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At least 451 records · Page 25Linked to original sources
PubMed1999

[Indications for imaging the inner ear with CISS-MRI].

BACKGROUND: High-resolution CT images are often unable to visualize the extent of possible cochlear obliteration after meningitis or after temporal bone fracture. The exact estimation of this extent, however, is crucial for cochlear implant surgery planning. Thus MR imaging of intralabyrinthine pathology is becoming an increasingly significant imaging modality. METHODS: The clinical relevance of the CISS (constructive interference in steady state) MR sequence is explained using 5 selected cases of different inner ear pathology. RESULTS: Two of the examined patients had unsuspicious inner ear signals, whereas in 3 cases MRI rendered relevant information about partial or total cochlear obliteration. CONCLUSIONS: These clinical examples illustrate how the ideal fluid and tissue contrast of CISS-MRI make this new technique suitable as a primary tool for evaluating inner ear obliteration before cochlear implant surgery.

Adult↗
PubMed1991

[Frequency dependence of the SISI test.(short increment sensitivity index). Clinical examples].

Experimental data on the influence of test frequency on the SISI-score are controversial. Comparability is limited by the diversity of experimental conditions. In a series of cases of pancochlear sudden hearing loss SISI-scores at 0.5 kHz and 3 kHz were compared. Some examples show that the sensitivity of the SISI-test at 0.5 kHz is much lower to that at 3 kHz. Low SISI-scores, of little evidence per se, have to be considered very critically in the low pitch range.

Audiometry, Pure-Tone↗
PubMed2000

Topical aminoglycoside ototoxicity: attempting to protect the cochlea.

Cochlear damage following topical application of aminoglycoside antibiotics to the round window membrane is a recognized phenomenon in both animal experiments and clinical reports. The authors have recently reported the ability of the free radical scavenging agent, alpha lipoic acid, to protect against the cochleo-toxic side effects of systemically administered aminoglycoside antibiotics. This study attempts to determine if the protective effect of this free radical scavenging agent is also seen following topical aminoglycoside application. Animals were implanted with osmotic pumps which delivered 2.5 microl/h solution of either neomycin 5% or neomycin plus alpha lipoic acid (50 mg/ml). Control animals received normal saline solution. Drug solutions were presented directly to the round window membrane over a 7-day period. Auditory sensitivity was monitored using compound action potentials (CAPs) of the auditory nerve recorded through an implanted chronic electrode terminating at the round window. Sixteen animals were entered into the study and randomized to one of the above groups. All animals receiving neomycin solution, with or without alpha lipoic acid, maintained normal thresholds for the first 3 days of the treatment period. Animals receiving neomycin solution alone experienced profound and rapid deterioration in auditory sensitivity, which was maximal by day 6. Animals receiving neomycin plus alpha lipoic acid also experienced significant cochlear damage; however, the rate of deterioration was slower than that seen in the group receiving neomycin alone. All control animals receiving saline maintained good hearing thresholds throughout the treatment period.

Administration, Topical↗
PubMed2000

Changes in 2f1 - f2 acoustic distortion products in humans during quinine-induced cochlear dysfunction.

Quinine is a suitable model substance for the study of otoacoustic emissions (OAEs) as it reversibly affects the outer hair cells, thus reducing sensitivity, frequency-selectivity and various forms of OAEs. The aim of this experiment was to study quinine-induced changes in the input/output (I/O) function of 2f1 - f2 distortion product OAE (DPOAE; f2/f1 = 1.22; 750-6,000 Hz). Six volunteers with normal hearing (26-39 years old) were intravenously infused to achieve pseudostable quinine plasma concentrations (approximately12 microM) inducing an average pure-tone threshold (PTT; 750-6,000 Hz) shift of 18 dB (5-30 dB) (frequency-independent and reversible). The mean quinine-induced DPOAE shift increased continuously with decreasing equal-level primary tones, e.g. from 1.0 dB at 70 dB sound pressure level (SPL) (n = 42) to 10.5 dB (n = 22) at 40 dB SPL (pooled data, no frequency dependence). According to recruitment, the mean slope of the DPOAE I/O function (at 30-60 dB SPL) increased from 0.86 to 1.35 dB/dB. The lack of correlation between shifts in DPOAE and PTT is in stark contrast to the excellent correlation reported between shifts in transient evoked OAE detection threshold and its corresponding psychoacoustic threshold. The highly vulnerable spontaneous OAEs, in combination with the less vulnerable DPOAEs, fit into a recently proposed taxonomic classification for OAEs.

