Sound induced fluid pressures directly activate vestibular hair cells: implications for activation of the cochlea.
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Acoustic Stimulation↗
Biomedical subjects
Haim Sohmer
Publications and source records attributed to Haim Sohmer.
The effects of positive and negative middle ear pressures on auditory threshold.
HYPOTHESIS: To assess the effects of positive and negative middle ear pressures on auditory threshold. BACKGROUND: Nonatmospheric middle ear pressures can alter auditory threshold by their effects on tympanic membrane and ossicular chain mobility. METHODS: Experiments were conducted on guinea pigs by inducing alterations in pressure (positive and negative) with a syringe connected to the middle ear bulla cavity, the magnitude of the pressure being assessed with a water manometer. Elevated middle ear fluid pressures were also induced by attaching a saline-filled vertical tube to the saline-filled middle ear. The effect of these altered middle ear air and fluid pressures were assessed by recording auditory nerve-brainstem evoked responses. RESULTS: There was no effect on auditory threshold of positive middle ear air pressures (up to 250 mm H2O). A negative middle ear air pressure of -50 mm H2O induced a significant 9.5-dB threshold elevation, whereas more negative pressures (up to -150 mm H2O) did not induce an additional threshold elevation. Filling the middle ear cavity with saline induced a 10- to 16-dB elevation, whereas additional fluid pressures (up to 200 mm H2O) did not induce further elevations. CONCLUSION: The major factor inducing threshold elevation in serious otitis media is not the alteration in middle ear pressure but rather the reduction in the volume of compressible air in the middle ear by the fluid.
Air Pressure↗
Quantitative experimental assessment of the factors contributing to hearing loss in serous otitis media.
OBJECTIVE: This study was designed to quantitatively assess the contribution of various factors to the conductive hearing loss in otitis media. BACKGROUND: In the conductive hearing loss seen in cases of serous otitis media, various volumes of fluid of different viscosities along with subatmospheric (negative) pressure are found in the middle ear. METHODS: To evaluate the contribution of each of these factors to hearing loss, various volumes of saline, whole blood, or glycerol were applied to the open middle ear cavity of guinea pigs for short periods of time and auditory function was evaluated by recording the threshold of auditory nerve-brainstem evoked responses. In some of the saline experiments, the bulla cavity was also sealed, allowing a subatmospheric (negative) pressure to develop in the cavity as water was osmotically absorbed because of the gradient in colloid osmotic pressure between saline and blood in the vessels lining the middle ear cavity. In other experiments, a thoracic drainage system was connected to the middle ear cavity to induce desired negative middle ear pressures. RESULTS: The degree of hearing loss increased as larger volumes of fluid were introduced into the middle ear, reaching a maximum of 15 to 16 dB. There was no difference in the degree of hearing loss induced by saline or by fluids with viscosities up to 1,000 times greater than that of water (glycerol). A subatmospheric pressure in the middle ear contributed only a small additional (1-2 dB) threshold elevation. CONCLUSION: The major factor contributing to hearing loss in serous otitis media is the volume of fluid in the middle ear, irrespective of its viscosity. The contribution of negative middle ear pressure is much smaller.
Analysis of Variance↗
Mechanism of cochlear excitation at low intensities.
In order to assess the mechanisms of cochlear activation, the cochlear fluids of one cochlea of a guinea-pig (I) were coupled to those of a cochlea of a second guinea-pig (II) by means of a saline-filled narrow bore tube, the ends of which were placed in the fluids around the opened round windows of both cochleae, thus joining the two cochleae from two different animals into a single, larger, unsealed fluid system. In response to air-conducted sound stimulation of cochlea I, auditory nerve-brainstem evoked responses could be recorded in animal II, not only when the coupling tube was filled with saline, but also when it was filled with ultrasound gel (viscosity 100,000 greater than that of water), when there was a very large hole encompassing a relatively large expanse of the cochlear shell of animal I, and even when animal I was no longer alive. The necessary control experiments were performed. Therefore, it is suggested that at low stimulus intensities, the passive, incoming basilar membrane traveling wave may not activate the cochlea. Instead the fluid pressures (condensation/rarefactions) induced in the cochlear fluids by vibrations of the stapes footplate may be adequate to directly activate the outer hair cells, which then generate an active component of basilar membrane displacement.
