Benign paroxysmal positional vertigo is repeated transient short—term attacks of systemic dizziness provoked by a change in the position of the head. They are associated with the presence of otoliths floating in the endolymph or fixed on the cupule. In addition to nausea and sometimes vomiting, attacks of paroxysmal dizziness are not accompanied by any other symptoms. The diagnosis is based on the patient’s complaints, a positive Dix–Hallpike test, and the results of a rotational test. Treatment consists in carrying out special therapeutic techniques of Epli or Semont, performing vestibular gymnastics.
General information
Benign paroxysmal positional vertigo (BPPG) is a benign paroxysmal systemic vertigo, lasting from several seconds to 0.5 minutes, occurring during head movements, more often in a horizontal position of the body. Described in 1921 by Robert Barani. In 1952 Dix and Hallpike suggested a link between the disease and disorders in the organ of balance and proposed a provocative diagnostic test for clinical use, which is still used by specialists in the field of neurology and vestibulology. Since benign paroxysmal positional vertigo is not associated with an organic lesion of the inner ear, but is caused only by a mechanical factor, “benign” is often added to its name. Benign paroxysmal positional vertigo is more common in women. The incidence is about 0.6% of the population per year. People over the age of 60 get sick 7 times more often than younger people. The age period most susceptible to BPPG is from 70 to 78 years.
Causes
The vestibular apparatus is formed by 3 semicircular channels and 2 sacs. The channels are filled with endolymph and sent out by hair cells — vestibular receptors that perceive angular accelerations. From above, the hair cells are covered with an otolith membrane, on the surface of which otoliths (otoconia) are formed — calcium bicarbonate crystals. During the vital activity of the body, the spent otoliths are destroyed and disposed of.
In case of metabolic disorders (hyperproduction or weakened utilization) of otoconias, their parts float freely in the endolymph of the semicircular canals, most often accumulating in the posterior canal. In other cases, the otoliths fall into the ampoules (extensions) of the channels and stick there to the cupule covering the receptor cells. During head movements, the otoconia move in the endolymph of the channels or displace the cupula, thereby irritating the hair cells and causing dizziness. After the end of the movement, the otoliths settle to the bottom of the channel (or stop shifting the cupula) and the dizziness stops. If the otoconia are located in the lumen of the channels, then they talk about canalolithiasis, if they are deposited on the cupula, then about cupulolithiasis.
Despite the thoroughly studied mechanism of the occurrence of BPPG, the causes of the formation of free otoconia in most cases remain unclear. It is known that in a number of patients otoliths are formed due to traumatic damage to the otolith membrane during traumatic brain injury. Etiofactors that cause paroxysmal positional dizziness also include previously transferred labyrinthitis of viral etiology, Meniere’s disease, spasm of the artery supplying the labyrinth (with migraine), surgical manipulations on the inner ear, taking ototoxic pharmaceuticals (primarily gentamicin antibiotics). In addition, BPPG can act as a concomitant pathology in other diseases.
Symptoms
The basis of the clinical picture is transient systemic dizziness — the sensation of objects moving in a horizontal or vertical plane, as if rotating around the patient’s body. Such a paroxysm of dizziness is provoked by head movements (turns, tilting). Most often occurs in a lying position, when turning over in bed. Therefore, most of the BPPG attacks occur in the morning, when patients lie in bed after waking up. Sometimes paroxysms of dizziness occur in a dream and lead to the awakening of the patient.
On average, the BPPG attack lasts no more than 0.5 minutes, although this period seems longer to patients, in their complaints they often indicate that dizziness lasts for several minutes. It is characteristic that the attack is not accompanied by tinnitus, headache, hearing loss (hearing loss). Nausea is possible, in some cases — vomiting. Within a few hours after the attack or periodically in the intervals between them, some patients note the presence of non—systemic dizziness – feelings of swaying, instability, “nausea”. Sometimes BPPG attacks are isolated in nature, but in most cases during the period of exacerbation they occur several times a week or a day. This is followed by a period of remission, in which there are no paroxysms of dizziness. It can last up to several years.