Adult↗
PubMed2006

Response of cochlear blood flow to prostaglandin E1 applied topically to the round window.

CONCLUSIONS: The increase in cochlear blood flow (CBF) after administration of prostaglandin E1 (PGE1) to the round window depends on increased blood flow through the anterior inferior cerebellar artery (AICA). OBJECTIVES: To evaluate the response of CBF to PGE1 applied topically to the round window, and to investigate the origin of blood flow changes after this topical application. MATERIAL AND METHODS: The response of CBF to topically applied PGE1 was measured by placing the tip of a laser Doppler probe on the bony wall of the basal turn of the cochlea after the middle ear mucosa over the cochlea had been removed in guinea pigs and rats. In rats, the CBF response to PGE1 administration was investigated after occlusion of the AICA or stapedial artery. RESULTS: CBF increased following PGE1 administration in both guinea pigs and rats. In rats, CBF increased from 100% to 132%+/-10% (mean+/-SD) after the topical application of 0.5 microl of a 0.014% PGE1 solution. CBF decreased after occlusion of the AICA or stapedial artery but did not increase after PGE1 administration during occlusion of the AICA. The CBF response to PGE1 administration was similar before and after occlusion of the stapedial artery.

Administration, Topical↗
PubMed2006

Triamcinolone acetonide protects auditory hair cells from 4-hydroxy-2,3-nonenal (HNE) ototoxicity in vitro.

CONCLUSION: Triamcinolone acetonide crystalline suspension (e.g. Volon A) was not ototoxic to the auditory hair cells present within organ of Corti explants and protected them from an ototoxic molecule, i.e. 4-hydroxy-2,3-nonenal (HNE), that is produced within the organ of Corti as a result of oxidative stress-induced damage. OBJECTIVES: To test the corticosteroid, triamcinolone acetonide, for ototoxicity and otoprotective capacity in organ of Corti explants. MATERIALS AND METHODS: Organ of Corti explants excised from 4-day-old rats were the test system, HNE was the ototoxin challenge. Hair cell integrity counts were performed with fluorescent microscopy on fixed explants stained with FITC-labeled phalloidin. Statistical significance was set at p<0.05. RESULTS: Triamcinolone acetonide did not affect hair cell integrity in the organ of Corti explants and it provided a high level of protection of hair cells against the ototoxic effects of a damaging level of HNE as determined by hair cell density counts.

Aldehydes↗
PubMed1998

The influence of an arterial and venous air embolism on the hearing level in laboratory mini pigs.

We examined the influence of an experimental venous and arterial air embolism on the hearing level in laboratory mini pigs. Before and after the injection of air a threshold ABR was measured in anaesthetized mini pigs (n=15). A venous air embolism was performed in 6 animals: no changes in the hearing level or in the interpeak latencies Jewett wave V-I were observed in any of the animals before, during or after the application of air. In 9 animals the arterial embolism was done, 2 animals died and had to be excluded. In 6 animals out of 7 a hearing loss was observed starting after the injection of 40 ml air and finally ending in deafness for these 6 animals. The detected hearing loss is probably of cochlear origin, as no prolongations of the interpeak latencies of Jewett wave V-I at 90 dB HL were observed prior to the deafness. Our results show that air bubbles in the arterial circulation lead to cochlear damage ending in deafness. Our research indicates that decompression sickness, which is comparable to the arterial air embolism, is more often the cause of a sensorineural hearing loss after diving than previously believed.

Animals↗
PubMed1999

Cell proliferation in spiral ligament of mouse cochlea damaged by dihydrostreptomycin sulfate.

Cell proliferation of the spiral ligament in the normal and drug-induced damaged mice cochleae was investigated using the mitotic tracer bromodcoxyuridine (BrdU). Only a few nuclei labelled by BrdU were seen in the spiral ligament of the control mouse. However, many BrdU labelled nuclei in the spiral ligament in the cochlea damaged by dihydrostreptomycin sulfate were found. The expression of fibroblast growth factor receptor and connexin 43 was detected in the spiral ligament where BrdU labelled cells were found. These results suggest that cell proliferation in the spiral ligament may occur after the drug-induced damage, and this process is probably related to the recovery of cochlear function.

