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PubMed2003

Hyperbaric compression in the guinea pig with perilymph fistula.

OBJECTIVE: The study goal was to evaluate the effects of hyperbaric therapy on the auditory and vestibular function of guinea pigs compromised by perilymph fistula (PLF). METHODS: Twenty-four pigmented guinea pigs underwent induction of bilateral eustachian tube dysfunction before the creation of a unilateral PLF. Half of the animals were randomly assigned to receive immediate hyperbaric compression treatment of 4 "dives" each. Hearing was tested electrocochleographically, and signs of vestibulopathy were recorded before and after compression. RESULTS: After accounting for the effects of PLF, compression was not associated with significant hearing loss (P = 0.5411). Vestibulopathy was seen only in ears with PLF, and its incidence was similar for compression and noncompression groups. CONCLUSION: Hyperbaric compression does not compromise auditory or vestibular function in guinea pig ears with experimental PLF. SIGNIFICANCE: Our observations support the relative safety of recompression in patients with PLF.

Animals↗
PubMed1996

Effects of brain stem lesions on cochlear function: mechanism of hearing improvement after removal of a brain stem tumor.

EOAEs are well correlated with changes of hearing sensitivity during the clinical course of brain stem lesions, as shown in this case study. They may serve as sensitive indicators to evaluate the possible effects of a brain stem lesion on cochlear function and monitor the attempted preservation of hearing during CPA or brain stem surgeries. It is thereby suggested that EOAEs should be included in an audiologic test battery in a differential diagnosis of retrocochlear lesions.

Audiometry, Pure-Tone↗
PubMed2000

Assessment of vestibular ototoxicity of ear drops by recording of vestibular evoked potentials to acceleration impulses.

INTRODUCTION: The cochlear ototoxicity of several ear drops is well documented in the literature, but very few studies exist on the vestibular ototoxicity of these topical drugs. GOAL OF STUDY: To develop an animal model for the assessment of the vestibular ototoxicity of ear drops. MATERIALS AND METHODS: Two animal groups, consisting of five fat sand rats (FSRs) each, underwent unilateral labyrinthectomy. Normal saline was topically applied into the middle ear cavity of rats in the first group for 7 days (control group). Rats in the second group were treated in the same way by topical gentamicin solution. Cochlear function was assessed by the recording of auditory evoked potential (ABPs) thresholds, and vestibular function was assessed by the recording of vestibular evoked potentials (VsEPs) to angular accelerations. RESULTS: In the control group, except for the amplitude of the first wave, there was no significant difference in the VsEPs recorded before and after topical application. In the gentamicin group, VsEPs could not be recorded after 7 days, and ABPs were recorded in one case only, with a threshold of 100 dB sound pressure level (SPL). CONCLUSION: VsEPs seem to be a reliable measure for evaluating the vestibular ototoxicity of topical ear drops.

Administration, Topical↗
PubMed2000

Changes of the compound action potential (CAP) and the expression of inducible nitric oxide synthase (iNOS/NOS II) in the cochlea under the inflammatory condition(1).

In this study, the effect of endotoxin on the guinea pig cochlea has been examined electrophysiologically and immunohistochemically. Bacterial lipopolysaccharide (LPS, 5 mg/ml, 0.2 ml) was injected into the middle ear trans-tympanically. The electrocochleograms were measured before, immediately upon, and 3, 6 and 12 h after the injection continuously with an electrode inserted into the facial canal. After each measurement, some of the animals were killed with an intracardiac perfusion of fixative, temporal bones were removed and were immunohistochemically examined for inducible nitric oxide synthase (iNOS/NOS II). On serial paraffin section, iNOS could be detected first after 3 h in the lateral wall, the supporting cells of the organ of Corti and in cells of the spiral ganglion and was observed up to 12 h. After the injection of LPS, the threshold of compound action potential became significantly worse after 12 h in the LPS group. These changes became evident first at higher frequency (8 kHz). These results suggest that iNOS-generated NO is involved in the cochlea dysfunction under inflammatory conditions.

