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Acoustic trauma was studied in experimental guinea pigs by combining gross auditory nerve recordings with single neurone (spiral ganglion) techniques and scanning electron-microscopy. Structural and functional changes caused by loud pure tones were assessed immediately after exposure and after varying recovery periods.
Following impulse noise trauma to chinchillas, observation of plastic-embedded surface preparations of the organ of Corti showed no consistent relationship between cochlear hair cell loss and permanent hearing loss (Hamernik et al. 1980). In some animals there was a loss of hearing when hair cells were present. The cochleas from that experiment were examined with transmission electron microscopy to determine at the ultrastructural level if there was damage to the sensory cells that would explain the change in threshold sensitivity. Ultrastructural changes in cochlear hair cells include an increase in lysosomes, multivesicular bodies, vacuolization of subsurface cisternae, and proliferation of Hensen bodies. These changes are observed in all experimented animals. Alterations to the ultrastructure of the stereocilia vary from animal to animal and on the outer hair cells, the changes include loosening of the stereocilia membranes, loss of stiffness, fusion of the stereocilia and disintegration of the rootlets. These changes are observed only in animals that have a permanent threshold shift after noise trauma.
The effects of ionizing irradiation on the cochlear microphonic response of guinea-pigs were studied. The cochlear microphonics (CM) of both ears were recorded in a total of 36 animals. Recording was carried out by the differential electrode technique on the basal turn of the cochlea. One week prior to recording, the left ear of each animal had been exposed to 35-70 Gy radiation in increments of 5 Gy. Doses of 40 Gy and above led to a reduction in CM response. After doses of 60 Gy or more, no CM response could be detected. Damage most probably occurred in the outer and inner hair cells.
Chronically implanted electrodes were used to record cochlear microphonics (CM) in awake rabbits. Test stimuli were sine waves of 1,250, 2,500, 5,000 and 10,000 Hz, with intensities increased from 40 to 100 dB SPL. By using this long-term method for registering the CM, we have found that the form of the input-output functions recorded is in agreement with that from acute experiments as described in the literature. Our method proved to be valid for recording CM with constant amplitudes over a period of 8-10 weeks. Our present results form a basis for further investigations concerning noise overload.
Evoked acoustic emissions (EAEs) and spontaneous acoustic emissions (SAEs) recordings hold some promise as a fast, objective and non-invasive audiological procedure, especially in children. However, accurate interpretation in the emission response must be based on the basic properties of the emissions present in a younger age group. In so doing, the properties of emissions were investigated in 49 ears from 26 children, whose ages varied between 2 days and 10 years. EAEs could be recorded in all normal ears, but the incidence of long-duration EAEs decreased with age. There were no statistically significant variations in recording the EAEs detection threshold with age. The incidence of SAEs also decreased with age.
Spontaneous cochlear emissions consist of one or more sinus tones. Oscillations and frequency shifts clearly widen averaged traces. Multiple peaks, if present, are spaced at intervals of 2-3% of the frequency, and increase with frequency. A frequency jump by the same amount was seen in one case. This appears to represent the distance between hair cells, and suggests that individual hair cells play a leading role in these oscillations.
Cochlear microphonics (CM) were recorded from awake rabbits with chronically implanted electrodes. Test frequencies used were 1,250, 2,500, 5,000 and 10,000 Hz, with intensities increased from 40 to 100 dB SPL. The rabbits were exposed to ten noise impulses of 144 dB SPL, which were then followed by impulse intensities of 153 and 164 dB SPL for the same animal. Input-output functions before and after each noise exposure were recorded, and recovery processes of the CM were tracked. After 144 dB SPL impulses, complete recovery of CM occurred; the effects of 153 dB SPL impulses varied from restitution up to complete CM loss. Impulses of 164 dB SPL caused an irreversible CM loss in all cases. Despite inter-individual differences, the threshold for irreversible CM loss in rabbits may occur between impulse noise intensities of 153 and 164 dB SPL.
