[Effects of strong whole body vibration on cochlear microphonics of the internal ear].
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Action Potentials↗
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Cochlear potentials in the study of cochlear physiology.
Cochlear potentials have been used for many years as probes of cochlear mechanics. Early studies of cochlear microphonics addressed the pattern of wave motion and linearity of the basilar membrane motion. Since the development of techniques to record from single receptor cells and sensory neurons, these potentials have also been used in studies of the mechanics. Although techniques exist for recording cochlear mechanical motion directly, cochlear potentials can be powerful supplements, since the methods used cause minimal damage to the cochlea and can be applied throughout the cochlear spiral. Unlike existing direct methods, cochlear potentials can be used to characterize the micromechanics of the organ of Corti.
Animals↗
Electrophysiological correlates of progressive sensorineural pathology in carboplatin-treated chinchillas.
Carboplatin produces progressive damage to auditory nerve fibers, spiral ganglion neurons (SGNs) and inner hair cells (IHC) in the chinchilla cochlea but leaves outer hair cells intact. Within 1 h after injection, many afferent terminals beneath IHCs and myelin lamellae surrounding SGN processes are vacuolated. One day after injection, approximately half of the nerve fibers are missing. IHCs are intact at 2 days, but 20-30% are missing at 3 days. We studied the electrophysiological correlates of this progressive morphological damage by recording cochlear microphonics (CM), distortion product otoacoustic emissions (DPOAE), summating potentials (SP), compound action potentials (CAP) and midbrain evoked potentials (IC-EVP) before and 1 h, 12 h, 1 days, 3 days, 5 days, 7 days and 14 days after carboplatin injection (75 mg/kg IP) in four chinchillas. CM and DPOAEs tended to be unchanged or enhanced. CAP and SP showed little change until Day 3, when amplitudes were reduced in all animals and CAP thresholds were elevated by 9 dB; amplitudes declined further between Days 3 and 5 but not thereafter. IC-EVP amplitudes decreased on Days 3 or 5 but thresholds were relatively unchanged. All animals showed some recovery of IC-EVP between Days 7 and 14, including one with 70% enhancement on Day 14. The results indicate that threshold and amplitude measures fail to detect peripheral pathology until some relatively high threshold level of damage has been exceeded. This has important implications for monitoring peripheral damage and interpreting electrophysiological test results in animals and humans.
Acoustic Stimulation↗
Cochlear microphonics in Ménière's disease.
The pathophysiology of hearing deterioration in Ménière's disease (MD) is unclear. Hair cell loss has been proposed to be the cause of severe hearing loss in Ménière's disease. The cochlear microphonic (CM) is known to be the receptor potential of the outer hair cells in the cochlea. This study measured the CM in Ménière's disease and investigated its relationship with the degree of hearing impairment and endolymphatic hydrops. Transtympanic electrocochleography (ECoG) using rarefaction (RAR) and condensation (CON) tonebursts at 1 kHz was performed on 130 ears of 119 patients. Ninety six ears were diagnosed to have MD and 34 were diagnosed non-Ménière's disease (NMD). The mean amplitude of the CM was 33.10 +/- 46.04 microV in the MD group and 13.15 +/- 12.77 microV in the NMD group (p < 0.001). Enlarged negative summating potential and action potential ratios (SP:AP > 40%) were found in 81.3% of the MD group and 17.6% of the NMD group. In the MD group, the CM in the group with an enlarged negative SP was 36.98 +/- 49.78 microV, and 16.31 +/- 15.88 microV in the group without (p < 0.01). The CM was 34.33 +/- 49.28 microV in the pure-tone average (PTA) < or = 25 dB group, 46.97 +/- 58.31 microV in the 26-40 dB group, 29.12 +/- 42.62 microV in the 41-70 dB group, and 26.20 +/- 22.41 microV in the > 70 dB group (p > 0.05). The CMs in 11 pairs of MD ears and sensorineural hearing loss (SNHL) ears with matching hearing (MD 44 dB, SNHL 45 dB) were measured. They were 71.42 +/- 75.94 microV and 7.90 +/- 5.89 microV, respectively (p < 0.01). Our study shows that the CM is higher in ears with endolymphatic hydrops, evidenced by an enlarged SP:AP ratio, than ears without and the CM shows no statistical difference in groups with different levels of hearing loss. These findings suggest that hearing loss with a large CM in Ménière's disease patients may be the result of an alteration of cochlear mechanics and only severe hearing loss with a small CM is caused by hair cell loss. The CM measurement, to evaluate the hair cell status, may be helpful in identifying patients whose hearing may be recoverable if the underlying hydrops can be corrected. Our data do not permit the conclusion that an enlarged CM can be used in the diagnosis of MD.