Acoustic Stimulation↗
Prior heat acclimation confers protection against noise-induced hearing loss.
Exposure to intense noise stress can cause a permanent noise-induced hearing loss which is thought to be due to elevation of reactive oxygen species in excess of the inherent antioxidant mechanisms of the cell. However, preconditioning to low levels of stress of one type can activate cellular mechanisms leading to the elevation of antioxidant levels so that the cell is then better able to tolerate subsequent severe stress of a different type. This has been called cross-tolerance. Here, we tested this hypothesis by acclimating rats to a moderate heat stress (30 days at 34 degrees C). The rats were exposed to 113 dB SPL noise for 3 days (12 h/day) in three different groups: heat acclimated then noise exposed; noise exposed and then heat acclimated; heat acclimated, then noise exposed and then heat acclimated again. Permanent changes in auditory function--auditory nerve brainstem evoked responses (ABR) and distortion product otoacoustic emissions (DPOAEs)--were evaluated in each of these animals and compared with those in rats exposed to noise only and in control groups of rats. Statistical evaluation of the results showed that when assessed with ABR, each of the heat-acclimated, noise-exposed groups was protected from the noise, even the group that was heat-acclimated after the noise exposure. When assessed with DPOAE, protection was statistically apparent only in the group that was heat acclimated, then exposed to noise, and not in the other groups. Thus, heat acclimation provides protection against permanent noise-induced hearing loss.
Acclimatization↗
Effect of an initial noise induced hearing loss on subsequent noise induced hearing loss.
The effect of previous noise induced hearing loss (NIHL) on subsequent NIHL was studied in rats. Three groups of animals were initially exposed to different durations of 113 dB SPL broad band noise (21 days, 3 days or 0 days--unexposed). Their permanent threshold shifts (PTS) from this exposure (PTS1) were evaluated using auditory nerve-brainstem evoked responses (ABR). All the animals were then noise-exposed for an additional 12 days, and the incremental PTS following this exposure (PTS2) was also assessed. The 21 day group showed the greater PTS1 [mean +/- SD: 27.03 +/- 6.78 dB, compared with 11.67 +/- 10.47 dB (3 day group)] and the lowest PTS2 [9.84 +/- 8.19 dB, compared with 13.33 +/- 14.60 dB (3 day group) and 24.04 +/- 12.4 dB (0 day group)]. This group also showed the highest total PTS and lowest SD following the two noise exposures [36.88 +/- 6.29 dB, compared with 25.00 +/- 12.68 dB (3 day group) and 26.35 +/- 11.93 dB (0 day group)]. The results may be explained by the lower effective intensity of the second noise exposure for the animals with a large PTS1 compared to those with little or no NIHL from the first noise exposure.
Animals↗
Further evidence for a fluid pathway during bone conduction auditory stimulation.
This study was designed to evaluate the suggestion that during bone vibrator stimulation on skull bone (bone conduction auditory stimulation), a major connection between the site of the bone vibrator and the inner ear is a fluid pathway. A series of experiments were conducted on pairs of animals (rats or guinea pigs). The cranial cavities of each pair of animals were coupled by means of a saline filled plastic tube sealed into a craniotomy in the skull of each animal. In response to bone conduction click stimulation to the skull bone of animal I, auditory nerve-brainstem evoked responses could be recorded in animal II. Various procedures showed that these responses were initiated in animal II in response to audio-frequency sound pressures generated within the cranial cavity of animal I by the bone conduction stimulation and transferred to the cranial cavity of animal II through the fluid in the plastic tube: they were not responses to air conducted sounds generated by the bone vibrator, were not induced in animal II by vibrations conveyed to it by the plastic tube and were not electrically conducted activity from animal I. Exposing the fluid in the tube to air was not accompanied by any change in threshold. These experiments confirm that during bone conduction stimulation on the skull, audio-frequency sound pressures (alternating condensations and rarefactions) can be conveyed by a fluid pathway to the cochlea and stimulate it.
