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PubMed2005

[Observation on the protective effect of MK-801 against hearing loss in acoustic trauma].

OBJECTIVE: To observe the protective effects of MK-801, an antagonist of N-methyl-D-aspartate (NMDA) receptor, against temporary (TTS) or permanent threshold shifts (PTS) in acoustic trauma. METHOD: Twenty guinea pigs were exposed to octave band noise with a central frequency of 4 kHz, 110 dB SPL for 3 h, and another twenty guinea pigs, to the same band noise at 115 dB SPL for 5 h. The test animals were given MK-801 (0.5 mg/kg, i. p. ) before and immediately after noise exposure; the control animals were treated with saline solution. Auditory brainstem responses (ABRs) of animals were recorded and ultrastructure of inner hair cells and afferent synapses were examined with transmission electron microscopy. RESULT: There was no significant difference in temporary threshold shifts immediately after noise exposure to 110 dB noise between the test and control group. The threshold shifts disappeared in one week after exposure in both groups. In 115 dB group, the threshold shifts of the test animals 7 days after exposure were significantly less than those of the control animals ( P >0.05) and 3 weeks after exposure, there was still this difference. The inner hair cell and afferent dendrites of the control animal exposed to 115 dB noise displayed many vacuoles. No vacuoles, however, were found in the inner hair cells or in the afferent dendrites of animals that were exposed to 110 dB noise or the test animals of 115dB group that received MK-801. CONCLUSION: MK-801 could partially protects against PTS, but not TTS in acoustic trauma through preventing from vacuole degeneration in inner hair cell and afferent dendrites.

Animals↗
PubMed1954

A device for prophylaxis of acoustic trauma.

Tests were made to determine whether protection against acoustic trauma was afforded by an ear-plug containing a valve designed to close under pressure of intensive noise. The hearing acuity of 34 persons was determined before they participated in target practice on a pistol firing range. Eighteen of them then wore the ear-plugs on the range and 16 did not. Hearing acuity was again determined after the target practice and it was noted that the loss of acuity was considerably less in subjects who had worn the plugs than in those who had not.

Auditory Perception↗
PubMed1986

[Need for rheologically active, vasoactive and metabolically active substances in the initial treatment of acute acoustic trauma].

Two rheologically active and 8 vasoactive and metabolically active substances were compared in eight independent studies, some of which were randomised and double blind, on 400 patients who had suffered acute acoustic trauma. The control group was given saline. Spontaneous recovery was excluded as far as possible. The following substances were tested: Dextran 40, hydroxyethyl starch 40/0.5, naftidrofurylhydrogenoxalate, Vinpocetin, betahistine, pentoxifylline, flunaricine, Regeneresen AU 4 and 0.9% saline. All groups showed superior results to the control group in both long-term and short-term tests with respect to hearing gain and tinnitis improvement. The rheologically effective substances showed no statistically significant variations. None of the vasoactive or metabolically active substances used as adjunctive therapy improved the results achieved with rheologically effective substances alone. These results demonstrate that acute acoustic trauma can be most effectively treated by rheologically active substances; vasoactive and metabolically active substances are unnecessary. Hyperbaric oxygenation is advantageous as an adjunctive therapy.

Adult↗
PubMed1999

The protective effect of the sympathetic nervous system against acoustic trauma.

OBJECTIVE: the cochlea is innervated by the sympathetic nerve fibers. However, the functions of those fibers in the cochlea are still controversial. The present study was designed to determine whether the sympathetic nervous system (SNS) exerts a protective or enhancing effect on acoustic trauma. METHODS: acoustic overstimulation (either of 110, 115, or 130 dB SPL for 10 min) was performed in guinea pigs during electrical stimulation of the ipsilateral cervical SNS, after its surgical elimination or in the non-treated condition. The threshold shift of the compound action potential (CAP) from the pre-exposure value was measured at 1 h and at 1 week after acoustic overstimulation. Two-way analyses of variance (ANOVAs) were completed for the SNS conditions and the frequencies. RESULTS: although no significant difference was found at 1 h after overstimulation among these three groups, the CAP threshold shift at 1 week (110 and 115 dB SPL) was significantly smaller in the SNS stimulation group than in the other two groups. CONCLUSION: a protective effect was observed in the SNS stimulation group 1 week after the exposure to acoustic overstimulation of moderate intensity (from 110 to 115 dB SPL for 10 min).

Acoustic Stimulation↗
PubMed2000

[Bilateral acoustic trauma after air bag inflation].

Airbag inflation is associated with a loud noise. This very short noise has a peak amplitude of 170 dB sound pressure level and can make otologic injuries. We report a case of acoustic trauma after airbag inflation. The 24-year-old man has hearing loss both side in the 3000- to 6000-Hz range and in the deep-frequency. The possibility of acoustic trauma from airbag noise are probably much more common and need more attention in the clinic.

