[Clinical observation of tinnitus caused by extrinsic causes--head trauma, acoustic trauma, etc].
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Acoustics↗
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Effects of acoustic trauma on acoustic enhancement of electrically evoked otoacoustic emissions.
Moderate acoustic trauma results in decreased cochlear sensitivity and frequency selectivity. This decrease is believed to be caused by damage to the cochlear amplifier that is associated with outer hair cells (OHCs) and their nonlinear electromechanical characteristics. A consequence of OHC nonlinearity is the acoustic enhancement effect, in which low-frequency electrically evoked otoacoustic emissions are enhanced by a simultaneous tone. The present study found that acoustic trauma reduced the acoustic enhancement effect and this reduction is correlated with the N1 threshold at the electrode site. This result is consistent with the theory that trauma affects the mechanoelectric transduction process, thus affecting cochlear mechanical nonlinearity. Acoustic trauma also reduced the cochlear microphonic in a way that suggests that the number of functioning tension-gated channels and the stiffness of the gating springs were decreased. In some cases, the electromechanical transduction process was also found to be affected by acoustic trauma.
Animals↗
Distortion Product Otoacoustic Emissions in acute acoustic trauma.
Acute acoustic traumas are caused by exposure to extremely high noise levels ranging from milliseconds to several hours' duration. In pure tone audiometry they range from the C5 dip to basomediocochlear sensorineural hearing loss. Their pathogenesis is assumed to consist of micromechanical-traumatic and biochemical-metabolic damage to the outer hair cells. In order to establish the changes to the DPOAE (distortion products of otoacoustic emissions), 17 patients were examined after sustaining acute acoustic trauma. The causes included firework explosions, anti-tank rocket launchers, vehicle tyre bursting, rock concerts, hand-gun shots, sub-machine gun fire, hand grenade explosion, exploding car battery. The pure tone audiogram, tympanogram, tinnitus maskability and DPOAE (both DP-gram and growth rate in various frequencies) were determined in all patients. If the event had occurred some time ago, measurements were taken only once; in acute cases measurements were repeated at different times. In nine patients with persistent hearing impairment, clear DPs were found in the unaffected frequencies but were completely absent in the affected frequency range. Four of these patients were unilaterally and two patients were bilaterally affected; three patients had a different (not noise-induced) hearing loss on the opposite side. In eight patients with regressive hearing loss, DPs were by contrast detectable throughout the entire frequency range, their amplitudes only rising slightly as hearing recovered. Of these eight patients, three were unilaterally and five bilaterally affected. DPOAE seem to indicate the likelihood of recovery of hearing threshold after an acute acoustic trauma. In cases with DPs completely absent in the affected frequency range, the prognosis seems to be much worse than in cases with present DPs in the frequency range of hearing.
Journal Article↗
Acute acoustic trauma.
Acute acoustic trauma is a clinical condition with immediate persistent hearing loss after impulse or blast wave noise. This condition is not well recognized in occupational medicine and probably not even in otolaryngology. We report 52 cases of acute acoustic trauma including information concerning the traumatic event. Most cases occurred within military service and in the shipbuilding industry. Except for immediate hearing loss, many patients experienced tinnitus and some pain and hyperacusis. Relatively few patients report immediately. Most patients have been met by a nihilistic approach to therapy, in most cases due to the fact that patients report long after the trauma. The aim of the report is to focus attention on this clinical condition, since there is some indication that the final outcome may improve if patients are taken care of and treated early.
Acute Disease↗
[Comparison of different treatments of acute acoustic trauma].
Comparison between different treatments of acute acoustic trauma. The acute acoustic trauma, induced tinnitus, hearing loss and an fickle otalgia, is a Permanent or a Temporary Threshold Shift. In a retrospect study of 184 patients, or 313 cases, the target of this research was to determinate a possible level of blood dilution resulted during normovolemic hemodilution, and an optimal therapeutic group. In fact, just the dilay of a starting treatment between 0 and 3 days permitted to obtain this group on qualitatives and quantitative criteria; efficiency of the treatment is better than the damages are important. We observed an important post normovolemic hemodilution effect on audition recovery and tinnitus evolution. In return, an optimal hematocrite value hadn't been found between 29 and 35%.