Action Potentials↗
PubMed2001

Role of nitric oxide in focal microcirculation disorder of guinea pig cochlea.

This study was designed to evaluate the role of endogenous nitric oxide (NO) in focal microcirculation disorder of the guinea pig cochlea. Focal microcirculation disorder was induced by a photochemical reaction at the lateral wall of the second cochlear turn. Saline or N omega-nitro-L-arginine methyl ester (L-NAME) was administered before the onset of photochemical reaction. Cochlear blood flow (CBF) was measured at the focal lesion (ischemic core), 1 mm from the lesion in the apical and basal direction (ischemic border zone) by using a novel non-contact laser blood flowmeter. NO synthase activities were measured by radioenzymeassay. In the saline pretreatment group, CBF was significantly decreased to 58.8+/-4.4% of the baseline at the ischemic core 30 min after the onset of photochemical reaction (P<0.01), while CBF showed no significant change at the ischemic border zone. In the L-NAME pretreatment group, CBF was significantly decreased not only at the focal lesion (48.3+/-6.5%, P<0.01), but also at the ischemic border zone (apical, 49.3+/-2.3%, P<0.05; basal, 58.7+/-7.1%, P<0.05, respectively). NO synthase III activity of cochlea was increased significantly (P<0.01) 15 min after microcirculation disorder. These findings suggest that formation of endogenous NO plays a key role in the maintenance of CBF in acute focal cochlear microcirculation disorder.

Animals↗
PubMed2001

Ultrastructural and physiological defects in the cochlea of the Mpv17 mouse strain. A comparison between young and old adult animals.

Ultrastructural investigations were performed in young (approximately 2 months) and old (7 months) Mpv17-negative and wild-type mice. The onset, the severity and the pattern of the degeneration significantly differed between both mice strains. In the wild-type mouse strain the degenerative changes of the cochlear structures were similar to the aging pattern described for other species. In contrast, the Mpv17 mutants showed degenerative changes of the cochlear structures already at the age of 2 months. The degenerative changes were patchy arranged throughout the entire length of the cochlea and involved the organ of Corti as well as the stria vascularis epithelia with alterations of the basement membrane of the capillaries. The severe sensorineural hearing loss and degenerative changes of the cochlear structures indicate that cochlear structures, especially the outer hair cells and the intermediate cells of the stria vascularis, are vulnerable to the missing Mpv17 gene product.

Aging↗
PubMed2001

Cortical reorganization in patients with high frequency cochlear hearing loss.

Animal research has shown that tonotopic representation in the auditory cortex is not statically fixed in the adult organism but can be altered after deafferentation. The present study examines the plasticity of the human auditory cortex in patients with high frequency cochlear hearing loss by means of magnetoencephalographic measurements. The data show that the cortical map can reorganize such that cortical neurons deprived of their usual most sensitive afferent input now respond to tone frequencies adjacent to the frequency range of the partial hearing loss. The results suggest that deafferentation due to cochlear damage in adults may lead to functional reorganization of auditory cortical structures.

Acoustic Stimulation↗
PubMed2002

The otolithic organ as a receptor of vestibular hearing revealed by vestibular-evoked myogenic potentials in patients with inner ear anomalies.

The human vestibule has preserved an ancestral sound sensitivity and it has been suggested that a reflex could originate from this property underlying cervical muscle micro-contractions secondary to strong acoustic stimulation. Previous studies have established that an early component of loud sound-evoked myogenic potentials from the sternocleidomastoid muscle originate in the vestibule. This is based on findings that the response can still be obtained from patients with complete loss of cochlear and vestibular (semi-circular canal) function. Our data confirm, in a more direct way, a saccular origin of this short-latency acoustic response and verifies that a saccular acoustic response persists in the human ear. The contribution of this response to the perception of loud sounds is discussed. It is concluded that vestibular response to sound might be used to assist in the rehabilitation of deafness.

