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PubMed2004

[The patterns of cell proliferation in the chick basilar papilla following severe acoustic trauma].

OBJECTIVE: To investigate the characteristics of cell proliferation in chick basilar papilla (BP) following severe acoustic trauma, and the orgin of precursor cell that can generate into new hair cell. METHOD: Chicks were continuously exposed to a 1.5 kHz pure tone at 120 dB SPL for 48 h, and they were intraperitoneally injected with bromodeoxyuridine (BrdU) at 40 h, 48 h after the onset of exposure. Then, cochlea were immunocytochemically labeled to detect BrdU, and examined the cell proliferative activity in BP. RESULT: 1. Labeled cells presented in the mid-proximal region of BP where hair cells have been damaged and lost following noise overstimulation; 2. The most cells in S phase were detected at 48 h after the onset of exposure; and 3. Both labeled hair cells and supporting cells can be seen in BP; In addition, the supporting cells may act as precursor cells that can generate into new hair cells. CONCLUSION: These findings suggest that auditory epithelial cells can be regenerated in chick cochlea after acoustic trauma, even though ongoing production of hair cells don't occur in BP, and supporting cells may be a source of newly generated hair cells under pathological conditions.

Acoustic Stimulation↗
PubMed1977

[Treatment of acute inner ear deafness (sudden deafness and acoustic trauma) (author's transl)].

The principal facts concerning therapeutic measures in cases of sudden deafness and acoustic trauma are outlined. Experiment data concerning the pharmacology of inner ear circulation are presented. There is sufficient evidence for a critical evaluation of a few treatments whose effect seems to be proven (experimental increase of inner ear circulation in normal animals) or at least possible (in normal animals no or dubious increase; effective under pathological conditions only?). Experimental and clinical experiences concerning the dextran treatment of sudden deafness and acoustic trauma are reported.

Acute Disease↗
PubMed1995

Hair cell regeneration in the chick inner ear following acoustic trauma: ultrastructural and immunohistochemical studies.

The regeneration of hair cells in the chick inner ear following acoustic trauma was examined using transmission electron microscopy. In addition, the localization of proliferation cell nuclear antigen (PCNA) and basic fibroblast growth factor (b-FGF) was demonstrated immunohistochemically. The auditory sensory epithelium of the normal chick consists of short and tall hair cells and supporting cells. Immediately after noise exposure to a 1500-Hz pure tone at a sound pressure level of 120 decibels for 48 h, all the short hair cells disappeared in the middle region of the auditory epithelium. Twelve hours to 1 day after exposure, mitotic cells, binucleate cells and PCNA-positive supporting cells were observed, and b-FGF immunoreactivity was shown in the supporting cells and glial cells near the habenula perforata. Spindle-shaped hair cells with immature stereocilia and a kinocilium appeared 3 days after exposure; these cells had synaptic connections with the newly developed nerve endings. The spindle-shaped hair cell is considered to be a transitional cell in the lineage of the supporting cell to the mature short hair cell. These results indicate that, after acoustic trauma, the supporting cells divide and differentiate into new short hair cells via spindle-shaped hair cells. Furthermore, it is suggested that b-FGF is related to the proliferation of the supporting cells and the extension of the nerve fibers.

Acoustic Stimulation↗
PubMed1994

Return of auditory function following structural regeneration after acoustic trauma: behavioral measures from quail.

After measuring baseline behavioral audiograms, three of four behaviorally trained quail and fifteen untrained cohorts were exposed to a 1.5-kHz octave-band noise at 116-dB SPL for 4 h. The trained birds were tested daily following the exposure and showed a steady recovery of absolute sensitivity with a return to normal absolute thresholds by post-exposure days 8-10. Thirteen untrained cohorts were sacrificed after various survival times to evaluate the structural condition of the ear. The cohorts all showed regeneration of sensory cells similar to that seen in chicks. The effects of repeated acoustic trauma on recovery of sensitivity were evaluated by re-exposing the three trained birds and two untrained cohorts 106 days after the first exposure. One of the trained birds was exposed a third time, 113 days following the second exposure. The findings demonstrate that, following acoustic trauma, normal sensitivity returns prior to complete structural regeneration of the sensory epithelium and that repeated acoustic trauma may increase the time course of recovery of normal hearing sensitivity.

