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PubMed1991

Absence of both auditory evoked potentials and auditory percepts dependent on timing cues.

An 11-yr-old girl had an absence of sensory components of auditory evoked potentials (brainstem, middle and long-latency) to click and tone burst stimuli that she could clearly hear. Psychoacoustic tests revealed a marked impairment of those auditory perceptions dependent on temporal cues, that is, lateralization of binaural clicks, change of binaural masked threshold with changes in signal phase, binaural beats, detection of paired monaural clicks, monaural detection of a silent gap in a sound, and monaural threshold elevation for short duration tones. In contrast, auditory functions reflecting intensity or frequency discriminations (difference limens) were only minimally impaired. Pure tone audiometry showed a moderate (50 dB) bilateral hearing loss with a disproportionate severe loss of word intelligibility. Those auditory evoked potentials that were preserved included (1) cochlear microphonics reflecting hair cell activity; (2) cortical sustained potentials reflecting processing of slowly changing signals; and (3) long-latency cognitive components (P300, processing negativity) reflecting endogenous auditory cognitive processes. Both the evoked potential and perceptual deficits are attributed to changes in temporal encoding of acoustic signals perhaps occurring at the synapse between hair cell and eighth nerve dendrites. The results from this patient are discussed in relation to previously published cases with absent auditory evoked potentials and preserved hearing.

Acoustic Stimulation↗
PubMed1986

Effects of temperature and elevated intracranial pressure on peripheral and brain stem auditory responses in dogs.

Far-field recordings of central (P2 through P4) and peripheral (cochlear microphonic; and compound action potential of the eighth nerve) auditory responses were used to assess changes in auditory function resulting from elevated intracranial pressure. Normative data for eight dogs were obtained. The relationship between response latency and core temperature was examined. A mean slope of -0.17 ms/degrees C resulted for the temperature range of 35.0 to 40.0 degrees C. Systemic arterial pressure was measured in order to identify the cerebral ischemic response. Responses were not altered significantly unless the intracranial pressure approached within 15 to 30 mm Hg of mean systemic arterial pressure. Changes in the response consisted of both enhancement and deterioration during intracranial pressure elevation and were accompanied by increases in systemic arterial pressure during that elevation. Supernormal amplitudes of the action potential also occurred during recovery periods. Results suggest that: (i) during elevated intracranial pressure, changes in both central and peripheral auditory function result from ischemia rather than pressure-induced distortion of the cochlea or central neural assemblies. (ii) Far-field auditory responses may include an O2-dependent cochlear microphonic. (iii) An unknown process causing enhancement of central and peripheral neural responses exists and operates in connection with intracranial hypertension. Possible mechanisms underlying enhancement of response components are discussed.

Animals↗
PubMed1979

An investigation of the auditory frequency-following responses as compared to cochlear potentials.

Comparisons were made of cochlear microphonics (CM) and scalp recorded frequency-following responses (FFR) from chinchilla and human. The latency of the scalp/ear-lobe recorded FFR was found to be nearly zero with respect to CM. Further, auditory nerve action potential were noted to diminish rapidly after death whereas the CM component in FFR reduced gradually. The decay of the CM component of FFR measured at the scalp after death followed an identical time course to that of the CM at round window. These observation lead to the conclusion that FFR does not originate in the brain stem but is essentially cochlear potentials picked up by electrodes located at the scalp.

Action Potentials↗
PubMed1995

Neurotransmitters of the olivocochlear lateral efferent system: with an emphasis on dopamine.

The olivocochlear lateral efferent system (OLES) of the adult mammalian cochlea uses variety of neuroactive substances, such as acetyl choline, GABA, dopamine (DA), enkephalins, dynorphins and CGRP. These neuroactive substances have been located within the efferent, small and dense matrix, fibers and terminals of the inner spiral and tunnel bundles. However, some of these neuroactive substances have also been found outside the OLES. Acetyl choline and CGRP, for instance, appear within the olivocochlear medial efferent fibers, and DA and CGRP may also be present in the perivascular innervation. A special case is GABA innervation at the apical coil, where nerve fibers containing GABA also make synapses with OHCs bodies. All these substances of the OLES could be involved in a highly selective filter modulating the activity of primary afferent fibers. For instance, sound stimulation results in an increase of cochlear DA turnover, indicating the release of DA from OLES fibers. DA probably acts on D-2 receptors since the administration of piribedil, a D-2 agonist, results in blocking of noise effects, while D-1 receptor stimulation does not modify cochlear DA turnover induced by noise. Therefore, DA could play an important role in the modulation and noise-protection of cochlear primary afferents. During cochlear development, all the aforementioned neuroactive substances appear a long time before the onset of hearing (evidenced by the recording of cochlear compound action potential and microphonic potentials). Thus, they may act during development on the late reorganization and plasticity on the afferent and efferent fibers. Moreover, the positive neurotrophic effect observed in cultured cochlear neurons, with GABA or glutamate, add new support to that hypothesis.