In humans, functional evidence based on recording cochlear microphonic, auditory nerve, and brain stem responses has shown that the site of lesion in hearing loss following neonatal hyperbilirubinemia is the auditory nerve (with sparing of the hair cells). Structural damage to the central nervous system (CNS) including the cochlear nuclei has been demonstrated in adult, homozygous Gunn rats which develop hyperbilirubinemia shortly after birth. In an attempt to use the Gunn rat as an experimental model for bilirubin-induced CNS damage, auditory nerve and brain stem responses (ABR) were recorded in jaundiced (homozygous) and non-jaundiced (heterozygous) Gunn rats and in Sabra (Wistar) rats. All of the rats including the jaundiced Gunn rats had normal ABR and responded behaviorally to sound stimuli. These results suggest that the adult jaundiced Gunn rat retains auditory function and in this way differs from human patients in whom neonatal jaundice has lead to hearing loss. Therefore, the adult homozygous Gunn rat probably cannot serve as a model for hearing loss due to hyperbilirubinemia.
Test series with both continuous and intermittent sound exposure to guinea pig ears yielded an area within the coordinates load frequency and load level in which a dose principle is valid more or less exactly. Exceeding the upper (level) borderline of this area provokes a damage of the organ of Corti nearly independent of the load dose. Sound levels of such order of magnitude mainly occur at sound impulses. However, to estimate the hair-cell damaging effect of a given sound impulse one needs its time or frequency function in addition to the peak level. A first order approximation seems to be possible by means of a 1/3-octave band level analysis.
(1) The loss of hair cells after pure tone exposure at the critical level of intensity shows an exact correlation to the frequency, the time of sound exposure, and time of recovery as regards the quality and quantity. (2) The total extent of the damage of sensory cells has to be estimated higher than the hair-cell loss as observed under the light microscope. Although an improvement of the function of the organ of Corti was determined electrophysiologically from the 5th to the 10th day of recovery, the hair-cell degeneration was progredient during this period. (3) The hair-cell damage is apically more strongly marked from the area of damage than basically. (4) Depending on the experimental conditions there are considerable degenerative alterations in the nerve fibres and in the connective apparatus of the organ of Corti besides hair-cell losses and damages.
Hypothermia during exposure to noise reduced hair-cell damage which, on the contrary, was prevented from recovering by narcosis and hypothermia. Hyperthermia is apparently able to eliminate the narcosis dependent limitation of metabolism. A noise damage happens to develop by decompensating the excessively overburdened metabolism, whereas recovery seems to depend on the availability of a highly intracellular level of biological energy.
The acoustical properties of the external ear of the barn owl (Tyto alba) were studied by measuring sound pressure in the ear canal and outer ear cavity. Under normal conditions, pressure amplification by the external ear reaches about 20 dB between 3-9 kHz but decreases sharply above 10 kHz. The acoustic gain curve of the outer ear cavity alone is close to that of a finite-length exponential horn between 1.2-13 kHz with maximum gain reaching 20 dB between 5-9 kHz. Pressure gain by the facial ruff produces a maximum of 12 dB between 5-8 kHz and decreases rapidly above 9 kHz. The directional sensitivity of the external ear was obtained from pressure measurements in the ear canal. Directivity of the major lobe is explained, to a first approximation, by the sound diffraction properties of a circular aperture. Aperture size is based on the average radius (30 mm) of the open face of the ruff. Above 5 kHz, the external ear becomes highly directional and there is a 26 degree disparity in elevation between the acoustic axis of the left and right ear. In azimuth, directivity patterns are relocated closer to the midline as frequency increases and the acoustic axis moves at a rate of 20 degree/octave between 2-13 kHz. Movement of the axis can be explained, to a first approximation, by the acoustical diffraction properties of an obliquely truncated horn, due to the asymmetrical shape of the outer ear cavity. The directional sensitivity of the barn owl ear was studied by recording cochlear microphonic (CM) potentials from the round window membrane. Between 3-9 kHz, CM directivity patterns are clearly different to the directivity patterns of the external ear; CM directionality is abruptly lost above 10 kHz. Above 5 kHz, CM directivity patterns are characterized by an elongated major lobe containing the CM axis, forming a tilted band of high amplitude but low directionality (CM axial plane), closely bordered by minima or nulls. The highest directionality is found in the CM directional plane, approximately perpendicular to the CM axial plane. The left and right ear axial planes are symmetrical about the interaural midline (tilted 12 degrees to the right of the midline of the head) and inclined by an average of 60 degrees to the left and right respectively. In azimuth, the CM axis moves towards the midline at a rate of 37 degrees/octave as frequency increases from 2-9 kHz, crossing into contralateral space near 7 kHz.(ABSTRACT TRUNCATED AT 400 WORDS)
Mongolian gerbils were examined for auditory nerve function at five ages, ranging from 90 to 730 days postpartum. Electrocochleograms were obtained in response to tone pips at frequencies ranging from 1 to 64 kHz. An age-related threshold increase was noted at all frequencies. The pattern of auditory loss is different from that observed in the aged rat, guinea pig, and mouse.
