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PubMed1979

[Auditory fatigue in individuals having sustained an acoustic trauma (author's transl)].

A comparison was made between losses of auditory sensitivity after a fatiguing sound exposure of the ear in two groups of subjects: audiometrically normal subjects and subjects with early acoustic trauma. Subjects with cochlear impairment sustained an auditory loss apparently less than that of normal subjects when this loss is measured at threshold level. However, at supraliminal levels the loss of sensitivity, as measured here, would seem to be equal in both groups of subjects. In fact, the dynamics of sonic variations, already reduced by the cochlear impairment, is even further decreased by the effects of fatigue.

Audiometry↗
PubMed1991

Cochlear efferent neurones and protection against acoustic trauma: protection of outer hair cell receptor current and interanimal variability.

We have measured the changes in neural and microphonic sensitivity in the basal turn of the guinea-pig cochlea produced by intense acoustic overstimulation (10 kHz, 115 dB SPL for 60 s and 150 s). As reported previously, the drop in neural and microphonic sensitivities observed after overstimulation were highly correlated [Patuzzi et al. (1989) Hear. Res. 39, 189-202]. Presentation of a non-traumatizing pure-tone to the contralateral ear (10 kHz, 80 dB SPL) during acoustic overstimulation reduced the amount of acoustic trauma measured using the neural response or the microphonic response. Transection of the medial olivo-cochlear system of efferent fibres at the floor of the fourth ventricle abolished this protective effect of contralateral sound and dramatically reduced the variability in the data. Since the low-frequency microphonic is a simple measure of the receptor current through the outer hair cells, and this current probably plays a part in enhancing the mechanical sensitivity of the cochlea, the protection of the microphonic we have observed suggests that the efferent system protects neural sensitivity by protecting the mechano-electrical transduction of outer hair cells. The drop in variability after sectioning the efferents also suggests that inter-animal variations in susceptibility to noise trauma may be a consequence of differing tonic activity of the efferents, and/or a variation in the sensitivity of the efferent pathway.

Action Potentials↗
PubMed1998

Acoustic trauma causes reversible stiffness changes in auditory sensory cells.

A common cause of hearing impairment is exposure to loud noise. Recent research has demonstrated that the auditory mechanosensory cells are essential for normal hearing sensitivity and frequency selectivity. However, little is known about the effect of noise exposure on the mechanical properties of the auditory sensory cells. Here we report a significant reduction in the stiffness and cell length of the outer hair cells after impulse noise exposure, suggesting that mechanical changes at the cellular level are involved in noise-induced hearing loss. There is a recovery of the cellular stiffness and cell length over a two-week period, indicating an activation of cellular repair mechanisms for restoring the auditory function following noise trauma. The reduced stiffness observed at the cellular level is likely to be the cause for the downward shift of the characteristic frequency seen following acoustic trauma. The deterioration and the recovery of the mechanical properties of outer hair cells may form important underlying factors in all kinds of noise-induced hearing loss.

Animals↗
PubMed2001

Otoacoustic emissions and medial olivocochlear suppression during auditory recovery from acoustic trauma in humans.

It is well known that the large inter-individual susceptibility to noise exposure makes it impossible to predict the degree of hearing loss which will develop after any given intense noise exposure. The acoustic trauma which sometimes occurs affects cochlear mechanisms, the damage being most probably due to deactivation of the active processes of the outer hair cells (OHCs), which receive direct efferent innervation. The present report is of a follow-up study involving young military personnel recovering auditively from impulse noise exposure, and seeks to assess changes in cochlear status by means of otoacoustic emissions (OAEs) and their modulation by the medial olivocochlear (MOC) system. The study investigated the relationship between recovery of cochlear function and variables that could serve as predictors of vulnerability to noise-induced hearing loss (NIHL). Thirty-six subjects with unilateral NHIL above 4 kHz were included. Normal and affected ears were compared with respect to click-evoked and spontaneous OAEs (CEOAEs and SOAEs, respectively) and for contralateral CEOAE suppression. Measurements were obtained: (i) just after the traumatic exposure (D0); (ii) 3 days after this first measurement (D3); and (iii) 30 days after (D30). Significant improvement in the 4, 6 and 8 kHz thresholds was observed for the affected ear, with large inter-subject variability. No significant change was observed in CEOAE amplitude or MOC suppression, whereas incidence of SOAE was found to increase in the affected ear, leading to higher SOAE prevalence on this side I month after the intense noise exposure. There was no significant correlation between NIHL at 4, 6 and 8 kHz and MOC functioning on D0, but significant correlations were obtained between audiometric threshold improvement by D3 and contralateral CEOAE suppression, with better recovery in subjects with greater MOC suppressive action. The MOC system could be an underlying mechanism in post-traumatic auditory threshold recovery.

