from the middle ear. Patients experience acute vestibular dizziness, nausea, hearing loss, fever, headache and ear pain. Purulent labyrinthitis is a dangerous disease that requires early diagnosis and antibiotic therapy.

2. Viral labyrinthitis. Damage to the auditory and vestibular organs is observed with various viral infections, including influenza, herpes, rubella, mumps, viral hepatitis, measles, and infection caused by the Epstein-Barr virus. Most patients recover on their own.

E. Functional vertigo occurs as a result of a disruption in the interaction between the vestibular, visual and somatosensory systems, which normally work together to provide spatial orientation. Dizziness can also be caused by physiological stimulation of normally functioning sensory systems.

1. Motion sickness is caused by unusual acceleration of the body or a discrepancy between afferentation entering the brain from the vestibular and visual systems. In a person in a closed cabin on a ship or in the back seat of a moving car, vestibular afferentation creates a sensation of acceleration, while visual afferentation indicates the relative immobility of surrounding objects. The intensity of nausea and dizziness is directly proportional to the degree of sensory mismatch. Motion sickness is reduced when there is sufficient panoramic visibility to verify the reality of the movement.

2. Visually caused dizziness occurs when observing moving objects - due to a mismatch of visual afferentation with vestibular or somatosensory (for example, when a person watches a movie with a car chase).

3. High-altitude vertigo is a common phenomenon that occurs when the distance between a person and the stationary objects he observes exceeds a certain critical value. The often observed fear of heights prevents adaptation to the physiological mismatch of vestibular and visual afferentation.

G. Transient ischemia of the brainstem

1. General information

A. Clinical picture

1) Vestibular dizziness and imbalance are the two most common symptoms of transient brainstem ischemia resulting from damage to the arteries of the vertebrobasilar region. At the same time, only in rare cases are they the only manifestations of this disease. If repeated attacks of dizziness are not accompanied by other signs of brainstem ischemia (diplopia, dysarthria, sensory disturbances of the face or limbs, ataxia, hemiparesis, Horner's syndrome or hemianopsia), then they are usually caused not by vertebrobasilar insufficiency, but by peripheral vestibulopathy.

2) Impaired balance and blurred vision occur both with vestibular neuronitis and with lesions of the trunk, and therefore do not allow us to clarify the localization of the lesion. Acute hearing loss is not typical for ischemic lesions of the brainstem; a rare exception is occlusion of the anterior inferior cerebellar artery, from which the internal auditory artery arises to the inner ear.

b. Differential diagnosis

1) Since transient brainstem ischemia requires active therapy aimed at preventing brainstem stroke, it is important to differentiate it from more benign disorders (in particular, vestibular neuronitis).

2) In the interictal period with transient ischemia of the brainstem, there are no signs of focal brain damage. However, during an attack, careful examination can reveal disorders such as Horner's syndrome, slight strabismus, internuclear ophthalmoplegia, central alternating or vertical nystagmus, etc., characteristic of damage to the trunk, but not the vestibular apparatus. With ischemia of the trunk, it is often possible to induce positional nystagmus. The Nilen-Barany test helps to distinguish central from peripheral lesions. Vestibular vertigo and imbalance may also occur with brainstem lesions of other etiologies, such as multiple sclerosis or tumors.

H. Cerebellar stroke

1. Clinical picture. Damage to the cerebellum due to ischemia or hemorrhage in the posterior inferior cerebellar artery can manifest as severe vestibular vertigo and imbalance, which can easily be mistaken for symptoms of acute vestibular neuronitis. Sometimes the lesion is limited to the cerebellar hemisphere, and in this case there are no signs of damage to the lateral medulla oblongata (dysarthria, numbness and paresis of the facial muscles, Horner's syndrome, etc.). Infarction in the superior cerebellar artery causes abasia and ataxia, which are usually not accompanied by severe dizziness.

