Dizziness. Diagnosis and treatment of dizziness

The diagnostics section of the site contains many examination methods. Moreover, all of them are of real diagnostic value, although they are not always available. The purpose of this article is to disclose an algorithm for examining patients with the presence of such a symptom as dizziness. The article presents a scheme for examining patients with existing dizziness, while the main research method and individual diagnostic stages are separately and succinctly reviewed.

Collection of complaints

Collecting complaints is the most important task when examining a patient with dizziness. After all, by dizziness, many people mean completely different sensations. It is important to evaluate and separate true (vestibular) dizziness, which is a sensation of rotation of the head or body in one plane, from non-systemic dizziness (more of a discomfort inside the head and some instability), from pre-syncope and other conditions.

Having assessed the nature of the dizziness (or having determined that the patient understands something completely different by “dizziness”), it is important to evaluate the provoking factors that cause or intensify the dizziness. Thus, indications of a change in head position help to suspect the presence of, sudden adoption of a vertical position -, being in public and emotional provoking factors -.

It is important to determine the presence of accompanying symptoms (nausea, vomiting, headache, etc.). Thus, a common cause of vestibular vertigo - sooner or later necessarily leads to the appearance of noise in the affected side and a decrease in (persistent) hearing. Often there are phenomena such as nausea and vomiting during an attack, there may be a typical migraine aura, etc.

It is important to assess the duration and nature of the attacks and recognize the many likely associated symptoms that people may present, which do not necessarily involve dizziness.

History taking

During the history, it is important to identify and exclude medications that may also cause dizziness. It is important to clarify how long ago and how often the attacks of dizziness occur, what provokes them and what, in the patient’s opinion, caused them for the first time.

It is necessary to identify hereditary risk factors in relation to certain diseases, clarify what treatment was carried out, what was its effectiveness, and also try to identify anamnestic information similar to current symptoms - after all, a person can often forget that over the past ten to fifteen years he has had several attacks of dizziness, which passed independently and quickly, while the seriality of attacks may be an indication of one or another process.

Objective examination

During an objective examination, it is necessary, first of all, to exclude orthostatic hypotension (orthotests) and the presence of arrhythmias (auscultation of the heart). It is also important to determine the presence of obvious signs of liver damage (protrusion beyond the borders, the presence of spider veins, etc.), the vessels of the lower extremities (their feeling of being cool to the touch, the absence of a pulse in the dorsal artery of the foot, the presence of obvious varicose veins and etc.) etc.

Neurological examination

In the neurological status, it is important to evaluate the performance of coordination tests (finger-to-toe, heel-knee tests), evaluate the marching walking test, conduct, but the greatest importance must be given. It is by studying nystagmus that one can with a high probability determine the level of damage. A thorough study of nystagmus, assessment of the fast and slow components, in measuring the duration and direction of nystagmoid movements in some cases (especially if technically impossible) allows one to abandon the procedure, although in expert cases it cannot be replaced.

It is also important to assess the general neurological status, identify focal symptoms that may indicate the central cause of dizziness (stroke, multiple sclerosis, traumatic brain injury, etc.).

Instrumental research methods

When approaching instrumental research methods, one should note the problems of over- and under-diagnosis of various diseases. Unfortunately, many doctors pay less attention to physical examination methods and focus on additional instrumental techniques. However, in the case of dizziness, this is completely wrong. In this section of the article I want to note two aspects - overdiagnosis of vascular vertigo and underdiagnosis of vestibular peripheral causes.

I think it’s no secret to anyone that above a certain age threshold, certain normal age-related changes begin to form. And these changes will be clearly reflected during the study, be it an MRI of the brain or. At the same time, it is not at all a fact that these reasons lead to the existing manifestations. It is also worth saying that a number of diseases (in particular, the above-mentioned BPPV) can imitate stroke. But an MRI will not help in this case.

That is why I would like to say that all instrumental techniques are important, but their implementation must be balanced. In the presence of a neurological deficit, an MRI of the brain should be performed; in case of repeated paroxysmal dizziness, accompanied by changes in hearing, show such a patient to an ENT doctor, as well as conduct audiometry, a caloric test, in the presence of nystagmus, the fast component of which is difficult to see with the eye, and there is also data for damage to the peripheral part of the vestibular system - videonystagmography is indicated.

In conclusion, I want to say this fact: despite some flaws and the general “cumbersomeness” of medicine in Russia, medical opinion should not be ignored. Trusting “competent” sources, in particular the Internet, as well as interpreting the available data, knowing that you have “osteochondrosis and these same plaques in the neck”, the patient’s opinion will not always be more correct, and in all cases of dizziness it is better to seek help from to a neurologist for the most optimal diagnosis.