Adolescent↗
PubMed1996

Regeneration after tall hair cell damage following severe acoustic trauma in adult pigeons: correlation between cochlear morphology, compound action potential responses and single fiber properties in single animals.

The time course of recovery of compound action potential (CAP) thresholds was observed in individual adult pigeons after severe acoustic trauma. Pigeons were overstimulated with a tone of 0.7 kHz and 136-142 dB SPL presented to one ear for 1 h under general anesthesia. Recovery of CAP audiograms was monitored at regular intervals after trauma. A new semi-stereotaxic approach to the peripheral part of the auditory nerve was developed. This permitted activity from single auditory nerve fibers to be recorded over a wide range of characteristic frequencies (CFs), including high CFs, without having to open the inner ear. Single unit recordings were made after three weeks and after 4 or more months of recovery. The time course of recovery, the single unit properties, and the morphological status of the basilar papilla were correlated. The CAP was abolished in all animals after overstimulation. Three groups of animals were identified according to the functional recovery of the CAP thresholds recorded at regular intervals with implanted electrodes: Group 1: Fast functional recovery starting immediately after trauma, followed by recovery to pre-exposure values within 3 weeks. Group 2: Slow functional recovery of threshold starting 1-2 weeks after trauma and ending 4-5 weeks after trauma. A mean residual hearing loss of 26.3 dB at 2 kHz remained. Group 3: No recovery of CAP thresholds up to 8 months after trauma. Three weeks after trauma, very few responsive neurons were found in groups 2 and 3. Tuning curves were very broad and sometimes irregular in shape. Thresholds were very high, around 120 dB SPL. Spontaneous firing rate was much reduced, especially in neurons with high CFs. After 4 or more months of recovery, the response properties of single units in group 1 had only partially recovered. Thresholds and sharpness of tuning of many single units were normal: however, in general they were still poorer than in control animals. Spontaneous firing rate was comparable to control animals. Neurons from animals in group 2 showed less recovery, especially at frequencies above the exposure frequency. Thresholds and sharpness of tuning were normal at frequencies below the exposure frequency, but were much poorer at frequencies above the exposure. Spontaneous firing rate was much reduced in fibers with high CFs. The basilar papilla in animals without recovery showed total loss of the sensory epithelium. The basal lamina of the basilar membrane, however, remained intact and was covered with cuboidal cells. In fast recovering animals, the papilla was repopulated with hair cells after 4 months. In slow recovering animals, short (abneural) hair cells were still missing over large parts of the papilla after 4 months of recovery. Residual short (abneural) hair cell loss was largest at two areas, one more basal and the other more apical to the characteristic place of the traumatizing frequency. The results show that functional recovery from severe damage to both short (abneural) and tall (neural) hair cells occurs in adult birds. However, the onset of recovery is delayed and the time course is slower than after destruction of short (abneural) hair cells alone. Furthermore recovery is incomplete, both functionally and morphologically. There are residual permanent hearing losses and regeneration of short (abneural) hair cells is incomplete.

Acoustic Stimulation↗
PubMed2003

Permanent bilateral acoustic trauma due to air bag deployment in a young female adult.

Air bag safety systems have significantly reduced the number of occupant injuries from road traffic accidents (RTA). However air bag deployment is also associated with unavoidable risks. We report the acoustic trauma incurred by a young female driver who was a heavy smoker as a consequence of air-bag deployment in a low speed RTA and the sparing of her child seated in the rear.

Accidents, Traffic↗
PubMed2003

Ebselen attenuates cochlear damage caused by acoustic trauma.

Ebselen (2-phenyl-1,2-benzisoselenazol-3(2H)-one), a seleno-organic compound, mimics glutathione peroxidase and reacts with peroxynitrite. It is reported to protect against gentamicin- and cisplatin-induced ototoxicity. We investigated whether it protects the cochlea from acoustic trauma. Male pigmented guinea pigs (250-300 g) with normal auditory brainstem response (ABR) thresholds were exposed for 5 h to 125 dB sound pressure level octave band noise centered at 4 kHz. One hour before and 18 h after exposure, they received orally 0.25 ml chloroform solution containing 0, 10, or 30 mg/kg ebselen (n=6, 5 and 5, respectively). The protective effect of ebselen was evaluated by ABR measurement and quantitative hair cell assessment. Treatment significantly (P<0.01) reduced the extent of permanent threshold shifts and outer hair cell loss. Interestingly, the protective effect of a 30 mg/kg dose was less than that of a 10 mg/kg dose. There were no adverse systemic or auditory function effects in three unexposed control subjects given 30 mg/kg ebselen. These findings indicate that ebselen attenuates noise-induced cochlear damage. The concentration that provides optimal protection against such damage has now to be determined.

