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PubMed2004

Protection against acoustic trauma by forward and backward sound conditioning.

The purpose of the present study was to determine if short-term sound conditioning provides protection when delivered either before (forward sound conditioning) or after (backward sound conditioning) a traumatic exposure in the guinea pig. Two different sound conditioning paradigms were studied (1 kHz, 81 dB SPL, 24 h; 6.3 kHz, 78 dB SPL, 24 h). The 1-kHz forward sound conditioning paradigm (81 dB SPL, 24 h) protected distortion product otoacoustic emissions (DPOAEs) against a short-duration acoustic trauma (2.7 kHz, 103 dB SPL, 5 min) compared to the group exposed to the acoustic trauma alone. The 1-kHz forward sound conditioning paradigm (81 dB SPL, 24 h) also protected both the auditory brainstem response (ABR) thresholds and DPOAEs against a longer-duration acoustic trauma (2.7 kHz, 103 dB SPL, 30 min). The group exposed to the acoustic trauma alone showed ABR threshold shifts between 15 and 24 dB, and DPOAE amplitude shifts between 11 and 24 dB, while the group with 1-kHz forward sound conditioning showed statistically significant protection at all ABR frequencies and at all DPOAE frequencies. The 1-kHz backward sound conditioning paradigm protected against acoustic trauma (2.7 kHz, 103 dB SPL, 30 min). The ABR thresholds were protected at 1, 2 and 4 kHz, and DPOAEs at all frequencies (except 8 kHz) when compared to the group exposed only to the acoustic trauma. The 6.3-kHz forward sound conditioning paradigm protected against acoustic trauma (5.5 kHz, 109 dB SPL, 30 min) at 6.3, 8 and 10 kHz. The 6.3-kHz backward sound conditioning paradigm showed no protection against acoustic trauma at any DPOAE frequency. Taken together, these findings are important for understanding how the auditory system can be modulated by acoustic stimulation and highlights the importance of the acoustic environment during the recovery process of the auditory system.

Acoustic Stimulation↗

PubMed2003

An auditory-periphery model of the effects of acoustic trauma on auditory nerve responses.

Acoustic trauma degrades the auditory nerve's tonotopic representation of acoustic stimuli. Recent physiological studies have quantified the degradation in responses to the vowel /E/ and have investigated amplification schemes designed to restore a more correct tonotopic representation than is achieved with conventional hearing aids. However, it is difficult from the data to quantify how much different aspects of the cochlear pathology contribute to the impaired responses. Furthermore, extensive experimental testing of potential hearing aids is infeasible. Here, both of these concerns are addressed by developing models of the normal and impaired auditory peripheries that are tested against a wide range of physiological data. The effects of both outer and inner hair cell status on model predictions of the vowel data were investigated. The modeling results indicate that impairment of both outer and inner hair cells contribute to degradation in the tonotopic representation of the formant frequencies in the auditory nerve. Additionally, the model is able to predict the effects of frequency-shaping amplification on auditory nerve responses, indicating the model's potential suitability for more rapid development and testing of hearing aid schemes.

Animals↗

PubMed2006

NF-kappaB mediated glucocorticoid response in the inner ear after acoustic trauma.

The inner ear of humans and experimental animals demonstrate an abundance of glucocorticoid receptors (GR). Glucocorticoids (GC) are widely used to treat different hearing disorders; yet the mechanisms of GC action on the inner ear are unknown. We demonstrate how GR can directly modulate hearing sensitivity in response to a moderate acoustic trauma that results in a hearing loss (10-30 dB). The GC agonist (dexamethasone) and the drugs (metyrapone + RU 486) showed opposing effects on hearing threshold shifts. GC agonist (dexamethasone) decreased the hearing threshold whereas pre-treatment with a GC synthesis inhibitor (metyrapone) in combination with a GR antagonist (RU 486) exacerbated auditory threshold shifts (25-60 dB) after acoustic trauma with statistically significant increase in GR mRNA and GR protein compared with the vehicle and acoustic trauma group. Acoustic trauma caused a significant increase in the nuclear transport of NF-kappaB, whereas pre-treatment with the drugs (metyrapone and RU 486) blocked NF-kappaB nuclear transport into spiral ganglion nuclei. An NF-kappaB inhibitor, pyrrolidine dithiocarbamate ammonium blocked the trauma-induced translocation of NF-kappaB and resulted in a hearing loss (45-60) dB. These results indicate that several factors define the responsiveness of the inner ear to GC, including the availability of ligand or receptor, and the nuclear translocation of GR and NF-kappaB. These findings will further our understanding of individual GC responsiveness to steroid treatment, and will help improve the development of pharmaceuticals to selectively target GR in the inner ear for individuals with increased sensitivity to acoustic trauma.

