ReviewHNO2026
Evolution of understanding and clinical practice of Ménière's disease.
Review in HNO, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since Prosper Ménière's original description more than 160 years ago, concepts of Ménière's disease (MD) pathophysiology and treatment have evolved through distinct phases. For much of the twentieth century, the field was dominated by the hydrodynamic paradigm, which attributed symptoms to pressure-driven endolymphatic hydrops and episodic membrane rupture. Over the past three decades, however, accumulating pathological, physiological, genetic, and imaging evidence has undermined this model. This review traces the transition from the classic hydrodynamic era to a modern framework that conceptualizes MD as a disorder characterized by endolymphatic sac (ELS) failure, leading to impaired inner-ear homeostasis. Recent temporal bone studies demonstrate that endolymphatic hydrops reflects proliferative epithelial growth rather than pressure-induced distension, while systematic analyses identify two major disease endotypes-hypoplastic and degenerative-defined by distinct endolymphatic sac pathologies, which are associated with differing clinical phenotypes. Advances in magnetic resonance imaging and computed tomography now allow for in vivo visualization of hydrops and ELS-related anatomy, enabling endotype stratification in living patients. Together, these developments support a new disease model analogous to renal insufficiency, with important implications for mechanistic research, animal modeling, diagnostic criteria, and personalized clinical management of MD.
Indexed as
Identifiers
42228080What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.