Adult↗
PubMed2004

The clinical free radical scavenger, edaravone, protects cochlear hair cells from acoustic trauma.

It is known that reactive oxygen species have toxicity to the cochlea. We investigated the effect of edaravone, a free radical scavenger for clinical use, on the cochleae of guinea pigs subjected to acoustic trauma. We assessed auditory brainstem response (ABR) thresholds to evaluate cochlear function and observed the sensory epithelium. After noise exposure (130 dB SPL, 3 h), we observed that the auditory brainstem response threshold shift in edaravone-treated ears was significantly less than that in untreated ears. This result suggests that edaravone protected the cochleae from acoustic trauma.

Animals↗
PubMed1993

Auditory degeneration after acoustic trauma in two genotypes of mice.

Two strains of mice, CBA/Ca and C57BL/6J, were exposed to a steady noise (2-7 kHz) of 120 dB SPL for 5 min at 1, 3, 6, or 12 months of age. Threshold shifts were determined by recording auditory brainstem response 1 month after exposure and thereafter up to the age of 16 months (C57BL) or 23-27 months (CBA). With increasing age of exposure, susceptibility to acoustic trauma at middle frequencies (6.3-12.5 kHz) 1 month after exposure decreased in CBA mice but remained constant in C57BL mice. With increasing age after exposure, threshold shifts were retained at the middle frequencies in CBA mice exposed at 1 month of age and in C57BL mice of all exposed groups. The progress of the interaction between the previous noise damage and aging effects was generally the same for the two strains, first an additivity and then a blocking-like interaction. The rate of the progress in post-noise hearing did not exceed the spontaneous rate of aging. The differences between exposed and non-exposed groups decreased with advancing age. The results indicate that the interaction of noise trauma and aging effects depends on the susceptibility of the individual to acoustic trauma, affected frequencies, and the severity of noise-induced PTS. A previous noise damage did not potentiate the auditory degeneration either in CBA/Ca or in C57BL/6J mice.

Acoustic Stimulation↗
PubMed1999

Acquired resistance to acoustic trauma by sound conditioning is primarily mediated by changes restricted to the cochlea, not by systemic responses.

Hearing loss caused by intense sound exposure can be significantly reduced by pre-exposing subjects to moderate-level acoustic stimuli. This phenomenon occurs in a variety of mammals. We investigated whether sound conditioning provides acquired resistance to acoustic trauma through local mechanisms selectively in the conditioned ears or if systemic mechanisms are involved that would yield contralateral protection in unconditioned ears. Guinea pigs (group I) in which one external ear canal was occluded were exposed to conditioning sound (2-20 kHz, 85 dB SPL, 5 h/day, 10 days). After removing the occlusion, the animals were then subjected bilaterally to intense noise (2-20 kHz, 110 dB SPL, 5 h) 5 days after the last conditioning exposure. Animals without ear canal occlusion were also exposed to the intense sound without conditioning (group II) or following the same conditioning exposure (group III). Intense sound exposure caused significantly greater permanent ABR threshold shifts at all frequencies tested (4, 8, 12, 16 and 20 kHz) in group II than in group III. In group I, the occluded ears showed significantly greater threshold shifts at all frequencies compared to the unoccluded ears. The threshold shifts in the occluded ears in group I were identical to those observed in group II; and the shifts in unoccluded ears in group I were identical to those in group III. Protective effects provided by sound conditioning were almost the same in group III and in the unoccluded ears in group I. The extent of hair cell damage supported the physiological findings. These results indicate that acquired resistance to acoustic trauma provided by sound conditioning is restricted to the cochlea exposed to conditioning sound, suggesting that conditioning protection is mediated primarily by the changes that occur locally within the conditioned cochlea. This animal model, with unilateral external ear canal occlusion during sound conditioning, is useful for studies of the mechanisms of conditioning protection.

Acoustic Stimulation↗
PubMed2005

Loss and recovery of sound-evoked otoacoustic emissions in young chicks following acoustic trauma.

Young and adult chickens exhibit substantial inner-ear damage and post-exposure deterioration in cochlear nerve activity following exposure to intense sound. Both the structural and functional losses largely recover in both age groups within 2-4 weeks after exposure. However, some aspects of acoustic trauma differ between the young and adult chicken ear. Overstimulation in the young chick causes considerable post-exposure loss and then recovery of the steady-state endocochlear potential, while in the adult animal there is little post-exposure effect on this potential. Moreover, in adults there is post-exposure loss but little recovery in the distortion product otoacoustic emission (DPOAE). The present study explores the possibility of an age difference in the effects of overstimulation on the DPOAE by examining these emissions in young chicks following exposure to an intense pure tone. Chicks exposed to intense sound were formed into groups at 0 and 12 days of recovery, and these were complemented by two additional groups of age-matched controls. The cubic difference tone emission (the 2f(1)-f(2) DPOAE component) was measured at 9 levels for 13 frequencies in all groups. Shortly after the exposure, the DPOAE reliably declined with the maximum loss at or above the exposure tone frequency. The exposed chicks examined 12 days after exposure showed complete recovery of the DPOAE. It would appear that 12 days of recovery sufficiently repaired inner ear damage to completely restore DPOAE production. This result is different from that in adult chicken and may be related to the greater severity of acoustic damage in the adult ear, a reduced susceptibility of the young ear to acoustic trauma, or the ability of the young animal to more successfully repair the inner ear.