Acoustic Stimulation↗

PubMed1994

Cell division in the gerbil cochlea after acoustic trauma.

The recent discovery of hair cell regeneration in the avian inner ear raises the possibility that hair cell regeneration might occur in the mammalian cochlea as well. The authors used 3H-thymidine labeling to detect mitotic activity in the cochleas of normal 3-week old gerbils exposed to acoustic trauma. Following an acoustic insult that caused progressively more severe damage in an apical to basal progression, 3H-thymidine was injected for 5 days. Control animals were not exposed to the acoustic insult. The gerbils' cochleas were sectioned and processed for autoradiography. In the control cochleas, there were extremely rare labeled cells in the stria, the spiral ligament, and the glial cells around the acoustic nerve fibers. In the damaged cochleas, no evidence of hair cell regeneration or of any cell division within the normal sensory epithelial structures was seen. Three labeled cells were seen in intercellular spaces within the sensory epithelium; they appeared to be macrophages. Frequent cell division was seen in numerous other regions of the damaged cochleas and among glial cells adjacent to the acoustic nerve fibers. It is concluded that there is no evidence for hair cell regeneration following acoustic trauma in the gerbil, but acoustic trauma does induce cell division in numerous other areas of the cochlea.

Animals↗

PubMed2004

Evaluation of various therapeutic schemes in the treatment of tinnitus due to acute acoustic trauma.

OBJECTIVES: We evaluated the effectiveness of various pharmaceutical therapeutic schemes in the treatment of tinnitus due to acute acoustic trauma. PATIENTS AND METHODS: This prospective study included 108 military personnel (all males; mean age 22 years; range 18 to 31 years) with complaints of tinnitus due to acute acoustic trauma following firearm use. Involvement was in the left ear in 61 patients, the right ear in nine patients, and in both ears in 38 patients. The mean duration from trauma to treatment was 26 days (range 1 to 110 days). Before and after treatment, complaints of tinnitus were evaluated using a questionnaire and a visual analog scale. Treatment was carried out for 15 days in four randomized groups: oral administration of trimetazidine, prednisolone, and vitamin B complex; trimetazidine alone; prednisolone and vitamin B complex; and intravenous piracetam and prednisolone. Unresponsive patients were further treated with trimetazidine for a month. Evaluations were made 15 days and 45 days after the institution of treatment. RESULTS: Thirteen patients (12%) had complete remission and 28 patients (25.9%) showed significant improvement. Further treatment with trimetazidine was beneficial in only seven (9.5%) patients. No significant differences were found between the groups in terms of tinnitus remission and improvement in hearing (p>0.05). Initiation of treatment, especially within the first week following acoustic trauma was significantly linked with higher rates of tinnitus regression (p<0.05). The degree of hearing improvement after medication did not correlate with improvement in tinnitus. Intravenous treatment was not advantageous over oral treatment. CONCLUSION: A timely initiation of therapy, especially within the first week following acoustic trauma, increases the chance of improvement in tinnitus patients.

Administration, Oral↗

PubMed1999

Hearing loss and tinnitus in acute acoustic trauma.

Despite extensive educational and protective measures, acute acoustic trauma continues to be a major problem in young military recruits. This retrospective study concern conscripts from eastern Austria who were referred to the Central Military Hospital for acute acoustic trauma (AAT) during the last 18 months. The study was designed to provide information on the profile of hearing loss and the presence of tinnitus after AAT. At the time when AAT occurred, hearing protection was not used in the majority of cases. In more than 75% of the ears hearing loss was registered in the high-frequency region (above 2 kHz). In the remaining 25% the speech frequency range under 2 kHz was also affected. Interestingly, the degree of hearing loss was independent of the type of firearm used, the number of shots and the use of hearing protection (ear plugs). Hearing loss occurred asymmetrically due to one-sided noise, whereas the distribution of tinnitus was symmetrical. The majority of patients experienced both, tinnitus and hearing loss as a consequence of AAT. Yet, in 6.2% of the subjects tinnitus was the only symptom. These results strongly suggest that tinnitus is as important a symptom of AAT as is hearing loss. Therefore, we believe that a tinnitus match should be performed in every patient with suspected AAT.

