Causes and treatment of benign paroxysmal positional vertigo. Benign paroxysmal positional vertigo (BPPV) Benign paroxysmal positional vertigo (BPPV)

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Definition

Benign paroxysmal positional vertigo (BPPV) is paroxysmal vestibular vertigo, the provoking factor of which is a change in the position of the head and body. It differs from other forms of positional vertigo in the effectiveness of treatment and the possibility of self-resolution.

Classification of BPPV

Depending on the location of the freely moving particles of the otolithic membrane in relation to the structures of the semicircular canal The most common forms of BPPV are:

• cupulolithiasis- particles are attached to the cupula of one of the channels of the vestibular receptor;
• canalolithiasis- particles of the macula are located freely in the canal cavity.
• When formulating a diagnosis, you should also indicate the side of the lesion and the semicircular canal (posterior, anterior, external) where the pathology was found.

Etiology of BPPV

In 50-75% of all cases of the disease, the cause cannot be determined, and therefore we are talking about an idiopathic form. Most likely reasons:

• injury
• neurolabyrinthitis
• Meniere's disease
• surgical operations (both general cavity and otological)

Pathogenesis of BPPV

Currently, there are two main theories of BPPV - cupulolithiasis and canalolithiasis, in some works united by the term “otolithiasis”. The mechanism of development of dizziness is associated with the destruction of the otolith membrane, the causes of which have not yet been elucidated, and the formation of freely moving particles in the otolith and ampullary receptors of the inner ear.

The development of positional vertigo and nystagmus in patients with otolithiasis is due to the fact that the cupula of the sensory epithelium of the ampullary receptor deviates due to the “piston effect” of freely moving particles of the otolithic membrane or a change in its position due to sagging of particles attached to it. This is possible by moving the head in the plane of the affected canal or the head and body at the same time.

Deviation of the cupula is accompanied by mechanical deformation of the hairs of the vestibular sensory epithelium, which leads to a change in the electrical conductivity of the cell and the occurrence of depolarization or hyperpolarization. In the unaffected vestibular receptor of the other side, such changes do not occur and the electrical activity of the receptor does not change. At this moment, a significant asymmetry occurs in the state of the vestibular receptors, which is the cause of the appearance of vestibular nystagmus, dizziness and autonomic reactions. It should be noted that with a slow change in the position of the head, the same slow movements of particles occur in the plane of the affected canal, which may not cause dizziness and positional nystagmus.

The “benign quality” of dizziness is due to its sudden disappearance, which, as a rule, is not affected by drug therapy. This effect is most likely due to the dissolution of freely moving particles in the endolymph, especially if the concentration of calcium in it decreases, which has been proven experimentally. In addition, particles can move into the vestibular sacs, although this occurs spontaneously much less frequently.

Positional vertigo with BPPV is usually greatest when the patient wakes up and then usually decreases throughout the day. This effect is due to the fact that acceleration when moving the head in the plane of the affected channel causes dispersion of clot particles. These particles are dispersed in the semicircular canal, and their mass is no longer sufficient to cause the initial hydrostatic changes in the endolymph during displacement, so positional vertigo decreases with repeated bending.

BPPV clinic

The clinical picture of BPPV is characterized by sudden vestibular dizziness(with a sensation of objects rotating around the patient) when the position of the head and body changes. Most often, dizziness occurs in the morning after sleep or at night when turning over in bed. Dizziness is characterized by great intensity and lasts no more than one or two minutes. If the patient returns to his original position at the time of dizziness, the dizziness stops faster. Provoking movements, in addition, can be throwing the head back and bending down, so most patients, having experimentally determined this effect, try to turn, rise from the bed and tilt the head slowly and not use the plane of the affected canal.

Like typical peripheral vertigo, an attack of BPPV may be accompanied by nausea and sometimes vomiting.

BPPV is characterized by the presence of a specific positional nystagmus, which can be observed when an attack of positional vertigo occurs. The specificity of its direction is due to the localization of particles of the otolithic membrane in a specific semicircular canal and the peculiarities of the organization of the vestibulo-ocular reflex. Most often, BPPV occurs due to damage to the posterior semicircular canal. Less commonly, the pathology is localized in the horizontal and anterior canal. There is a combined pathology of several semicircular canals in one or both ears of one patient.

Important for the clinical picture of BPPV is the complete absence of other neurological and otological symptoms, as well as the absence of changes in hearing in patients due to the development of this dizziness.

Diagnosis of BPPV

Physical examination

Specific tests for establishing BPPV are the Dix-Hallpike, Brandt-Daroff, etc. positional tests.

The Dix-Hallpike positional test is performed as follows: the patient sits on the couch and turns his head 45° to the right or left. Then the doctor, fixing the patient’s head with his hands, quickly moves him to a supine position, while the patient’s head, held by the doctor’s hands, hangs over the edge of the couch at 45° and is in a relaxed state. The doctor observes the patient's eye movements and asks him if he is feeling dizzy. It is necessary to warn the patient in advance about the possibility of the appearance of his usual dizziness and convince him of the reversibility and safety of this condition. The resulting nystagmus, typical of BPPV, necessarily has a latent period, which is associated with some delay in the movement of the clot in the plane of the canal or deviation of the cupula when the head is tilted. Since the particles have a certain mass and move under the influence of gravity in a liquid with a certain viscosity, the settling rate increases over a short period.

Typical of BPPV is a positional rotational nystagmus that is directed toward the ground (geotropic). This is typical only for pathology of the posterior semicircular canal. When you move your eyes away from the ground, you can observe vertical movements. Nystagmus, characteristic of the pathology of the horizontal canal, has a horizontal direction; for the pathology of the anterior canal, it is torsional, but directed from the ground (ageotropically).

The latent period (time from tilting to the appearance of nystagmus) for pathology of the posterior and anterior semicircular canals does not exceed 3-4 s, for pathology of the horizontal canal - 1-2 s. The duration of positional nystagmus for canalolithiasis of the posterior and anterior canal does not exceed 30-40 s, for canalolithiasis of the horizontal canal - 1-2 minutes. Cupulolithiasis is characterized by longer-lasting positional nystagmus.

The typical positional nystagmus of BPPV is always accompanied by dizziness, which occurs along with nystagmus, decreases and disappears along with it. When a patient with BPPV returns to the original sitting position, reverse nystagmus and dizziness can often be observed, directed in the opposite direction and, as a rule, less intense than when bending over. When the test is repeated, nystagmus and dizziness recur with proportionally reduced characteristics.

When examining the horizontal semicircular canal to determine BPPV, it is necessary to turn the head and body of a patient lying on his back, respectively, to the right and left, fixing the head in extreme positions. For horizontal canal BPPV, positional nystagmus is also specific and is accompanied by positional vertigo.

Patients with BPPV experience the greatest balance disorder in a standing position at the moment of throwing back or turning the head in the plane of the affected canal.

Instrumental studies

It is recommended to use devices that enhance visual observation of nystagmus and eliminate gaze fixation: Blessing or Frenzel glasses, electrooculography, videooculography.