Animals↗
PubMed1988

Help for the hearing-impaired. Early evaluation, advanced technology, improved management.

Nearly one in ten Americans has some degree of hearing loss. The primary care physician generally is the first to evaluate patients who complain of hearing loss and thus has the first opportunity to determine the need for treatment or referral to an otolaryngologist or otologist. New technology provides better management of hearing loss than ever before. Virtually every case of hearing loss can now be corrected or improved.

Amplifiers, Electronic↗
PubMed2000

Inhibition of inducible nitric oxide synthase lowers the cochlear damage by lipopolysaccharide in guinea pigs.

Endotoxin-treated cochleas of the guinea pig were examined electrophysiologically and immunohistochemically concerning the expression of inducible nitric oxide synthase (iNOS/NOS II). One mg of bacterial lipopolysaccharide (LPS, 5 mg/ml) or mixed solution of 1 mg of LPS plus 1 mg of N(G)-nitro-L-arginine methyl ester (L-NAME, 5 mg/ml) (L-NAME/LPS) was injected into the middle ear of guinea pigs transtympanically. The electrocochleograms were measured prior to, immediately and 48 h after the injection. Immunohistological studies for iNOS followed after fixation, embedding and sectioning of the temporal bones. The threshold and amplitude of the compound action potential (CAP) became significantly worse in the LPS treated group. In contrast, the changes of the threshold and amplitude of CAP were decreased in the L-NAME/LPS group. iNOS was expressed in the stria vascularis, the spiral ligament, the organ of Corti and the spiral ganglion in the LPS group. These immunoreactivities in the L-NAME/LPS group were less intense than that in the LPS group. These results indicate that LPS has an ototoxic effect on the cochlea and that this effect could be mediated by iNOS produced high nitric oxide under inflammatory conditions.

Animals↗
PubMed2003

Myo15 function is distinct from Myo6, Myo7a and pirouette genes in development of cochlear stereocilia.

The unconventional myosin genes Myo15, Myo6 and Myo7a are essential for hearing in both humans and mice. Despite the expression of each gene in multiple organs, mutations result in identifiable phenotypes only in auditory or ocular sensory organs. The pirouette (pi) mouse also exhibits deafness and an inner ear pathology resembling that of Myo15 mutant mice and thus may be functionally related to Myo15. In order to investigate possible interactions between Myo15 and Myo6, Myo7a, and the gene affected in pirouette, we crossed Myo15(sh2/sh2) mice to the three other mutant mouse strains. Hearing in doubly heterozygous mice was similar to age-matched singly heterozygous animals, indicating that partial deficiency for both Myo15 and one of these other deafness genes does not reduce hearing. Viable double mutants were obtained from each cross, indicating that potential overlapping functions between these genes in other organs are not essential for viability. All critical cell types of the cochlear sensory epithelium were present in double mutant mice and cochlear stereocilia exhibited a superimposition of single mutant phenotypes. These data suggest that the function of Myo15 is distinct from that of Myo6, Myo7a or pi in development and/or maintenance of stereocilia.

Animals↗
PubMed2003

Acrylonitrile produces transient cochlear function loss and potentiates permanent noise-induced hearing loss.

