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Perilymph fistulas are a known cause of sudden hearing loss. The two cases presented illustrate round window ruptures secondary to acoustic trauma. The important considerations are early diagnosis and treatment, the possibility of associated congenital anomalies, and future protection against sound.
In a retrospective study 103 patients with acute acoustic trauma (AAT) were investigated. The control group (53 patients) was treated with Dextran 40 (10% solution), neurotrop vitamins and Betahistin. Bencyclan was administered additionally in the test group (50 patients). Statistical analysis of the audiometric data showed the following results: 1. Mean hearing levels of the test group showed better improvement of threshold shifts, if the therapy started within 2 days or after more than 10 days after the AAT. 2. Regression-and correlation coefficients, however, in a regression analysis of absolute hearing gains and hearing losses before therapy, did not indicate a substantial effect of Bencyclan. 3. Neither did statistical tests with relative hearing gains show any significant differences between test-and control groups. Consequently Bencyclan is not likely to have a positive effect in AAT, if it is administered in the above mentioned way.
A simple-to-use classification system is presented for expressing the hearing loss resulting from acoustic trauma. They system is based upon the implications for social hearing as seen the pure tone air conduction hearing test, which is classified according to specifically segmented areas of the audiogram. A study of the audiometric results of 102 ex-army men with AcT and 25 controls with normal hearing included a detailed questionnaire to relate the patients' functional complaints to their audiograms, and the clinical picture was then completed by the administration of speech audiometry tests both in quiet backgrounds of various signal-to-noise ratios. Three main severity categories of hearing impairment were established. These are described and illustrated.
A prospective study was performed in all Finnish conscripts who were referred to the Central Military Hospital for acute acoustic trauma (AAT) in 1989-93. The study was designed to provide information on hearing protection at the time of AAT and also on the general habits of using hearing protection at shooting drills and combat training in the field. Altogether 449 conscripts with verified AAT were included. According to their statements, all conscripts always used hearing protectors at shooting drills on the range and 97% always or nearly always during combat training in the field. At the moment when AAT occurred, hearing protectors were not used in 83% of cases. Accidental shots or explosions (25.6%), unforeseen exposure to impulse noise, e.g. during combat training (17.5%), and loss of applied protectors (14.9%) were the most common reasons for absence of hearing protection. AATs can be avoided by improving instruction in handling firearms, planning combat training more carefully and making sure that application of earplugs is properly taught and mastered.
This is a new method devised by the AA. in order to produce a laboratory experimental acoustic trauma, using a recorded noise. So it is possible to produce at will a noise strong enough to provoke a cochlear damage with the rythm, the frequency spectrum and duration chosen.
The vulnerability of inner hair cells (IHCs) and outer hair cells (OHCs) to acoustic overstimulation is still controversially discussed. The present study was undertaken to investigate the vulnerability of IHCs and OHCs and the relation between chronological changes of auditory threshold shifts and stereocilia damages on IHCs and OHCs in guinea pigs after moderate acoustic trauma, caused by a single continuous exposure to pink noise (20 Hz to 20 kHz) of around 106 +/- 2 dB SPL for 44 h. Stereocilia changes and threshold shifts of auditory brainstem responses (ABR) were assessed at regular intervals after noise exposure for 9 weeks. Scanning electron microscopy demonstrated the morphological changes of stereocilia as early as 1 day after noise exposure. The morphological changes included fused, bent, collapsed, and even missing stereocilia. These damages were more prominent on IHCs than on OHCs. The shift of ABR threshold was not parallel to the chronological change of the stereocilia on IHCs as well as OHCs. The elevation of the ABR threshold (40-60 dB SPL) was greatest on the 1st day after noise exposure, whereas the stereocilia showed the most damage 7 days after noise exposure. Combined with the results from previous studies, we conclude that moderate-level (around 105-110 dB) noise tends to induce more damage to the stereocilia of IHCs than of OHCs. Other damage (e.g., metabolic disturbance) than morphological damage of hair cell stereocilia may contribute partially to the hearing threshold shift induced by moderate acoustic overstimulation.