G. D. Weiss

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. General algorithms for diagnostic tactics for dizziness are given in rice. 4.1 And rice. 4.2.

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 vertigo(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-fainting state. 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 (see. rice. 4.1), and the tactics for these conditions are completely different than for vestibular vertigo.

B. Balance imbalance characterized by instability, a shaky (“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. Uncertain 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. 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.

G. Neelen-Barany test for positional vertigo (see. Ch. 4, paragraph III.B.2).

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 - 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. Labyrinth lesions 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 may occur in 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 (see. table 4.1).

D. Stabilography- balance testing 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- complex and time-consuming 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(cm. table 4.2). 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. Treatment symptomatic.

A. Medicines. IN table 4.3 lists medications that reduce dizziness in vestibular neuronitis, motion sickness and other vestibular disorders (vestibulolytic drugs). For severe nausea, medications are prescribed in suppositories or parenterally. Indications for hospitalization include severe imbalance, as well as persistent vomiting requiring rehydration.

read also the post: How to recognize a stroke in a patient with isolated acute dizziness? (to the website)

The specifics of work (including that of a neurologist) in a multidisciplinary healthcare institution imply the most accurate determination of the causes of the disease at the emergency department level. It is very important when receiving an emergency, where the patient’s main complaint is dizziness, to correctly determine the cause of the disease and hospitalize it in the appropriate department: a vascular center for patients with acute cerebrovascular accidents (ACVA), or hospitalization and observation in the general neurology department will be sufficient.

Everyone knows the fact that dizziness is the second complaint after headache, requiring detail and careful diagnosis, and therefore some skills in a specific otoneurological examination of patients.

Vestibular vertigo is true or systemic vertigo associated with damage to the peripheral or central vestibular apparatus. The complaints of patients are concentrated on the sensation of rotation of their own body or surrounding objects in front of their eyes, combined with instability and vegetative manifestations (nausea, vomiting, increased sweating, a feeling of fear). For differential diagnosis, the distinction between central and peripheral vestibular vertigo is important. [ 1 ] Central vertigo occurs when the structures of the vestibular analyzer outside the temporal bone are damaged. These include: the intrastem part of the VIII pair of cranial nerves to the vestibular nuclei, the vestibular nuclei in the medulla oblongata and cerebellum, the auditory and vestibular pathways of the brain, the temporal zone of the cerebral cortex. [ 2 ] Peripheral dizziness is called dizziness, which occurs when the inner ear, consisting of the auditory and vestibular apparatus, is damaged. [ ! ] Determining the level of damage to the vestibular apparatus is the key to successful treatment and further recovery and rehabilitation period.

Currently, doctors have the ability to diagnose dizziness, including specific tests and instrumental studies, such as magnetic resonance imaging (MRI), magnetic resonance angiography (MR-AG), X-ray computed tomography (X-ray computed tomography, synonym: CT), videonystagmography , Doppler ultrasound examination of the main arteries of the head, duplex scanning, hearing examination, acoustic brainstem evoked potentials, vestibular myogenic evoked potentials.

However, the listed studies are simply not available in the emergency department, and often a thorough history and neurological examination is sufficient to make a correct diagnosis.

Collection of complaints and medical history. When collecting complaints and medical history, some mandatory points should be clarified. First, the patient must describe the dizziness in his own words, how he feels it, what it is like. Here it is important not to overestimate the importance of concomitant cerebrovascular pathology and diseases of the cervical spine. The time of day when dizziness occurs is also of great importance (for example, in the morning after waking up). The duration of the attack and the factors that provoke dizziness are of differential diagnostic importance. Vestibular vertigo, which occurs with changes in head position and lasts several minutes, is characteristic of benign paroxysmal positional vertigo (BPPV) and vestibular paroxysmia. In addition to BPPV, diseases such as perilymphatic fistula and acute labyrinthitis can also be accompanied by dizziness when changing the body, but dizziness does not stop when returning the head to its original position. An attack of Meniere's disease (up to 24 hours), migraine with perilymphatic fistula usually lasts for several hours. Transient ischemic attacks (TIA) are accompanied by vertigo from several minutes to an hour.