Acoustic Stimulation↗
Semicircular canal fenestration - improvement of bone- but not air-conducted auditory thresholds.
Auditory stimulation can, under certain circumstances, activate the vestibular end organs and this is facilitated by fenestration of a semicircular canal (SCC). Several fenestrated profoundly deaf patients reported improvements in their bone- (BC) but not air-conducted (AC) thresholds. Bone conduction auditory thresholds have been reported to be better than normal in several patients with thinning or absence of bone over a SCC (dehiscence). This phenomenon was carefully studied in the fat sand rat (Psammomys obesus) by recording auditory brainstem evoked responses to BC and AC auditory stimulation, before and after SCC fenestration. Fenestration would be expected to decrease the pressure difference across the cochlear partition, causing a reduction in the amplitude of the classical base to apex input traveling wave, and should therefore lead to an elevation in AC and BC thresholds. Instead, BC thresholds decreased (i.e. improved) following fenestration (by 7.0+/-4.2 dB; P<0.005), while AC thresholds did not change. Thus the cochlea becomes more sensitive to BC, but not AC, stimulation in the presence of a SCC fenestration. This may be due to the removal by the fenestration of a factor impeding BC cochlear responses, or by the addition of a facilitating factor. The result that the SCC fenestration did not affect AC threshold provides support for the concept that at low intensities the outer hair cells are directly activated by components of the fluid pressures surrounding them, which alternate at audio-frequencies. These cochlear fluid audio-frequency pressures are induced by stapes footplate movement and not by a base to apex input traveling wave. The audio-frequency pressures would not be affected by SCC fenestration. The outer hair cell motility thus induced somehow excites the inner hair cells and the auditory nerve fibers. At low intensities the outer hair cell motility causes localized displacement at the appropriate position on the basilar membrane.
Acoustic Stimulation↗
Changes in the auditory nerve brainstem evoked responses in a case of maple syrup urine disease.
Maple syrup urine disease (MSUD) is a rare metabolic disease due to deficiency in the enzyme that breaks down branched chain amino acids. Lack of the enzyme causes accumulation of these amino acids and, if untreated, causes severe neurological damage. A case study of a 10-day old female infant, born after 40 weeks' gestation with a birthweight of 2740 g with MSUD hospitalized in the acute stage with respiratory failure and severe brain oedema is described. As part of the neurological evaluation, auditory nerve brainstem evoked response testing was conducted and revealed bilateral presence of the first wave from the auditory nerve, with no later brainstem waves. Over the course of days when her condition improved following dialysis treatment and a diet to reach balanced levels of branched chain amino acids, the later brainstem waves appeared on one side, and several weeks later they were also observed on the other side. The possible mechanisms of the reversibility of the appearance of brainstem waves in this case are discussed.
Acute Disease↗
New approach for implantable hearing aids: a feasibility study.