Differential diagnosis of BPPV

Diseases of the posterior cranial fossa, including tumors, which are characterized by the presence of neurological symptoms, severe balance disorders and central positional nystagmus.

Central positional nystagmus is characterized primarily by a special direction (vertical or diagonal); fixation of gaze does not affect it or even strengthens it: it is not always accompanied by dizziness and is not exhausted (it lasts as long as the patient remains in the position in which it appeared).

Positional nystagmus and dizziness may accompany multiple sclerosis and vertebrobasilar circulatory insufficiency, but neurological symptoms characteristic of both diseases are recorded.

Treatment of BPPV

Non-drug treatment

1. Brandt-Daroff method. Most often it is performed by the patient independently. According to this technique, the patient is recommended to perform exercises three times a day, five bends in both directions in one session. If dizziness occurs at least once in the morning in any position, the exercises are repeated during the day and evening. To perform the technique, the patient must, after waking up, sit in the center of the bed with his legs hanging down. Then he lies on either side, with his head turned upward by 45°, and remains in this position for 30 seconds (or until the dizziness stops). After this, the patient returns to the original sitting position, in which he remains for 30 seconds, after which he quickly lies down on the opposite side, turning his head upward by 45°. After 30 s, he returns to his original sitting position. In the morning, the patient makes five repeated bends in both directions. If dizziness occurs at least once in any position, bending should be repeated during the day and evening.
   The duration of such therapy is selected individually. Cannot be completed unless the positional vertigo that occurs during Brandt-Daroff exercises does not recur within 2-3 days.
2. Semont maneuver. Performed with the help of a doctor or independently. Starting position: sitting on the couch, legs hanging down. While sitting, the patient turns his head in a horizontal plane 45° to the healthy side. Then, fixing the head with the hands, the patient is placed on his side, on the affected side. He remains in this position until the dizziness stops. Next, the doctor, quickly moving his center of gravity and continuing to fix the patient’s head in the same plane, places the patient on the other side through the “sitting” position without changing the position of the patient’s head (i.e., forehead down). The patient remains in this position until the dizziness completely disappears. Next, without changing the position of the patient’s head, he is seated on the couch. If necessary, you can repeat the maneuver. It should be noted that the peculiarity of this method is the rapid movement of the patient from one side to the other, while the patient with BPPV experiences significant dizziness, and autonomic reactions in the form of nausea and vomiting are possible; therefore, in patients with diseases of the cardiovascular system, this maneuver should be performed carefully, resorting to premedication if necessary. For this you can use betahistine (24 mg once 1 hour before the procedure). In special cases, thiethylperazine and other centrally acting antiemetics are used for premedication.
3. Epley maneuver(with pathology of the posterior semicircular canal). It is advisable to have it performed by a doctor. Its feature is a clear trajectory, slow movement from one position to another. The patient's starting position is sitting along the couch. First, the patient's head is turned 45° towards the pathology. The doctor fixes the patient's head in this position. Next, the patient is placed on his back, head tilted back 45°. The next turn of the fixed head is in the opposite direction in the same position on the couch. Then the patient is placed on his side, and his head is turned with the healthy ear down. Next, the patient sits down, the head is tilted and turned towards the pathology, after which it is returned to its usual position - looking forward. The patient’s stay in each position is determined individually, depending on the severity of the vestibulo-ocular reflex. Many specialists use additional agents to speed up the deposition of freely moving particles, which increases the effectiveness of treatment. As a rule, 2-4 maneuvers during one treatment session are enough to completely stop BPPV.
4. Lempert maneuver(for BPPV of the horizontal semicircular canal). It is advisable to have it performed by a doctor. The patient's starting position is sitting along the couch. The doctor fixes the patient's head during the entire maneuver. The head is turned 45° and horizontally towards the pathology. Then the patient is placed on his back, successively turning his head in the opposite direction, and after that - on his healthy side, the head, accordingly, is turned with his healthy ear downwards. Next, the patient’s body is turned in the same direction and placed on his stomach; the head is given a position with the nose down; As you turn, the head turns further. Following this, the patient is placed on the opposite side; head - sore ear downwards; The patient is seated on the couch through the healthy side. The maneuver can be repeated. It is important that after performing the maneuver the patient follows the mode of limiting bending, and on the first day sleeps with the head of the bed raised by 45-60°.

Surgery

Shown when ineffectiveness of treatment maneuvers in 0.5-2% of cases:

• Filling the affected semicircular canal with bone chips.
• Selective neurectomy of the vestibular nerves.
• Labyrinthectomy.
• Laser destruction of the labyrinth.

Forecast
Favorable, with full recovery. The disability of a patient with BPPV lasts for about a week. In the case of cupulolithiasis, these periods may be extended.

One of the most common causes of systemic dizziness is a pathology called “benign paroxysmal positional vertigo” (BPPV). Instant manifestation of signs of this disease is observed during squats and bends, as well as when performing other physical exercises.

The condition of a patient diagnosed with BPPV is characterized by short attacks of dizziness, which are provoked by a change in the position of the body in space, its movement (sometimes it is enough to turn the head sharply for it to start spinning). This reaction of the body is called orthostatic hypotension.

The presence of otolithiasis may be due to the following reasons:

• middle ear infections;
• TBI (traumatic brain injury);
• compliance with prolonged bed rest;
• otological surgical interventions;
• Meniere's disease;
• the effect of certain antibacterial drugs (gentamicin);
• constant migraine attacks provoked by dystonic and spasmodic phenomena in the arteries running in the labyrinth.

In older adults, BPPV becomes more likely after labyrinthine infarction. In half of the cases, the cause of the disease remains unknown. Women experience this pathology 2 times more often than men.

A characteristic feature of the clinical picture of BPPV is cupulolithiasis (crystallized calcium clot). The pressure it exerts affects the ampullary receptor responsible for the perception of angular acceleration.

For this reason, positional vertigo occurs when the head and torso are in a certain position. Under the influence of gravity, otolith fragments move into the semicircular canal (cupulolithiasis) or settle on the cupula of the ampullary receptor. Most often, clots are localized in the posterior semicircular canal of the labyrinth, since these areas are in the plane of gravity.

The onset of a BPPV attack occurs during a latency period of 10 seconds. At first the dizziness will be severe. It is accompanied by various vegetative symptoms. This sensation lasts only 1 minute, and if you do not turn your head, it quickly passes.

After several changes of position, BPPV disappears, but prolonged rest leads to its reappearance, however, no additional symptoms are noted.

Differential diagnosis

For treatment to be effective, it must be prescribed only after the diagnosis has been made as accurately as possible. There are several diseases that are similar in their manifestations to BPPV or accompany it, creating a misconception about a person's condition.

Benign positional vertigo may resemble a migraine aura (one of the symptoms of osteochondrosis) or an infectious pathology. Differential diagnosis, which is the most detailed and accurate, helps to draw the right conclusions in such cases.