Adult↗
Cochlear implantation in patients with auditory neuropathy of varied etiologies.
OBJECTIVES/HYPOTHESIS: Auditory neuropathy is a relatively recently described pattern of hearing loss characterized by preservation of outer hair cell function despite absent brainstem auditory evoked responses. Intact outer hair cell function is demonstrated by the presence of otoacoustic emissions and/or a measurable cochlear microphonic on electrocochleography, whereas no synchronous neural activity (absent action potentials) is seen on acoustically evoked brainstem auditory evoked response testing. The study reviews the authors' experience with six patients diagnosed with auditory neuropathy, four of whom have undergone cochlear implantation. MATERIALS AND METHODS: A retrospective review of all medical and audiological charts at the University of Virginia Hospitals (Charlottesville, VA) was performed to identify patients who have undergone cochlear implantation or have been diagnosed with auditory neuropathy, or both. RESULTS: Six patients with hearing loss attributable to auditory neuropathy were identified, four of whom have undergone cochlear implantation. Causes varied, including congenital, infectious, and idiopathic origins. Adults demonstrated subjective auditory perception on promontory stimulation, whereas no repeatable brainstem auditory evoked response waveforms could be demonstrated on pediatric promontory stimulation testing. Patients with implants demonstrated implant-evoked brainstem auditory evoked responses and improved audiological performance. CONCLUSIONS: The six cases presented in the study represent varied causes and, probably, varied sites of lesions of auditory neuropathy. Promontory stimulation has been valuable, particularly in adults. Cochlear implantation allows the opportunity to provide a supraphysiological electrical stimulation to the auditory nerve, with the hope of reintroducing synchronous neural activity. Greater confidence and enthusiasm for cochlear implantation in appropriately selected patients with auditory neuropathy are gained through experience with such diverse cases.
Adult↗
Hereditary auditory, vestibular, motor, and sensory neuropathy in a Slovenian Roma (Gypsy) kindred.
Members of a Roma (Gypsy) family with hereditary motor and sensory peripheral neuropathy (HMSN) and concomitant auditory and vestibular cranial neuropathies were identified in Kocevje, Slovenia. The illness begins in childhood with a severe and progressive motor disability and the deafness is delayed until the second decade. There are no symptoms of vestibular dysfunction. The family structure is consistent with an autosomal recessive pattern of inheritance and the genetic locus for the disorder is linked to the same region of chromosome 8q24 as other Roma families with HMSN and deafness from Lom, Bulgaria (HMSN-Lom). The present study shows that the deafness is caused by a neuropathy of the auditory nerve with preserved measures of cochlear outer hair cell function (otoacoustic emissions and cochlear microphonics) but absent neural components of auditory brainstem potentials. The hearing loss affects speech comprehension out of proportion to the pure tone loss. Vestibular testing showed absence of caloric responses. Physiological and neuropathological studies of peripheral nerves were compatible with the nerve disorder contemporaneously affecting Schwann cells and axons resulting in both slowed nerve conduction and axonal loss. Genetic linkage studies suggest a refinement of the 8q24 critical region containing the HMSN-Lom locus that affects peripheral motor and sensory nerves as well as the cranial auditory and vestibular nerves.
Acoustic Stimulation↗
Intracochlear perfusion of pneumolysin, a pneumococcal protein, rapidly abolishes auditory potentials in the Guinea pig cochlea.