2. Diagnostics. Impaired balance with a tendency to fall towards the lesion is observed with damage to both the vestibular system and the cerebellar hemispheres and does not help in the differential diagnosis. Central alternating nystagmus, the fast phase of which is directed towards gaze, and hemiataxia indicate damage to the cerebellar hemisphere. A CT scan can diagnose cerebellar hemorrhage, but may not detect a heart attack (especially if the test is performed immediately after the onset of symptoms). A more reliable method for diagnosing cerebellar infarction is MRI.

3. Current. Cerebellar infarctions and hemorrhages are often limited in size and the outcome is favorable. Typically, gradual recovery occurs and the residual defect is minimal. More extensive lesions, accompanied by cerebellar edema, can cause compression of the trunk and fourth ventricle. This severe complication requires surgical decompression, but it can be prevented by timely dehydration, so early diagnosis and careful monitoring in the acute phase are extremely important for cerebellar strokes.

I. Oscillopsia is the illusion of vibration of stationary objects. Oscillopsia in combination with vertical nystagmus, instability and vestibular vertigo is observed with craniovertebral anomalies (for example, Arnold-Chiari syndrome) and degenerative lesions of the cerebellum (including olivopontocerebellar atrophy and multiple sclerosis).

K. Vestibular epilepsy. Dizziness can be the leading manifestation of simple and complex partial seizures if they occur in the vestibular areas of the cortex (superior temporal gyrus and association areas of the parietal lobe). Dizziness in this case is often accompanied by noise in the ear, nystagmus, and paresthesia in the contralateral limbs. The attacks are usually short-lived and can easily be confused with other diseases that manifest as vestibular vertigo. In most cases, such seizures are combined with typical manifestations of temporal lobe epilepsy. The diagnosis is confirmed by EEG changes. Treatment: anticonvulsants or resection of the affected area of the brain.

L. Migraine

1. Clinical picture. Dizziness can be a leading symptom of basilar migraine. During an attack, visual and sensory disturbances, disturbances of consciousness, and intense headache are also noted.

2. Diagnostics. Recurrent attacks of vestibular vertigo (in the absence of other symptoms) may be a manifestation of dissociated migraine. The diagnosis of migraine in this case is possible only if all other causes are excluded; it is more likely if there are other manifestations of this disease.

M. Chronic vestibular dysfunction

1. General information. The brain is able to correct the disrupted connection between vestibular, visual and proprioceptive signals. Thanks to central adaptation processes, acute dizziness, regardless of its cause, usually resolves within a few days. However, sometimes vestibular disorders are not compensated due to damage to the brain structures responsible for the vestibulo-ocular or vestibulospinal reflexes. In other cases, adaptation does not occur due to concomitant visual or proprioceptive impairments.

2. Treatment. Constant dizziness, impaired balance and coordination of movements can cause disability for the patient. Drug therapy in such cases is usually ineffective. Patients with persistent vestibular dysfunction are shown a set of special exercises (vestibular gymnastics).

A. Exercise goals

1) Reduce dizziness. 2) Improve your balance. 3) Restore self-confidence.

b. Standard complex of vestibular gymnastics

1) Exercises to develop vestibular adaptation are based on the repetition of certain movements or postures that cause dizziness or imbalance. It is believed that this should promote adaptation of the vestibular structures of the brain and inhibition of vestibular reactions.

2) Balance exercises are designed to improve coordination and use information from multiple senses to improve balance.

Causes of involuntary movements

All causes of nystagmus can be divided into two groups - the pathology can be congenital or acquired as a result of other diseases. Note that in any of these cases, the primary cause is disturbances in the functioning of the motor system of the eye. There are a number of factors and diseases that can influence the formation of nystagmus:

various eye diseases;
ear infections;
head injuries, vestibular dysfunction;
inflammatory diseases of different parts of the brain, pituitary gland;
overstrain of the central nervous system;
intoxication with drugs and other chemicals.