Typical signs of BPPV:

• paroxysmal (dizziness occurs for no apparent reason and ends similarly);
• the duration of the attack is no more than a day;
• there are vegetative symptoms (feeling of nausea, pale skin, hyperhidrosis, fever);
• at the end of the attack, the condition becomes completely normal and quite acceptable;
• The occurrence of tinnitus, deafness and headache is unlikely.

The body’s recovery after overcoming the disease occurs very quickly, and treatment requires no more than 30 days.

Diagnosis (in case of damage to the posterior semicircular canal)

Canalolithiasis of the posterior semicircular canal can be diagnosed in a patient using a special test. When testing the right labyrinth, the patient is asked to turn his head approximately 45˚ to the left.

After fulfilling the set conditions, the specialist as quickly but carefully places the patient on his right side and waits for 10 seconds of the latent period to pass. Next, the subject experiences dizziness and nystagmus (twitching) directed toward the right ear.

After the symptoms become maximum, their severity will subside. As soon as all discomfort disappears, the patient will be asked to quickly change position and sit down again.

Usually, in this case, signs of the disorder appear again, although with less force, and the nystagmus is directed in the direction opposite to the right ear.

Checking the channel of the left labyrinth is carried out according to a similar principle. This procedure is called the Dix-Hallpike positional vertigo test. In addition to this, you will need to do:

• MRI of the brain;
• X-ray of the cervical spine;

If the horizontal semicircular canals are affected, then the technique for checking the patient’s condition will be slightly different.

Diagnostics (for damage to the horizontal semicircular canal)

This variant of the disease is detected much less frequently, only in 10-20% of cases. In this case, different semicircular canals may be affected on the ears (for example, on the left - horizontal, on the right - vertical), in addition, due to the actions of specialists, they can transform into one another.

If it is the horizontal semicircular canal that is affected, the patient usually feels paroxysmal dizziness when he tilts his head in different directions while lying on his back. This symptom is most noticeable after proper rest and when turning the face towards the sore ear.

Such diagnostics are convenient because they can be carried out independently.

The latent period of BPPV with damage to the horizontal semicircular canal is short (5 seconds), and the attack itself has a long duration. Often the pathology is accompanied by vomiting.

Treatment

At the moment, the treatment of otolithiasis often involves actions that facilitate the extraction of the otolith from the semicircular canal back into the vestibule. This allows you to relieve existing symptoms, but does not guarantee that the attack will not recur.

In situations where removal of the otolith is impossible, specialists resort to the method of repeated provocation of dizziness, which makes it possible to reduce the severity of symptoms (or even get rid of them altogether) thanks to central compensation.

After the attending physician has carried out the necessary actions, it is usually necessary to reduce vestibular excitability. For this purpose, special vestibulolytic drugs are used.

Most often, specialists prescribe betahistine dihydrochloride (Betaserc) to patients. The medication affects histamine receptors located in the inner ear and the vestibular nuclei of the central nervous system.

Betaserc improves blood flow and normalizes lymphatic pressure inside the cochlea and labyrinth. In addition, the drug helps increase serotonin levels, which also makes the vestibular nuclei less active. The optimal dosage of the drug is 24 mg twice a day.

In addition, the doctor may prescribe additional medications that will help eliminate nausea, dizziness and emotional stress, and will also help normalize blood circulation in general.

One of the most significant points regarding overcoming a disorder of the vestibular system is associated with performing sets of exercises that represent special vestibular gymnastics.

It is equally important to begin treatment as early as possible, as well as to provide rational psychotherapy, since in some cases (as, for example, with phobic pastural vertigo), the main cause of the disease can be psychological disorders, without eliminating which the entire process will be meaningless. It should also be taken into account that patients may require not only medication, but also surgical treatment.

Health-improving gymnastics

First of all, we are talking about rotatory (facing the affected ear) tilts of the head. A lying or bending person holds the position for 10-15 seconds. Then he sits down, simultaneously turning his head in the direction opposite to the painful area.

You can also make turns by vertically rocking forward and backward. The desired result is felt already 1-2 days later in approximately 75% of patients.

• Epley maneuver.

You need to sit on the couch in a sitting position and turn your head approximately 45° towards the sore ear. The specialist fixes the resulting position and places the patient on his back, also tilting his head to 45°. After this, you need to turn it in the opposite direction, and the entire body on the side where the healthy ear is.

The last step is to take the starting position, tilt your head and turn to where you feel dizzy. Repeat the entire complex 3-4 times.

While sitting, keep your legs perpendicular to the ground. Turn your face 45° towards the ear that does not hurt. Fix the pose with your hands and lie on the side opposite to the side in which you turned your face.

You must remain in this position until the attack completely passes, and then, with the help of a doctor, lie on the other side without changing the position of your head. Wait until the attack is over again, then take the starting position. Repeat as needed.

Sitting on the couch, turn your head at the standard angle for such exercises in the direction where the pathological area is located. The physician must hold the patient's head throughout the maneuver. The person needs to be placed on his back and his face turned in the opposite direction. Then turn your head to where your ear is great.

Next, the body of the person who came to the appointment is turned so that he lies on his stomach. The head should be turned so that the nose points perpendicularly downwards. Turn the patient on the other side, and place the head so that its painful side is facing down. Return to the starting position through the healthy side.

Such techniques are usually quite sufficient to overcome the disease, so you should not resort to independently obtained folk recipes for treating dizziness, especially without obtaining the approval of a specialist.

Bottom line

It is necessary to cure BPPV, since this will allow you not to be afraid of being in conditions of excessive depth or height, where strong pressure changes are recorded, and it will also be possible to minimize the likelihood of relapses. The only thing that is required from the patient in this case is to consult a doctor in a timely manner so that he can prescribe the necessary medications, exercises or surgery (if necessary).

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Relevance. Benign paroxysmal positional vertigo (BPPV) is the most common cause of vertigo (VPO) in patients of all age groups. According to various authors, BPPV accounts for up to 35% of all causes of dizziness, approximately every third person over 70 years of age has experienced an attack of positional vertigo at least once, and the overall prevalence in the population is 2.4%. And, nevertheless, despite the high prevalence of BPPV, its vivid and quite characteristic clinical picture (see below), it is paradoxical that this disease is one of the most common NOT diagnosable causes of GC.

