[Clinical observation of tinnitus caused by extrinsic causes--head trauma, acoustic trauma, etc].
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Acoustics↗
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Immune cell recruitment following acoustic trauma.
Acoustic trauma induces cochlear inflammation. We hypothesized that chemokines are involved in the recruitment of leukocytes as part of a wound healing response. The cochleas of NIH-Swiss mice, exposed to octave-band noise (8-16 kHz, at 118 dB) for 2h, were examined after the termination of exposure. Leukocytes were identified immunohistochemically with antibodies to CD45 and F4/80. Gene array analysis followed by RT-PCR was performed on cochlear tissue to identify up-regulation of chemokine and adhesion molecule mRNA. The expression of the adhesion molecule ICAM-1 was also investigated immunohistochemically. Few CD45- or F4/80-positive leukocytes were observed in the non-exposed cochlea. Following acoustic trauma however, the number of CD45-positive cells was dramatically increased especially after 2 and 4 days, after which time the numbers decreased. F4/80-positive cells also increased in number over the course of a week. Gene array analysis indicated increased expression of monocyte chemoattractant protein 5 (MCP-5), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein-1beta (MIP-1beta) and ICAM-1. RT-PCR, performed using primers for the individual mRNA sequences, confirmed the increased expression of MCP-1, MCP-5, MIP-1beta, and ICAM-1 relative to non-exposed mice. In the normal cochlea, ICAM-1 immunohistochemical expression was observed in venules, spiral ligament fibrocytes and in endosteal cells of the scala tympani. Expression increased to include more of the spiral ligament and endosteal cells after acoustic trauma. A cochlear inflammatory response is initiated in response to acoustic trauma and involves the recruitment of circulating leukocytes to the inner ear.
Animals↗
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↗
Mononuclear phagocytes migrate into the murine cochlea after acoustic trauma.
Acoustic injury results in destruction of hair cells and numerous nonsensory cells of the cochlea. How these injured structures undergo repair is not well understood. This study was designed to examine the cochlea for the presence of mononuclear phagocytes after tissue injury caused by noise damage. We used octave band noise (8--16 kHz) at three levels (106, 112, and 120 dB) for 2 hours and studied the mice at 1, 3, 7, and 14 days after noise exposure to determine how noise affected hearing thresholds, hair cell number, and tissue injury in the cochlea. Furthermore, we assessed the cochlea for presence of inflammation by performing immunohistochemistry for CD45, common leukocyte antigen. We counted the number of CD45(+) cells that were present in the cochlea at the above-mentioned time points after noise. CD45 is present on all bone marrow-derived white blood cells and is not otherwise expressed in the inner ear. We found that, after noise exposure, there is a large increase in CD45(+) cells. These marrow-derived cells are concentrated in the spiral ligament and spiral limbus, areas that are known to be susceptible to acoustic injury. It is possible that this inflammatory response plays a role in propagating cellular damage in these areas. Immunohistochemistry demonstrates that these cochlear cells are derived from the monocyte/macrophage lineage and serve a phagocytic function in the inner ear.
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↗
[Effectiveness of pharmacologic therapy combined with hyperbaric oxygen in sensorineural hearing loss following acute acoustic trauma. Preliminary report].
UNLABELLED: Exposure to loud sounds can cause acute acoustic trauma and permanent sensorineural hearing loss. The aim of the study was to evaluate effectiveness of pharmacological treatment combined with the hyperbaric oxygen (HBO) in the treatment of sensorineural hearing loss following acute acoustic trauma for patients treated in the Department of Otolaryngology of Military Institute of Health Service and Warsaw Center for Hyperbaric Therapy and Wounds Treatment. MATERIAL AND METHODS: Group of 12 patients (22 damaged ears) with acute acoustic trauma (10 men and 2 women), 16-67 years of age, mean age 28 years, was involved in our study. Patients with tinnitus and sensorineural hearing loss of minimum 15 dB at 0.25-8 kHz were included in the treatment group. Hearing gain of minimum 10 dB at 0.25-8 kHz and decrease in the intensity of tinnitus was considered as an improvement. 4 days was the mean time interval between acoustic trauma and starting the pharmacological treatment, 7 days was the mean time interval for the hyperbaric oxygen therapy commencement. RESULTS: Statistically significant difference in Pure Tone Audiometry results obtained before and after the treatment was noted in 4 kHz when considering all damaging factors that caused acoustic trauma and in 6 kHz only for damage resulting form shooting. Statistically significant difference was noted in 6 kHz if the HBO therapy was continued over 10 days (p < 0.00001). Statistically significant difference was noted in 4, 6, 8 kHz when treatment was started within 5 days since the acoustic trauma (p < 0.000001). CONCLUSIONS: Hyperbaric oxygen therapy is the unique method of increasing concentration of oxygen in the inner ear fluids thus facilitates the regeneration process. Hyperbaric oxygen therapy combined with steroids is an effective method of sensorineural hearing loss treatment following acute acoustic trauma.