Acute Disease↗

PubMed1995

The emergence of free radicals after acoustic trauma and strial blood flow.

The effect of acoustic trauma on cochlear strial circulation was investigated immunohistologically in the guinea pig. Kanamycin was used as a tracer of blood flow. Moreover, histochemical examinations were made to reveal the emergence of free radicals in the cochlea following acoustic trauma. At 5 min (5 min after intense sound exposure 120-125 dB SPL, 3 h) the blood flow in the stria vascularis was greatly diminished. At 2 h the strial blood flow started to recirculate and at 6 h it appeared to have returned to normal. Superoxide anion radicals (O2-) emerged along the luminal membrane of the marginal cells of the stria vascularis at 5 min. O2- disappeared at 30 min, but reappeared at 2 h. The cause of its emergence at 5 min was obscure. However, the strange phenomenon that O2- emerged again at 2 h seemed ascribable to the re-circulation of strial blood flow after sound exposure.

Animals↗

PubMed2003

Is there a relation between acoustic trauma or noise-induced hearing loss and a subsequent appearance of Ménière's Disease? An epidemiologic study of 17245 cases and a review of the literature.

OBJECTIVE: To explore whether acute acoustic trauma or noise-induced hearing loss may cause the later development of Ménière's Disease. STUDY DESIGN: Retrospective search of a military medical data bank. SETTING: Medical records of 17245 Israel Defense Force veterans who were recognized as being disabled as a result of acoustic trauma or noise-induced hearing loss. PATIENTS: Eleven cases of late-onset Ménière's Disease were retrieved from these files. MAIN OUTCOME MEASURES: Documented symptoms and audiograms. RESULTS: Eleven of the 17425 veterans appeared to have typical Ménière's Disease. Their symptoms included attacks of vertigo, lasting between half an hour and a few hours and no more than 24 hours; the sensation of aural fullness; and tinnitus accompanied by a fluctuating or permanent low-tone hearing loss. Four of the 11 patients had a documented previous noise-induced hearing loss, and the remaining 7 had experienced acute acoustic trauma. The Ménière's Disease was bilateral in three cases. The average period between the first documented hearing loss and the onset of Ménière's Disease was 15.8 years (standard deviation, +/- 6.6 years). This yielded a prevalence of 1.9:100000 of Ménière's Disease in a population with acoustic trauma or noise-induced hearing loss-a figure comparable to that in the general population. CONCLUSIONS: No support was found for the hypothesis that Ménière's Disease may be causally related to previous acoustic trauma or noise-induced hearing loss.

Adolescent↗

PubMedDate not supplied

Acute acoustic trauma. A retrospective study of influencing factors and different therapies in 268 patients.

The files of 268 patients with acute acoustic trauma acquired during military service were analysed in a retrospective study. The following factors were examined: age, profession, degree of hearing loss, audiometric contour, and drug treatment. No influence of age or profession on recovery of hearing loss could be detected. The absolute hearing gain, defined as the difference between the hearing loss at onset and, on average, 7 days later, was dependent on the degree of initial hearing loss. The relative hearing gain, defined as absolute hearing gain divided by initial hearing loss, was independent of the degree of initial injury. The audiometric contour after the acoustic trauma had no prognostic relevance. Nine different types of drug treatment were compared in a subgroup of patients (n=199), in all of whom treatment was started within 2 days of the acoustic trauma. There were no significant differences in relative hearing gain between the nine types of treatment. Patients receiving early treatment had significantly better hearing one week after the acoustic trauma, as compared with the group of patients (n=69) not receiving treatment during the first 7 days. However, it was not possible to determine retrospectively whether this difference was due to treatment effects, or whether it was due to the exclusion of spontaneous remissions among those who were neither examined nor treated within the first 7 days.

Adult↗

PubMed1987

Regeneration of the tectorial membrane in the chick cochlea following severe acoustic trauma.