The objective of this study was to test the feasibility of a new kind of implantable hearing device based on a cerebrospinal fluid hydroacoustic pathway by which sound waves are conducted from the dura mater to the inner ear by cerebrospinal fluid. In this prospective animal study, a piezoelectric bimorph was implanted into 2 guinea pigs and 1 dog between the skull bone and the dura at the parietal area. The bimorph was connected transdermally by wires to a click generator. The auditory brain stem response was recorded after stimulation of the piezoelectric device by the click generator. In the 3 animals, the auditory brain stem response could be recorded in response to a stimulus intensity of 135 dB peak equivalent (pe) sound pressure level (SPL; instrument setting), corresponding to 3.8 V activating the device. The auditory brain stem response disappeared during white noise masking, proving that the origin of the response was in the inner ear. The threshold was 125 and 115 dB pe SPL in the 2 guinea pigs and 135 dB pe SPL in the dog (instrument setting). We conclude that transmission of sound waves by a cerebrospinal fluid hydroacoustic pathway to the inner ear is possible. Such a device would have advantages over more traditional implantable hearing devices: it would not be necessary to couple it to the ossicular chain, and it could be used in patients with infected middle ears.
Animals↗
Cochlear activation at low sound intensities by a fluid pathway.
In order to assess the mechanisms responsible for cochlear activation at low sound intensities, a semi-circular canal was fenestrated in fat sand rats, and in other experiments a hole was made in the bone over the scala vestibuli of the first turn of the guinea-pig cochlea. Such holes, which expose the cochlear fluids to air, provide a sound pathway out of the cochlea which is of lower impedance than that through the round window. This should attenuate the pressure difference across the cochlear partition and thereby reduce the driving force for the base-to-apex traveling wave along the basilar membrane. The thresholds of the auditory nerve brainstem evoked responses (ABR) and of the cochlear microphonic potentials were not affected in the fenestration experiments. In addition, holes in the scala vestibuli of the first turn did not cause ABR threshold elevations. These results contribute further evidence that at low sound intensities the outer hair cells are probably not activated by a base-to-apex traveling wave along the basilar membrane. Instead it is possible that they are excited directly by the alternating condensation/rarefaction fluid pressures induced by the vibrations of the stapes footplate. The activated outer hair cells would then cause the localized basilar membrane movement.
Acoustic Stimulation↗
Mechanisms responsible for postnatal middle ear amniotic fluid clearance.
Neonatal guinea pigs show signs of a temporary conductive hearing loss during the first few days after birth. It has been suggested that this is due mainly to the presence of amniotic fluid in the middle ear (ME) cavity at birth and its subsequent clearance. This study was designed to try to identify the mechanisms responsible for the amniotic fluid clearance from the ME after birth by means of several experiments in guinea pigs. The osmolarity of the blood, amniotic fluid and the fluid in the ME cavity of guinea pig fetuses was measured. Serum and normal saline were introduced into the ME of older animals and fluid clearance was monitored short- and long-term by microscopic observation, tympanometry and estimation of residual fluid. Following instillation of 1/5 normal saline and normal saline into the ME cavity, the osmolarity of the remaining fluid was determined, short- and long-term. Clear osmotic pressure gradients were found between amniotic fluid (low pressure), fetal blood (higher pressure) and the fluid in the fetal ME (intermediate between them). The MEs into which normal saline had been introduced developed negative pressure and, over several days, were cleared of fluid. When serum was applied, ME pressure remained close to atmospheric and the fluid was not cleared. Hypotonic saline application led to an increase in the osmotic pressure in the fluid remaining in the ME. It is concluded that most of the amniotic fluid is cleared from the neonatal ME cavity by water outflow into the blood due to osmotic pressure gradients.
Acoustic Impedance Tests↗
The effect of hydrogen peroxide applied to the middle ear on inner ear function.
