Acute Acoustic Trauma Research Articles

Occurrence and Persistence of Tinnitus after Acute Acoustic Trauma by Gunshot

Background and Objectives：Acute acoustic trauma (AAT) by gunshot can be the cause of hearing loss and tinnitus. Tinnitus after AAT frequently disappears with time. But the prognosis of this injury is very difficult to predict. This study tried to identify the factors influencing on tinnitus to occur and persist after AAT. Subjects and Method：A group of 268 military subjects who get the gunshot training with K-2 rifle once after conscripted was asked to answer the questions: age, otologic history, number of firing, usage of earplugs, presence of tinnitus after gunshot and its characteristics, relapsed time after firing, Tinnitus Severity Index (TSI) questionnaire. Physical examination and pure tone audiometry were conducted to the subjects with existing tinnitus on the questionnaire. Results：95 patients (36.4%) experienced tinnitus immediate after gunshot among 261 subjects. It is obvious that wearing earplugs could prevent immediate tinnitus after AAT. There was statistical significance between tinnitus with earplug and without it (p=0.000). At the time of questionnaire, 27 (10.3%) were complaining of tinnitus. Among factors such as age, number of firing, wearing earplugs, severity of tinnitus and relapsed time after firing, only severity of tinnitus has the significant effect with the persistence of tinnitus (p=0.046). Conclusion：Wearing earplugs can prevent tinnitus immediately after AAT, but does not seem to be the factor decreasing the prevalence of tinnitus. It was the only factor related to severity of tinnitus and to existing tinnitus. (Korean J Otorhinolaryngol-Head Neck Surg 2009;52:113-7)

Hyperbaric oxygen therapy seems to enhance recovery from acute acoustic trauma

Hyperbaric oxygen therapy seems to enhance recovery from acute acoustic trauma

Effects of Explosive Blast Trauma on Sleep Quality and Quality of Lives of the Workers in Ammunition Factory

We investigated the effects of explosive acoustic trauma on sleep quality and quality of lives (QOLs) of the workers in Ammunition Factory. Forty-one male workers exposed to explosive acoustic trauma in Ammunition Factory 12 years ago constructed the study group (Group 1). Thirty-eight male workers of Ammunition Factory who were not exposed to the explosion, were included into the control group (Group 2). We used the Mini Sleep Questionnaire (MSQ) and SF-36 questionnaire. In workers of the study group who had experienced psychological and sleep problems; hearing loss and acute tinnitus just after explosion; and had higher education levels, some of the sleep and QOL parameters got worse. Workers, adjacent to the explosion site and not used earpluggs during explosion, had more impaired sleep quality results (p<0.05). We may conclude that acute explosive acoustic trauma may affect negatively some items of sleep quality and quality of the lives of the workers. Workers should be educated to use ear muffs and ear plugs. For post-explosion sleep problems and other psychological problems, psychological support should be given to the workers by the health-team and their families.

Clinical Characteristics of Acoustic Trauma Caused by Rifle Gunshot Noise

Background and Objectives：One of the major occupational hazards of working in the military service is being subjected to intense impulse noise, hence acoustic trauma. Acute acoustic trauma is a preventable disease, but the effective treatment modality has not been established yet. Acute acoustic traumas caused by exposure to rifle gunshot noise are common in young Korean males in the military service because of conscription policy. Through the analysis of the clinical presentation of acoustic traumas caused by rifle gunshot noise, we suggest effective preventive modalities. Subjects and Method：165 soldiers who had otologic symptoms after performing regular rifle gunshot exercise without any hearing protective measures were analyzed. They all had been tested with K2 rifle. History taking, physical examination, pure-tone audiometry, and impedence audiometry, temporal MRI, and Newmann’s tinnitus inventory questionnaire survey were performed. Results：Most common and annoying symptom was tinnitus. The average outcome of postexposure air conduction thresholds were 22.3dB HL in the affected ear and 11.8dB HL in the unaffected ear. There was no correlation between severity of tinnitus and severity of hearing loss. Asymmetry of hearing loss related to head position during gunshot was not found. This may be due to the fact that during the mass gunshot training, each patient can be influenced by the gunshot noise of the adjacent gunner’s shooting. Conclusion：Widening the distance between firing lanes and providing bilateral hearing protective devices against acoustic trauma must be taken into serious consideration. (Korean J Otorhinolaryngol-Head Neck Surg 2008;51:699-704)