OBJECTIVE: Bacterial meningitis and chronic suppurative otitis media caused by Streptococcus pneumoniae are associated with considerable otological morbidity. Specifically, sensorineural hearing loss is a permanent sequela in a third of those who contract pneumococcal meningitis. Pneumolysin, a pneumococcal protein, has been implicated as one of the main virulence/cytotoxic factors. Its pathogenicity is intimately dependent on an ability to form transmembrane pores on binding with cholesterol in target tissues. MATERIAL AND METHODS: We perfused wild-type pneumolysin, at a number of different concentrations, into the guinea pig cochlea and used electrocochleography to characterize the effects of this cytolytic exotoxin in the organ of Corti. RESULTS: Intracochlear perfusion of pneumolysin (10 microg/50 microl) reduced the compound action potential of the auditory nerve within seconds. The cochlear microphonics (f1=8 kHz, f2=9.68 kHz) and their distortion product (2f1-f2) were also reduced, albeit in a slightly less dramatic fashion. At lower concentrations (1 microg/50 microl), a selective and earlier effect on inner hair cells was observed. CONCLUSIONS: These results clearly show that significant ototoxicity ensues when sensory cells of the organ of Corti are exposed to pneumolysin (and complete cochlear death when the concentration is high enough). Toxicity is dose-dependent and appears to be site-sensitive. This may have implications for any possible future protective strategies against pneumococcal disease in the ear.
Acoustic Stimulation↗
Case of recurrent, reversible, sudden sensorineural hearing loss in a child.
This paper describes audiologic, electrophysiologic, and medical test results for a now 10-year-old girl who has had 45 episodes of reversible, sudden sensorineural hearing loss over the last 8 years. Episodes have lasted from 6 to 72 hours and often have been accompanied by a mild illness. Acoustic immittance measures have been consistent with normal middle-ear function with the exception of absent ipsilateral and contralateral acoustic reflexes. Mechanically evoked perioral reflex activity was markedly asymmetric following lower lip stimulation. The asymmetry of R1 activation between right and left side lower lip inputs raises questions about the integrity of central connections within the brain stem, including internuncial pathways coursing between trigeminal sensory relay nuclei and the facial motor nucleus. An electrocochleographic evaluation revealed cochlear microphonic but absent or markedly abnormal whole nerve action potentials. Auditory brainstem responses (ABR) have been either absent or poorly formed and significantly delayed, regardless of hearing sensitivity. Middle and late auditory evoked potentials were essentially normal. Both transient-evoked and distortion-product otoacoustic emissions were present regardless of peripheral auditory sensitivity. All medical tests have been essentially normal. Although no definitive diagnosis has been reached, beta blockers have been used with some success. Taken together, these data document a very unusual case of fluctuating hearing loss. The electrocochleographic and otoacoustic emission data suggest that the outer hair cells are functioning normally and that the loss is not cochlear in origin.(ABSTRACT TRUNCATED AT 250 WORDS)
Audiometry, Evoked Response↗
Auditory neuropathy in systemic sclerosis: a speech perception and evoked potential study before and after cochlear implantation.
We report the results of speech perception and electrophysiological evaluation of the auditory periphery performed before and after cochlear implantation in a 18-year-old girl with systemic sclerosis (SS) who presented the clinical picture of auditory neuropathy. Transtympanic electrocochleography (ECochG) in response to 0.1 ms clicks was recorded 1 month before cochlear implantation on both sides while the electrically evoked neural response was obtained intraoperatively in the right ear through cochlear implant stimulation. The ECochG recordings revealed the presence of the cochlear microphonic with normal amplitude and threshold on both sides. A compound action potential was only detected in the left ear at high stimulation intensity, while the electrically evoked neural response was clearly identifiable at all the recording sites during neural response telemetry. Standardized speech perception tests were performed 1 month before cochlear implantation and several times after cochlear implant connection. Speech perception scores were close to chance before cochlear implantation while they showed a remarkable improvement thereafter. The results of this study show that subjects affected by SS could present the clinical picture of auditory neuropathy which is possibly underlain by lesions involving the distal portion of auditory nerve fibers and/or synapses with inner hair cells. The restoration of synchronous neural discharge could be achieved by electrical stimulation through cochlear implant.
Adolescent↗
Contribution of BK Ca2+-activated K+ channels to auditory neurotransmission in the Guinea pig cochlea.