Young hamsters pass through a developmental stage during which they are unusually susceptible to acoustic trauma. This sensitive period occurs after apparent structural and functional maturation of the ear and appears to be dependent on unidentified developmental changes within the cochlea.
This article deals with the shift in audiometric tracings brought about by the discharge of firearms (acute acoustic trauma). The study included 60 subjects with normal hearing, between 18 and 20 years of age. Each individual shot 25 bullets in about 5 minutes, at an intensity level calculated at 163 dB. None of them related antecedents of sensorineural deafness. The audiometric examinations were performed as follows: the first one prior to the experiment, the second immediately after the series of shots, and others 8 and 40 hours later. These are the conclusions drawn out by the AA.: the most important and lasting deafness was verified in the left ear. The 6000 c/s frequency was the most affected. Recovery of the previous hearing level was total in 80.5% of the cases within 40 hours. Two subjects having otosclerotic relatives showed certain difficulties in recovering.
Changes in spontaneous activity, recorded over 15-min periods before, immediately after and within hours after an acute acoustic trauma, were studied in primary auditory cortex of ketamine-anesthetized cats. We focused on the spontaneous firing rate (SFR), the peak cross-correlation coefficient (rho) and burst-firing activity. Multi-units (MUs) were grouped according to characteristic frequency (CF): MUs with a CF below the trauma-tone frequency (TF) were labeled as Be, those with a CF within 1 octave above the TF were labeled as Ab1 and those with a CF more than 1 octave above the TF were labeled as Ab2. Immediately after the trauma, the SFR was not significantly changed. The percentage of time that neurons were bursting, the mean burst duration, the number of spikes per burst and the mean inter-spike interval in a burst were enhanced. rho was locally increased in the Ab1-Ab2 and Ab2-Ab2 groups. A few hours post trauma, the SFR was increased in the Be and Ab2 groups, whereas burst-firing returned to pre-exposure levels. Moreover, rho was elevated in the Be-Ab2, Ab1-Ab2 and Ab2-Ab2 groups; this increase was significantly correlated to the changes in SFR. The results are discussed in the context of a neural correlate of tinnitus.
We investigated the prevalence, characteristics and subjective perceived handicap caused by long-term tinnitus induced by acute acoustic trauma (AAT) in 418 former military conscripts. They had been treated between 1984 and 1989 because of AAT from exposure to impulse noise caused by firearm shooting. All 418 patients reported tinnitus after the AAT. At discharge from the military service, 122 (29%) still reported tinnitus. In 1999, of these 122 patients, 101 were reached and 66 still had tinnitus. The Tinnitus Handicap Questionnaire demonstrated various difficulties in life because of tinnitus, not attributable only to tinnitus loudness. Psychological factors also seem to play an important role. The effects of AAT and possible compensation have been evaluated so far mostly by audiometric findings, but in some cases tinnitus may be an even more serious threat to life satisfaction than mild hearing impairment.
An audiological and clinical study was carried out on 433 soldiers suffering from symptomatic acute acoustic trauma (AAT). The severity of AAT was similar following exposure to different types of firearms. The typical subjective complaints were tinnitus and hearing loss and the more severe the objective hearing loss, the more frequent were the typical subjective symptoms. It seems that there are critical sound pressure levels and critical frequencies below which the remnants of infectious processes in the middle ear may have a protective effect on the cochlea in cases of exposure to noise, whereas above these critical levels and frequencies the injurious influence of noise appears to be enhanced. The best known treatment for AAT seems to be removal from further exposure to noise. Further exposure to noise had a significant worsening influence on the average hearing status, while removal from noise significantly improved the audiometric status.
Six selected human cochleae showing definite signs of mechanical damage caused by exposure to high intensity noise (acute acoustic trauma) are reviewed. Patterns of degeneration of cochlear hair cells were compared with the functional audiometric examinations. Tonotopic relations, mechanism of damage to the organ of Corti as well as pathological changes of the tectorial membrane are discussed.