Acetylcholinesterase↗
PubMed1987

Preservation of cochlear potentials in a deaf patient fifteen months after excision of an acoustic neuroma.

Intraoperative electrocochleographic monitoring has been used in an attempt to protect cochlear nerve function during acoustic neuroma excision. One patient is presented with an apparently intact cochlear nerve and waves N1 and N2 preserved at the end of surgery, but no hearing on subsequent testing. Fifteen months after operation, cochlear microphonics and the summating potential were still present, but N1 and N2 had disappeared. There had been no improvement in her hearing and there were no consistent brainstem auditory evoked potentials on the affected side. A possible explanation for these findings is given.

Adult↗
PubMed1981

Effect of anesthesia on maximal cochlear microphonics.

During prolonged periods of pentobarbital anesthesia (6-8 h), cochlear microphonics (CM) in cats became reduced by approximately 6 dB, but only in the region of maximal responses ("truncation"). For the following reasons, this change is held to be neurally mediated, specifically by an impairment of the olivocochlear bundle (OCB): (1) Its onset coincided with the disappearance of efferent action potentials, normally superimposed on low-frequency CM. (2) OCB stimulation augments CM by approximately 6 dB, once more only in the region of maximal responses [4]. (3) Sectioning of the OCB reduces maximal CM responses [8]. (4) Truncation was produced by two neural blocking agents, azide and DFP [10], most likely also resulting from OCB impairments. (5) At the high input levels required to produce maximal responses, CM ought to become slightly elevated by acoustically-evoked OCB activity. This elevation should cease to occur on impairment of OCB under the effect of pro-longed anesthesia; thus there would be an apparent truncation.

Anesthetics↗
PubMed1985

A comparative study of the physiological properties of the inner ear in Doppler shift compensating bats (Rhinolophus rouxi and Pteronotus parnellii).

Cochlear microphonic (CM) and evoked neural (N-1) potentials were studied in two species of Doppler shift compensating bats with the aid of electrodes chronically implanted in the scala tympani. Potentials were recorded from animals fully recovered from the effects of anesthesia and surgery. In Pteronotus p. parnellii and Rhinolophus rouxi the CM amplitude showed a narrow band, high amplitude peak at a frequency about 200 Hz above the resting frequency of each species. In Pteronotus the peak was 25-35 dB higher in amplitude than the general CM level below or above the frequency of the amplitude peak. In Rhinolophus the amplitude peak was only a few dB above the general CM level but it was prominent because of a sharp null in a narrow band of frequencies just below the peak. The amplitude peak and the null were markedly affected by body temperature and anesthesia. In Pteronotus high amplitude CM potentials were produced by resonance, and stimulated cochlear emissions were prominent in Pteronotus but they were not observed in Rhinolophus. In Pteronotus the resonance was indicated by a CM afterpotential that occurred after brief tone pulses. The resonance was not affected by the addition of a terminal FM to the stimulus and when the ear was stimulated with broadband noise it resulted in a continual state of resonance. Rapid, 180 degree phase shifts in the CM were observed when the stimulus frequency swept through the frequency of the CM amplitude peak in Pteronotus and the frequency of the CM null in Rhinolophus. These data indicate marked differences in the physiological properties of the cochlea and in the mechanisms responsible for sharp tuning in these two species of bats.

Anesthesia, General↗
PubMedDate not supplied

Ototoxicity of ethanol in the tympanic cleft in animals.

This work was undertaken to study the ototoxicity of topically applied ethanol in quantitative terms. Using guinea pigs, ethanol was administered (1) on the round window for 10 min, (2) instilled in the middle ear cavity for 24 hours, and (3) perfused into the cochlear canal (into the scala tympani) at the rat of 10 microliter/min for 10 min. Cochlear microphonics from the electrode on the round window were recorded. The critical concentration (the maximum dilution ratio) of the ethanol that appears to be ototoxic in the experimental condition mentioned above was determined to be (1) 50%, (2) 10%, (3) 0.1% respectively. Using chinchillas, the effect of ethanol with round window application on the Endocochlear Potential (EP) was studied. Simultaneous recording of EP from the 1st and 3rd turn of the cochlea showed a more marked decline in EP in the 1st turn. 70% ethanol caused an irreversible, plateauing decline in EPO, while 35% ethanol caused a reversible decline in EP.