BPPV is a disease of the peripheral part of the vestibular analyzer (vestibular apparatus of the inner ear), which is manifested by attacks of systemic positional GC due to the movement of fragments of the otolithic membrane of the utriculus (oval, synonym: elliptical, sac of the vestibular vestibule of the labyrinth) into the semicircular canals of the inner ear (scheme of the structure of the peripheral part of the vestibular analyzer ]). note: BPPV is called “benign,” thereby emphasizing the peripheral nature of the disease and the possibility of relieving GC attacks without treatment; the term “paroxysmal” indicates the suddenness of the attack; HA is “positional” because its occurrence is associated with a change in the position of the patient’s head, or rather not with the position as such, but with the very process of moving the head from one position to another. BPPV as a separate nosological form was described by M.R. Dix and C.S. Hallpike in 1952

ANATOMICAL STRUCTURE OF THE INNER EAR[INCREASE ]

According to etiology, BPPV can be divided into 2 forms: [ 1 ] idiopathic (iBPPV) or degenerative (more than 90% of all cases) and [ 2 ] symptomatic (sBPPV), which is usually caused by traumatic brain injury (i.e., post-traumatic BPPV; can be bilateral), vestibular neuronitis, labyrinthitis, otoinfection, vascular pathology of the inner ear, etc. BPPV is associated with osteopenia, osteoporosis and reduced vitamin D levels in blood plasma, as well as with migraine and with previous acute vestibular dysfunction of vascular origin (which developed against the background of a hypertensive crisis or circulatory discirculation in the vertebrobasilar system, which provokes degenerative changes in the otolithic membrane, and in the immediate delayed period - within 1 month , - as primary acute vestibular dysfunction and ataxia subside, BPPV develops). The proportion of iBPPV exceeds the proportion of sBPPV, for example post-traumatic BPPV, while the former predominate in elderly patients, the latter in young patients. Among the groups and risk factors for BPPV are: age from 50 to 70 years, weather dependence, stress, lack of sleep, professions associated with barotrauma (divers, pilots, etc.).

read also the post: Post-traumatic paroxysmal positional vertigo(at laesus-de-liro.live-journal.com)

The pathogenetic substrate of BPPV (according to the theory of canalolithiasis, proposed by L.S. Parnes and J.A. McClure in 1991) is the presence of spots (macula) of the elliptical sac of otolith deposits (inorganic crystals) separated under the influence of gravity (when the position of the head changes) from the otolithic membrane, which move freely in the membranous labyrinth (in the endolymph) of the inner ear and penetrate into one or more semicircular canals [SC], which is canalolithiasis (the elliptical sac connects to three PCs - lateral, anterior and posterior). As a result, each change in the position of the head in the plane of the affected PC leads to a displacement of otolithic deposits and irritation of the ampullary receptor of the PC (i.e., the sensory epithelium of the ampullar ridge of the PC), in response to which an attack of GC occurs (otoliths or otoconia are layered pebbles consisting predominantly made of calcium carbonate crystals, like nacre or pearls; they are immersed in a jelly-like layer enveloping the hairs of sensitive cells on the surface of the spherical and elliptical sacs of the vestibular analyzer). Most often, with BPPV, the posterior PC is affected due to its anatomical location relative to the direction of gravity (high probability of otoliths getting into it due to gravitational forces). BPPV of the posterior PC accounts for up to 75 - 90% of all cases. However, some researchers believe that the prevalence of horizontal BPPV remains underestimated, since with this type of BPPV self-healing often occurs. BPPV of the anterior PC is extremely rare, probably due to its superior location, which prevents retention of otoliths in it (the anterior PC opens vertically into a common pedicle with the posterior semicircular canal, so otoliths often come out of it on their own and dizziness stops on its own in a short time).

Thus, there are 3 pathogenetic forms of BPPV: due to the involvement of PC [ 1 ] posterior [z-BPPV] (75 - 90%); [ 2 ] horizontal [g-BPPV] (10 - 20%); [ 3 ] anterior [p-BPPV] (1 - 5%); [ !!! ] note: one patient may have a combination of lesions of different PCs (for example, g-BPPV can be combined with s-BPPV of the opposite ear).

However, in addition to the variant of BPPV in the form of canalolithiasis (i.e. the presence of free-floating otoliths in the lumen of the PC), a less common variant of BPPV in the form of cupulolithiasis is possible, i.e. the presence of particles (otoliths) adhered to the cupula of the PC (i.e., adhered to the ampullary receptor of the PC - to the sensory epithelium of the ampullary ridge of the PC) [the term “cupulolithiasis” was introduced into scientific use by H.F. Schuknecht, 1973]. Normally, thanks to the balance between the formation and resorption of the layers that make up the otoliths, their renewal is ensured, as well as the resorption of detached otoliths. If this balance is disturbed (as a result of any pathological process indicated above), one of the otoliths adhering to the cupula (to the ampullary ridge) acquires large sizes (2 - 4 times larger than neighboring cells), a large mass leads to greater displacement along compared to adjacent fixed otoliths, which is a source of irritation to the vestibular system. It should be noted that dome lithiasis (unlike canalolithiasis) is characterized by a longer course (several months) and no effect from vestibular maneuvers.

In both canalolithiasis and cupulolithiasis, asymmetrical signal input to the brain during unilateral stimulation of the vestibular apparatus disrupts the illusion of balance, which is created by the interaction of the vestibular, visual and proprioceptive systems (the latter receives signals from the muscles and ligaments that evaluate the position of limb segments). There is a feeling of GC. Sensitive cells of the vestibular analyzer (in the macula and/or cupula) send a signal of maximum intensity to the brain during the 1st second of stimulation, then the signal strength decreases exponentially, which underlies the short duration of BPPV symptoms.

Thus, the clinical picture of BPPV is determined by canal or cupulo lithiasis. In the first case, otoconia (otoliths) move freely along the semicircular canal under the influence of gravitational forces, in the second they are motionlessly attached (“stick”) to the cupula. BPPV can be unilateral or bilateral, the latter option usually observed after traumatic brain injury.

The clinical picture of BPPV is characterized by [ acute peripheral vestibular syndrome:] a feeling of pronounced rotation of the surrounding space - objects, sometimes a feeling of rotation inside the head and/or the patient himself in various planes (the so-called systemic HA), which (the feeling of HA) occurs acutely when changing the position of the head and/or body in space (in including when lying in bed on one side; often the patient wakes up from a feeling of pronounced HA) and which is accompanied by a specific positional [vertical-torsional or horizontal] nystagmus (an objective sign of the patient having a [systemic] HA), the direction of which depends on the which of the semicircular canals is affected (nystagmus associated with a harmonious deviation of the torso and arms towards the slow component). note: nystagmus in BPPV is characterized [usually] by a torsional component and a latent period (relative to the provocative movement) lasting 1 - 5 s (during which the displacement of the cupula caused by the otoliths becomes sufficient to activate the receptor cells). The attack may be accompanied by oscillopsia (the illusion of motionless objects vibrating) and pronounced autonomic reactions (nausea, vomiting, sweating, palpitations, changes in breathing, paleness or redness of the face; less commonly, presyncope and syncope), supported by a feeling of fear, anxiety (it is worth noting that This group of patients is also characterized by anxiety-depressive psycho-emotional disorders). Remember: with BPPV, as a rule, there is no tinnitus (ear noise) - hearing impairment (in rare cases, patients complain of the presence of ear noise on the affected side, the occurrence of which coincides with the onset of BPPV; there is a mention of a combination of BPPV with acute sensorineural hearing loss and tinnitus), there are absolutely no focal neurological disorders (except in cases where focal symptoms are a manifestation of actual comorbid neurological pathology or are a consequence of previous neurological diseases).