Disruption of Balanced Cortical Excitation and Inhibition by Acoustic Trauma

Sensory deafferentation results in rapid shifts in the receptive fields of cortical neurons, but the synaptic mechanisms underlying these changes remain unknown. The rapidity of these shifts has led to the suggestion that subthreshold inputs may be unmasked by a selective loss of inhibition. To study this, we used in vivo whole cell recordings to directly measure tone-evoked excitatory and inhibitory synaptic inputs in auditory cortical neurons before and after acoustic trauma. Here we report that acute acoustic trauma disrupted the balance of excitation and inhibition by selectively increasing and reducing the strength of inhibition at different positions within the receptive field. Inhibition was abolished for frequencies far below the trauma-tone frequency but was markedly enhanced near the edges of the region of elevated peripheral threshold. These changes occurred for relatively high-level tones. These changes in inhibition led to an expansion of receptive fields but not by a simple unmasking process. Rather, membrane potential responses were delayed and prolonged throughout the receptive field by distinct interactions between synaptic excitation and inhibition. Far below the trauma-tone frequency, decreased inhibition combined with prolonged excitation led to increased responses. Near the edges of the region of elevated peripheral threshold, increased inhibition served to delay rather than abolish responses, which were driven by prolonged excitation. These results show that the rapid receptive field shifts caused by acoustic trauma are caused by distinct mechanisms at different positions within the receptive field, which depend on differential disruption of excitation and inhibition.

Potential efficacy of early treatment of acute acoustic trauma with steroids and piracetam after gunshot noise

The purpose of this randomized study was to evaluate the early effect of the treatment of acute acoustic trauma (AAT) with steroids and piracetam in a sample of 52 young soldiers who were exposed to intense gunfire noise (G3 rifle). These patients were divided into three groups: (1) group A (20 patients) in which the treatment began within the first hour after the AAT, (2) group B (17 patients) in which the treatment started more than 1 h later and less than 16 h after the AAT and (3) group C (15 patients) in which the treatment began after 24 h or more. One month after the treatment onset, 36 (69%) patients of all the groups showed hearing improvement (complete-partial recovery) in the pure tone audiometry. The greater number of patients who showed complete recovery after AAT was noted in group A (65%) compared to group B (23.5%) and C (13.3%). Moreover, in group A, in the final audiogram, the averaged hearing threshold was statistically better (P < 0.001) than that of groups B and C. In spite of the lack of control group, our data demonstrated the possible effectiveness of the immediate onset of treatment of AAT.

Effectiveness of 4-hydroxy phenyl N-tert-butylnitrone (4-OHPBN) alone and in combination with other antioxidant drugs in the treatment of acute acoustic trauma in chinchilla

Acute acoustic trauma (AAT) results in oxidative stress to the cochlea through overproduction of cellular reactive oxygen, nitrogen, and other free radical species appearing from 1 h to 10 days after noise exposure. It has been shown that N-acetyl-L-cysteine (NAC), a glutathione prodrug, and acetyl-L-carnitine (ALCAR), a mitochondrial biogenesis agent, are effective in reducing noise-induced hearing loss. Phenyl N-tert-butylnitrone (PBN), a nitrone-based free radical trap, appears to suppress oxidative stress in a variety of disorders and several biological models. In this study, we tested whether 4-hydroxy PBN (4-OHPBN), a major metabolite of PBN, administered 4 h after noise exposure is effective in treating noise-induced hearing loss and whether a combination of antioxidant drugs (4-OHPBN plus NAC and 4-OHPBN plus NAC plus ALCAR) provides greater efficacy in attenuating AAT since each agent addresses different injury mechanisms. Chinchilla were exposed to a 105 dB octave-band noise centered at 4 kHz for 6 h. 4-OHPBN and combinations of antioxidant drugs were intraperitoneally administered beginning 4 h after noise exposure. Hearing threshold shifts in auditory brainstem responses and missing outer hair cell counts were obtained. 4-OHPBN reduced threshold shifts in a dose-dependent manner while both drug combinations showed greater effects. These results demonstrate that 4-OHPBN and combinations of antioxidants can effectively treat acute acoustic trauma and drug combinations may increase the effectiveness of treatment and decrease the required individual medication dose.

