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PubMedDate not supplied

Lymphocytic streaming as an indicator of inner ear compartmentalization.

Despite a great deal of anatomic and physiologic data in animals, controversy still exists over whether or not the perilymphatic space in man is directly connected to the intracranial space via a patent cochlear aqueduct or other fluid channel. Human physiologic data are limited, indirect, and conflicting. Anatomic and pathologic data have heretofore been inadequate for answering the question convincingly. The temporal bones of a 19-year-old woman with central nervous system lymphoblastic leukemia are discussed. The passive-appearing movement of lymphoblasts between cerebrospinal fluid and perilymphatic spaces suggests both a functionally patent cochlear aqueduct and alternate pathways.

Adult↗
PubMed1986

The state of tinnitus after inner ear surgery.

A retrospective study of several procedures--for either treatment of vertigo or resection of acoustic neuromas--was performed to determine their effect on tinnitus. Subjective ratings of the state of tinnitus (resolution, improvement, maintenance, or deterioration) were obtained by questionnaire. Surgical procedures performed for correction of vertigo frequently alter tinnitus. In general, procedures that conserve hearing--namely, retrolabyrinthine vestibular neurectomy (RVN), middle fossa vestibular neurectomy (MFVN), and endolymphatic shunt procedures (ELS)--have a 50% to 65% chance of helping relieve tinnitus and up to a 22% chance of worsening tinnitus. When there is no serviceable hearing, cochleovestibular neurectomy (CVN) offers the best cure rate for tinnitus (76%) and the least chance of worsening tinnitus (3%). When hearing is minimal and the patient complains of tinnitus, a CVN--rather than a labyrinthectomy--should be recommended. However, when useful hearing is present, a CVN is not usually recommended for relief of tinnitus, since the actual cure rates are only 35%. When vertigo is not a complaint, there is currently no surgical procedure known that can be recommended for the treatment of tinnitus.

Diagnosis, Differential↗
PubMed1978

A detection method for lactic dehydrogenase activity in the inner ear.

A method for the detection of lactic dehydrogenase enzymatic activity in outer hair cells of the rabbit is described. The membranous labyrinth with temporal bone was prefixed in glutaraldehyde. After being placed into the incubation medium, it was postfixed in osmium tetroxide. Specimens of the organ of Corti were removed. Then the specimens were embedded in water-soluble glycol and cut with a cryostat for light microscopy, and also they were embedded in Epon and cut for light and electron microscopy. Sectioning of the membranous labyrinth was very easily made when the specimens were embedded in both the water-soluble glycol and the Epon. The structures of the frozen sections as well as the Epon-embedded ones were well preserved. In the frozen sections the preservation and localization of reaction products were thoroughly kept, but monoformazan of the Epon-embedded sections was soluble.

Animals↗
PubMed2003

Brn3c null mutant mice show long-term, incomplete retention of some afferent inner ear innervation.

BACKGROUND: Ears of Brn3c null mutants develop immature hair cells, identifiable only by certain molecular markers, and undergo apoptosis in neonates. This partial development of hair cells could lead to enough neurotrophin expression to sustain sensory neurons through embryonic development. We have therefore investigated in these mutants the patterns of innervation and of expression of known neurotrophins. RESULTS: At birth there is a limited expression of BDNF and NT-3 in the mutant sensory epithelia and DiI tracing shows no specific reduction of afferents or efferents that resembles neurotrophin null mutations. At postnatal day 7/8 (P7/8), innervation is severely reduced both qualitatively and quantitatively. 1% of myosin VIIa-positive immature hair cells are present in the mutant cochlea, concentrated in the base. Around 20% of immature hair cells exist in the mutant vestibular sensory epithelia. Despite more severe loss of hair cells (1% compared to 20%), the cochlea retains many more sensory neurons (46% compared to 15%) than vestibular epithelia. Even 6 months old mutant mice have some fibers to all vestibular sensory epithelia and many more to the cochlear apex which lacks MyoVIIa positive hair cells. Topologically organized central cochlea projections exist at least until P8, suggesting that functional hair cells are not required to establish such projections. CONCLUSION: The limited expression of neurotrophins in the cochlea of Brn3c null mice suffices to support many sensory neurons, particularly in the cochlea, until birth. The molecular nature of the long term survival of apical spiral neurons remains unclear.