Physical examination. The physical examination requires assessment of the following parameters. Initially, nystagmus is assessed, which determines the level of damage to the vestibular apparatus. Vestibular nystagmus has 5 characteristics: plane, direction, degree, amplitude, ratio of fast and slow phases of nystagmus. Peripheral vertigo is accompanied by horizontal or horizontal-rotatory nystagmus, which decreases with gaze fixation, and there are no symptoms of damage to the brain stem and cerebellum. If, in addition to the vestibular nerve, the auditory nerve is also affected, then tinnitus, hearing loss, and ringing are observed. Central vertigo (cerebellar, ocular, brainstem) is accompanied by alternating, horizontal nystagmus, which does not decrease when the gaze is fixed, and there are no auditory symptoms. A characteristic disorder is the ability to smoothly follow - when trying to follow an object, saccades occur.

After assessing nystagmus, it is necessary to perform a Head-Impulse test [Halmagi test] (ask the conscious patient to look at the bridge of the nose of the doctor and sharply turn the head to the left/right). Normally, the gaze remains fixed on the starting point. With peripheral vestibular disorders, a series of saccades appears - a sign of Halmagi. An interesting fact is that if the patient, according to complaints and history, has a peripheral lesion, and there are no deviations during the Head-Impulse test, then this is a sign of a central lesion, and the patient urgently needs to undergo neuroimaging to exclude cerebellar or brainstem infarction.

The Head-Shaking test (head shaking test) is quite simple to perform and an indicator for diagnosing a central lesion, when, after performing a maneuver (turning the head in a horizontal plane from side to side with an amplitude of 30° for 20 s), prolonged vertical nystagmus or unconjugate eye movement.

The Dix-Hallpike test is a mandatory test for all patients complaining of dizziness, although it is a diagnostic test for BPPV. BPPV is the most common diagnosis in patients with vestibular vertigo. After performing a test on both ears, the appearance of nystagmus is determined and analyzed, which, if the test is positive, has the following characteristics: rotatory, geotropic, develops after a short latent period, lasts less than 1 minute, “gets tired” with repeated tests. If, during the test, nystagmus appears, which does not at all satisfy these characteristics, then most likely the diagnosis of “BPPV” is excluded and pathological conditions associated with impaired cerebral circulation in individual branches of the vertebral and basilar arteries are assumed. In this case, it is advisable to conduct additional research methods, such as angiography.

The outstretched arms test is a method for assessing tonic vestibular reactions, when, when assessing the test, a deviation of the arms towards the slow component of nystagmus (Wodak-Fisher reaction) is observed in a patient with damage to the labyrinth. Hand deviation is a component of the peripheral vestibular syndrome and occurs in Meniere's disease and labyrinthitis.

In the Barani index test (finger-finger), the accuracy of the patient's index finger hitting the doctor's index finger is assessed. When the vestibular apparatus is damaged, the slow component of nystagmus is missed. If there is deviation of only one arm or deviation of the arms in different directions, then this indicates damage to the cerebellum. In the finger-nose test, in case of labyrinth disease, a spontaneous miss is observed, directed towards the slow component.

“Writing” tests (tests of vertical and horizontal writing) are highly sensitive in cases of changes in labyrinthine tonic reflexes; they make it possible to determine “pre-nystagmus” signs of vestibular dysfunction.

If there is no time for an interview and a neurological examination in the emergency department, it makes sense to conduct a 20-point scale for rapid diagnosis of motor coordination disorders. This scale includes quantitative assessment of complaints, Uemura test (standing on one leg with eyes closed), Fukuda step test (hundred steps in place with eyes closed), Fukuda written test (writing the number 33 in a column), tracking (tracking a small a bright object moving in horizontal and vertical directions), pointing test (hitting a target at arm's length). Based on the results of all tests, the balance function is assessed from 0 to 20 points. The sensitivity of all tests reaches 93.64%.

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

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.

D. Uncertain 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.
G. Neelen-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.

D. Hearing loss and noise in the ears can occur with diseases of the peripheral part of the vestibular system (inner ear or vestibular-cochlear 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.

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.

E. Functional vestibular tests, electronystagmography and stabilography - complex and time-consuming 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).

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 are apparently in most cases 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. 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. Clinical picture 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. Current 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 dropsy). 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 operation 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 disruption of the interaction between the vestibular, visual and somatosensory systems, which normally jointly provide spatial orientation. Dizziness can also be caused by physiological stimulation of normally functioning sensory systems.

1. Motion sickness 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 related vertigo 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- 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 area. 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- 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 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.

Dizziness- one of the most common complaints with which patients turn to a neurologist. Indeed, there is no person who has never experienced dizziness.

