Over 150 years have elapsed since Prosper Meniere’s described for the first time the clinical symptoms of the disease that is called by his name at the present time. Nevertheless, the etiology of this pathological condition remains unknown. It has been believed during many decades that the cause of Meniere’s disease Is the presence of an excess fluid (hydrops) in the endolymphatic space of the inner ear leading to the rupture of membranes responsible for hearing impairment and vestibular disorders. The recent histopathological studies have demonstrated that endolymphatic hydrops (RH) is not necessarily associated with the clinical manifestations of Meniere’s disease. During the last decades, certain authors have undertaken attempts to elaborate new theories of etiology, pathogenesis, and mechanisms underlying the development of dizziness associated with Meniere’s disease. These are the theory of genetic predisposition to this condition, the viral and autoimmune theories, and the theory of disturbance of the longitudinal endolymph flow. However, none of these theories was adequately substantiated. The ongoing experimental and morphological studies appear to give evidence that the aquaporin water channels may play a role in the formation of hydrops. Moreover, the mechanisms underlying episodes of dizziness remain to be elucidated. In the light of recent progress in normal physiology and pathological physiology of the ear, the theory of ruptures proposed by H. Schuknecht tends to be considered increasingly less attractive and appears to be replaced by new hypotheses providing an alternative explanation for the mechanism behind the development of Meniere’s disease giving priority to the role of contamination of perilymph with calcium ions.