**5. Physiology in Meniere's disease**

The pathophysiology of Meniere's disease is tied to the physiology of the hydrops, which can be induced in experimental models by obliteration or blockage of the duct and/or sac in animals at a success rate approaching 100% in guinea pigs but with more variability in other species. The experimental animal models remain deficient, with no acute attacks of MD and lack of reported vestibular dysfunction despite severe hydrops, cautioning against direct equivalence from animal to human theories. This induced hydrops, despite being an incom‐ plete model, is used to study the effects on the labyrinthine and cochlear physiology such as electrolyte homeostasis in the fluids and membranes, pressures and potentials.

#### **6. Ionic homeostasis and hydrops**

Despite logistical and technical difficulties in obtaining tissues and fluid (as composition is usually disturbed during surgical procedures), some human and animal studies show a change in the sodium‐potassium levels of the cochlear and vestibular endolymphatic fluids in MD and experimental hydrops, respectively [20]. In addition to the theory of ruptures caus‐ ing spillage of potassium ions into the perilymph, another possible explanation for the ionic and fluid imbalances in hydrops was postulated to be the Na, K‐ATPase enzymes found in the cochlear lateral wall. However immunohistochemical studies of human temporal bones did not show statistically significant differences in hydropic ears consistent with the normal func‐ tioning of the stria vascularis in patients with MD [21]. Possible theories diverging from the traditional disruption of Guild's principle of longitudinal endolymphatic flow include ionic disequilibrium being responsible for the hydrops. Cellular changes in Reissner's membrane are postulated to cause disruption of the endolymphatic flow and thus lead to ionic imbal‐ ance, a possible mechanism of hearing loss in endolymphatic hydrops [22].