An experimental model for emotional stress is described. Emotional stress can affect hearing if severe enough or if it lasts long enough. The noxious effect on the ear can be explained by the high level of blood catecholamines and exaggerated activity of the cochlear sympathetic innervation.
The present experiment investigated whether or not auditory responses of the middle and/or inner ear in guinea pigs to low frequency sound stimuli [ 60 Hz-2 kHz at 90-120 dB(SPL) ] exhibited the harmonic distortion phenomenon resulting from cochlear microphonics (CM). Measurement of CM leading in turn I by the differential electrode recording method involved measurement of 50 microV isopotential responses, output voltages and CM wave form distortion at each constant sound pressure. The results obtained were as follows: (1) On the 50 microV isopotential response curve and the output voltage curves, the changes at 60-90 Hz were different from those at higher frequencies. (2) At stimuli of 90 or 100 dB(SPL), CM wave form distortion appeared frequently at frequencies below 120 Hz, but were less pronounced above approximately 200 Hz. (3) When raised to 110 and 120 dB(SPL), almost all CM wave forms were distorted at all test frequencies between 60 and 500 Hz. (4) The patterns of CM wave form distortion at frequencies below approximately 120 Hz showed peak clipping and triangular wave distortions, while those at frequencies above approximately 200 Hz showed little of these distortions.
The effects on CM induced by 46.5 h exposure to low-frequency sound of 0.125 kHz at 115 dB (SPL) and 100 dB (SPL), which frequency is considered to be in the vicinity of the lowest limit of audiofrequency for guinea pigs, were investigated by the sound pressure levels at which CM output voltages produced 50 microV (50 microV isopotential responses) at test frequencies of 0.06, 0.08, 0.12, 0.18, 0.25, 0.5, 1, 2, and 4 kHz, and by the intensity function measured from 65 to 120 dB (SPL) at test frequencies of 0.06, 0.08, 0.12, 0.18, 0.25, 0.5, 1, and 2 kHz. The results obtained were as follows. In 50 microV isopotential responses measured at about 30 min after the termination of sound exposure, the mean dB in the 115 dB-exposed group tended to elevate at all test frequencies of 0.06 kHz to 4 kHz as compared with those in the control group. Significant dB elevations were especially observed at 0.06, 0.12, 1, 2, and 4 kHz. In the 100 dB-exposed group, however, no significant dB elevations were observed at any test frequencies as compared with those in the control group. In the intensity function measured at about 40-60 min after the termination of sound exposure, the mean output voltages in the 115 dB-exposed group induced by test stimuli of 0.18 kHz-2 kHz at higher intensities showed significant depression in comparison with those in the control group (by over 110 dB at 0.18 and 0.25 kHz, and by over 90 dB at 1 and 2 kHz).(ABSTRACT TRUNCATED AT 250 WORDS)
A new tubal transducer (NC-3) for measuring cochlear microphonics (CM) in extratympanic electrocochleography (ECochG) was developed by improving the common hearing aid earphone. Using a human forearm as a dummy ear, the artifact contamination generated from the NC-3 tubal transducer was tested and the possibility of measuring the CM at a non-shielded bedside was studied. An HN-5 electrode was fixed to a subject's forearm, and a sound stimulus of 90 dBnHL was delivered through the tube of the NC-3. When the earphone of the transducer was placed at a right-angle to the electrode on either a vertical or horizontal plane and the electrode was placed in direct contact with the tip of the tube, contamination from electromagnetic induction and CM-like mechanical vibration were prevented. Using the HN-5 electrode and NC-3, extratympanic ECochG-CM was recorded from normal-hearing subjects in both a shielded soundproof room and a non-shielded ordinary, quiet room. No differences were found between CMs measured in the two rooms. These results suggest that the NC-3 overcomes the shortcomings of a loudspeaker system and allows CM to be recorded accurately at non-shielded bedsides.
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