Adolescent↗
PubMed2002

Electrophysiological characteristics of inferior colliculus neurons in mutant mice with hereditary absence of cochlear outer hair cells.

One strain of homozygous Kit(W-v) mice (formerly known as W(v)/W(v)) lack 98% of the cochlear outer hair cells (OHCs) from birth. Inner hair cells (IHCs) and supporting cells develop normally. Thus, this strain is an attractive model to study the effect of complete OHC absence on central frequency representation. Frequency threshold curves were recorded along the tonotopic axis of inferior colliculus (IC) in mutant and control mice of the genetic background strain (C57BL/6J) and a different outbred strain (NMRI/wild mouse hybrids) known to be free of any cochlear pathology. The average threshold level of neurons in the mutants was 100 dB sound pressure level, 60 dB higher than in C57BL/6J and NMRI mice. Their tuning curves lacked the sharply tuned tip. In the C57BL/6J mice, although younger than four months, abnormal tuning curves were found for about 30% of the neurons, especially in the high frequency range. No abnormal tuning curves were found in the NMRI mice. The bandwidth of the tuning curves, measured at 10 dB above threshold, was on average 1.27 octaves in mutants, 0.62 octaves in C57BL/6J mice, and 0.34 octaves in NMRI mice. The range for the high cut-off frequency of the tuning curves at 10 dB above threshold was 6.4-61.1 kHz in the NMRI and 7-59.5 kHz in C57BL/6J. In the mutants, the range was limited to 11.1-41.7 kHz. The tonotopic gradient based on the cut-off frequency was less steep in the IC of the mutants than in both control groups.

Action Potentials↗
PubMed2003

Effect of cochlear damage on the detection of complex temporal envelopes.

Recent studies have demonstrated that the detection of complex temporal envelopes relies - at least partially - on the perception of a distortion component generated by a peripheral (cochlear) and/or central (post-cochlear) non-linearity. In the present study, first- and second-order amplitude modulation (AM) detection thresholds were obtained in normally hearing (NH) and hearing-impaired (HI) listeners using a 2-kHz pure-tone carrier. In both groups of listeners, first-order AM detection thresholds were measured for AM rates fm ranging between 4 and 87 Hz, and second-order AM detection thresholds were measured for second-order AM rates fm' ranging between 4 and 23 Hz, using a fixed first-order 'carrier' AM rate fm of 64 Hz. When the sound pressure level was adjusted in order to yield equal detectability in both groups for the 64-Hz first-order carrier modulation, (i) first-order AM detection thresholds for the HI listeners were normal at fm=87 Hz, and better-than-normal at fm=4 and 16 Hz, and (ii) second-order AM detection thresholds were identical at all modulation rates in NH and HI listeners. Similar results were obtained when the audibility of the 2-kHz pure-tone carrier was equated for both groups, i.e. when listeners were tested at the same sensation level. These results demonstrate clearly that cochlear damage has no effect on the detection of complex temporal envelopes, and indicate that the distortion component must be generated by a more central non-linearity than cochlear compression, transduction, or short-term adaptation.

Acoustic Stimulation↗
PubMed2003

Cochlear damage caused by continuous and intermittent noise exposure.

We compared the extent of permanent threshold shifts (PTS) and cochlear hair cell damage caused by continuous noise exposure with those caused by intermittent noise exposure. Twenty male pigmented guinea pigs that had been exposed to a one-octave band of noise at 4 kHz for 5 h were placed in four groups: exposure to 115 dB SPL continuous noise (group 1, n=5), 115 dB SPL intermittent noise (group 2, n=5), 125 dB SPL continuous noise (group 3, n=5), and 125 dB SPL intermittent noise (group 4, n=5). PTS at 2, 4, 8, and 16 kHz were assessed by means of auditory brainstem responses measured before noise exposure and 10 days after. The guinea pigs were killed 15 days after noise exposure, and the number of hair cells missing counted in surface preparations of the organs of Corti stained with rhodamine phalloidin. Groups 1 and 3 had significantly greater PTS (P<0.05) at all frequencies than intermittent groups 2 and 4. Group 3 had the greatest PTS at all the frequencies. Intermittent 125 dB noise total energy was greater than that of continuous 115 dB noise, but the latter elicited more PTS than the former. The extent of hair cell damage was comparable to the physiological findings. This indicates that continuous noise causes greater damage to the cochlea than intermittent noise of the same intensity and that, at the intensities tested, damage to the cochlea is not proportional to the total noise energy.