Adolescent↗
Otoacoustic emissions and persistent tinnitus after acute acoustic trauma.
OBJECTIVES: To follow up the auditory status of military personnel after an acute acoustic trauma and to identify the possible predictive value of hearing thresholds and otoacoustic emissions during the first 24 hours after the acoustic trauma. STUDY DESIGN: A group of 24 young military subjects, aged 22 +/- 2.3 years, without any otologic problem before the acoustic trauma, were examined at three time intervals after an accidental acoustic trauma caused by the discharge of a firearm: 24 hours, 72 hours, and 15 days. METHODS: Each subject was submitted to medical examination and to a questionnaire detailing the circumstances of the acoustic trauma. Pure tone audiometry was performed from 1 to 8 kHz per half octave. Transiently evoked otoacoustic emissions were recorded in the nonlinear mode at 80 dB pSPL, and distortion product otoacoustic emissions were recorded from 1 to 6 kHz, using a distortion product-gram type procedure, at 65/55 dB SPL, with f2/f1 = 1.22. Two groups of subjects were defined: group 1 (n = 8) represented subjects with short-lasting tinnitus (<72 h) and group 2 (n = 16) subjects with long-lasting tinnitus (>72 h). RESULTS: Hearing thresholds did not differ significantly between these two groups 24 hours after the acoustic trauma. However, otoacoustic emissions showed significantly lower amplitudes 24 hours after the acoustic trauma in subjects showing a longer lasting tinnitus. CONCLUSION: Otoacoustic emissions appear to be a better predictor of the persistence of tinnitus than hearing thresholds alone 24 hours after an acute acoustic trauma.
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↗
Glucocorticoid receptor and nuclear factor-kappa B interactions in restraint stress-mediated protection against acoustic trauma.
The role of glucocorticoid receptors (GRs) in the protective effect of restraint stress (RS) before acoustic trauma was studied in spiral ganglion neurons of CBA mice. RS increased corticosterone and protected against elevated auditory brain stem thresholds caused by acoustic trauma. This protection was inhibited by the pretreatment with a corticosterone synthesis inhibitor, metyrapone (MET), and a GR antagonist (RU486). RS followed by acoustic trauma caused an immediate increase in corticosterone that triggered nuclear translocation of GR, without a change in the expression of GR protein. RU486 + MET before RS and acoustic trauma caused an immediate increase in GR mRNA followed by increased GR protein expression (24 h after trauma). GR signaling was further characterized by analyzing nuclear factor-kappaB (NF kappaB) nuclear translocation and protein expression. NF kappaB nuclear translocation was reduced after acoustic trauma or pretreatment with RU486 + MET before RS and acoustic trauma. On the contrary, RS protected against the trauma-induced NF kappaB reduction of its nuclear translocation in inhibitory-kappaB (I kappaB)-dependent manner. RU486 + MET caused a simultaneous decreased I kappaB expression and NF kappaB nuclear translocation, demonstrating an interference with the I kappaB-mediated activation of NF kappaB. In summary, RS protects the cochlea from acoustic trauma by increasing corticosterone and activating GRs. These results emphasis how GR activity modulates hearing sensitivity and its importance for the rationale use of glucocorticoids in inner ear diseases.
Animals↗
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↗
Vestibular evoked myogenic potentials in acute acoustic trauma.
OBJECTIVES: Anatomical proximity of the saccule to the stapedial footplate points to the possibility of acoustic trauma associated with saccular dysfunction. Therefore, it was the authors' premise that abnormal vestibular evoked myogenic potential (VEMP) after acute acoustic trauma may be caused by saccular damage from very high intensity noise; consequently, irreversible hearing loss ensued. The aim of this study was to investigate the VEMP responses in those with acute acoustic trauma. STUDY DESIGN: A prospective study. SETTING: University hospital. PATIENTS: Twenty patients (29 ears) without previous ear disorders diagnosed as acute acoustic trauma were enrolled in this study. MAIN OUTCOME MEASURES: Before treatment, each patient underwent pure tone audiometry and caloric and VEMP tests. Correlations between the hearing outcome and mean hearing level, sources of noise, caloric responses, or VEMP results were investigated. RESULTS: After 3 months of medication, complete recovery was achieved in 4 ears and hearing improvement in 4 ears, whereas hearing in 21 ears (72%) remained unchanged. Eighteen ears presenting normal VEMPs revealed hearing improvement in eight ears (44%) and unchanged hearing in ten ears (56%). However, hearing loss remained unchanged in all 11 ears (100%) with absent or delayed VEMPs, exhibiting a significant relationship between VEMP results and hearing outcome. Thus, VEMP test can predict the hearing outcome after acute acoustic trauma with a sensitivity of 44% and a specificity of 100%. CONCLUSION: The greater the noise intensity, the severer damage on the cochlea and saccule is shown. Absent or delayed VEMPs in ears after acute acoustic trauma may indicate poor prognosis with respect to hearing improvement, whereas normal VEMP is not a powerful indicator for expectation of hearing improvement.
Adult↗
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↗