Animals↗
PubMedDate not supplied

Therapeutic efficacy of magnesium in acoustic trauma in the guinea pig.

Comparative functional and morphological tests were performed in two groups of impulse noise-exposed guinea pigs treated either with magnesium (Mg) or isotonic saline as a placebo to extend the knowledge on the therapeutic efficacy of Mg in acoustic trauma demonstrated recently. The permanent threshold shifts were significantly lower in the Mg than in the placebo group as measured by auditory brainstem response audiometry, distortion product otoacoustic emissions and compound action potentials (CAPs) 1 week after exposure. This also applies to the damage to hair cell stereocilia tested with scanning electron microscopy. There were frequency-related differences in the individual functional responses. The CAP threshold shifts reflected the morphological damage most obviously.

Animals↗
PubMed1980

Comparative method for the study of structural damage in acoustic trauma.

The traumatic dose 50 (TD50), similar to the lethal dose (LD50) widely used in pharmacology, was determined in guinea pigs for varying intensities and varying durations of exposure to a band of noise. The method proposed permits the comparison of results in studies of acoustic trauma caused by noises of various characteristics in different species of experimental animals.

Animals↗
PubMedDate not supplied

[Relationship between auditory disability and auditory threshold in acute acoustic trauma: pilot study].

The aim of this study was to determine the relationship existing between auditory disability, according to WHO 1980, and pure tone audiometry threshold in noise induced hearing loss. Disability was evaluated on the basis of a questionnaire submitted to 286 subjects with acoustic trauma. Answers obtained were considered reliable on the basis of statistical analysis. Results showed that subjects with disability have an higher pure tone threshold than subjects without auditory disability. However it appears difficult to determine a precise threshold level ever which auditory disability may be considered present. The Authors suggest that this limit could be determined on the basis of pure tone threshold at the 10th centile of the group of subjects with disability or at the 90th centile of subjects without disability.

Adult↗
PubMed1978

[The acoustic trauma in animal experiment: I. Morphological reaction in the guinea pig cochlea after traumatisation by shots (a scanning microscopical study) (author's transl)].

Guinea pigs were exposed to shots of a pistol under standardized experimental conditions. The organs of Corti were examined by SEM after surviving times of 5 min, 1, 5 and 10 days. In correlation to the acoustic trauma we found mainly three different ways of morphological reaction of sensory cells. After 1--3 shots alterations and even losts of stereocilia were observed mainly in the 2nd (and 1st) coil from base. Only the rows III and II of outer hair cells (OHC) were concerned while changes in inner hair cells (IHC) were not observed. 5--10 shots regularly caused more severe alterations in the 1st, 2nd (and 3rd) coils of the organ of Corti. The three rows of outer hair cells degenerated within 2--5 days, while inner hair cells did not show any changes of the surface when the pillar cells remained intact. (20) 40 or even 100 shots most often caused a complete damage of all sensory--and supporting cells. The cell detritus was abolished within 5 days. At this time the damaged organ of Corti was replaced by a flat epithelium on the intact basilar membrane.

Animals↗
PubMed1985

Differential susceptibility of avian hair cells to acoustic trauma.

Five groups of 10-day-old chicks were continuously exposed to either 500 or 1500 Hz pure tone at 125 dB for 4 or 12 h and killed 10 days later. The basilar papillae were fixed, embedded in plastic, sectioned, and hair cells were counted according to type: tall or short. Short hair cells were found to be more susceptible to acoustic overstimulation than tall hair cells. Further, the position of maximum short hair cell loss varied along the length of the basilar papilla as a function of the exposure frequency while the position of tall hair cell loss did not. Similarities between morphological response of short hair cells in avians after acoustic trauma and outer hair cells in mammals are discussed.

Animals↗
PubMed1983

Tinnitus pitch and acoustic trauma.

56 Subjects complaining of tinnitus underwent an audiometric test and a test for identifying the analogous pitch of their tinnitus. All of the subjects reported that they had been exposed to noise in the past. The subjects were divided into two groups on the basis of their audiometric test results. Group P was composed of subjects who showed a sensorineural hearing loss typical of acoustic trauma. Group N was composed of subjects whose hearing was within normal limits. The pitch of the tinnitus in group P was concentrated in the high-frequency range, whereas in group N tinnitus pitch values were distributed over the low and mid-audiometric frequency spectrum. It was deduced that different processes are involved in the generation of tinnitus in the two groups.

