Benign paroxysmal vertigo: causes and pathogenesis

Causes of benign paroxysmal dizziness

In 50-75% of all cases, the cause can not be established and therefore it is an idiopathic form. Possible cause of benign paroxysmal positional dizziness can be: trauma, labyrinthitis, Meniere's disease, surgical operations (both general and otologic).

Pathogenesis of benign paroxysmal dizziness

At the present time, there are two main theories of benign paroxysmal positional dizziness of cupulolithiasis and canalolithiasis, in some works combined by the term "otolithiasis". The mechanism of development of vertigo is associated with the destruction of the otolith membrane, the causes of which have not yet been elucidated. The cause is a violation of some factors of the calcium metabolism or the substance that binds it. Therefore, some researchers associate the development of benign paroxysmal positional vertigo with osteoporosis and osteopenia, although this point of view is not supported by all. Probably, the prospect of establishing the cause of the destruction of the otolith membrane is included in the study of a protein that binds calcium.

Freely moving particles on the threshold of the labyrinth, having mass and being in the zindolim, tend to precipitate. Since their mass is small, and the endolymph has a certain density, otolithic sacs settle to the bottom slowly. Any movement of the head, which often occurs during the day, provokes the process of moving particles. The best period for the deposition of otolith particles is the phase of human sleep. Head position the time of sleep unfolds the particles in such a way that contributes to their entry into the entrance of the semicircular canals. The free-moving particles of the otolith membrane have a charge, which leads to their association with slow deposition and the formation of a "bunch", which will have a mass considerably greater than the weight of the individual particles. The mass of particles that can cause dizziness is theoretically calculated. So, for cupulolithiasis it is 0.64 μg, for canalolithiasis it is 0.087 μg.

Development of dizziness and positional nystagmus in patients with otolithiasis is caused by the "piston effect" of moving particles when the head moves in the plane of the affected canal, located in the membranous part of the semicircular canal, or by the deviation of the cupula when the particles are placed on it. With the subsequent movement of the body and head in the plane of this channel, a displacement of such a clot occurs, which causes hydrostatic changes in the semicircular canal from the massive particle. This, in turn, leads to depolarization or hyperpolarization of the cupula. On the opposite side, there are no changes. A significant asymmetry in the state of the vestibular receptors is the cause of the appearance of vestibular nystagmus, dizziness and negative reactions. It should be noted that slow movement of particles in the plane of the affected canal can not cause dizziness.

"Benign" dizziness due to a sudden disappearance, which, as a rule, is not affected by ongoing medical therapy. This effect is most likely associated with the dissolution of freely moving particles in the endolymph, especially when the concentration of calcium and her were reduced, which was proved experimentally. In addition, particles can move and pouches of the vestibule, although spontaneously it happens much less often.

As a rule, positional dizziness in benign paroxysmal positional vertigo is most pronounced after the patient wakes up, and then during the day, as a rule, decreases.

This effect is due to the fact that acceleration when the head moves in the plane of the affected channel leads to the dispersion of the bunch particle. These particles are dispersed in a semicircular canal, their masses are no longer sufficient for the initial hydrostatic changes in the endolymph to be displaced, so when the inclinations are repeated, the positional vertigo decreases.

[1], [2], [3], [4], [5], [6]