The term “dizziness” describes completely different sensations: from a feeling of lightheadedness and impending loss of consciousness to the rotation of one’s own body or surrounding objects.
Dizziness is this incorrect awareness of your body in space or the sensation of imaginary rotation or movement of the body in space. Dizziness is a symptom of various neurological and somatic diseases and occurs in almost 80 different pathologies. Dizziness can occur with diseases of the cardiovascular system, eye and ear diseases, blood diseases, mental and neurological diseases. Dizziness is an extremely unpleasant subjective symptom that significantly reduces a person’s quality of life. It is customary to distinguish between systemic (true) and non-systemic dizziness.

True dizziness they call the illusion of movement of one’s body or objects around (this happens if you spin quickly, for example, on a carousel). True dizziness is accompanied by: nausea, vomiting, pale skin, sweating, anxiety. True, systemic vertigo is associated with irritation of certain areas of the vestibular analyzer and, depending on the level of damage, can be peripheral or central. The most common causes of true dizziness are impaired blood supply to the brain and inner ear, inflammatory and degenerative processes in the organs of hearing and balance, and intoxication.

Unsystematic dizziness called a feeling of instability of the surrounding space, a feeling of instability. This type of dizziness occurs with presyncope, emotional disorders, damage to the visual analyzer, and cerebellar disorders.

Most often in neurological practice, dizziness occurs with vascular diseases of the brain, pathology of the cervical spine and emotional disorders.

Pathology of the cervical spine. The vestibular system reacts very sharply to a lack of blood supply. The inner ear and vestibular centers of the brain receive their blood supply from the vertebral artery system. The vertebral arteries pass through narrow canals in the cervical spine. Instability, trauma, and osteochondrosis of the cervical vertebrae often lead to spasm or compression of these arteries; and therefore – to a lack of blood flow in them and to dizziness. The main symptoms of such diseases are: dizziness, unsteadiness, aggravated by turning or tilting the head; spots and “ripples” in the eyes, decreased vision in the dark; pain, tension or discomfort in the neck, lower back of the head, temples; fatigue, irritability; possible increase in blood pressure, accompanied by nausea and vomiting.

Emotional disorders. Neurotic disorders, depression, and simply overwork can imitate almost any symptoms of “physical” diseases. Moreover, the only symptom may be dizziness, noise or “fog” in the head, ringing or noise in the ear. Dizziness in these diseases is accompanied by constant fixation of attention on one’s well-being, severe fatigue, bad mood and tearfulness, combined with increased anxiety, disturbances in appetite and sleep.

For vascular lesions of the brain dizziness can occur both as a result of hypertension and atherosclerotic artery damage. A prolonged increase in blood pressure leads to damage to the small arteries of the brain. The arteries become narrow and inelastic. As a result, the flow of arterial (oxygen-rich) blood to the brain is limited, which leads to dizziness, noise in the head and ears. With atherosclerosis, plaques appear on the inner walls of the arteries - bulges that gradually block the flow of blood. Plaques in the arteries of the brain are especially dangerous. In the area of plaques, blood movement can be turbulent, which limits the flow of arterial blood to the brain, auditory nerves, and receptors that perceive auditory stimuli. Dizziness with CVP is characterized by a combination with noise in the head or ear, the presence of pre-syncope and balance disorders, increased fatigue, and decreased memory. When cerebral circulation is impaired, dizziness is the first and sometimes the only complaint.

Diagnosis of dizziness. If dizziness occurs, you should consult a neurologist and otolaryngologist. For the first time an attack of dizziness occurs, hospitalization is indicated to clarify the diagnosis and select therapy. The diagnostic program includes computed tomography or magnetic resonance imaging of the brain, x-ray examination of the cervical spine, Doppler ultrasound of the brachiocephalic arteries and Doppler scanning of the vessels of the head, vestibular tests (caloric test, rotational tests). To diagnose a possible disease of the hearing aid, tone threshold audiometry and acoustic impedance measurements can be performed.

Treatment. Treatment of dizziness depends on its cause, and only after it is clarified, a treatment strategy for the disease is chosen. If dizziness occurs against the background of a current somatic disease, then first of all it is necessary to treat it. Treatment of dizziness itself as a phenomenon includes drug therapy and physical exercise (special sets of exercises for vestibular training).

You should contact a specialist if any alarming symptoms appear – immediately! If qualified diagnosis and treatment is necessary, he invites you to a consultation with a neurologist in Moscow at the clinic of the Central Clinical Hospital of the Russian Academy of Sciences. An appointment with a neurologist can be made on the website, as well as by telephone.