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PubMedDate not supplied

Classification of endolymphatic hydrops.

Ménière's disease is but one member of a family of disorders linked by the common pathophysiologic substrate of endolymphatic hydrops. The authors evaluated both clinical cases and temporal bone specimens and conclude that endolymphatic hydrops is a pathologic condition that is the final common manifestation of a variety of otologic insults. They present a logical classification which, on the basis of clinical data, distinguishes symptomatic and asymptomatic forms. The hallmarks of the symptomatic form are fluctuating hearing loss and episodic vertigo. The asymptomatic form is clinically silent. Each form may be further subclassified into embryopathic, acquired, and idiopathic types. The embryopathic type comprises those cases in which a noxious influence disrupts labyrinthine development in utero. The acquired type includes those cases in which a documented insult, either inflammatory or traumatic, is suffered by a previously normal labyrinth. The idiopathic type encompasses all those cases in which the event precipitating the endolymphatic hydrops is unknown. Ménière's disease is redefined as idiopathic, symptomatic endolymphatic hydrops.

Adolescent↗
PubMedDate not supplied

Animal models of endolymphatic hydrops.

Endolymphatic hydrops in the animal can be produced by various methods. The most promising is obliteration of the endolymphatic duct in the guinea pig. The extent of hydrops is similar to that of Ménière's disease specimens, but the animals are asymptomatic. A better model, utilizing a less invasive method and having the ability to elicit episodic vestibular symptoms, is needed. There is a reasonable doubt that one of the causes for Ménière's disease lies in the abnormal endolymphatic duct and sac. A wide ablation of such pathologic tissue may provide additional pathogenetic information.

Animals↗
PubMedDate not supplied

Hydrostatic pressure measurement of endolymph and perilymph in the guinea pig cochlea.

Hydrostatic pressures of endolymph and perilymph were measured with a servo-micropipet system. The validity of the experiment was assessed by observation of endolymphatic pressure changes during and after 3 minutes of anoxia. Simultaneous recording of endocochlear DC potential confirmed the location of the electrode tip. Following verification of the efficacy of the system, measurements of endolymphatic or perilymphatic pressures were made in ten guinea pigs in which the middle ears had been filled with a saturated sodium chloride solution. Both endolymphatic and perilymphatic measurements showed gradual declines in pressure, with minimum pressure at 15 to 20 minutes and slow recovery during the next 20 minutes.

Animals↗
PubMedDate not supplied

Experimental perilymphatic fistula.

Perilymphatic fistula was produced in guinea pigs by injecting artificial perilymph into the subarachnoid space of the posterior fossa. Rupture of the round window was confirmed by direct observation of the round window membrane under a surgical microscope during the injection. The animals were either vitally fixed or kept alive for one to three months before fixation. Conventional celloidin embedding method was used for serial sectioning. In immediate observation, nine cochleas showed hydrops, seven showed collapse, and 20 of 36 cochleas showed no change. Changes in the vestibular apparatus varied, with collapse of the membranous vestibular labyrinth as the main change. Delayed observation revealed 16 normal cochleas and four collapses and no hydrops out of 20 ears. Of these 20, nine ears showed normal vestibular apparatus, nine collapse, and two saccule hydrops. Loss of the outer hair cells was observed in five of 20 cochleas. Marked compression of the organ of Corti was seen in both immediate and delayed observations.

Animals↗
PubMedDate not supplied

An electrophysiologic study of experimental perilymphatic fistula.

This study was undertaken to elucidate the mechanism that causes sensorineural hearing loss in clinical cases with perilymphatic fistula. Perilymph was experimentally aspirated through the round window membrane in 17 guinea pigs. The extent of cochlear damage was examined electrophysiologically as well as histopathologically. Immediately after aspiration, several types of changes in summating potential (SP) were observed. Two animals without a polarity change of the SP showed only slight threshold changes in both cochlear microphonic and action potentials, and no specific histopathologic changes in the cochlea. Reversed polarity of the SP was observed in three animals, of which one showed a high-amplitude negative SP followed by rapidly progressive hearing loss. Bulging of Reissner's membrane was confirmed histopathologically in this case. The SP disappeared in the remaining 12 animals. In animals with profound electrophysiologic changes, bulging or rupture of Reissner's membrane and damaged hair cells were observed. These findings suggest that an abrupt change in perilymphatic pressure produces morphologic changes in the membranous labyrinth, causing changes in the vibration function of the cochlear partition and in the function of the organ of Corti. Abrupt pressure imbalance may be a causative factor of sensorineural hearing loss in the case of perilymphatic fistula.

Acoustic Stimulation↗
PubMed2003

An in vivo tracer study of noise-induced damage to the reticular lamina.

An in vivo tracer was used to determine if the reticular lamina and/or the cell membranes abutting the endolymphatic space are temporarily disrupted after intense noise exposure (4-kHz OBN, 108-dB SPL, 1.75 h). Using a double-barreled micropipette, the endolymphatic potential (EP) was recorded and artificial endolymph containing 10% carbon particles was injected into the endolymphatic space either 0 days or 28 days post-exposure. The cochleae were fixed 30-45 min post-injection, then dehydrated, embedded in plastic and dissected as flat preparations. Damage in the organ of Corti (OC) was quantified, the location of carbon was determined, and some OC segments were then sectioned radially. EP averaged 72+/-5 mV in five controls. These cochleae had carbon tracer in the endolymphatic space only. Four of five noise-exposed chinchillas examined 3-4 h post-exposure had a low EP (30+/-6 mV). The cochleae from these 0-day animals had several focal lesions in which nearly all outer hair cells had just degenerated. At these lesions, carbon was attached to cell membranes and debris between the reticular lamina and basilar membrane. By transmission electron microscopy, discontinuities were found in the apical membranes of sensory and supporting cells. Carbon particles were found in the cytoplasm of these cells. Four of five animals examined at 28 days had an average EP of 70+/-11 mV. The cochleae from these animals had multiple lesions in the basal turn, all of which were healed by phalangeal scars or squamous epithelial cells. In these cochleae, no carbon was found within the OC. Acute disruption of the reticular lamina and the apical membranes of sensory and supporting cells from noise appears to be a major mechanism to account for degeneration in the cochlea that spreads or continues for days to weeks post-exposure.

Animals↗