Attacks of positional vertigo do not pose a danger to the life or health of the patient. The exception is cases when paroxysm occurs when a person is at a high altitude, underwater diving or driving a vehicle. In addition, repeated attacks can negatively affect the psycho-emotional state of the patient, provoking the development of hypochondria, depressive neurosis, neurasthenia.
Diagnostics
The diagnosis of BPPG is based primarily on clinical data. In order to confirm it, a neurologist or vestibulologist conducts a Dix–Hallpike test. Initially, the patient sits with his head turned 45 degrees to the affected side and fixing his gaze on the bridge of the doctor’s nose. Then the patient is abruptly transferred to a lying position, while throwing his head back by 30 degrees. After a latent period (1-5 seconds), systemic dizziness occurs, accompanied by rotatory nystagmus. To register the latter, video oculography or electronystagmography is necessary, since peripheral nystagmus is suppressed when the gaze is fixed and may not be visually fixed. After the disappearance of the nystagmus, the patient is returned to the sitting position, which is accompanied by light dizziness and rotatory nystagmus directed in the opposite direction to the previously caused one.
The provocative test is performed from 2 sides. A bilateral positive Dix–Hallpike test, as a rule, occurs in BPPG of traumatic genesis. If both dizziness and nystagmus were absent during the test, it is considered negative. If there was dizziness without nystagmus, then the test is considered positive, the so-called “subjective BPPG” is diagnosed. After repeated repetition of the sample, the nystagmus is depleted, dizziness does not occur, because as a result of repeated movements, the otoliths disperse along the semicircular channel and do not form a cluster capable of affecting the receptor apparatus.
An additional diagnostic test is a rotational test, which is carried out in a lying position with the head thrown back by 30 degrees. With a positive test, after a sharp turn of the head after a latent interval, a horizontal nystagmus occurs, which is well recorded by visual observation. In the direction of nystagmus, it is possible to distinguish canalolithiasis from cupulolithiasis and diagnose which semicircular canal is affected.
Differential diagnosis of BPPG should be carried out with positional vertigo in arterial hypotension, vertebral artery syndrome, Barre–Lieu syndrome, Meniere’s disease, vestibular neuritis, labyrinth fistula, CNS diseases (multiple sclerosis, neoplasms of the posterior cranial fossa). The basis of diffdiagnosis is the absence, along with positional dizziness, of other symptoms characteristic of these diseases (hearing loss, “darkening” in the eyes, neck pain, headaches, ear noise, neurological disorders, etc.).
Treatment
Conservative therapy is recommended for most patients, which depends on the type of PPG. So, with cupulolithiasis, vestibular Semont gymnastics is used, and with canalolithiasis, special therapeutic techniques are used to change the location of the otoconias. With residual and mild symptoms, exercises for training the vestibular apparatus are recommended. Pharmacotherapy may make sense during periods of exacerbation. It is based on such drugs as cinnarizine, ginkgo biloba, betahistine, flunarizine. However, drug therapy can only serve as a supplement to treatment with special techniques. It should be said that some authors express great doubts about its expediency.
The most common therapeutic methods include the Epli technique, which consists in sequentially fixing the head in 5 different positions. The technique allows you to move the otoliths from the canal into the oval pouch of the labyrinth, which leads to the relief of symptoms of PPG in 85-95% of patients. When taking Semont, the patient is transferred from a sitting position with his head turned to the healthy side to a lying position on the affected side, and then, without changing the rotation of the head, through the sitting position to the lying position on the healthy side. Such a rapid change in the position of the head allows you to free the cupula from the otoliths that have settled on it.
In severe cases with frequent attacks of positional vertigo, which is not stopped by the use of Epley and Semont techniques, the issue of surgical treatment is considered. Surgical intervention may consist in filling the affected semicircular canal, selective intersection of individual vestibular fibers, laser destruction of the labyrinth.