Causes of Meniere's Disease

The causes of Meniere's disease are not known. The term "idiopathic" takes the first place in the definition of this disease; the main cause (or causes) of this nosological unit depends on a number of factors that can lead to the development of endolymphatic dropsy. Among them - viral infections, vascular disorders, autoimmune processes, allergic reactions, trauma, endocrine diseases, etc.

[1], [2], [3], [4], [5], [6], [7]

Pathogenesis of Meniere's disease

For the first time, the symptom complex, including dizziness and auditory disorders (hearing impairment and tinnitus), was described by Prosper Mehner in 1861, and it was he who suggested the relationship of these symptoms to the condition of the inner ear of a person. Further studies confirmed the validity of these assumptions, so the disease got its name after the author, Proscher Menier, who first described a typical symptom complex, which is a very complex clinical problem for doctors both in the diagnosis aspect and in the aspect of the treatment effectiveness of the disease.

At present, there is a lot of evidence that, with typical clinical diseases, there is a hydrops in the inner ear. According to morphological studies, the membrane of the vestibule and the volume of fluid in the endolymphatic space are stretched. Endolymph is completely isolated by walls of membranous labyrinth and is surrounded by perilymph, which has a communication with cerebrospinal fluid through the vestibule of the vestibule. Theoretically, the pressure of the cerebrospinal fluid can be transmitted to the endolymph via the vestibule of the vestibule, although there is no free interaction. Intracranial vascular pressure can affect the fluids of the inner ear, since the vessels are in direct contact with these fluids. In this case, thin-walled venules have a more significant effect on the transfer of pressure in comparison with thick-walled, elastic arteries.

There is a certain disagreement in the views on the source of endolymph products. The following mechanisms of its formation are proposed:

• sweating of fluid from the blood plasma through the capillaries of the vascular stria:
• sweating of fluid from the perilymph through the epithelium of the membranous labyrinth;
• maintaining the existence of the endolymph in a greater degree than its secretion, that is, the homeostasis of the endolymph,

Theories concerning the current of the endolymph include:

• the longitudinal current mechanism at which the endolymph is produced in the cochlea flows into the spherical sac of the membranous labyrinth and is finally absorbed in the endolymphatic sac;
• the radial current mechanism, in which the endolymph is secreted and absorbed in the cochlear path.

In favor of the longitudinal current theory of the endolymph, mainly data obtained with the help of dyes or markers, which after the introduction of the cochlea into the endolymph, were quickly detected in the endolymphatic sac. Evidence in favor of the radial theory is presented by data according to which the damage to the cochlea leads to disturbances only in the area of injury, while maintaining the intraluminal potential and the endolymph in the areas proximal and distal to the damage mast. It is likely that both of these mechanisms occur, but with different representations and significance for different people.

Endolymphatic hydrops can occur as a result of a number of mechanisms. Based on the theory of the longitudinal boom, the development of endolymphatic dropsy may be the result of the discoordination of the "production-absorption" process, in which the absorption of the endolymph does not correspond to the production. This idea seems too simplistic, since such discoordination should lead to a change in the composition of the endolymph, which in reality is not observed either in patients with Meniere's disease or in animals with experimental endolymphatic dropsy. Another mechanism of hydrocele development involves the excessive accumulation of certain ions or substances with a large molecular weight, which leads to the appearance of an osmotic gradient, an increase in the volume of the endolymph with a corresponding increase in pressure, and, as a result, to dropsy. The diametrically opposite concept is the assumption that the perilymph volume is insufficient, which could lead to endolymphatic edema.

Based on the concomitant changes in the temporal bone of endolymphatic hydrocephalus, a mechanism was proposed for the venous insufficiency of the endolymphatic passage and sac, as well as the insufficiency or absence of the vein near the anterior tubule.

The proposed mechanisms for the occurrence of Meniere's disease may also be accompanied by an increase in venous pressure, which, in turn, will disrupt the outflow of venous blood from the endolymphatic sac. The study of the ultrastructure of the inner ear and the peculiarities of the exchange of fluids in it continues. In particular, the scientists' observations of the sick Meniere's disease with the labyrinth hydrosome showed that the dissection of the endolymphatic duct in the area of its exit to the posterior surface of the temporal bone pyramid (before entering the endolymphatic sac) stably eliminates factors leading to attacks of dizziness and sensorineural hearing loss. Dissection of the endolymphatic duct was made by 152 patients. Attacks of dizziness stopped in all patients, 26% improved hearing by 10-20 dB, noise in the ear stopped. No one repeated treatment for a 20-year period was not. It is important to note that in 20 years, 94 patients have been repeatedly questioned - Meniere's attacks have not been resumed. These data allow us to conclude that the non-endolymphatic sack eliminates the endolymphatic gypsum and thereby normalizes the labyrinth functions, while the endolymph passes through the endolymphatic duct under the dura mater. These facts indicated that the cause of the hydrops could be the stenosis of the endolymphatic duct in the region distal to its exit from the pyramid's bone, or the deterioration in the absorption of the endolymph by the epithelium of the endolymphatic sac.