Acoustic Stimulation↗
PubMed1997

Effects of acoustic trauma on the representation of the vowel "eh" in cat auditory nerve fibers.

A population study of cat auditory-nerve fibers was used to characterize the permanent deficits induced by exposure to 110-115 dB SPL, narrow-band noise. Fibers in the region of acoustic trauma (roughly 1-6 kHz) showed a loss of sensitivity at best frequency (BF) of about 50-60 dB and an increased tuning bandwidth. A correlation between weakened two-tone suppression and loss of sensitivity was found for fibers with BFs above 1 kHz. Single-fiber responses to the vowel "eh" were recorded at intensities ranging from near threshold to a maximum of about 110 dB SPL. In normal cochleas, the temporal response patterns show a capture phenomenon, in which the first two formant frequencies dominate the responses at high sound levels among fibers with BFs near the formant frequencies. After acoustic trauma, fibers in the region of threshold shift synchronized to a broad range of the vowel's harmonics and thus did not show capture by the second formant at any sound level used. The broadband nature of this response is consistent with the broadened tuning observed in the damaged fibers, but may also reflect a weakening of compressive nonlinearities responsible for synchrony capture in the normal cochlea.

Animals↗
PubMed1992

Additivity of threshold losses produced by acute acoustic trauma.

We have previously [Patuzzi and Rajan, Hear. Res. 60, 165-177, 1992] formulated a model to describe how the threshold elevations produced by a variety of independent, short-term cochlear manipulations add when the manipulations are combined. The manipulations were presumed to affect only the 'active process' in the cochlea. The present report applied this model to the effects observed after acute acoustic trauma in normal-hearing guinea pigs and in guinea pigs with idiopathic threshold losses. Successive loud pure-tone exposures were presented to the normal-hearing guinea pigs, while only a single exposure was presented to the guinea pigs with idiopathic hearing losses. Various parameters of exposure and inter-exposure delays were used to create a variety of threshold elevations, and the total hearing losses observed in the various groups were compared to the total hearing losses predicted by the model. In most cases a statistically-valid 1:1 relationship was obtained between the predicted values and the observed values. In cases where the model's predictions were found not to fit the data, this appeared to be due to inclusion of data previously defined to be outside the scope of the model. When such data were excluded, there was good agreement between the model's predictions and the observed data. The model was further tested by comparing its predictions with data obtained in studies of acute noise trauma in chinchillas and humans by other researchers. The model's predictions were found to agree with these data as well. Thus, across a number of different types and conditions of exposures, the model appears to provide a very good description of the additivity of threshold losses produced by acute acoustic trauma. The generality of and constraints on the model are discussed.

Acoustic Stimulation↗
PubMed1980

Recovery of the endocochlear potential and the K+ concentrations in the cochlear fluids after acoustic trauma.

Intense noise stimulation (142 dB, 1/3-octave-band noise centred at 1 kHz for 1 h) causes damage mainly in the second turn of the cochlea. Several hours (3-5) after the noise exposure, the endocochlear potential (EP) was found to be very low (5.7 +/- 6.0 mV). Similarly, the K+ concentration in the endolymph (Ke+) had decreased to low values (18.9 +/- 9.5 mM). The return of EP and Ke+ to normal values took 5-20 days. In contrast to the Ke+ changes, the perilymph K+ concentration (Kp+) increased slightly after the noise exposure to 4.5 +/- 1.7 mM and returned to normal values one day after the exposure. Differences were found in the time course of the EP, Ke+ and Kp+ changes after the arrest of ventilat ion when animals with acoustic trauma were com,ared with normal healthy individuals. The anoxic EP in noise-exposed animals never decreased to values more negative than -20 mV. The results imply that the inner ear mechanisms maintaining positive EP, Ke+ and Kp+ are severely damaged after acoustic trauma and that their function is restored in 5-20 days. With respect to some parameters (decrease of the EP during anoxia, the value of anoxic negative EP, EP overshoot after reventilation) the inner ear mechanisms are, however, still abnormal.

Acoustic Stimulation↗
PubMed2000

Changes to low-frequency components of the TEOAE following acoustic trauma to the base of the cochlea.