Action Potentials↗
PubMed2002

Transtympanic electrocochleography: a 10-year experience.

OBJECTIVE: To report the authors' experience with transtympanic electrocochleography during the past 10 years. STUDY DESIGN: Retrospective case review. SETTING: Otology/neurotology referral center. PATIENTS: Transtympanic electrocochleography was performed on 2,421 ears of 2,140 patients from May 1990 to April 2000. INTERVENTION: Clicks and tonebursts were used in electrocochleography testing. Summating potential/action potential ratio was calculated. Action potential latency shift by rarefaction and condensation clicks was measured. Cochlear microphonic was recorded. MAIN OUTCOME MEASURE: An enlarged summating potential/action potential ratio (>0.40), broadened action potential waveform (>3 msec) or prolonged action potential latency shift (>0.2 msec) was considered to be indicative of endolymphatic hydrops. The presence of cochlear microphonic indicated hair cell survival. RESULTS: In response to clicks, an enlarged summating potential/action potential ratio was found in 76.1% of ears and a broadened action potential waveform in 70%. Either an enlarged summating potential/action potential ratio or a broadened action potential waveform was observed in 78.4% of ears. In response to tonebursts, an enlarged summating potential/action potential ratio was found in 64.8%. The combined use of clicks and tonebursts yielded an enlarged summating potential/action potential ratio in 81.7%. Electrocochleography using tonebursts had the advantage of frequency selectivity. A prolonged action potential latency shift was found in 62.2% of ears with Ménière's disease. A significant association between an enlarged summating potential/action potential ratio and an action potential latency shift was noted (chi = 5.357, p = 0.021). An enlarged summating potential/action potential ratio was found 71% in Stage 1 of Ménière's disease, 82% in Stage 2, 85% in Stage 3, and 90% in Stage 4 (chi = 19.442, p = 0.000). An enlarged summating potential/action potential ratio was associated with the duration of the disease, 43% in the under 1-year group, and 100% in the more than 30-years group (chi = 33.555, p = 0.000). A large cochlear microphonic was present in 69% of ears with hearing levels greater than 40 dB. CONCLUSION: Transtympanic electrocochleography using clicks and tonebursts is a reliable test to detect the presence of endolymphatic hydrops in Ménière's disease. A prolonged action potential latency shift evoked by rarefaction and condensation clicks is a useful addition to the application of electrocochleography in the diagnosis of Ménière's disease.

Action Potentials↗
PubMed1997

Estimating mechanical responses to pulsatile electrical stimulation of the cochlea.

This study estimated the mechanical response of the cochlea to pulsatile electrical stimulation of the scala tympani of the cat. The auditory nerve compound action potential evoked by an acoustic probe was forward-masked by a train of charge-balanced biphasic current pulses. Masking as a function of probe frequency reflected the excitation pattern of the response to the masker and resembled the spectrum of the electrical stimulus. Both pulse rate and pulse width influenced the degree of masking. The vibration of a region of the basilar membrane was estimated by recording the local cochlear microphonic evoked by biphasic pulses. The amplitude of the cochlear microphonic was proportional to the amplitude of the spectral component of the electrical stimulus to which the local cochlear microphonic was tuned. These results are consistent with the generation of a mechanical response to the electrical stimulus.

Acoustic Stimulation↗
PubMedDate not supplied

Hearing loss in experimental cytomegalovirus infection of the guinea pig inner ear: prevention by systemic immunity.

Guinea pig cytomegalovirus (GPCMV) has been used to establish a reproducible model of viral labyrinthitis and hearing loss. Cochlear function was assessed by electrophysiological recordings of cochlear microphonic (CM) and eighth nerve N1 compound action potential (AP) thresholds prior to and up to eight days following inoculation of the scala tympani. Inner ear inoculation of seronegative subjects with live GPCMV produced profound elevations in CM and AP thresholds: 70% of these subjects had their thresholds raised to the limits of the sound system throughout the tested frequency range of 0.10 to 32 kHz. Histopathologic effects associated with CM and AP threshold shifts were primarily limited to the perilabyrinthine compartment, and were greatest in the most basal cochlear turns. Systemic infection with GPCMV produced an immune response, but did not affect CM or AP thresholds. Subsequent inoculation of the inner ear of these seropositive animals with live GPCMV did not result in either CM or AP threshold shifts, or cochlear histopathology. Inoculations of inactivated virus into the inner ears of seronegative and seropositive animals produced only moderate CM and AP threshold effects. Primary GPCMV labyrinthitis thus results in significant cochlear dysfunction and histopathologic changes which are prevented by prior systemic infection with GPCMV.