Adult↗
Clinical and animal experiment studies to optimise the therapy for acute acoustic trauma.
Despite extensive educational measures and improved ear protection, acute acoustic trauma still represents a major problem for the young soldier in the Federal Armed Forces. The aim of the investigation was thus to establish the optimum therapeutic scheme that could be applied by the generally young and still inexperienced unit medical officer to patients who had suffered acute acoustic trauma and to demonstrate the therapeutic scheme in animal experiments. In the clinical section, ten studies conducted on 500 patients who had suffered acute acoustic trauma made it possible to show that the combination of low-molecular dextran, or low-molecular hydroxyethyl starch, and hyperbaric oxygenation produced the best therapeutic results in terms of hearing gain and tinnitus elimination by a statistically significant margin. The studies only included patients who showed no tendency towards spontaneous recovery, with strict exclusion criteria being applied. Through animal experiments, it was seen that hyperbaric oxygenation, in the manner in which we conducted it (100% oxygen at 2.5 bar), leads to an increase in the oxygen partial pressure in the perilymph of the guinea pig cochlea. This is due partly to diffusion and partly to the blood flow. In a further experimental approach using animals, it proved possible to show that 60 hours after damage by acoustic trauma and hyperbaric oxygenation, the number of inner ear sensory cells that had suffered morphological damage in the animal was lower than without the hyperbaric oxygenation by a statistically significant margin. At the same time, valuable information was gained on the epidemiology of acute acoustic trauma.
Acute Disease↗
Acute acoustic trauma: dynamics of hearing loss following cessation of exposure.
The natural history of individuals with acute acoustic trauma who ceased to be exposed to impact noise was examined. Retrospective follow-up was carried out for 4 years on patients who were qualified as disabled following acoustic trauma with permanent threshold shift. Eight hundred forty-one individuals (1682 ears) were examined, of which 1514 ears with acoustic trauma were included in the study group; 150 individuals (300 ears) who continued to be exposed to impact noise even after discovery of acoustic trauma comprised the control group. In the latter, as long as exposure to gunfire continued, the severity of acoustic trauma increased. In the study group, during the first year after injury, changes were observed in hearing, whether improvement or deterioration; after this period, hearing loss appeared to be final. We suggest that, after 1 year following acute acoustic trauma, the associated hearing loss be considered as final, provided there is no further exposure to noise. This finding holds great importance from the medicolegal standpoint, an aspect that is unclear in the literature. It clarifies that beyond the period of 1 year after initial exposure, the pathologic process ceases (as long as there is no additional exposure to noise or gunfire). Further hearing deterioration beyond this period is not related to the initial acoustic trauma but rather to other factors.
Acute Disease↗
Progressive hearing loss after single exposure to acute acoustic trauma.
Progressive hearing loss after single episodes of acute acoustic trauma (Knalltrauma) has been reported in only a few cases. Many authors dispute such a progressive evolution. Since this question is of obvious importance in cases evolving into lawsuits, its occurrence also arouses scientific interest. The present study reports 58 bilateral and 17 unilateral cases of acute acoustic trauma showing progression of more than 20 dB at least at one frequency. The mean follow-up time was more than 20 years. The incidence was estimated as less than 1% of cases involving acute acoustic trauma. The evolution of the progressive hearing loss did not show a specific pattern; in the unilateral group, there were no statistically significant differences between the progression in both ears. The findings clearly indicate that late progression of hearing loss due to single episodes of acute acoustic trauma does not exist unless the affected ear is exposed to additional damage not related to the initial trauma.
Adolescent↗
Bilateral hearing loss as a sequel to unilateral acoustic trauma.
Within the framework of a study on the natural history of acoustic trauma, over 600 soldiers were examined. A higher rate of bilateral acoustic trauma was observed among soldiers with longer service. Comparison between unilateral and bilateral acoustic trauma showed a greater severity of damage in both ears of the latter group. Comparison of the progression of the damage in the same persons on two consecutive examinations suggested the same trend. It is suggested that bilateral acoustic trauma may be a later and more severe stage in some types of noise-induced damage.
