An Experimental Study on the Mechanism of the Ménière’s Attack: The Influence of High Perilymphatic Potassium Concentration on the Vestibular System

Abstract

Clinical characteristics of Ménière’s disease are episodic vertigo and fluctuating hearing loss, the origin of which is still obscure. It is well known that nystagmus is always present during the attack, as described by Aschan and Stahle [1], but whose character is not always the same. According to a previous study [2], irritative, paralytic, and reversal nystagmus were observed during the Ménière’s attack in 25%, 36%, and 39% of patients, respectively. To explain such complicated clinical manifestations, Schuknecht’s membrane rupture theory [3] would be most acceptable. He ascribed the episodic vertigo and fluctuating hearing loss to the rupture and repairing process in the endolymphatic system. His findings were supported by Silverstein [4], who provoked nystagmus by perfusing the perilymphatic space with artificial endolymph. Silverstein thought that sensorineural excitability might be altered by high perilymphatic potassium concentration. Dohlman [5] theorized that, on the basis of the membrane rupture theory, an initial ipsilateral nystagmus could occur due to partial depolarization of the vestibular nerve by the leaking endolymph, and then as the depolarization became more complete, the direction of nystagmus would turn to the contralateral side. Molinari [6] considered that the irritative nystagmus was due to the excitation of the vestibular receptor cells, and that the paralytic nystagmus was due to the inhibitory rebound in the central nervous system. Meissner [7] speculated that the potassium concentration in perilymph determined the extent of depolarization of the sensorineural synpase and brought about the tonus imbalance of the vestibular nuclei followed by ipsior contralateral nystagmus.