Animals↗
PubMed1987

Timing of spike initiation in cochlear afferents: dependence on site of innervation.

1. The phase of excitation of inner hair cells (IHCs) relative to basilar membrane motion has been estimated as a function of best frequency (BF) (or, equivalently, cochlear location) by recording responses to tones (100-1,000 Hz) from chinchilla cochlear afferent axons at their central exit from the internal auditory meatus. 2. The time of IHC excitation (i.e., the time of chemical transmitter release) was derived from the neural recordings at near-threshold levels by applying a correction for the latency of synaptic processes and the propagation time of action potentials. 3. The phase of basilar membrane motion at the appropriate innervation site was estimated on the basis of previously measured basilar membrane responses at a location close to the basal end of the cochlea and estimates of mechanical travel time from the basal end to the innervation site, derived from the neural latencies to intense rarefaction clicks, as a function of BF. 4. The derived near-threshold excitation of basal IHCs leads basilar membrane displacement toward scala tympani by approximately 40-60 degrees. 5. At BFs corresponding to midcochlear locations (2-6 kHz) there is an abrupt phase transition. The derived excitation for IHCs located at more apical locations (BFs large in relation to stimulus frequency) corresponds approximately to peak velocity of the basilar membrane toward scala vestibuli. 6. Although the derived response phases of apically located IHCs are consistent with intracellular recordings from IHCs, the derived near-threshold response phases of basal IHCs may be inconsistent with intracellular IHC recordings. 7. The foregoing results, based on responses of nearly 1,000 cochlear afferents to tones 100-1,000 Hz at near-threshold stimulus levels, amply confirm our previous conclusions that were based on a smaller sample of responses to very low frequency tones (less than or equal to 100 Hz): there is a spatial transition at midcochlear regions in the mode of excitation of IHCs, which does not seem to simply reflect the macromechanics of the basilar membrane. 8. It has been proposed that both the paradoxical response phases of high-BF afferents and the spatial phase transition arise from an influence of cochlear microphonics on the transmembrane potential of IHCs. The present results, which show that the spatial phase transition occurs for frequencies at least as high as 400 Hz, would appear to make such an electrical influence of outer hair cells on IHCs less likely. An alternative explanation might be that the phase transition has a mechanical basis, perhaps localized to micromechanical events in the subtectorial regio

Acoustic Stimulation↗
PubMed1975

[Clinical interpretation of microphonic potentials by electrocochleography].

The clinical electrocochleography essentially allows the registration of the global action potential of the acoustic nerve. The use of acoustic stimulations with alternating polarity eliminates the cochlear microphonics. In severe deafness, where no action potential can be registered, even not with maximal acoustic impulses, it can be interesting to register the microphonic potentials. This can be done by using acoustic stimulations with the same polarity. If some microphonic potentials can be registered by this technique, one can assume that the ciliated cells are -- at least partially -- unaffected and that the cause of the deafmess in neurogenic. This test thus allows a primary differentiation between sensory and neural deafness. Some clinical cases illustrate this phenomenon.

Action Potentials↗
PubMed1995

Effects of kanamycin ototoxicity and hair cell regeneration on the DC endocochlear potential in adult chickens.

High doses of aminoglycoside antibiotics cause massive damage to the avian basilar papilla. The resulting functional loss could conceivably arise from the reduction in the DC endocochlear potential (EP) due to impairment of the tegmentum vasculosum (TV) or to shunting of current through the damaged sensory epithelium. To test this hypothesis, the EP was measured in adult chickens after destroying hair cells in the basal half of the cochlea with a high dose (400 mg/kg per day for 10 days) of kanamycin (KM). KM treatment caused an increase in the steady-state EP from +18.1 to +23.3 mV and a decrease in the magnitude of the negative EP from -42.0 to -19.2 mV. The EP showed almost no change between 1 and 2 days and 1 week post-KM treatment. After 4 weeks of recovery, most hair cells had regenerated; however, the steady-state EP was still elevated by 13% and the negative EP was depressed by 37%. These results suggest that functional loss as shown by the large reduction in cochlear microphonic (CM) and the elevated thresholds of compound action potential (CAP) following KM treatment is not due to a reduction in the EP but may arise from functional deficits in the hair cells and/or the auditory nerve.

Animals↗
PubMed1979

Maintenance of cochlear function with artificial oxygen carriers.