Damage to the tectorial membrane caused by acoustic trauma was examined with scanning and transmission electron microscopy immediately after exposure and at selected time points over a 10 day recovery period. At 0 h of recovery the structure of the tectorial membrane overlying the region of hair cell damage was severely disrupted and connections between the membrane and the basilar papilla were lost. By 24 h of recovery, regeneration of the tectorial membrane was evident in the secretion of new matrix materials by the supporting cells of the basilar papilla. By 10 days of recovery a new honeycomb-like matrix had replaced the segment of damaged tectorial membrane, re-established connections with hair cell stereocilia and become fused with adjacent regions of undamaged tectorial membrane. However, the regenerated segment included only the honeycomb-like structure of the lower layer of the normal tectorial membrane. The laterally-oriented fibers which form the upper layer of the membrane were not regenerated over the damaged region. These findings indicate that the tectorial membrane is regenerated in parallel with the hair cells during recovery from acoustic trauma but the full extent of this recovery and its effect on cochlear function are not yet clear.

Animals↗

PubMed1989

Possible precursors of regenerated hair cells in the avian cochlea following acoustic trauma.

Hair cell regeneration following acoustic trauma to the avian cochlea has been documented using DNA labeling with tritiated thymidine. The goal of this study was to identify potential precursor cell populations for regenerating hair cells. Chicks were exposed in pairs to a 1500 Hz pure tone at 120 dBSPL for 18 h. The animals received repeated injections of 3H-thymidine over a survival period of 6, 15, or 24 h, 3 days or 30 days after the completion of noise exposure. One cochlea from each animal was processed for autoradiography and the other for scanning electron microscopy. Labeled, regenerated hair cells were present by 3 days after exposure and recovery from injury was nearly complete by 30 days. Examination of animals in short survival groups suggest that two precursor populations may exist. For inferior sensory epithelial damage, cuboidal or hyaline epithelial cells appear to serve as the precursor cell population for the regeneration of both hair cells and supporting cells. With isolated superior damage, however, supporting cells may be the precursor population.

Animals↗

PubMed2000

Efficiency of hyperbaric oxygen therapy in experimental acute acoustic trauma from firearms.

In acute acoustic trauma (AAT), excessive noise exposure causes rupture of cell membranes and decreased cochlear blood flow. This leads to decreased oxygen tension in inner ear fluids and reduction of a variety of different oxygen-dependent cellular activities. Hyperbaric oxygen treatment (HBO) may help the cells suffering from hypoxia to survive. We exposed male Wistar rats to 60 impulses of 162-dB SPL from a 7.62-mm assault rifle equipped with a blank adaptor. After the exposure, 15 animals were given HBO treatment for 90 min daily for 10 consecutive days at 0.25 MPa. After a survival time of 4 weeks, auditory brainstem responses were measured and the left cochleae processed for light microscopy. The impulse noise caused permanent damage to the cochlea of all animals, with the most severe lesions in the lower middle coil, where a significantly smaller number of hair cells was missing in the HBO-treated group. The morphological damage was also reflected in function, as measured by auditory brainstem responses, which showed the greatest threshold shifts at 6.0, 8.0 and 10.0 kHz.

Acute Disease↗

PubMed2000

[Noise from a car airbag as a cause of acute acoustic trauma].

A case of acute acoustic trauma in 32 year male, caused by a noise from car airbag, was described. The symptoms occurring directly after the airbag shot were tinnitus and hearing loss in right ear. Patient was admitted to ENT Clinic in Gdańsk just after 5 months after an accident. Treatment--vasodilatators and oxygen hyperbaric therapy--was ineffective. Review of literature, concerning the side effects of car airbag shot, was made. A mechanism of airbag action was presented as a source of short time noise.

Acute Disease↗

PubMed1988

Hair cell regeneration after acoustic trauma in adult Coturnix quail.

Recovery of hair cells was studied at various times after acoustic trauma in adult quail. An initial loss of hair cells recovered to within 5 percent of the original number of cells. Tritium-labeled thymidine was injected after this acoustic trauma to determine if mitosis played a role in recovery of hair cells. Within 10 days of acoustic trauma, incorporation of [3H]thymidine was seen over the nuclei of hair cells and supporting cells in the region of initial hair cell loss. Thus, hair cell regeneration can occur after embryonic terminal mitosis.