Hyperbaric oxygen therapy seems to enhance recovery from acute acoustic trauma

Conclusion. The average recovery of hearing and cessation of tinnitus was significantly better after hyperbaric oxygen therapy (HBOT) than after normobaric oxygen therapy (NBOT). HBOT can be valuable adjuvant therapy for patients with acute acoustic trauma (AAT). Objectives. AAT was one of the early indications for the use of HBOT. The rationale of administering oxygen to patients with AAT is based on experimental studies showing that noise exposure results in cochlear hypoxia, which could be compensated by HBOT. The aim of this study was to investigate the efficacy of HBOT in patients with AAT. Patients and methods. We compared the recovery from hearing impairment and tinnitus in 60 ears treated with HBOT with 60 ears treated with NBOT. The HBOT was given daily for 1–8 days. There were no significant differences in clinical or audiological data between HBOT and NBOT groups. Results. The average recovery of hearing both at high and speech frequencies was significantly better and tinnitus persisted less commonly after the HBOT than after the NBOT. Normal hearing at the end of the follow-up period was regained in 42 ears in the HBOT group and in 24 ears in the NBOT group (p<0.01).

Akute einseitige Ertaubung und pathologische Vestibularisbefunde nach Knalltrauma durch Gewehrschüsse

Acute acoustic trauma is usually acquired during military service after exposure to impulse or blast wave noise. The typical audiometric shape is a notch centered at about 4 kHz with some recovery above this frequency. This is the first case of an immediate induced unilateral total hearing loss in a young soldier following exposure to gunfire noise. A 25-year-old right-handed army officer during military training, after realizing a series of five shots with a rifle (G3), immediately experienced on the right ear otalgia, tinnitus and severe hearing loss, without imbalance or dizziness. The pure tone audiogram revealed a cophosis on the right ear without any residual remnants. In order to estimate the extent of the labyrinth damage, a caloric test and vestibular evoked myogenic potentials (VEMPs) were performed, which were both abnormal. The possible mechanical and metabolic damage effects on the cochlea from the intense gunfire noise were discussed. As the caloric test showed directional preponderance and the VEMPs were totally abolished, it has been concluded that the saccule and to a lesser degree the posterior labyrinth have been also found affected. The importance of wearing hearing protectors such as ear plugs and ear muffs during exposure to intense noise was underlined.

Hyperbaric oxygenation with corticoid in experimental acoustic trauma

Among possible therapies after acute acoustic trauma, hyperbaric oxygenation (HBO) combined with corticoid was found effective in several animal studies. Such evidence was obtained for moderate 20–25 dB losses. The aim of this study was to further assess this therapy for noise-induced hearing losses greater than previously examined. Sixty-five ears from thirty-six adult guinea pigs were used. Acoustically evoked responses from intracranial electrodes chronically implanted bilaterally into the ventral cochlear nucleus were used to assess acoustic sensitivity alterations. Trauma sound was a third-octave noise-band around 8 kHz presented bilaterally at 115 dB SPL for 45 min. One control group received no treatment, one group was treated with HBO only and another with corticoid only both starting within one day post-trauma, two groups were treated with both HBO and corticoid starting for one group within one day post-trauma, and for the second group at 6 days post-trauma. Acoustic thresholds were measured between the 6th and the 16th days after acoustic trauma. Animals treated with HBO alone or corticoid alone did not differ from controls. Combined HBO and corticoid therapy provided significant protection from noise-induced loss of auditory thresholds, especially when started one day post-exposure. Hearing loss reduction induced by HBO combined with corticoid was of similar magnitude (about 10–15 dB) as in previous studies although the induced hearing loss was considerably greater (about 40 dB instead of 20–25 dB).

Seitendifferente Schallempfindungsschwerhörigkeit durch seitengleichen knalltraumatischen Schalldruck

Due to diffraction, acute acoustic trauma usually causes symmetrical hearing loss. Acoustical shadow effects are relevant only at distances greater than 1 m to the sound source and frequencies greater than 1000 Hz. In case of pronounced asymmetrical hearing loss causal connection to acute acoustic trauma is unlikely. We describe two cases with pronounced asymmetrical hearing loss in spite of symmetrical acute acoustic trauma. In the first case two patients headed an exploding giant tyre in a distance of approximately 1-2 m. One of them--as expected--got a symmetrical inner ear damage. On the other hand the other patient, which stayed directly besides him, got a pronounced asymmetrical inner ear damage. In an additional case we found also asymmetrical inner ear damage after symmetrical noise exposure. In this case it was detected, that years ago the patient suffered from a menieriform attack in the now worse ear. Occult inner ear damage is discussed as a reason for the phenomenon of pronounced asymmetrical inner ear damage after symmetrical noise exposure.