Large-conductance calcium-activated potassium (BK) channels are known to play a prominent role in the hair cell function of lower vertebrates where these channels determine electrical tuning and regulation of neurotransmitter release. Very little is known, by contrast, about the role of BK channels in the mammalian cochlea. In the current study, we perfused specific toxins in the guinea pig cochlea to characterize the role of BK channels in cochlear neurotransmission. Intracochlear perfusion of charybdotoxin (ChTX) or iberiotoxin (IbTX) reversibly reduced the compound action potential (CAP) of the auditory nerve within minutes. The cochlear microphonics (CM at f1 = 8 kHz and f2 = 9.68 kHz) and their distortion product (DPCM at 2f1-f2) were essentially not affected, suggesting that the BK specific toxins do not alter the active cochlear amplification at the outer hair cells (OHCs). We also tested the effects of these toxins on the whole cell voltage-dependent membrane current of isolated guinea pig inner hair cells (IHCs). ChTX and IbTX reversibly reduced a fast outward current (activating above -40 mV, peaking at 0 mV with a mean activation time constant tau ranging between 0.5 and 1 ms). A similar block of a fast outward current was also observed with the extracellular application of barium ions, which we believe permeate through Ca2+ channels and block BK channels. In situ hybridization of Slo antisense riboprobes and immunocytochemistry demonstrated a strong expression of BK channels in IHCs and spiral ganglion and to a lesser extent in OHCs. Overall, our results clearly revealed the importance of BK channels in mammalian cochlear neurotransmission and demonstrated that at the presynaptic level, fast BK channels are a significant component of the repolarizing current of IHCs.
Acoustic Stimulation↗
Origin of the receptor potential in inner hair cells of the mammalian cochlea--evidence for Davis' theory.
The primary sensory hair cells of the mammalian cochlea are located in the organ of Corti, a sensory epithelium which separates fluids of widely differing chemical composition. The apical, sensory surfaces of the hair cells are exposed to the potassium-rich endolymph of the scala media and their lateral and ventral surfaces are exposed to the perilymph of the scala tympani whose chemical composition resembles that of other extracellular fluids. The high potassium concentration of the endolymph (150 mM) is believed to result from the activity of electrogenic potassium pumps located in the stria vascularis which lines the lateral walls of the cochlea. These pumps are also the source of the positive endocochlear potential of about +80 mV which can be recorded from the scala media. When the ear is stimulated with sound, receptor potentials may be recorded extracellularly from the fluid-filled spaces of the cochlea, and intracellularly from the rows of inner and outer hair cells. According to the 'resistance microphone' theory of Davis, these receptor potentials are derived from the pre-existing polarization of the hair cells by a change in the ohmic resistance of the mechanosensitive portion of the cell membrane (Fig. 1). This procedure potential changes in the scala tympani and scala media of opposite phase, thus giving rise to the cochlear microphonic (CM). Evidence is presented here to support this theory. When sufficient depolarizing current is injected into inner hair cells to cancel the polarizing voltage, the receptor potentials disappear, and their phase is reversed when the polarizing voltage across the apical membranes of the hair cells is reversed.
Acoustic Stimulation↗
Cochlear function in mice with only one copy of the prestin gene.
Targeted deletion of the prestin gene reduces cochlear sensitivity and eliminates both frequency selectivity and outer hair cell (OHC) somatic electromotility. In addition, it has been reported by Liberman and colleagues that F2 generation heterozygotes exhibit a 6 dB reduction in sensitivity, as well as a decrease in protein and electromotility. Considering that the active process is non-linear, a halving of somatic electromotility would be expected to produce a much larger change in sensitivity. We therefore re-evaluated comparisons between heterozygotes and wildtype mice using both in vivo and in vitro electrophysiology, as well as molecular biology. Data reported here for F3-F5 generation mice indicate that compound action potential thresholds and tuning curves, as well as the cochlear microphonic, are similar in heterozygotes and wildtype controls. Measurements of non-linear capacitance in isolated OHCs demonstrate that charge density, as well as the voltage dependence and sensitivity of motor function, is indistinguishable in the two genotypes, as is somatic electromotility. In addition, both immunocytochemistry and western blot analysis in young adult mice suggest that prestin protein in heterozygotes is near normal. In contrast, prestin mRNA is always less than in wildtype mice at all ages tested. Results from F3-F5 generation mice suggest that one copy of the prestin gene is capable of compensating for the deleted copy and that heterozygous mice do not suffer peripheral hearing impairment.