Acoustic Stimulation↗
PubMed1994

Return of auditory function following structural regeneration after acoustic trauma: behavioral measures from quail.

After measuring baseline behavioral audiograms, three of four behaviorally trained quail and fifteen untrained cohorts were exposed to a 1.5-kHz octave-band noise at 116-dB SPL for 4 h. The trained birds were tested daily following the exposure and showed a steady recovery of absolute sensitivity with a return to normal absolute thresholds by post-exposure days 8-10. Thirteen untrained cohorts were sacrificed after various survival times to evaluate the structural condition of the ear. The cohorts all showed regeneration of sensory cells similar to that seen in chicks. The effects of repeated acoustic trauma on recovery of sensitivity were evaluated by re-exposing the three trained birds and two untrained cohorts 106 days after the first exposure. One of the trained birds was exposed a third time, 113 days following the second exposure. The findings demonstrate that, following acoustic trauma, normal sensitivity returns prior to complete structural regeneration of the sensory epithelium and that repeated acoustic trauma may increase the time course of recovery of normal hearing sensitivity.

Animals↗
PubMed1985

Hyperbaric oxygen therapy for acute acoustic trauma.

We conducted a study on the effect of hyperbaric oxygen therapy on 122 soldiers following acute acoustic trauma. The patients included in this study, after the effect of spontaneous recovery had largely been excluded, were randomly allocated to four treatment groups. The results of our studies show that hyperbaric oxygen therapy shortens the course of healing with respect to high-pitch perception dysacusis. The results of treatment after an observation period of 6 weeks is also more favorable when patients are treated with oxygen when compared to patients given infusions or vasoactive substances. Similarly, the use of hyperbaric oxygen therapy also reduces the frequency of relapse following discharge from hospital. In contrast, the vasoactive substance chosen in our studies (betahistine) failed to have a favorable effect on the course of healing. Our study has also shown that no method can compare with hyperbaric therapy in eliminating tinnitus following acoustic trauma.

Adult↗
PubMed2002

Acoustic trauma induces reemergence of the growth- and plasticity-associated protein GAP-43 in the rat auditory brainstem.

We explored the consequences of unilateral acoustic trauma to intracochlear and central nervous system structures in rats. An acoustic trauma, induced by applying click stimuli of 130 dB (sound pressure level; SPL) for 30 minutes, resulted in an instant and permanent threshold shift of 95.92 +/- 1.08 dB (SEM) in the affected ear. We observed, as a consequence, a structural deterioration of the organ of Corti. Deprivation-dependent changes of neurons of the auditory brainstem were determined using antibodies against neurofilament and the growth-associated protein GAP-43 and compared with those following cochleotomy, studied earlier. By 231 days posttrauma, spiral ganglion cell bodies and their processes were almost entirely lost from all cochlear regions with destroyed organ of Corti. In the lateral superior olive (LSO) ipsilateral to the trauma, cell bodies of lateral olivocochlear neurons turned transiently GAP-43 positive within the first 1.5 years posttrauma. The time course of emergence and disappearance of this population of neurons was similar to that found after cochleotomy. Additionally, after noise trauma, principal cells in contralateral LSO and in medial superior olive (MSO) on both sides of the brainstem developed an expression of GAP-43 that began 3 and 16 days posttrauma, respectively, and lasted for at least 1 year. Such cells were rarely observed after cochleotomy. An unequivocal rise in GAP-43 immunoreactivity was also found in the neuropil of the inferior colliculus and the ventral cochlear nucleus, both preferentially on the acoustically damaged side. We conclude that the degree and specific cause of sudden unilateral deafness entail specific patterns of plasticity responses in the auditory brainstem, possibly to prevent the neural network dedicated to locate sounds in the environment from delivering erroneous signals centralward.

Acoustic Stimulation↗
PubMed1999

Treatment of acoustic trauma.

The aim of this study is to determine the actual efficiency of the present medical treatments of acoustic trauma. Untreated and treated groups of guinea pigs are exposed to a traumatic noise exposure, inducing up to 60-dB threshold shift. The recovery is followed for up to 14 days. The first results indicate that in some animals the recovery of the threshold shifts are complete despite the fact that significant areas of hair cells are damaged. The most widely used medical treatments of acoustic trauma (oxygenotherapy, carbogen, hyperbaric oxygen, vasoactive agents, and corticotherapy) have been tested. Preliminary results indicate that pure oxygen and carbogen seem ineffective, hyperbaric oxygen used alone is dangerous, and corticoids and combined corticoid/hyperbaric oxygen seem to improve functional and morphological recovery. This study will be taken as a reference to look for new treatments that will be applied directly to the cochlea by means of an implanted osmotic micropump.