Adult↗
Evidence for supporting cell mitosis in response to acoustic trauma in the avian inner ear.
Acoustic overstimulation can lead to sensory cell (hair cell) loss in the auditory epithelium. Damaged hair cells in the organ of Corti (the mammalian auditory end-organ) degenerate and are replaced by non-sensory cells (supporting cells) which construct an irreversible scar. In birds, however, auditory hair cells which are damaged by acoustic trauma or ototoxic drugs may be replaced by new hair cells. As first step in determining the mechanism of hair cell regeneration, we developed an assay for cell divisions in the auditory epithelium after acoustic trauma. The results of these experiments demonstrate that supporting cells in damaged regions of the auditory epithelium incorporate the DNA-specific marker bromodeoxyuridine as early as one day after noise exposure. We provide direct evidence that following acoustic insult to the avian inner ear, supporting cells which reside within the sensory epithelium divide near the luminal surface and repopulate the epithelium. These results suggest that supporting cells participate in scar formation during hair cell degeneration, and produce new cells for regeneration.
Animals↗
Riluzole rescues cochlear sensory cells from acoustic trauma in the guinea-pig.
Acoustic trauma is the major cause of hearing loss in industrialised nations. We show in guinea-pigs that sound exposure (6 kHz, 120 dB sound pressure level for 30 min) leads to sensory cell death and subsequent permanent hearing loss. Ultrastructural analysis reveals that degeneration of the noise-damaged hair cells involved different mechanisms, including typical apoptosis, autolysis and, to a lesser extent, necrosis. Whatever the mechanisms, a common feature of noise damage to hair cells was mitochondrial alteration. Riluzole (2-amino-6-trifluoromethoxy benzothiazole) is a neuroprotective agent that prevents apoptosis- and necrosis-induced cell death. Perfusion of riluzole into the cochlea via an osmotic minipump prevents mitochondrial damage and subsequent translocation of cytochrome c, DNA fragmentation, and hair cell degeneration. This was confirmed by functional tests showing a clear dose-dependent reduction (ED(50)=16.8 microM) of permanent hearing loss and complete protection at 100 microM. Although less efficient than intracochlear perfusion, intraperitoneal injection of riluzole rescues the cochlea within a therapeutic window of 24 h after acoustic trauma.These results show that riluzole is able to prevent and rescue the cochlea from acoustic trauma. It may thus be an interesting molecule for the treatment of inner ear injuries.
Acoustic Stimulation↗
A randomized, double-blind, placebo-controlled study of dextran/pentoxifylline medication in acute acoustic trauma and sudden hearing loss.
The effectiveness of any therapy in acute acoustic trauma or sudden hearing loss of unknown origin has not been demonstrated convincingly. The assessment is difficult because of a relatively high rate of spontaneous recovery. Nevertheless, many different forms of treatment are recommended. We tested one form, treatment with rheoactive substances, in a prospective, randomized, double-blind trial and compared treatment with (a) infusions of dextran-40 with pentoxifylline, (b) saline infusions with pentoxifylline, and (c) saline infusions with placebo medication. Pure-tone hearing thresholds served as control parameters and were taken before treatment and at 1 and 4 weeks after the onset of therapy. Three hundred eighty-two patients were included in the trial, 331 (87%) could be analyzed, 184 patients were treated because of sudden hearing loss, 147 because of acute acoustic trauma. The three treatment groups were comparable in their basic characteristics including the amount of initial hearing loss. In patients with sudden hearing loss, no significant differences of hearing recovery were detected between the three treatment groups. Hearing recovery was also similar in patients with acute acoustic trauma. A power analysis of the study revealed that possible true treatment differences of a hearing recovery of 10 dB would have lead to significance with a probability of over 90%. It is concluded that there were, in fact, no clinically relevant differences in hearing gains of sudden hearing loss or acute acoustic trauma between treatments with saline infusions together with placebo medication and treatment with dextran-40 and/or pentoxifylline.
Acoustic Stimulation↗
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↗
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↗
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↗
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↗
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↗
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↗