Further remarks on the mechanism producing the symptoms of Ménière's disease.

The characteristic symptoms of a Ménière attack--low-tone hearing loss; and nystagmus of long duration, often beating in an ipsilateral direction, eventually changing to a contralateral direction, with a return to normal function between attacks--have all been reproduced in animal experiments by increasing the potassium concentration of the interstitial fluid surrounding the afferent nerve branches from the sensory areas of the inner ear. Several recent experiments of other investigators have shown that a low potassium concentration may increase the action potential frequency. This would explain an ipsilateral nystagmus. Raising the concentration further depresses the action potential frequency, resulting in a contralateral nystagmus. Furthermore, there is evidence indicating that cochlear microphonics might not be affected by increases in the potassium concentration. This seems to indicate that the nerves, and not the hair cells, are engaged in the production of those symptoms dependent on potassium increase. The clinical signs of a similar reaction of the cochlear hair cells in Ménière's cases seem to support the assumption of a similar cause. All the objective symptoms of a Ménière attack, thus, seem to comply with the experimental findings of an endolymphatic potassium contamination of the perilymph spaces around the afferent nerve branches.