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Past theories that have been proposed to account for the attacks of vertigo during the course of Meniere disease are reviewed. In the past, vascular theories and theories of perilymph and endolymph mixing due to ruptures or leakages were proposed. Recent research concerning the basic mechanisms of the inner ear anatomy and function cast doubt on these theories. The anatomy, physiology, and pathophysiology of the inner ear, and in particular of the endolymphatic sac and endolymphatic duct are reviewed. Recent studies suggest that in people the endolymph ionic content is replenished without any flow of fluid and that longitudinal endolymph flow only occurs in response to volume excess. Furthermore audiological and electrophysiological studies have revealed little or no change in the cochlear function during episodes of vertigo. The longitudinal drainage theory attempts to encompass the recent research findings. The theory hypothesizes that endolymph draining too rapidly from the cochlear duct (pars inferior) causes attacks of vertigo. The endolymph overfills the endolymphatic sinus and overflows into the utricle (pars superior), stretching the cristae of the semicircular canals, causing the attacks of vertigo., (Crown Copyright 2010. Published by Elsevier Inc. All rights reserved.)

It is well established that endolymphatic hydrops plays a role in Ménière disease, even though the precise role is not fully understood and the presence of hydrops in the ear does not always result in symptoms of the disease. It nevertheless follows that a scientific understanding of how hydrops arises, how it affects the function of the ear, and how it can be manipulated or reversed could contribute to the development of effective treatments for the disease. Measurements in animal models in which endolymphatic hydrops has been induced have given numerous insights into the relationships between hydrops and other pathologic and electrophysiological changes, and how these changes influence the function of the ear. The prominent role of the endolymphatic sac in endolymph volume regulation, and the cascade of histopathological and electrophysiological changes that are associated with chronic endolymphatic hydrops, have now been established. An increasing number of models are now available that allow specific aspects of the interrelationships to be studied. The yclical nature of Ménière symptoms gives hope that treatments can be developed to maintain the ear in permanent state of remission, possibly by controlling endolymphatic hydrops, thereby avoiding the rogressive damage and secondary pathologic changes that may also contribute to the patient's symptoms., (Copyright 2010 Elsevier Ltd. All rights reserved.)

In summary, fluctuant hearing loss is defined as a disorder of the inner ear characterized by fullness, roaring tinnitus, and fluctuations in hearing. It is believed to be caused by an inadequate absorption of endolymph from the endolymphatic sac, with or without one or more metabolic disorders, that interferes with the delicate balance between the production and absorption of endolymph and thus produces cochlear hydrops. This triad of fullness, roaring tinnitus, and fluctuant hearing loss resulting from cochlear hydrops is much more common than the quadrad of true turning vertigo, fullness, roaring tinnitus, and fluctuant hearing loss due to vestibular and cochlear hydrops known as Meniere's disease. Although patients with fluctuant hearing loss only may eventually develop vertigo as the chief complaint and then be said to have Meniere's disease, it is remarkable how many patients continue to suffer mainly from cochlear symptoms at all times. It would appear, because of the greater frequency of fluctuant hearing loss than in Meniere's disease, that the cochlear labyrinth is more susceptible to hydrops than the vestibular labyrinth. For the purposes of diagnosis and treatment it is very useful to separate patients into those with fluctuant hearing loss and those with Meniere's disease.