There is growing evidence that agents that produce oxidative stress in the cochlea have significant ototoxic potential by themselves and can potentiate noise-induced hearing loss as well. Acrylonitrile (ACN) metabolism entails conjugation with glutathione, resulting in rapid and pronounced depletion of this important antioxidant in many organs including brain, liver, and kidney. ACN metabolism also results in cyanide (CN) formation through a secondary oxidative pathway. The results of two physiological experiments are reported here. First, the acute effects of ACN (50 mg/kg sc) on auditory sensitivity are assessed using a within subject study. In the second study, persistent effects of ACN alone (50 mg/kg, sc and 2 x 50 mg/kg, sc) and ACN in combination with noise exposure (8 h, 108 dB octave-band noise) are evaluated using threshold sensitivity as the dependent measure. Auditory threshold shift and absolute thresholds were determined using the compound action potential (CAP) amplitude. Acute ACN administration produces a loss in auditory threshold sensitivity that reached a maximum 10-20 min following sc injection. Auditory thresholds returned to control levels 75-100 min following exposure. In the study of permanent auditory threshold shifts, ACN plus noise increased auditory threshold impairment relative to rats receiving noise only when thresholds were assessed 3 weeks following exposure. ACN by itself did not produce permanent threshold impairment 3 weeks following administration. Assays were undertaken in separate groups of rats to track the elevation in blood CN and the depletion of total glutathione in cochlea, brain, and liver following ACN treatment. Systemic blood CN levels were not significantly elevated until 60-120 min following injection, and cochlear glutathione levels showed significant depletion as little as 15 min after injection and remained depressed for about 4 h. The results confirm the prediction that ACN is acutely ototoxic and can enhance noise-induced hearing loss.

Acrylonitrile↗
PubMed2000

Acoustic trauma enhances DNA binding of transcription factor AP-1 in the guinea pig inner ear.

Radiolabeled probes for the transcription factor, activator protein-1 (AP-1), bound differentially to nuclear fractions of discrete structures of the guinea pig cochlea (organ of Corti, lateral wall tissues, and spiral ganglion). Noise exposure (4 kHz octave band, 115 dB, for 5 h) significantly increased AP-1 binding in both the organ of Corti and lateral wall tissues but not in the spiral ganglion. Supershift analysis using an antibody against c-Fos protein demonstrated that enhancement of AP-1/DNA binding was at least in part due to the expression of c-Fos protein. These results suggest that AP-1 is involved in the molecular mechanism(s) mediating noise-induced cochlear damage.

Animals↗
PubMed2001

Hypothermia reduces glutamate efflux in perilymph following transient cochlear ischemia.

The effect of hypothermia on ischemic injury of the cochlea in gerbils was studied with particular regard to glutamate efflux in the perilymph. Under normothermic conditions interruption of the blood supply to the cochlea for 15 min caused a remarkable elevation of the compound action potential (CAP) threshold, and an increase in perilymphatic glutamate. The CAP threshold recovered to some extent with reperfusion, but not to preischemic levels. CAP thresholds, under hypothermic conditions and with reperfusion, recovered promptly to near pre-ischemic levels, while glutamate concentration did not change. These results, together with electron microscopy studies, suggest that hypothermia prevents hearing loss primarily through reduction of glutamate efflux at the synopses between inner hair cells and primary afferent auditory neurons.

Animals↗
PubMed2001

The role of acidic fibroblast growth factor in recovery of acoustic trauma.

We administered acidic fibroblast growth factor (aFGF) to the perilymph of the guinea pig cochlea after exposure to intense sound to investigate its effect on the process of recovery after acoustic trauma. We assessed auditory brain stem response (ABR) thresholds to evaluate cochlear function and observed the sensory epithelium using confocal laser-scanning microscopy. After noise exposure (120 dB SPL, 5 h), the ABR threshold showed an increase of approximately 50 dB SPL that recovered after 14 days. Cochlear function in aFGF treated ears recovered more quickly than that in control ears. These results suggest that aFGF may play an important role in cochlear recovery after acoustic injury.

Animals↗
PubMed2002

Adenoviral and adeno-associated viral vector mediated gene transfer in the guinea pig cochlea.

Peripheral sensorineural hearing loss is a very common inner ear disorder affecting nearly 10% of the population. At present there is no cure for this disorder but gene therapy has been suggested as a potentially effective method for clinical treatment in the future. Thus we investigated the effectiveness of adenoviral (Ad) and adeno-associated viral (AAV) vectors to transduce the cochlea of guinea pigs. After direct injection into the basal turn of the cochlea, we found that both Ad and AAV vectors coding for the reporter genes lacZ or GFP readily transduced spiral ganglion cells. In addition, some transgene expression was detected in the stria vascularis after AAV-GFP injection. Gene expression persisted at least 8 weeks after viral vector injection. Present findings will help to develop future gene therapy protocols in the inner ear by using Ad and AAV coding for neurotrophins such as NT-3, BDNF, GDNF and VEGF.

Adenoviridae↗