Animals↗
Development of early auditory-evoked responses in the cat.
The post-natal development of the auditory-evoked responses to 1- and 4-kHz tone bursts has been studied in the cat with subcutaneous electrodes and signal-averaging techniques. A cochlear microphonic response antedates the earliest appearance of brain stem potentials by 1 or 2 days, and can be recorded in some animals on the first post-natal day with the 4-kHz stimulus. The earliest brain stem response consists of three or four low-voltage waves,which increase to six in the 2nd week. Latency shortening and amplitude growth occur for all waves, but are most pronounced in the later part of the response. The characteristics of the summating potential, and the variable influence of rate effects on wave amplitude are described for the different age-groups.
Acoustic Stimulation↗
Mechanism of the short-term poststimulatory depression of the cochlear microphonics (hysteresis).
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Animals↗
Protective effects of phenyl-N-tert-butylnitrone on the potentiation of noise-induced hearing loss by carbon monoxide.
Free radical injury has been implicated in cochlear damage resulting from exposure to high-intensity noise and due to carbon monoxide (CO) hypoxia. Although exposure to noise plus CO is common in occupational settings and noise-induced hearing loss (NIHL) is enhanced in the presence of CO, potential mechanisms resulting in auditory impairment have not been studied. This study evaluates protective effects of the free radical scavenger phenyl-N-tert-butylnitrone (PBN) against potentiation of NIHL by CO. Three PBN administration protocols have been evaluated in subjects exposed to noise plus CO or noise alone. Long Evans hooded rats were exposed to octave band noise at 100 dB(Lin), center frequency (cf) = 13.6 kHz for a duration of 2 h. The level of CO used was 1200 ppm. Endpoints used to detect permanent auditory impairment were compound action potential (CAP) threshold and 1 microV root mean square (RMS) cochlear microphonic (CM). Testing was done 4 weeks following exposure. PBN administration prior to and following simultaneous exposure provided significant protection against auditory impairment in subjects receiving noise plus CO. Partial protection was observed in the protocols where PBN was injected following noise plus CO exposure. PBN administration appeared to reduce auditory impairment in animals exposed to noise alone, but the difference was not found to be statistically significant. Protective effects of PBN following simultaneous exposure to noise plus CO suggest that free radicals may be generated during combined exposure.
Animals↗
[Cochlear Implant Mini-System 22 for the management of deaf preschool children].
The long-term reliability and the overall good results achieved with cochlear implants in adults have led us to consider whether this method could also be applied in small children. This though was supported by the work of House, who has been providing children with cochlear implants for many years, although using a monochannel device with only one electrode, which is inserted only a few millimetres into the scala tympani. Our considerations were also prompted by technical progress which has resulted in the so-called Mini System 22. In this system, the implant is only 6 mm thick with a speech processor of a mere 9 x 6 x 1.9 cm and weighs not more than 100 g. From the point of view of the surgical technique, small children do not present any specific difficulties, except for the necessity of fixing the array of electrodes as closely as possible to the cochlea, in order to avoid its slipping out of the cochlea during skull growth. Positive results with single reimplantations indicate that such patients will also be able to benefit from technical progress in future decades. To differentiate between inner ear and nerve deafness the promontory test has to be replaced by electrocochleography. This indicates a neural genesis of the hearing impairment in cases of cochlear microphonics of more than 50-60 nHL and possibly even a summation potential can be recorded. Additionally, we consider it mandatory to use objective parameters as a basis for the first tune-up of the speech processor.(ABSTRACT TRUNCATED AT 250 WORDS)
Audiometry, Evoked Response↗
On the derivative relationship between stapes movement and cochlear microphonic.
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Animals↗
[Effect of acetazolamide on the cochlear microphonics].
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Acetazolamide↗