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At least 217 records · Page 12Linked to original sources
PubMed1980

Distribution of marked perilymph to the subarachnoidal space.

In guinea pigs the tympanic perilymph of the basal turn was marked with fluorescing rhodamine. In the first series one drop of a 2% solution of the dye was applied onto the round window membrane. Since the perilymphatic space was not opened, the physiologic state of the communicating fluids perilymph and CSF was maintained. The dye appeared within 3-5 min via cochlear aqueduct in the subarachnoidal space. In the dead animal the speed of distribution was significantly less. This most probably indicates a weak physiologic flow of the perilymph through the aqueduct to the subarachnoidal space in living animals. In the second series, 2 ng of lyophilized rhodamine was instilled directly into the tympanic perilymph near the round window. Though hardly any additional volume was brought into the perilymph, the distribution of the dye was distinctly greater as a sign of the considerable sensitivity of the fluid system, even by the slightest manipulation.

Animals↗
PubMed1997

Mode shapes of a damaged and repaired tympanic membrane as analysed by the finite element method.

This work makes use of recent finite element discretization of the human tympanic membrane where the known anisotropy of the tympanic membrane is implemented by a series of thin beam elements superimposed on thin shell membrane elements. These thin beam elements were introduced in order to simulate the fibre structure of the tympanic membrane. The onset of tympanosclerosis has been modelled as a gradual increase in tympanic membrane density and modulus in the affected area. This increased density results in a fall of 55% of the first natural frequency for only a 16% area of drum sclerosis. Additionally the amplitude response is significantly reduced. Repair of the membrane was simulated by removal of the fibre system from the affected area. Under these circumstances the natural frequencies virtually return to the healthy state but the mode shapes of vibration do not. The repair to the membrane, although not significantly altering frequency values, has resulted in a disruption to the normal mode shape patterns with consequences in the movements conveyed to the stapes and cochlear fluids.

Cochlea↗
PubMedDate not supplied

Ototoxicity of neomycin and its penetration through the round window membrane into the perilymph.

The ototoxicity of neomycin and its concentration in the perilymph after direct application on the round window membrane were studied. After placing 5 mg of neomycin on the round window membrane of guinea pigs for various time intervals, concentration of the drug in the perilymph was determined by high performance liquid chromatography, and the cochlea was examined by light microscopy. Neomycin penetrated the round window membrane quite easily, and its concentration in the perilymph became extremely high in a short time and then decreased gradually. This indicates that high concentration of neomycin in the perilymph can be attained by application of a small amount of the drug on the round window membrane. Ototoxicity of neomycin was observed after application for 4 hours. Cochlear damage increased as neomycin application time became longer, but no consistent relationship was noted between the concentration of neomycin and the amount of damage. This result is discussed from the point of concentration and persistence of the drug in the inner ear fluids.

Animals↗
PubMed1997

Anatomy of the normal human cochlear aqueduct with functional implications.

There is great variation in published descriptions of the shape, size, and patency of the human cochlear aqueduct. The first part of this paper describes the anatomy of the normal human cochlear aqueduct as determined from a study of 101 temporal bones. Nineteen bones aged 0-1 years and approximately 10 bones per decade of life until age 100 years were examined. The aqueduct was found to have a funnel shaped aperture at the cranial end with a dural sheath extending into it for a varying distance. The rest of the aqueduct was filled with a meshwork of loose connective tissue, often with a central lumen within it. Four types of patencies were noted: central lumen patent throughout length of aqueduct (34%), lumen filled with loose connective tissue (59%), lumen occluded by bone (4%), and obliteration of the aqueduct (3%). The mean value (+/- SD) of the narrowest portion was 138 (+/- 58) microns which occurred 200-300 microns from the cochlear end of the aqueduct. There was no correlation between age and narrowest diameter, or between age and category of patency. In the second part of this paper, we propose quantitative models of aqueduct function, based on measurements of ductal dimensions and known acoustical properties of the inner ear. Our model analyses suggest that in normal ears, the aqueduct (1) cannot support fluid flows large enough to explain stapedectomy gushers, (2) does filter out cardiac- and respiration-induced pulses in CSF and prevents them from affecting cochlear function, and (3) has little effect on normal ossicular transmission of sound for frequencies above 20 Hz. In pathological ears, such as those with ossicular disruption or after a type IV tympanoplasty, a patent aqueduct might affect hearing for frequencies below 150 Hz.

Acoustics↗