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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.

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