Age Factors↗
PubMed2004

Effect of gravity on the caloric stimulation of the inner ear.

Robert Barany won the 1914 Nobel Prize in medicine for his convection hypothesis for caloric stimulation. Microgravity caloric tests aboard the 1983 SpaceLab 1 mission produced nystagmus results that contradicted the basic premise of Barany's convection theory. In this paper, we present a fluid structural analysis of the caloric stimulation of the lateral semicircular canal. Direct numerical simulations indicate that on earth, natural convection is the dominant mechanism for endolymphatic flow. However, in the microgravity environment of orbiting spacecraft, where buoyancy effects are mitigated, an expansive convection becomes the sole mechanism for producing endolymph motion and cupular displacement. Transient 1 g and microgravity case studies are presented to delineate the different dynamic behaviors of the 1 g and microgravity endolymphatic flows. The associated fluid-structural interactions are also analyzed based on the time evolution of cupular displacements.

Biophysical Phenomena↗
PubMed2000

Molecular analysis of the Pendred's syndrome gene and magnetic resonance imaging studies of the inner ear are essential for the diagnosis of true Pendred's syndrome.

Pendred's syndrome is a combination of congenital sensorineural hearing loss and iodine organification defect leading to a positive perchlorate test and goiter. Although it is the commonest form of syndromic hearing loss, the variable clinical presentation contributes to the difficulty in securing a diagnosis. The identification of the disease gene (PDS) prompts the need to reevaluate the syndrome to identify possible clues for the diagnosis. To this purpose, in three Italian families presenting with the clinical features of Pendred's syndrome, the molecular analysis was accompanied by full clinical, biochemical, and radiological examination. A correlation between genotype and phenotype was found in the only patient with enlargement of vestibular aqueduct and endolymphatic duct and sac at magnetic resonance imaging. This subject was a compound heterozygote for a deletion in PDS exon 10 (1197delT, FS400) and a novel insertion in exon 19 (2182-2183insG, Y728X). The present study demonstrates for the first time the value of the combination of clinical/radiological and genetic studies in the diagnosis of Pendred's syndrome. The positivity of a perchlorate discharge test and the malformations of membranous labyrinth fit well with the recent achievements on the role of pendrin in thyroid hormonogenesis and the maintenance of endolymph homeostasis.

Adolescent↗
PubMed2005

The Notch ligands DLL1 and JAG2 act synergistically to regulate hair cell development in the mammalian inner ear.

The mammalian auditory sensory epithelium, the organ of Corti, contains sensory hair cells and nonsensory supporting cells arranged in a highly patterned mosaic. Notch-mediated lateral inhibition is the proposed mechanism for creating this sensory mosaic. Previous work has shown that mice lacking the Notch ligand JAG2 differentiate supernumerary hair cells in the cochlea, consistent with the lateral inhibitory model. However, it was not clear why only relatively modest increases in hair cell production were observed in Jag2 mutant mice. Here, we show that another Notch ligand, DLL1, functions synergistically with JAG2 in regulating hair cell differentiation in the cochlea. We also show by conditional inactivation that these ligands probably signal through the NOTCH1 receptor. Supernumerary hair cells in Dll1/Jag2 double mutants arise primarily through a switch in cell fate, rather than through excess proliferation. Although these results demonstrate an important role for Notch-mediated lateral inhibition during cochlear hair cell patterning, we also detected abnormally prolonged cellular proliferation that preferentially affected supporting cells in the organ of Corti. Our results demonstrate that the Notch pathway plays a dual role in regulating cellular differentiation and patterning in the cochlea, acting both through lateral inhibition and the control of cellular proliferation.

Animals↗