note! It is believed that BPPV occurs under the influence of trigger movements, and outside of these movements, patients feel good, no vestibular disorders are noted. However, some patients note various symptoms even in the non-attack period in the form of non-systemic hypertension, mild instability and uncertainty when walking.

read also (on the website) post: Nystagmus, post: Clinical assessment of the oculomotor system

With BPPV of the posterior PC (the most common type of BPPV), patients note the occurrence of systemic HA when performing certain movements: [ 1 ] turning in bed; [ 2 ] transition from a lying position to a sitting position or vice versa; [ 3 ] when throwing the head back or tilting it forward; [ 4 ] when tilting the head and torso towards the affected ear; [ 5 ] with any sudden or rapid turns of the head. Nystagmus with damage to the posterior PC is rotatory-vertical, lasting from 5 to 20 s, depleting. The clinical differences between canal and cupulolithiasis of the posterior PC are that with the latter, nystagmus occurs without a latent period, since the otoconia are already on the cupula; there is no phenomenon of exhaustion of nystagmus (lasting more than 1 minute). Cupulolithiasis rarely develops due to the anatomical features of the posterior PC.

note! A characteristic feature of BPPV is that it is “nighttime” dizziness of a “horizontal position”. The maximum manifestation of symptoms is observed at night when turning in bed and in the morning when trying to get out of bed. During the day, being in an upright position, patients feel quite satisfactory - they work, perform their daily duties. In a relatively small percentage of BPPV cases, patients experience unsteadiness, nausea, and occasional daytime dizziness.

There are 3 degrees of severity of BPPV: [ 1 ] mild - the patient experiences minor spontaneous GCs, nausea when changing the position of the head, minor disorders of the vestibular apparatus, autonomic reactions; [ 2 ] moderate - the patient experiences frequent attacks of positional GC with loss of balance in the intervals between them, more pronounced autonomic reactions; [ 3 ] severe - almost constant HA with disequilibration (impaired equilibration [lat. aequilibris - in balance]), caused by any movement of the head, the patient cannot fully move and is disoriented in space.

note! HA is characterized by [ 1 ] high intensity (and, as a rule, accompanied by nausea and vomiting), short duration - no more than a minute (classic attack of BPPV); in this case, the duration of one attack usually does not exceed 5 - 30 s (maximum duration - 60 s), which is explained by the time required for the movement of otoliths to the lowest point of the canal (depending on the size and composition of the otoliths, it often takes 10 s), and the time , necessary to return the cupula to a state of rest; [ 2 ] however, attacks (episodes) of HA can follow one after another with short intervals (creating a false sense of continuity of HA), if instead of avoiding unnecessary movements, the patient begins to actively move, change the position of the head (the indicated course of BPPV is possible in patients with unstable psycho-emotional state and limitation of cognitive functions: patients may complain of continuous systemic dizziness with constant instability; however, a thorough survey makes it possible to clarify that the maximum severity is associated with certain movements); [ 3 ] in some cases, more often in elderly patients, instead of the classic positional [paroxysmal] GC, the following are noted: a feeling of instability [including permanent] and imbalance.

The reason for the unusual clinical manifestations of BPPV in old age is unclear. One explanation may be age-related degeneration of the sensory epithelium and efferent nerve fibers of the vestibular-cochlear nerve with a subsequent decrease in the sensitivity of the receptors of the peripheral vestibular analyzer. The resulting irritation of the ampullary receptor in canalolithiasis in elderly patients does not necessarily lead to a rotational HA, but may manifest as more or less significant instability.

note! It should be remembered that in some patients the severity of dizziness depends on the duration of the disease: at the onset, dizziness in more than half of the patients is dramatic in nature - intense rotation in the horizontal or vertical planes with pronounced vegetative manifestations; Over time, the severity of the attacks usually decreases.

read also the article “Dizziness and anxiety disorders in the elderly” by O.V. Kotova, M.V. Zamergrad; State Budgetary Educational Institution of Higher Professional Education “First Moscow State Medical University named after. THEM. Sechenov”, Moscow, Russia (magazine “Therapeutic Archive” No. 9, 2016) [read]

Often the medical history of a patient with BPPV develops according to the following scenario. At the moment of an attack of hypertension, thinking about a stroke, the patient calls an ambulance. The clinical picture can be complicated by the fact that BPPV attacks can follow one after another, creating a false impression of a constant long-term hypertension, and, due to the autonomic reaction and feelings of fear, blood pressure can increase to high numbers, creating a false impression of acute cerebrovascular accident (ACVA) or hypertensive crisis. Due to the absence of changes according to neuroimaging data and the rapid regression of HA, a diagnosis of “Transient ischemic attack” is made and the patient remains “stigmatized” with the diagnosis of stroke for life. At the same time, drug treatment for BPPV is ineffective, GC attacks continue (if self-healing does not occur), the patient is diagnosed with “Blood circulation failure in the vertebrobasilar system,” and he continues to receive inadequate treatment. The situation is aggravated by the fact that after the first attacks of BPPV, an anxious phobic GC can join the underlying disease, thereby closing the classic circulus vitiosus (Latin vicious circle), from which it is very difficult for the patient to get out. Also, in elderly patients (due to the peculiarities of the manifestation of BPPV in them - without GC [see above]), a constant feeling of instability and fear (often not unreasonable) of a possible fall, combined with a longer chronic course of the disease, creates the preconditions for the development of anxiety and depression. Delayed diagnosis, when a patient with this relatively benign lesion of the peripheral vestibular analyzer is mistakenly treated for cerebrovascular disease for a long time, aggravates the situation.

The following variant of the development of the medical history of a patient with BPPV is also possible. The occurrence of BPPV is preceded by acute vestibular dysfunction of vascular origin, which develops against the background of a hypertensive crisis or circulatory discirculation in the vertebrobasilar system. The patient experienced systemic dizziness (vertigo) for several days, mild neurological symptoms (in this case, the patient is usually hospitalized). As primary acute vestibular dysfunction and ataxia subside in the immediate delayed period (within 1 month), BPPV develops, which can be explained by discirculation of blood circulation in the vertebrobasilar system, provoking degenerative changes in the otolithic membrane (relationship between BPPV and the state of blood circulation in the vertebrobasilar system noted in a number of works; it also cannot be excluded that in this case we are talking about Lindsay-Hemenway syndrome, which develops with ischemia in the anterior vestibular basin [due to its occlusion] and is characterized by the development of BPPV and a decrease or complete disappearance of nystagmus in the caloric test after initial acute vestibular dysfunction).

The diagnosis of BPPV is made based on the characteristic clinical picture of the disease and the results of specific tests (positive Dix-Hallpike test, roll test, Brandt-Daroff, etc.). The Dix-Hallpike test is most often used to diagnose lesions of the posterior PC (up to 90% of all cases of BPPV according to various authors). It is carried out as follows: from a sitting position with the head turned 45 degrees to the side, the patient is quickly placed on his back so that the head hangs over the edge of the couch. In this case, after a short latent period, first increasing, then decreasing nystagmus occurs, directed towards the affected ear of the patient.