Adult↗
PubMed1976

[Comparative study of acoustic trauma caused by blasts, treated by vasodilators or by a combination of vasodilators and hyperbaric oxygenation].

The authors had comparated two series of patients with noise induced hearing loss treated by vasodilatators or vasodilatators and hyperbaric oxygen. This therapy seems to give better results than the vasodilatators only, but the patients had to be treated before ten days after the noise exposition. In the two series of acoustic trauma we see rarely a complete recovery from the hearing loss.

Adult↗
PubMed1979

Supra-normal susceptibility to acoustic trauma of the rat pup cochlea.

1 Young and adult rats were exposed to a continuous 120 dB SPL white noise for 30 min. 2 Animals exposed before the 40th postnatal day showed drastic and permanent threshold shifts (PTS) at high frequencies (between 6 and 20 kHz). 3 After 60 days of age, only temporary threshold shifts (TTS) were noticed, which lasted 7 days. 4 Thus the sensory structures of the rat cochlea showed a supra-normal susceptibility to acoustic trauma, during and just after their anatomical differentiation. 5 These results support previous data obtained on hamsters and guinea-pigs and are discussed in terms of anatomo-functional relationships.

Aging↗
PubMed2000

Activities of Na(+),K(+)-ATPase and Ca(2+)-ATPase in cochlear lateral wall after acoustic trauma.

Na(+),K(+)-ATPase and Ca(2+)-ATPase are well known participants in the active transport of ions in the inner ear. These two enzymes play an important role in maintaining cochlear function. Although changes in these enzymes' activities in the cochlea have been implicated in noise-induced hearing loss, no evidence of quantitative alteration of Na(+),K(+)-ATPase or Ca(2+)-ATPase activities has ever been shown. The present study was undertaken to determine the quantitative alterations of their activities by microcolorimetric assay in the cochlear lateral wall after acoustic trauma. Adult albino guinea pigs were exposed to white noise at 105+/-2 dB A for 10 min or 40 h. The age-matched control animals were not exposed to noise. Noise exposure resulted in a significant threshold shift of the auditory brainstem response (P<0.001). Significant decreases in activities of Na(+),K(+)-ATPase and Ca(2+)-ATPase were found in the cochlear lateral wall after noise exposure (P<0.001). Statistical analysis indicated that a good correlation held not only between the decline of these enzyme activities and noise-induced hearing loss, but also between the gradual partial recovery of these parameters during the first 10-day recovery period. The present findings suggest that metabolic damage and ionic disturbance may contribute, at least partially, to noise-induced hearing threshold shift.

Animals↗
PubMed1995

Transient-evoked otoacoustic emissions and high-frequency acoustic trauma in the guinea pig.

Transient-evoked otoacoustic emissions (TEOE) disappear when hearing loss exceeds 40 dB in the range 1-4 kHz, due to impairment of cochlear outer hair cells. Early screening of sensorineural hearing losses is based on this finding. However, little is known as to the frequency specificity of TEOE abnormalities in a damaged cochlea. TEOE were recorded in 18 normally hearing guinea pigs in a range from 1.5 to 5 kHz before and after exposure to loud pure tones (3-10 kHz, 95-105 dB SPL, 1-10 min). The thresholds of eighth-nerve compound action potentials (CAP) were monitored with a round-window electrode; it was confirmed that acoustic overexposure resulted in typical high-frequency threshold elevations (10 to 50 dB). Most TEOE components were found at lower frequencies at which CAP thresholds did not change. However, a significant linear regression was found between their amplitudes and the percentage of basal cochlea with unaltered CAP thresholds (r = 0.69, p < 0.0001). Two alternative hypotheses are proposed to account for this correlation. Either acoustic trauma induced some minute cochlear damage at places tuned to low frequencies and TEOE were more sensitive to it than CAP thresholds, or significant contributions to lower-frequency TEOE came from the most damaged cochlear places tuned to much higher frequencies.

Acoustic Stimulation↗
PubMed1998

Protecting the Inner Ear from Acoustic Trauma.

Calcium activated proteases, or calpains, play an important role in neurodegeneration. In some cases, neural degeneration can be significantly reduced by leupeptin, a potent calpain inhibitor. To determine if leupeptin could protect against noise-induced hearing loss and hair cell loss, we infused leupeptin into scala tympani of one cochlea before, during and after a 14-day exposure to a 100 dB SPL, octave band noise centered at 4.0 kHz. Hearing loss, assessed with the auditory evoked response, was less in the leupeptin-treated ear than in the control ear during the early stage of recovery from acoustic trauma. In addition, hair cell loss in the leupeptin-treated ear was significantly less than in the control ear. These preliminary results suggest that leupeptin may protect against noise-induced hearing loss.

Journal Article↗