Mechanism of the Ménière Attack

Abstract

A survey of experimental evidence showing the influence of an increase in potassium concentration in the perilymph on cochlear and vestibular nerve branches is discussed. Informations have indicated that a concentration lower than 20–30 mM produced an increase in action potential frequency in nerve preparations and that a low potassium concentration in animal experiments produced an ipsilateral nystagmus. Increasing the concentration of potassium in the endolymph to values not over the normal endolymph concentration, blocked the conduction of action potentials in the vestibular nerve branches resulting in a reversible contralateral nystagmus. From these results it may be concluded that all objective symptoms of a Ménière attack can be experimentally reproduced by one single factor: the potassium concentration in the perilymph. The known ruptures in the distended walls in a hydrops, with a diffusion of endolymph potassium into the perilymph surrounding the nerve branches to the vestibular and cochlear areas have consequently been assumed to produce the basis for Ménière attacks.

Meniere’s, migraine, and motion sickness

“…Visual and vestibular sensory conflicts occur in Meniere's disease during vertiginous symptoms and also during motion sickness [16,17]. Prolonged and recurrent episodes of vertigo in Meniere's disease cause a progressive loss of accurate vestibular perceptions and unstable vestibular gain levels [18].…”

Vestibular evoked myogenic potentials: optimal stimulation and clinical application

“…One is membrane rupture theory, which mainly occurs on the Reissner's membrane, and the other is membrane distension theory, indicating that the utricular or saccular membrane herniates into the semicircular canal. Most patients with Meniere attacks revealed abnormal VEMPs, indicating that the saccule ''participates'' in the event of Meniere attack, an important idea that stimulates consideration of the mechanism of Meniere attack [34,39]. Abnormal VEMPs may or may not normalize after Meniere attack depending on the individual saccular pathology [40,41].…”

Ante mortem Ruptures of the Endolymphatic Membranes in Children: Real Finding or Artifact?

“…Typically the histopathological study of temporal bones from patients with Ménière's disease demonstrates bulging of the endolymphatic membranes [1]. Dohlman [8] was the first who theorized that the sudden episodes of vertigo in Ménière's disease are caused by a mixture of endolymph with perilymph after rupture of the endolymphatic membranes. Endolymphatic hydrops, however, can occur in adults [12] and children [9] without clinical Ménière's disease, but it is still not known whether a slowly increasing volume of endolymph will result in spontaneous ruptures, especially because the endolymph/perilymph system is a low-pressure system [13].…”

“…Ruptures of the endolymphatic membranes have been reported in several histopathological studies in humans with Ménière's disease [5][6][7]. This has generated the concept that increasing endolymphatic pressure causes ruptures with subsequent mixing of perilymph and endolymph, triggering the sudden onset of vertigo in Ménière's disease [8]. The existence of membrane ruptures, however, has been doubted because no reproducible ruptures after induced endolymphatic hydrops occurred in the experimental animals [3,4].…”