Several studies have shown that acoustic trauma to the base of the cochlea can result in loss of transient-evoked otoacoustic emission (TEOAE) energy at frequencies much lower than those affected in the audiogram. We have extended these studies to show that the low-frequency emission energy was substantially affected if the transient stimulus included frequencies within the range affected by the trauma, otherwise the change observed was small. In keeping with the suggestion that TEOAEs are predominantly comprised of intermodulation distortion energy (Yates and Withnell, Hear. Res. 136 (1999) 49-64), trauma to the basal region of the cochlea was found to affect emission energy across a broad frequency range in response to a wide-band acoustic stimulus. Further, group delay measurements demonstrated that the dominant contribution to the TEOAE originated from the basal region of the cochlea.

Acoustic Stimulation↗
PubMed2006

Negative effect of immediate hyperbaric oxygen therapy in acute acoustic trauma.

OBJECTIVE: The functional evaluation of the effect of the hyperbaric oxygen therapy (HBOT) onset time on cochlea by using distortion product otoacoustic emission. STUDY DESIGN: Animal study. METHODS: Twenty-four Wistar albino rats were divided into six groups and their right ears were directly exposed to a 110-dB sound pressure level (1-12 kHz) white noise for 25 minutes. The first group was considered the control group. HBOT was started at 1 hour postexposure for the second group, at 2 hours postexposure for the third group, at 6 hours postexposure for the fourth group, at 24 hours postexposure for the fifth group, and at 48 hours postexposure for the sixth group. Signal-to-noise ratios (SNRs) were recorded before the noise exposure; immediately after the noise exposure; and on the 3rd, 7th, and 10th day of postexposure. RESULTS: SNRs at 6 to 8 kHz were significantly decreased after the acoustic trauma. The evaluation on the third day of postexposure showed that recovery begun in all groups except the group in which the HBOT was started at 1 hour postexposure. SNRs in the control group and HBOT groups were back to the preexposure levels at 10 days postexposure, except the 1- and 2-hour postexposure groups. However, in the group in which the HBOT was started at 1 hour postexposure, distortion product otoacoustic emissions were lost except at 4 kHz. The recovery of the SNRs in hyperbaric oxygen administration at 2 hours postexposure almost completed on the 10th day after noise exposure. CONCLUSION: Immediate HBOT in acoustic trauma treatment is not necessary; on the contrary, it has an adverse effect.

Acute Disease↗
PubMed1988

Acute acoustic trauma. An emergency condition.

This paper reviews 16 selected patients reporting for acute acoustic trauma (AAT). All patients had a fairly recent pre-accident audiogram. Most of the patients were tested audiologically immediately after the acoustic accident. All patients were men, with ages varying between 16 and 50 years. Eight patients received pharmacological treatment with low-molecular-dextran intravenously, papaverin perorally and prednisolone perorally. The high-frequency pure-tone average (3-4-6 kHz) was more affected than the pure-tone average (0.5-1-2 kHz). In 2 patients, the converse was true. The most affected frequencies were 3, 4, and 6 kHz. The initial maximum hearing loss varied between 15 and 70 dB. In 6 patients, extra-high-frequency audiometry (8-20 kHz) was performed and in all patients an asymmetry was demonstrated. Younger patients had somewhat more hearing improvement after AAT than older patients. It also appears that patients reporting early had a somewhat better healing course than patients reporting later.

Accidents↗
PubMed1988

Acoustic trauma caused by the telephone. Report of two cases.

Two patients with acoustic trauma resulting from the use of telephones have been evaluated. Both patients used a particular type of telephone which had the ringing device located in the ear receiver and no automatic gain control in the circuit. The output of the bell recorded on one of these telephones was in the 139-dB range on the A scale. The auditory insult resulted, in the case involving a cord-type telephone, from the transmission of a loud, extraneous sound probably due to a misfunction of the circuit and, in the second case, from the patient holding his cordless telephone against his ear when ringing occurred.

Female↗
PubMedDate not supplied

[Acute acoustic trauma in military personnel. Evaluation of 1 year epidemiologic surveillance].

OBJECTIVES: Acute acoustic trauma (AAT) refers to damage to sensitive cochlear structures caused by excessive exposure to impulse noise. The aim of this study was to 1) assess the incidence of ATT in French soldiers and 2) to clarify the circumstances under which AAT occurs. PATIENTS AND METHODS: We carried out a prospective study of AAT events reported to medical officers in 1998. RESULTS: The incidence of AAT was 156 per 100,000 person-years (150-161). It was higher in conscripts and in soldiers aged under 31 years. Fifty-seven percent were wearing hearing protectors when the accident took place. CONCLUSION: According to these results, specific preventive programs were planned and should be assessed by epidemiological surveillance of exposed populations.

Adult↗