Age Factors↗

PubMed2001

The efficacy of medication on tinnitus due to acute acoustic trauma.

Seventy-two young males suffering from acute acoustic trauma with tinnitus due to gunshots were included prospectively in the study. Forty of the subjects had the left ear affected, four the right ear and the remaining 28 sustained bilateral acoustic traumas. The mean time of admission after onset of symptoms was 28 days (5-88 days). The subjects were randomly categorized into three groups: group A received trimetazidine, prednisolone and complex B vitamins; group B were treated only with trimetazidine; and group C received prednisolone and complex B vitamins. At 3-month follow up, tinnitus had been completely eradicated in only eight subjects and had in 17. No statistically significant difference was found between the three groups concerning improvement of tinnitus. However, it was found that early admission predisposed towards better prognosis. The degree of hearing improvement after medication did not seem to correlate with the relief of tinnitus.

Acute Disease↗

PubMed2004

Cochlear administration of adenosine triphosphate facilitates recovery from acoustic trauma (temporary threshold shift).

BACKGROUND: Adenosine triphosphate (ATP) has often been used in the treatment of acoustic trauma although evidence supporting its clinical use was lacking. The aim of this study was to evaluate the chronic effects of ATP on acoustic trauma in guinea pigs. METHODS: We infused ATP into the perilymph of the guinea pig cochlea concurrently with intense noise exposure to investigate the effect of ATP on the process of recovery after acoustic trauma. We assessed auditory brainstem response (ABR) thresholds to evaluate cochlear function. RESULTS: After noise exposure (120 dB SPL, 5 h), ABR thresholds showed an increase of approximately 50 dB SPL that returned to normal after 14 days. Cochlear function in ATP-treated ears recovered more quickly than in control ears. The effect of ATP was inhibited by the administration of the ATP receptor antagonist: pyridoxal- phosphate-6-azophenyl-2',4'-disulfonic acid. CONCLUSION: These results suggest that ATP mitigates the effects of noise trauma through the ATP receptor.

Adenosine Triphosphate↗

PubMed1981

Characteristics of tinnitus in acoustic trauma.

Several parameters of tinnitus were investigated in a group fo 102 subjects suffering from acoustic trauma. These parameters were then compared to the results of the hearing tests and subjective complaints. The frequency and intensity of tinnitus were established by the usual matching technique with a clinical audiometer. The most effective masking of the tinnitus due to acoustic trauma was by pure tones. There seems to be a correlation between the tinnitus level and the hearing loss level at the frequency at which the hearing loss was most severe. A significant association was found between the matched tinnitus level and its description by the patient. There is also an association between the severity of the acoustic trauma and the perceived loudness of the tinnitus, as well as other subjective complaints.

Adolescent↗

PubMed1995

Therapeutic effect of hyperbaric oxygenation in acute acoustic trauma.

Retrospectively 78 patients with uni- or bilateral acute acoustic trauma (AAT) were evaluated to assess the therapeutic effect of hyperbaric oxygenation (HBO). All subjects received saline or dextran (Rheomacodrex) infusions with Ginkgo extracts (Tebonin) and prednisone. Thirty six patients underwent additional hyperbaric oxygenation at a pressure of 2 atmospheres absolute for 60 minutes once daily. Both treatment groups were comparable as far as age, gender, initial hearing loss and prednisone dose are concerned. The delay of therapy onset was 15 hours in both groups and treatment was started within 72 hours in all cases. Control audiometry was performed after 6.5 days, when the HBO group had had 5 exposures to hyperbaric oxygenation. The average hearing gain in the group without HBO was 74.3 dB and in the group treated additionally with HBO 121.3 dB (P < 0.004). It is concluded, that hyperbaric oxygenation significantly improves hearing recovery after AAT. Therefore acute acoustic trauma with significant hearing threshold depression remains an otological emergency. Minimal therapy involving waiting for spontaneous recovery, which is mostly incomplete leaving a residual C5 or C6 and handicapping tinnitus, is not the treatment of choice. Randomized prospective clinical trials with a larger patient series are needed and further experimental studies are required to understand the physiological mechanisms of HBO responsible for the clinical success in AAT.

Acute Disease↗