||The earliest change in the vestibular labyrinth consists of a dilatation of the saccule. Over time the saccule may distend to such an extent that it displaces the utricle posterosuperiorly. With continued distension the utricle may herniate into the semicircular canals. The distended saccule may bring the saccular membrane into contact with the stapes footplate. There is a correlation between the amount of dilatation of the vestibular contents and decreased response of the ear to caloric irrigation.
The increased volume and pressure of the endolymph may cause spontaneous ruptures or breaks in Reissner's membrane or in the walls of the saccule, or utricle. Ruptures occur more frequently in Reissner's membrane than in the vestibular membranes.
Ruptures of the membranous labyrinth seem to be an explanation for acute episodes of vertigo. The hearing loss and decreased vestibular function result from the admixture of endolymph and perilymph, which alters the electrochemical properties of these two separate fluids.
The increased pressure produced by the excess of endolymph is also believed to be responsible for the dysfunction of the cochlear hair cells, and of the cupulae of the semicircular canals. The deformation and herniation of the vestibular membranes may precipitate the attacks of vertigo.
Whereas the acute attacks of Meniere's disease are characterized by hydropic distension of the endolymphatic membranous labyrinth with subsequent rupture and collapse, long-term changes are those of permanent hair cell damage and sensorineural hearing loss. The cause of this permanent cochlear and vestibular dysfunction is not known. It may be due to ischemia from prolonged pressure, or it may be metabolic or toxic in nature.