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Ménière’s disease is a complex disorder of the inner ear, characterized by recurrent episodes of vertigo, progressive hearing loss, tinnitus, and aural fullness. The pathophysiology of this condition is dominated by endolymphatic hydrops, reflecting imbalances in fluid regulation and pressure within the membranous labyrinth, which impair cellular function and the transmission of vestibular and auditory signals. Although genetic predisposition provides a susceptible background, recent studies emphasize that non-genetic factors act as critical triggers of clinical events, determining both the onset of symptoms and the modulation of their severity. These factors directly influence pathophysiology by disrupting endolymphatic homeostasis and altering the intracellular and tissue dynamics of the membranous labyrinth, thereby contributing to the phenotypic variability observed among patients. The key to this process lies in the synergistic interaction between genetic predisposition and external or contextual influences, which determines the threshold at which the compensatory mechanisms of the inner ear fail, triggering the characteristic episodes. Understanding this interdependence, as well as the underlying disease mechanisms, provides essential insights for the identification of preventive and therapeutic strategies aimed not only at symptom control but also at modulating the factors that influence susceptibility to endolymphatic imbalance.
Iațentiuc et al. (Sat,) studied this question.