Action Potentials↗
PubMed2004

Expression of connexin 26 in the lateral wall of the rat cochlea after acoustic trauma.

OBJECTIVE: Although the mutation in the Gap Junction Beta 2-encoding gap junction protein connexin 26 (Cx26) has been related to hereditary non-syndromic deafness and maturation of cochlear development, the physiological role of Cx26 in the cochlear lateral wall remains unclear. It has been suggested to be responsible for the recycling of K+ in the endolymph and for maintenance of the endocochlear potential (EP). In noise-induced hearing loss, alterations in the EP and the K+ concentration in endolymph have been observed. Thus Cx26, which is widely expressed in the cochlear lateral wall, may play a role in the mechanism of acoustic trauma. MATERIAL AND METHODS: We used a rat model of noise-induced hearing impairment to detect changes in Cx26 expression in the cochlear lateral wall. By means of immunofluorescent staining and Western blotting, we investigated whether Cx26 was involved in the pathophysiological mechanism of acoustic trauma. RESULTS: The results indicated that abundant Cx26 protein was found on fibrocytes of the spiral ligament in the cochlear lateral wall. Protein extract of cochlear lateral wall expressed Cx26 with a molecular weight of approximately 21 kDa. After noise exposure, with an increasing threshold of the auditory brainstem response (ABR) of approximately 54.2 +/- 21.8 dB SPL, the expression of Cx26 protein increased significantly (p < 0.05) as revealed by semi-quantitative analysis from Western blotting. CONCLUSION: Cx26 protein was present in the cochlear lateral wall of rats and was upregulated when the ABR threshold shifted after intense noise exposure. Cx26 protein was involved in the pathogenesis of acoustic trauma.

Animals↗
PubMed2004

Effects of an acute acoustic trauma on the representation of a voice onset time continuum in cat primary auditory cortex.

Here we show that hearing loss associated with an impairment of speech recognition causes a decrease in neural temporal resolution. In order to assess central auditory system changes in temporal resolution, we investigated the effect of an acute hearing loss on the representation of a voice onset time (VOT) and gap-duration continuum in primary auditory cortex (AI) of the ketamine-anesthetized cat. Multiple single-unit activity related to the presentation of a /ba/-/pa/ continuum--in which VOT was varied in 5-ms step from 0 to 70 ms-- was recorded from the same sites before and after an acoustic trauma using two 8-electrode arrays. We also obtained data for gaps, of duration equal to the VOT, embedded in noise 5 ms after the onset. We specifically analyzed the maximum firing rate (FRmax), related to the presentation of the vowel or trailing noise burst, as a function of VOT and gap duration. The changes in FRmax for /ba/-/pa/ continuum as a function of VOT match the psychometric function for categorical perception of /ba/-/pa/ modeled by a sigmoid function. An acoustic trauma made the sigmoid fitting functions shallower, and shifted them toward higher values of VOT. The less steep fitting function may be a neural correlate of an impaired psychoacoustic temporal resolution, because the ambiguity between /ba/ and /pa/ should consequently be increased. The present study is the first one in showing an impairment of the temporal resolution of neurons in AI caused by an acute acoustic trauma.

Acute Disease↗
PubMed2002

On prediction of hearing recovery after acute acoustic trauma caused by impulse noise.

The present study investigates the prediction of how successfully hearing returns to normal after an acute acoustic trauma caused by a firearm shot, an explosion or other impulse noise. Study material consisted of 113 conscripts who had suffered an acute acoustic trauma during their military service. A logistic regression model was formed to predict hearing recovery. From several possible variables at least five were found to be important among our dataset, which is still rather limited. However, more data will be acquired later in order to elaborate the research more widely by using other methods also.

Adolescent↗
PubMedDate not supplied

Sensitive period to acoustic trauma in the rat pup cochlea. Histological findings.