Intratympanic treatment of acute acoustic trauma with a cell-permeable JNK ligand: a prospective randomized phase I/II study

Objectives. Intratympanic administration of a cell-permeable JNK ligand has been shown to prevent hearing loss after acute acoustic trauma in animal models. Conclusions. Functional and morphological analysis of the treated ears revealed that AM-111 had an excellent otoprotective effect, even when administered hours after the noise exposure. Blocking the signal pathway with D-JNKI-1 is therefore a promising way to protect the morphological integrity and physiological function of the inner ear in various conditions involving acute sensorineural hearing loss. Subjects and methods. For the first application of AM-111 in humans, we organized a clinical phase I/II trial in patients with acute acoustic trauma after exposure to firecrackers in Berlin and Munich on New Year's Eve 2005/2006. We randomly selected 11 patients for intratympanic treatment with AM-111 at a concentration of 0.4 mg/ml or 2 mg/ml within 24 h after noise exposure. Pure tone audiometry and otoacoustic emissions were assessed before treatment and on days 3 and 30 thereafter. Results. Based on clinical experience and on a calculation using an empirically derived exponential hearing recovery function AM-111 seems to have had a therapeutic effect. A total of 13 adverse events were reported in 5 study participants. None of the adverse events were serious or severe.

Ostry uraz akustyczny i termiczny ucha spowodowany awarią telefonu komórkowego

The case of acute acoustic and burn ear trauma caused by mobile phone failure is presented. A woman aged 24 after dialling a phone number and putting a phone into the ear heard a sound of high frequency and intensity. At the same time she felt a pain and heat and there was also a smoke from the phone. With otoscopic examination a burn of external acoustic duct (I0) and sensitive hearing loss (examination made with tuning forks) were stated. The patient did not agree to stay in hospital and she was administered prednizone, trimetazidin and xantylol nicotinate. Audiometric examination, which was made on another day, showed hearing loss of 30 dB for frequency 4000Hz. After 2 days she started to hear a sound like a sea noise in her right ear. In the control examination, made 2 weeks after injury, no abnormalities in audiogram were stated but the patient steal heard ear noise. She continued to take trimetazidin and betahistin and after one month all symptoms of ear injury relieved. Patient is still under control of otolaryngologist. Unfortunately our efforts to explain the cause of such accident from phone producer were ineffective. Described case proves that mobile phone failure can be a cause of acute ear injury.

NAC for noise: From the bench top to the clinic

Noise-induced hearing loss (NIHL) is an important etiology of deafness worldwide. Hearing conservation programs are in place and have reduced the prevalence of NIHL, but this disorder is still far too common. Occupational and recreational pursuits expose people to loud noise and ten million persons in the US have some degree of noise-induced hearing impairment. It is estimated that 50 million in the US and 600 million people worldwide are exposed to noise hazards occupationally. Noise deafness is still an important and frequent cause of battlefield injury in the US military. A mainstay of hearing conservation programs is personal mechanical hearing protection devices which are helpful but have inherent limitations. Research has shown that oxidative stress plays an important role in noise-induced cochlear injury resulting in the discovery that a number of antioxidant and cell death inhibiting compounds can ameliorate deafness associated with acoustic trauma. This article reviews one such compound, N-acetylcysteine (NAC), in terms of its efficacy in reducing hearing loss in a variety of animal models of acute acoustic trauma and hypothesizes what its therapeutic mechanisms of action might be based on the known actions of NAC. Early clinical trials with NAC are mentioned.

Vestibular Evoked Myogenic Potentials in Acute Acoustic Trauma

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. A prospective study. University hospital. Twenty patients (29 ears) without previous ear disorders diagnosed as acute acoustic trauma were enrolled in this study. 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. 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%. 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.

09:00 AM: Cochlear Base-Apex Differences in Cell-Death Following Noise

09:00 AM: Cochlear Base-Apex Differences in Cell-Death Following Noise

09:20 AM: Optimal Treatment of Acute Acoustic Trauma in the Chinchilla

09:20 AM: Optimal Treatment of Acute Acoustic Trauma in the Chinchilla

Otoacoustic Emissions and Persistent Tinnitus after Acute Acoustic Trauma

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. 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. 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). 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. Otoacoustic emissions appear to be a better predictor of the persistence of tinnitus than hearing thresholds alone 24 hours after an acute acoustic trauma.

Negative Effect of Immediate Hyperbaric Oxygen Therapy in Acute Acoustic Trauma

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

Negative Effect of Immediate Hyperbaric Oxygen Therapy in Acute Acoustic Trauma

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