title: Hypothetical mechanism for vertigo in Meniere's disease.
abstract: 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.
authors: Department of Surgery/Otolaryngology, The University of Sydney, New South Wales 2006, Australia. wpr_gibson@bigpond.com
authors: William P R
authors: WP
authors: Gibson
mesh_terms: D001301:Audiometry, Pure-Tone; D001309:Auditory Threshold / Q000502:physiology; D003051:Cochlea / Q000502:physiology; D004710:Endolymph / Q000378:metabolism; D004711:Endolymphatic Duct / Q000033:anatomy & histology; D004712:Endolymphatic Sac / Q000033:anatomy & histology / Q000502:physiology / Q000601:surgery; D006801:Humans; D008575:Meniere Disease / Q000503:physiopathology*; D009759:Nystagmus, Pathologic / Q000503:physiopathology; D012444:Saccule and Utricle / Q000502:physiology; D013577:Syndrome; D009626:Terminology as Topic; D014717:Vertigo / Q000209:etiology / Q000503:physiopathology