OBJECTIVES/HYPOTHESIS: The objective was to assess the effect of hydrogen peroxide applied to the middle ear on cochlear and vestibular function. STUDY DESIGN: Prospective animal study. METHODS: Sand rats underwent a right-side total labyrinthectomy, and a polyethylene tube was inserted into the left-side middle ear. Following baseline recordings of vestibular evoked potentials in response to linear acceleration stimuli and auditory brainstem response, each experimental animal received five daily applications of hydrogen peroxide into the left-side middle ear. Two control groups received saline and gentamicin, respectively. Subsequently, recordings were repeated and compared with baseline measurements. RESULTS: Saline administration affected neither vestibular evoked potentials nor auditory brainstem response. In contrast, both responses could not be recorded following gentamicin application. After hydrogen peroxide administration, auditory brainstem response could not be recorded in 25% (3 of 12) of the animals, whereas in the remaining nine animals the average auditory brainstem response threshold was significantly elevated by 55 dB (P =.000002). Linear vestibular evoked potentials could not be recorded in 42% (5 of 12) of the animals. CONCLUSION: It appears that topical hydrogen peroxide adversely affects both cochlear and vestibular function of the sand rat. The study demonstrated the effect of a reactive oxygen species on inner ear function and may be useful in the study of mechanisms responsible for this damage and its protection. Clinically, although an animal model was used in the present study, caution should be exercised when large amounts of hydrogen peroxide are applied to a dry, perforated ear.
Administration, Topical↗
The differential vulnerability of the inner ear end-organs to several external factors.
In a number of recently conducted animal studies, the effect of various external factors such as ototoxic substances, different types of noise and systemic disease on the different end-organs of the inner ear has been investigated. These studies are distinguished by the use of short latency vestibular evoked potentials (VsEPs) (to both linear and angular acceleration), an objective method for directly assessing the function of the different vestibular end-organs. In addition, the well known auditory brainstem response (ABR) was used to assess cochlear function. The studies are reviewed and it appears that the general pattern of effect is as follows: ABR (cochlea) is the most sensitive to the various external factors; angular VsEPs (semicircular canals) the least sensitive; linear VsEPs (otolith organs) intermediate between them.
Diabetes Complications↗
Use of ABR threshold and OAEs in detection of noise induced hearing loss.
OBJECTIVE: To determine which measure is the most sensitive to noise induced hearing loss (NIHL): auditory nerve brainstem response (ABR), distortion product otoacoustic emission (DPOAE) or transient evoked otoacoustic emission (TEOAE), and how to assess possible changes in these responses. SUBJECTS & METHODS: Four groups of rats were exposed to various durations of 113 dB SPL broadband noise: 5 or 10 minutes (temporary changes in cochlear function), and 3 or 4 hours (permanent changes). Group means and data from individual animals were compared before and after exposure. RESULTS: Mean group DPOAE amplitude reduction showed no clear advantage over mean ABR threshold elevation in detection of temporary and permanent NIHL. Data from individual rats, however, indicated a clinical advantage for DPOAEs in detecting slight temporary, but not permanent, changes. TEOAEs were more sensitive in detecting changes in individual rats than as a group measure. CONCLUSIONS: TEOAE and DPOAE monitoring may improve detection of NIHL, though it should be used in conjunction with audiometric threshold monitoring.
Acoustic Stimulation↗
Analysis of visual evoked potentials and background electroencephalographic activity in young and elderly subjects.
OBJECTIVE: New techniques developed in this laboratory to overcome the loss of information involved in conventional evoked potential averaging are applied here to visual evoked potential (VEP) in young and elderly normal subjects. METHODS: The techniques are based on statistical descriptions of the times and amplitudes of the electroencephalographic deflections recorded before (background) and after (evoked) a series of pattern reversal visual stimuli. RESULTS: The elderly had a higher rate of background deflections at all electrode sites, but lower amplitudes at the occipital electrodes. The elderly had a lower rate of deflections during the period of evoked activity compared with the background period. The young had a higher degree of response deflection time locking and amplitude. The mean amplitude of the deflections recorded during the period of evoked activity was significantly greater in amplitude than the background deflections and greater than the amplitudes of the conventionally averaged VEP derived from the same data. Thus the lower amplitude VEPs seen in the elderly are due to their poor time locking and reduced amplification. Only 79% of the stimulus trials contributed deflections to the P1 response component in both young and elderly subjects and 63% to the N1. In young subjects, several of the new response parameters showed the presence of evoked response components that were not apparent in the conventionally averaged VEP derived from the same data. CONCLUSIONS: The novel methods presented here provide a great deal of additional information that is unavailable when analyzing data using only conventional evoked potential averaging.