Acoustic Stimulation↗
PubMed1998

A semiquantitative analysis of the effects of cisplatin on the rat stria vascularis.

Cisplatin (CDDP) is a very effective chemotherapeutic agent but is highly ototoxic. Most studies have focused on the effects of CDDP on the outer hair cells. The purpose of this study was to examine changes in the stria vascularis in cisplatin treated male Wistar rats and to provide semiquantitative analysis of the results. We removed a section of the stria vascularis from the basal turn of five control and five CDDP (16 mg/kg) treated rats. Using transmission electron microscopy (TEM) we analyzed: (1) changes to the strial tissue as a whole; and (2) intracellular changes in the marginal cells. We also subjected the samples to semiquantitative analysis using the MCID, focusing on three aspects of strial profile abnormalities; the number of abnormal marginal cells in CDDP treated tissue, intracellular strial edema and densitometry. Controls appeared normal, but many pathologic changes were apparent in the experimental group. Results from the semiquantitative analysis indicate cisplatin has a deleterious effect on the stria vascularis including strial edema; bulging, rupture and/or compression of the marginal cells and depletion of the cytoplasmic organelles.

Animals↗
PubMed1998

Evidence for loss and recovery of chick brainstem auditory neurons during gentamicin-induced cochlear damage and regeneration.

It is well documented that damage to the chick cochlea caused by acoustic overstimulation or ototoxic drugs is reversible. Second-order auditory neurons in nucleus magnocellularis (NM) are sensitive to changes in input from the cochlea. However, few experiments studying changes in NM during cochlear hair cell loss and regeneration have been reported. Chicks were given a single systemic dose of gentamicin, which results in maximal hair cell loss in the base of the cochlea after 5 days. Many new hair cells are present by 9 days. These new hair cells are mature but not completely recovered in organization by 70 days. We counted neurons in Nissl-stained sections of the brainstem within specific tonotopic regions of NM, comparing absolute cell number between gentamicin- and saline-treated animals at both short and long survival times. Our data suggest that neuronal number in rostral NM parallels hair cell number in the base of the cochlea. That is, after a single dose of gentamicin, we see a loss of both cochlear hair cells and NM neurons early, followed by a recovery of both cochlear hair cells and NM neurons later. These results suggest that neurons, like cochlear hair cells, can recover following gentamicin-induced damage.

Animals↗
PubMed1999

Endocochlear potential in focal lesions of the guinea pig cochlea.

To estimate the correlation between the cochlear lateral wall and endocochlear potential (EP), the EP was measured at different time intervals up to 3 weeks at cochlear focal lesions made in the guinea pig. Lesions were produced by a photochemical reaction between systemically administered Rose Bengal and green light illumination in the second cochlear turn. Focal strial lesions (mean diameter 975 microm) became apparent under a scanning electron microscope 60 min after illumination, and degeneration of the organ of Corti was recognized at 3 days. The EP was measured continuously for 1 h following onset of the reaction in eight ears. In the other ears, EP measurements were done after various intervals of time up to 3 weeks. The EP showed two declines from pre-illumination level. The first started soon after illumination, reached a minimum value at 25 min, and then slightly recovered by 1 h. The second decline appeared at 3 days after illumination. In contrast to evident focal morphological degeneration 2 weeks post illumination, the EP values had recovered to almost normal. We suggest that the sequential changes in the EP were produced depending on the degeneration and then repairing processes of the endolymphatic boundary tissues.

Animals↗