Benign paroxysmal vertigo - Causes and pathogenesis

Causes of benign paroxysmal vertigo

In 50-75% of all cases of the disease, the cause cannot be determined and therefore we are talking about an idiopathic form. Possible causes of benign paroxysmal positional vertigo may be: trauma, labyrinthitis, Meniere's disease, surgical operations (both general cavity and otological).

Pathogenesis of benign paroxysmal vertigo

At present, there are two main theories of benign paroxysmal positional vertigo: cupulolithiasis and canalolithiasis, which are united by the term "otolithiasis" in some works. The mechanism of dizziness development is associated with the destruction of the otolith membrane, the causes of which have not yet been clarified. The cause is a violation of some factors of calcium metabolism or a 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 everyone. Probably, the prospect of establishing the cause of the destruction of the otolith membrane is included in the study of the protein that binds calcium.

Freely moving particles in the vestibule of the labyrinth, having mass and being in the endolymph, tend to settle. Since their mass is small, and the endolymph has a certain density, sedimentation on the bottom of the otolith sacs occurs slowly. Any head movements, which more often occur during the daytime, provoke the process of particle movement. The best period for the sedimentation of otolith particles is the human sleep phase. The position of the head during sleep unfolds the particles in such a way that it promotes their entry into the entrance of the semicircular canals. Freely moving particles of the otolith membrane have a charge, which leads to their connection during slow sedimentation and the formation of a "clot", which will have a mass significantly exceeding the weight of individual particles. The mass of particles that can cause dizziness has been theoretically calculated. Thus, for cupulolithiasis it is 0.64 μg, for canalolithiasis - 0.087 μg.

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

The "benignity" of vertigo is due to its sudden disappearance, which is usually not affected by the drug therapy. This effect is most likely associated with the dissolution of freely moving particles in the endolymph, especially with a decrease in the concentration of calcium and it, which has been proven experimentally. In addition, particles can move and vestibular sacs, although this occurs spontaneously much less often.

As a rule, positional vertigo in benign paroxysmal positional vertigo is most pronounced after the patient awakens, and then usually decreases during the day.

This effect is due to the fact that accelerations during head movement in the plane of the affected canal lead to dispersion of the clot particle. These particles are dispersed in the semicircular canal, their mass is no longer sufficient to cause initial hydrostatic changes in the endolymph during displacement, therefore, with repeated tilts, a decrease in positional vertigo occurs.

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