Recordings from single neurons in the dorsal cochlear nucleus (DCN) of unanesthetized (decerebrate) cats were done to characterize the effects of acoustic trauma. Trauma was produced by a 250 Hz band of noise centered at 10 kHz, presented at 105-120 dB SPL for 4h. After a one-month recovery period, neurons were recorded in the DCN. The threshold shift, determined from compound action-potential audiograms, showed a sharp threshold elevation of about 60 dB at BFs above an edge frequency of 5-10 kHz. The response maps of neurons with best frequencies (BFs) above the edge did not show the typical organization of excitatory and inhibitory areas seen in the DCN of unexposed animals. Instead, neurons showed no response to sound, weak responses that were hard to tune and characterize, or "tail" responses, consisting of broadly-tuned, predominantly excitatory responses, with a roughly low-pass shape similar to the tuning curves of auditory nerve fibers with similar threshold shifts. In some tail responses whose BFs were near the edge of the threshold elevation, a second weak high-frequency response was seen that suggests convergence of auditory nerve inputs with widely separated BFs on these cells. Spontaneous rates among neurons with elevated thresholds were not increased over those in populations of principal neurons in unexposed animals.
The therapy results of inhalation of carbon dioxide (oxycarbon) together with the infusion therapy (Dextran, a.s.o.) carried out on 63 patients having acute acoustic trauma are presented and discussed. These results are superior to the results obtained by carbon dioxide therapy only or by infusion therapy only.
We administered acidic fibroblast growth factor (aFGF) to the perilymph of the guinea pig cochlea after exposure to intense sound to investigate its effect on the process of recovery after acoustic trauma. We assessed auditory brain stem response (ABR) thresholds to evaluate cochlear function and observed the sensory epithelium using confocal laser-scanning microscopy. After noise exposure (120 dB SPL, 5 h), the ABR threshold showed an increase of approximately 50 dB SPL that recovered after 14 days. Cochlear function in aFGF treated ears recovered more quickly than that in control ears. These results suggest that aFGF may play an important role in cochlear recovery after acoustic injury.
Any loss of cochlear hair cells has been presumed to result in a permanent hearing deficit because the production of these cells normally ceases before birth. However, after acoustic trauma, injured sensory cells in the mature cochlea of the chicken are replaced. New cells appear to be produced by mitosis of supporting cells that survive at the lesion site and do not divide in the absence of trauma. This trauma-induced division of normally postmitotic cells may lead to recovery from profound hearing loss.
Etiological factors and otological and audiological findings were analysed retrospectively in 361 Finnish conscripts who had suffered acute acoustic trauma (AAT) from firearms shooting during their military service. The most common cause of AAT was shooting with hand-held weapons without ear-protectors (50%). Other common causal weapons were antitank guns (25%) and cannons (12%). Explosions had caused AAT in one-tenth of the cases. The tympanic membrane had been ruptured in 22 subjects (6%). The frequency at which hearing loss was severest was most commonly 6.0 kHz, followed by 8.0 kHz and 4.0 kHz in that order. Speech frequencies were involved in about 25% of the ears. A flat type of audiometric configuration was observed in about 20% and a rising type (low-tone loss) in about 5% of the ears. Impulse noise from large-calibre guns seemed to cause low-tone hearing loss more often than shooting with hand-held weapons.
The paper analyzes the 8 KHz threshold in subjects with noise-induced hearing loss. The study group consisted of 315 subjects occupationally exposed to noise and suffering from acoustic trauma, which was considered as a mean threshold of more than 25 dB at 2, 3 and 4 KHz. The mean shape of audiograms was characterized by a neurosensory deficit which was more elevated at 4 and 6 KHz whereas the threshold at 8 KHz was better. However, this pattern was found in 60% of the cases whereas in the remaining 40% the threshold at 8 KHz was worse. Subjects with the most impaired audiometric threshold at 8 KHz were mainly older, although cases were found in a low percentage of younger subjects. The results demonstrate that in individual cases it is impossible, on the basis of the shape of the audiogram, to establish whether a hearing loss is due to noise or age.