A simpler (for diagnosing posterior PC dysfunction) is the “side lying” maneuver. The patient sits across the couch, head turned 45° in the opposite direction from the affected ear. The doctor, with a relatively sharp movement, places the patient on his side so that the face remains turned upward, and records the presence of characteristic nystagmus.

The McClure-Pagnini test allows you to determine damage to the horizontal PC. When performing this test, the patient is placed on his back, his head is raised 30º. Next, the doctor turns his head to one side by 90º and waits for at least 30 seconds for dizziness and nystagmus to appear, noting their duration and direction. Then the procedure is repeated in the opposite direction.

Read also the article “Diagnostics and treatment of benign paroxysmal positional vertigo” Likhachev S.A., Alenikova O.A.; Republican Scientific and Practical Center of Neurology and Neurosurgery, journal “Medical Panorama” No. 5, 2008) [read]

note! Performing diagnostic tests (and treatment maneuvers) is often frightening for patients, especially those who have previously been incorrectly diagnosed with repeated transient ischemic attacks () or cervicogenic dizziness. In this regard, before performing any diagnostic test and then a therapeutic maneuver [ !!! ] it is important to explain to the patient the essence of the movements being performed, and also to instruct not to close the eyes, even with severe HA.

Sometimes patients complain of short-term episodes of positional GC, but diagnostic tests do not give a positive result. In such cases, a thorough neurological examination is necessary to rule out other causes. However, even with a negative Dix-Hallpike test, therapeutic maneuvers are highly effective, since nystagmus in 25% of cases can be slightly expressed or suppressed by gaze fixation. Its amplitude can decrease significantly after repeated trials (exhaustion phenomenon). The use of Frenzel glasses or videonystagmography increases the chances of detecting nystagmus during diagnostic tests. Some authors call BPPV without nystagmus subjective.

First of all, the differential diagnosis of BPPV is carried out with other diseases accompanied by acute systemic vertigo: with cerebral stroke, vestibular neuronitis, vestibular migraine and Meniere's disease (but above all with central positional vertigo caused by neurological diseases affecting the brain stem and cerebellum). The distinctive features of these diseases are presented in the table:

Remember! In addition to HA, patients with central positional HA have neurological disorders (focal symptoms). In addition, central positional nystagmus can be strictly vertical (without the torsional component characteristic of BPPV), monocular, have no latency period, do not fade over time, or not be accompanied by GC.

Benign paroxysmal positional vertigo is a disease of the vestibular system characterized by sudden attacks of dizziness. Four words from the name convey the main essence of this problem: “benign” means the absence of consequences and the possibility of self-cure, “paroxysmal” indicates the paroxysmal nature of the disease, “positional” indicates dependence on the position of the body in space, and “dizziness” is the main symptom . However, behind the apparent simplicity there are many subtleties hidden. You can learn about everything related to benign paroxysmal positional vertigo, the basic information and subtleties of this disease by reading this article.

In general, it is a very nonspecific symptom. Offhand, we can name more than 100 diseases that can manifest themselves as dizziness. But benign paroxysmal positional vertigo has some clinical features, thanks to which the correct diagnosis can be established already during the initial examination by a doctor.

Benign paroxysmal positional vertigo (BPPV) is considered a fairly common condition. Western European countries provide the following statistics: up to 8% of their population suffers from this disease. The CIS countries, unfortunately, do not have reliable statistical data on this problem, but it is unlikely that they would differ significantly from European ones. Up to 35% of all cases of vestibular vertigo may be associated with BPPV. The numbers are impressive, aren't they?

BPPV was first described by the Austrian otolaryngologist Robert Barany in 1921 in a young woman. And since then, the symptoms of BPPV have been identified as a separate disease.

Causes and mechanism of development of BPPV

To understand why and how this disease develops, it is necessary to delve a little deeper into the structure of the vestibular apparatus.

The main part of the vestibular apparatus is three semicircular canals and two sacs. The semicircular canals are located almost at right angles to each other, which makes it possible to record human movements in all planes. The channels are filled with liquid and have an extension - an ampulla. The ampoule contains a gelatin-like substance, cupula, which has a close connection with the receptors. The movements of the cupula, together with the flow of fluid inside the semicircular canals, create a sense of position in space in a person. The upper layer of the cupula may contain calcium bicarbonate crystals - otoliths. Normally, otoliths are formed throughout life and then destroyed during the natural aging of the body. Destruction products are utilized by special cells. This situation is normal.

Under certain conditions, spent and obsolete otoliths are not destroyed and float in the form of crystals in the fluid of the semicircular canals. The appearance of additional objects in the semicircular canals, naturally, does not go unnoticed. The crystals irritate the receptor apparatus (in addition to normal stimuli), resulting in a feeling of dizziness. When the crystals settle in an area under the influence of gravity (usually the area of ​​the sacs), the dizziness disappears. The described changes are the main mechanism for the occurrence of BPPV.

Under what conditions are otoliths not destroyed, but sent “free floating”? In half of the cases the cause remains unclear, the other half occurs when:

• (due to traumatic detachment of otoliths);
• viral inflammation of the vestibular apparatus (viral labyrinthitis);
• surgical manipulations on the inner ear;
• taking ototoxic antibiotics of the gentamicin series, alcohol intoxication;
• spasm of the labyrinthine artery that supplies blood to the vestibular apparatus (for example, during migraine).

Symptoms

BPPV is characterized by specific clinical features that form the basis for the diagnosis of this disease. So, BPPV is characterized by:

• sudden attacks of severe dizziness that occur only when changing body position, that is, dizziness never appears at rest. Most often, an attack is provoked by a transition from a horizontal to a vertical position after sleep, or by turning in bed during sleep. The leading role in this case belongs to the change in the position of the head, and not the body;
• dizziness can be felt as the movement of one’s own body in space in any plane, as the rotation of objects around, as a feeling of falling or lifting, swaying on the waves;
• the duration of the dizziness attack does not exceed 60 seconds;
• sometimes dizziness may be accompanied by nausea, vomiting, slow heart rate, diffuse sweating;
• An attack of dizziness is accompanied by nystagmus - oscillatory involuntary movements of the eyeballs. Nystagmus can be horizontal or horizontal-rotational. As soon as the dizziness stops, the nystagmus immediately disappears;
• attacks of dizziness are always the same, never change their “clinical coloring”, and are not accompanied by the appearance of other neurological symptoms;
• attacks are more pronounced in the morning and in the first half of the day. Most likely, this is due to the dispersion of crystals in the fluid of the semicircular canals during constant head movements. The crystals break down into smaller particles in the first half of the day (motor activity is much higher during the waking period than during sleep), so in the second half, symptoms practically do not occur. During sleep, the crystals “stick together” again, leading to increased symptoms in the morning;
• upon examination and thorough examination, no other neurological problems are ever detected. There is no tinnitus, no hearing loss, no headache - no additional complaints;
• Spontaneous improvement and disappearance of attacks of dizziness are possible. This is probably due to the spontaneous dissolution of detached calcium bicarbonate crystals.