Adolescent↗
The effect of noise exposure in the presence of canal fenestration on the amplitude of short-latency vestibular evoked potentials.
BACKGROUND: Exposure to high-intensity noise causes little, if any, reduction in vestibular function in normal animals as shown by short-latency vestibular evoked potentials (VsEPs). OBJECTIVE: To investigate the effect of noise exposure on VsEPs following fenestration of the horizontal semicircular canal. DESIGN AND METHODS: Psammomys obesus (fat sand rat) underwent labyrinthectomy in 1 ear, while the lateral semicircular canal in the other ear was fenestrated. Control VsEPs to linear acceleration (approximately 3g; rise time, approximately 1-2 milliseconds) were recorded immediately after the operation. The experimental group animals were then subjected to loud white noise (113-dB sound pressure level) for 1 hour. Immediately after the noise exposure in the experimental group animals, VsEPs were once more recorded. RESULTS: The VsEPs in the experimental group animals were significantly reduced immediately following the noise exposure, while there was no change in the recordings from the control group animals (fenestrated but not noise exposed; noise exposed but not fenestrated), even though the noise exposure induced a mean 47-dB threshold elevation of the auditory brainstem response. CONCLUSIONS: The presence of the fenestration caused the vestibular end organs to become vulnerable to noise exposure. The fenestration may create a pathway enabling pressure release through the vestibular end organs during noise exposure, thus increasing the possibility of damage to the vestibular end organs. This did not occur in the intact, nonfenestrated animals.
Analysis of Variance↗
Lateralization during the Weber test: animal experiments.
OBJECTIVES/HYPOTHESIS: The objective of this study were to present an assessment of a new theory to explain lateralization during the Weber test using an animal model. This theory is based on the discovery that a major pathway in bone conduction stimulation to the inner ear is through the skull contents (probably the cerebrospinal fluid [CSF]). The placement of a bone vibrator or tuning fork on the skull excites the inner ear by the classic osseous pathway and by the suggested CSF pathway. We assume that there is a phase difference between the stimulation mediated by the ossicular chain (inertial and occlusion mechanisms) and the one mediated by the CSF. The presence of a conductive pathology will decrease the magnitude of the sound energy mediated by the ossicular chain. Thus, the out-of-phase signal arriving through the bony pathways will be decreased, hence increasing the resultant sound intensity stimulating the cochlea. STUDY DESIGN: Prospective animal study. METHODS: The experiment was performed on 10 fat sand rats, which had undergone unilateral cochleostomy and a small craniotomy. The auditory nerve brainstem response (ABR) thresholds were measured to air-conducted stimulation, to stimulation with the bone vibrator applied to the skull, and to stimulation with the bone vibrator applied directly to the brain through the craniotomy. The ossicular chain of the second ear was then fixed to the middle ear walls with cyanoacrylate glue to induce a conductive hearing loss. The ABR thresholds to the same three stimuli were then measured again. RESULTS: After ossicular chain fixation, the ABR threshold to air-conducted stimulation increased, to bone vibrator stimulation on the bone decreased (hearing improvement), and to bone vibrator stimulation directly on the brain remained unchanged. CONCLUSIONS: This experiment confirms the proposed theory. During clinical bone conduction stimulation, there is a phase difference between sound energy reaching the inner ear through the middle ear ossicles and from the CSF. A middle ear conductive pathology removes one of these components, thus increasing the effective sound intensity in the affected ear. On the other hand, when the bone vibrator is applied on the brain, the inner ear is stimulated only through the CSF, so ossicular chain fixation does not change the ABR threshold. Moreover, this study proves that lateralization during the Weber phenomenon is the result, at least in part, of an intensity difference between sound energy reaching the two cochleae.
Acoustic Stimulation↗