In a previous paper we demonstrated physiologically a sensitive period for acoustic trauma in the rat pup cochlea, with a maximum at 22 days of age. Seven or 60 days after noise exposure these 22-day exposed rats were used for light and electron microscopy. At 7 days, surface preparation revealed restricted damage to the basal cochlear coil, while with electron microscopy signs of cytoplasmic degeneration appeared in the great majority of basal coil structures. Two months after noise exposure these structures have completely degenerated. These results were discussed in terms of mechanical versus metabolic explanations of the critical period for acoustic trauma.

Animals↗
PubMed1987

[Calcium antagonists and damage to the organ of Corti in acoustic trauma].

The protective effect of Ca2+ antagonists in acoustic trauma was evaluated by morphometric analysis of the guinea pig cochlea. Damage to the outer and inner hair cells was significantly reduced. Ca2+ antagonists may exert a beneficial influence on the cellular membrane of the sensory cell or on the cochlear vasculature if given in advance and in the early post-traumatic phase.

Animals↗
PubMed1996

Acoustic trauma caused by lightning.

Lesions produced by exposure to noise are frequent in everyday life. Injuries may be found in all systems of the human body, from the digestive to the endocrine, from the cardiovascular to the nervous system. Many organs may be damaged, the ear being one of them. It is known that noise produced by factories, airports, musical instruments and even toys can cause auditory loss. Noises in nature can also cause acoustic trauma. This report is the case history of acoustic trauma caused by lightning. The patient was studied with CAT scan, electroencephalogram, and brain mapping, impedance audiometry with tympanogram and acoustic reflex, audiometry and evoked otoacoustics emissions: distortion products and transients.

Acoustic Impedance Tests↗
PubMed1988

[Development of hearing following damage from acoustic trauma with reference to a subsequent workplace].

60 patients were subjected to follow-up examination approximately one year after they had suffered initial damage due to acute acoustic trauma and received immediate in-patient therapy, in order to determine loss of hearing and development of tinnitus. The result of the study shows that both improvements in hearing and a disappearance of the tinnitus noise can be observed over the year, this being often closely associated with the noise level in the occupation pursued after in-patient treatment. At the same time, instances of progressive deterioration in hearing were also measured, which were virtually independent of the noise level. It is not possible to predict the development of hearing and tinnitus on the basis of the initial damage due to acoustic trauma.

Adult↗
PubMedDate not supplied

Diltiazem for prevention of acoustical trauma during otologic surgery.

100 patients were tested in a prospective, randomized, double-blinded study to assess the perioperative efficacy of a calcium channel blocker (diltiazem) in preventing acoustical trauma during otologic surgery. The patients were randomly divided into a therapy group (diltiazem) and a control group (placebo). Bone conduction hearing thresholds were examined preoperatively and again 1 day and 3 months postoperatively. Frequency-dependent changes in postoperative bone conduction and the number of patients with various degrees of postoperative hearing loss in both groups were statistically analyzed. The results indicated only a small postoperative hearing loss after ear surgery in both groups. There was a tendency for better results in the therapy group, but this was not statistically significant. Despite favorable results in animal trials utilizing different types of noise and the prophylactic application of diltiazem, further studies in humans are needed to determine the role of calcium antagonist drugs in the prophylaxis or treatment of acoustical trauma.

Adult↗
PubMed1999

Discriminability of vowel representations in cat auditory-nerve fibers after acoustic trauma.

This paper attempts to connect deficits seen in the neural representation of speech with perceptual deficits. Responses of auditory-nerve fibers were studied in cats exposed to acoustic trauma. Four synthetic steady-state vowels were used as test signals; these stimuli are identical, except that the second format (F2) resonator in the synthesizer was set to 1.4, 1.5, 1.7, or 2 kHz, producing four spectra that differ mainly in the vicinity of the F2 frequency. These stimuli were presented to a large population (523) of auditory-nerve fibers in four cats with sloping high-frequency threshold shifts that reached 50-70 dB at 2-4 kHz. In normal animals, May et al. [Auditory Neurosci 3, 135-162 (1996)] showed previously that the discharge rates of fibers with best frequencies near the F2 frequencies provide enough information to allow discrimination of these stimuli at the performance levels shown by cats in behavioral experiments. Here it is shown that, after acoustic trauma, there is essentially no rate information which would allow the vowels with different F2 frequencies to be discriminated. However, information that could allow discrimination remains in the temporal (phase-locked) aspects of the responses.

Animals↗