BPPV is more common in people over 50 years of age. Perhaps by this time the natural processes of resorption of calcium bicarbonate crystals are slowing down, which is the reason for the more frequent occurrence of the disease at this age. According to statistics, women suffer from BPPV 2 times more often than men.

Diagnostics

Already at the stage of questioning, the doctor may suspect the cause of dizziness.

The clinical features of BPPV make it possible to come close to the correct diagnosis already at the stage of questioning the patient. Clarification of the time of onset of dizziness, provoking factors, duration of attacks, absence of additional complaints - all this suggests BPPV. However, more reliable confirmation is needed. For this purpose, special tests are performed, the most common and simple of which is the Dix-Hallpike test. The test is carried out as follows.

The patient is seated on the couch. Then turn (do not tilt!) the head in one direction (presumably towards the affected ear) by 45°. The doctor seems to fix the head in this position and quickly places the patient on his back, maintaining the angle of rotation of the head. In this case, the patient’s torso should be positioned in such a way that the head hangs slightly over the edge of the couch (that is, the head should be thrown back slightly). The doctor observes the patient's eyes (anticipating nystagmus) and at the same time asks about the feeling of dizziness. In essence, the test is a provocative test for a typical attack of BPPV, since it causes displacement of crystals in the semicircular canals. In the case of BPPV, approximately 1-5 seconds after the patient is laid down, nystagmus and typical dizziness occur. The patient is then returned to a sitting position. Often, when returning to a sitting position, the patient again experiences a feeling of dizziness and nystagmus of less intensity and the opposite direction. This test is considered positive and confirms the diagnosis of BPPV. If the test is negative, then the test is performed with the head turned in the other direction.

In order to notice nystagmus during the test, it is recommended to use special Frenzel (or Blessing) glasses. These are glasses with a high degree of magnification, which eliminate the influence of arbitrary fixation of the patient's gaze. For the same purpose, a videonystagmograph or infrared recording of eye movements can be used.

It should be borne in mind that when the Dix-Hallpike test is repeated, the severity of dizziness and nystagmus will be less, that is, the symptoms seem to be exhausted.

Treatment

Modern approaches to the treatment of BPPV are mainly non-pharmacological. Just 20 years ago, things were different: the main treatment was medications to reduce dizziness. When the mechanism of development of the disease became known to scientists, the approach to treatment also changed. Free-floating crystals cannot be dissolved or immobilized with the help of medications. That is why the dominant role today belongs to non-drug methods. What are they?

These are so-called positional maneuvers, that is, a series of successive changes in the position of the head and torso, with the help of which they try to drive the crystals into a zone of the vestibular apparatus from where they can no longer move (the zone of the sacs), and therefore will not provoke dizziness. During such maneuvers, BPPV attacks may occur. Some maneuvers can be performed independently, while others can only be performed under the supervision of a doctor.

The following positional maneuvers are currently considered the most common and effective:

• Brandt-Daroff maneuver. It can be carried out without the supervision of medical personnel. In the morning, immediately after sleep, a person needs to sit on the bed with his legs dangling. Then you need to quickly take a horizontal position on one side, with your legs slightly bent. The head must be turned 45° up and lie in this position for 30 seconds. Afterwards, take a sitting position again. If a typical attack of BPPV occurs, then in this position you need to wait until the dizziness stops and only then sit down. Similar actions are then performed on the other side. Next, you need to repeat everything 5 times, that is, 5 times on one side and 5 times on the other. If dizziness does not occur during the maneuver, then the next time the maneuver is performed the next morning. If an attack of dizziness does occur, then you need to repeat the maneuver in the daytime and evening;
• Semont maneuver. Its implementation requires the supervision of medical personnel, since pronounced autonomic reactions in the form of nausea, vomiting and transient cardiac arrhythmias may occur. The maneuver is carried out as follows: the patient sits on the couch with his legs dangling. The head turns 45° to the healthy side. The doctor fixes the head in this position with his hands and the patient is placed on the couch on his side on the painful side (the head is thus turned slightly upward). He should remain in this position for 1-2 minutes. Then, maintaining the same fixed position of the head, the patient quickly returns to the original sitting position and immediately lies down on the other side. Since the head has not changed its position, when lying on the other side, the face turns down. You need to stay in this position for another 1-2 minutes. And then the patient returns to the starting position. Such sudden movements usually cause severe dizziness and vegetative reactions in the patient, so doctors have a twofold attitude towards this method: some find it too aggressive and prefer to replace it with more gentle maneuvers, others, agreeing with its severity for the patient, are the most effective (especially in severe cases). cases of BPPV);
• Epley maneuver. It is also advisable to carry out this maneuver under the supervision of a physician. The patient sits on the couch and turns his head to the painful side at an angle of 45°. The doctor fixes the head with his hands in this position and places the patient on his back while simultaneously throwing back the head (as with the Dix-Hallpike test). Wait 30-60 seconds, then turn your head to the opposite side to the healthy ear and then turn your torso on its side. The head turns ear down. And again wait 30-60 seconds. After which the patient can take the original sitting position;
• Lempert maneuver. It is similar in technique to the Epley maneuver. In this case, after turning the patient’s torso on its side and the head with the healthy ear down, the rotation of the torso continues. That is, the patient then takes a position lying on his stomach with his nose down, and then on the sore side with the sore ear down. And at the end of the maneuver, the patient again sits in his original position. As a result of all these movements, the person seems to rotate around an axis. After the Lempert maneuver, it is necessary to limit the inclination of the torso during life activities and on the first day sleep with the head of the bed raised by 45°-60°.

In addition to the basic maneuvers, there are also various modifications. In general, when positional gymnastics are carried out correctly, the effect occurs after just a few sessions, that is, only a few days of such therapy are needed, and BPPV will recede.

Drug treatment for BPPV today involves the use of:

• vestibulolytic drugs (Betagistin, Vestibo, Betaserc and others);
• antihistamines (Dramina, motion sickness tablets);
• vasodilators (Cinnarizine);
• herbal nootropics (Ginkgo biloba extract, Bilobil, Tanakan);
• antiemetic drugs (Metoclopramide, Cerucal).

All these drugs are recommended for use in the acute period of severe attacks of BPPV (accompanied by severe dizziness and vomiting). Then it is recommended to resort to positional maneuvers. Some doctors, on the contrary, say that the use of medications for BPPV is unjustified, citing the inhibition of their own mechanisms for compensating for vestibular disorders, as well as a decrease in the effect of positional maneuvers while taking medications. Evidence-based medicine does not yet provide reliable data on the use of drugs for BPPV.

A set of vestibular exercises is used as a consolidating therapy, so to speak. Their essence is to perform a series of movements with the eyes, head and torso in those positions in which dizziness occurs. This leads to stabilization of the vestibular apparatus, increased endurance, and improved balance. In the long term, this leads to a decrease in the intensity of BPPV symptoms when the disease recurs.