By means of vascular perfusion via the anterior inferior cerebellar artery with a blood substitute containing the perfluorochemical FC 47 as oxygen carrier, it is possible to maintain normal or near normal levels of the cochlear microphonics and the endolymphatic potential of the guinea pig for perios of 90 min, or longer. Following 60 min. of perfusion with artificial blood, the levels of ATP and 5' AMP in the stria vascularis and the organ of Corti are comparable to those of nonperfused control animals maintained at optimal metabolic conditions. Following the same period of perfusion, the appearance of the organ of Corti is normal, but small vacuoles, presumably deposits of FC 47, are visible in the marginal cells of the stria vascularis. Preliminary experiments concerning the survival time and the revival time of the cochlear potentials, as well as the response to furosemide, ouabain, and mersalyl are presented to illustrate the value of this method in elucidating various biochemical and pharmacological problems of the cochlea.

Adenosine Monophosphate↗
PubMedDate not supplied

[Effects of aminoglycoside antibiotics on various structures of the acoustic analyzer].

Aminoglycoside antibiotics decrease the microphone potential amplitude and the auditory nerve potential in response to acoustic stimulation. These drugs suppress the bioelectrical activity of medulla, cerebral cortex, and olivo-cochlear efferent system. The experiments on freely moving cats showed that cortical response to electric stimulation of thalamocortical fibers originating from medial geniculate body are more sensitive to aminoglycoside antibiotics than the microphone potential and the auditory nerve potential.

Action Potentials↗
PubMed1999

Successful treatment of noise-induced cochlear ischemia, hypoxia, and hearing loss.

Cochlear blood flow (CoBF), perilymphatic partial pressure of oxygen (PL-pO2), cochlear microphonics (CMs), compound action potentials of the auditory nerve (CAPs), and auditory brainstem responses (ABRs) were studied in noise-exposed guinea pigs during and after the following treatments: intravenous infusion of isotonic saline (placebo); blood flow promoting drugs (hydroxyethyl starch = HES, pentoxifylline, betahistine, gingko biloba, naftidrofuryl); antiinflammatory agents (prednisolone, diclofenac sodium, histamine H1-receptor antagonist); isobaric oxygenation (IBO); and hyperbaric oxygenation (HBO) with and without supplements (simultaneous infusion of isotonic saline, pentoxifylline, prednisolone, or HES). It was found that PL-pO2 declined simultaneously with deterioration of CM, CAP, and ABR amplitudes after exposure to broad-band noise (bandwidth 1-12 kHz, 30 min, 106-dB SPL). CoBF decreased only 30 min after cessation of broad-band noise and progressed with cochlear hypoxia, while the hearing loss showed no further signs of deterioration and no recovery up to 3 h after exposure. Treatment (60 min) started 60 min after cessation of noise and was studied for a further 60 min. Isotonic saline did not influence the measuring parameters. Noise-induced cochlear hypoxia was compensated by IBO and more effectively by HBO with and without supplements, while other treatments had no sustained effect. A sustained therapeutic effect on noise-induced cochlear ischemia was achieved only by HES, HBO + HES, and pentoxifylline. However, the best therapeutic effect on noise-induced hearing loss was achieved with a combination of HBO and prednisolone, followed by monotherapy with prednisolone or HES with the result that not only did the CAPs and ABRs completely recover, the CMs also showed significant improvement, although full recovery did not occur. All other therapies were significantly less effective or did not improve noise-induced reduction of auditory evoked potentials.

Action Potentials↗
PubMed1994

The disconnected ear: phenomenological effects of a large acoustic tumor.

OBJECTIVE: To document the existence of a peripheral auditory disconnection syndrome in a 23-yr-old male with a large tumor of the right cerebellopontine angle using contemporary behavioral, electroacoustic, and electrophysiologic auditory tests. DESIGN: Single subject with repeated measures. RESULTS: In spite of a profound hearing loss in an ear with a large cerebellopontine angle tumor determined by behavioral audiometry, distortion product otoacoustic emissions, surface recorded brain stem auditory evoked potentials, and transtympanic electrocochleography (click evoked compound action potentials and tone evoked cochlear microphonics) demonstrated that the cochlea was intact and functional over a broad bandwidth and intensity range. CONCLUSIONS: A peripheral auditory disconnection syndrome is demonstrated in a 23-yr-old male with a large tumor of the cerebellopontine angle. In this instance, the tumor effectively deafferentated the peripheral from central auditory nervous system, resulting in profound hearing loss of presumed neural origin. It is suggested that other pathologic conditions/mechanisms could produce similar findings.

Adult↗