Sometimes BPPV symptoms may resolve spontaneously. Most likely, these cases are associated with the independent entry of crystals into the “silent” vestibular zone during normal head movements or with their resorption.

In 0.5-2% of cases of BPPV, positional exercises have no effect. In such cases, surgical correction of the problem is possible. Surgical treatment can be carried out in various ways:

• selective cutting of vestibular nerve fibers;
• filling of the semicircular canal (then there is simply nowhere for the crystals to “float”);
• destruction of the vestibular apparatus using a laser or its complete removal from the affected side.

Many doctors are also ambivalent about surgical methods of treatment. After all, these are operations with irreversible consequences. It is simply impossible to restore cut nerve fibers or the entire vestibular apparatus after destruction and, especially, removal.

As you can see, BPPV is an unpredictable disease of the inner ear, the attacks of which usually take a person by surprise. Due to sudden and severe dizziness, sometimes accompanied by nausea and vomiting, the sick person becomes afraid of the possible causes of his condition. Therefore, if such symptoms appear, it is necessary to consult a doctor as soon as possible so as not to miss other more dangerous diseases. The doctor will dispel all doubts regarding the symptoms that have arisen and explain how to overcome the disease. BPPV is a safe disease, so to speak, because it is not fraught with any complications and certainly not life-threatening. The prognosis for recovery is almost always favorable, and in most cases only positional maneuvers are required for the disappearance of all unpleasant symptoms.

Ph.D. A. L. Guseva reads a report on the topic “Benign paroxysmal positional vertigo: features of diagnosis and treatment”:

Clinic of Professor Kinzersky, educational video about benign paroxysmal positional vertigo:

BPPV was first described by Robert Barany in 1921. It is believed that this type of disorder of the peripheral part of the vestibular analyzer occurs in 17-35% of patients who consult a doctor with a complaint of dizziness. People aged 50-60 years are most susceptible to it (40% of cases). In women, benign positional paroxysmal vertigo is diagnosed 2 times more often than in men.

Causes

The causes of benign positional paroxysmal vertigo have not been established. Presumably, it could result from:

• traumatic brain injury;
• viral infection affecting the inner ear (labyrinth);
• Meniere's disease;
• taking antibiotics with ototoxic effects;
• ear surgery;
• spasm of the labyrinthine artery.

However, doctors believe that in more than half of the cases the causes of BPPV are not pathological. There are several theories explaining the mechanism of benign positional vertigo. The main one is cupulolithiasis.

The vestibular analyzer, responsible for maintaining balance, consists of two sections - central, located in the brain, and peripheral, located in the inner ear. The peripheral section includes the semicircular canals and the vestibule.

At the ends of the channels there are extensions - ampoules in which receptor hair cells are located; their clusters are called cupules (flaps). The cavities of the inner ear are filled with fluids - perilymph and endolymph. When moving, the pressure of fluids changes and irritation of receptors occurs, as a result a signal is sent to the brain about a change in the position of the body or head in space.

In the vestibule of the internal one there are two sacs - the utriculus and the sacculus, communicating with the semicircular canals. They contain accumulations of calcareous cells - the otolithic apparatus. The processes of nerve cells are immersed in the otoliths. According to the theory of cupulolithiasis, the causes of BPPV lie in the fact that when the head is turned, tiny particles are torn off from the otoliths, which then stick to the cupula, it becomes heavier and deviates, causing dizziness. During the reverse movement, the particles fall away from the receptor cells, and the attack passes.

This theory is confirmed by the fact that during pathological examination, a basophilic substance was found on the cupulae of patients suffering from positional vertigo. Doctors believe that the high incidence of BPPV in older people is due to otolith degeneration during aging.

Symptoms

What is the diagnosis of BPPV? What signs does it show? The main symptom of BPPV is short-term dizziness when changing head position. Most often, attacks occur when a person is lying down and suddenly turns over or throws his head back. The duration of dizziness is no more than a minute, then a feeling of instability may be felt for some time. Sometimes BPPV occurs during sleep and can be so severe that the person wakes up with discomfort.

Other symptoms of benign positional paroxysmal vertigo are nausea and vomiting, but these are rare. Headache and hearing loss are not typical for this condition.

As a rule, BPPV proceeds benignly: periods of exacerbations, during which attacks occur frequently, are replaced by a stable long-term remission - up to 2-3 years. In rare patients, the disease is accompanied by regular episodes of dizziness and severe autonomic disorders.

In general, benign positional paroxysmal vertigo is not dangerous for humans, but it can lead to fatal consequences if an attack occurs while driving, while at height, in water, and so on.

Diagnostics

Benign positional paroxysmal vertigo is diagnosed based on the patient's complaints. The diagnosis is confirmed by a positive Dix-Hallpike test. It is carried out like this. The patient sits on the couch and focuses his gaze on the doctor's forehead. The doctor turns the patient’s head to the right 45°, sharply lays him on his back and tilts his head back 30°. If a person experiences dizziness and nystagmus (oscillating eye movements), the test is assessed as positive. Then it is repeated on the other side. Nystagmus does not always appear.

BPPV is differentiated from vestibular neuronitis, labyrinthine fistula and vestibular type of Meniere's disease.

Additional diagnostic methods:

• test using a stabilometric platform;
• MRI of the brain;
• CT or X-ray of the cervical spine.

Treatment

How is BPPV treated? In the past, doctors advised patients to avoid head positions that cause dizziness and to take medications as symptomatic treatment. As a rule, Meclozin was prescribed, a drug with antihistamine and anticholinergic properties. But practice shows the low effectiveness of drugs in the treatment of BPPV.

In recent years, the treatment of benign paroxysmal vertigo (BPPV) has been practiced with the help of various exercises that promote the return of otolith particles to their place - in the sacs. The Epley technique is considered the most effective way to restore inner ear mechanics and normalize balance control. Its algorithm:

• The patient sits straight on the couch and turns his head towards the affected ear by 45º, then lies on his back, staying in this position for 2 minutes.
• The doctor turns the patient’s head in the opposite direction (90º) and fixes it for 2 minutes.
• The patient slowly turns his torso in the direction of turning his head, pointing his nose down and staying in this position for 2 minutes, then returns to the starting point.

The person may feel dizzy throughout the exercise. Usually 3 repetitions are required, after which there is a steady improvement in the condition. The number of procedures is determined by the doctor. Relapses occur in 6-8% of cases.

Another way to treat benign paroxysmal positional vertigo is vestibular gymnastics using the Semont method. Its essence lies in successive sharp changes in the position of the patient’s head and torso. It typically causes severe dizziness and is considered too aggressive by many doctors and is rarely prescribed.

If conservative treatment is ineffective and the disease is severe, neurosurgical surgery is performed on the inner ear.

Forecast

The prognosis for BPPV is favorable: in most cases, adequate treatment leads to stable remission.

Prevention

Measures to prevent BPPV have not been developed because the causes of the disease have not been established.

Video: exercises for BPPV using the Epley method