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Results for “Cochlear Microphonic Potentials”

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At least 181 records · Page 10Linked to original sources
PubMed1975

[Evoked response audiometry of the guinea pig before and after drop in hearing induced by furosemid (author's transl)].

Using particular surface electrodes evoked response audiometry (ERA) can be applied to small laboratory animals without any sedation or anaesthesia. In addition to other methods we have studied in this way the influence of extreme doses of Furosemid on the guinea pig inner ear. 6-20 mg Furosemid per 100 g of bodyweight (about 100 times the human therapy dose) were applicated i.v. within 5 min resulting in a drop of hearing immediately. For the anaesthesized animal the cochlear microphonic potentials (CM) decrease simultaneously, indicating Furosemid to act at the inner ear itself. By both methods recovery of inner ear function is seen to start about 10 min later according to the little biological half life of Furosemid. As being restricted in respect of time for the CM-measurements we are sure about reversibility only by the ERA-method.

Animals↗
PubMed1989

[Frequency-dependent cochlear microphonics in inner ear hearing loss with various pitch thresholds].

Promontory recordings of the cochlear microphonics (CM) after stimulation with 0.5, 1 and 2 kHz tone bursts at 120 dB SPL were performed on normal subjects and patients with various, levels of sensory hearing loss. A significant correlation was found between frequency-related CM amplitudes and the configuration of the pure-tone audiogram. Such recordings provide objective information on hearing abilities at low and middle frequencies and are thus a relevant tool in clinical audiometry.

Auditory Threshold↗
PubMed1986

[The promontory test and electrocochleography in deafness caused by mumps].

Contradictory histological findings in patients with deafness following mumps led us to conduct electrophysiological investigations. Promontory testing (PT) and measurement of cochlear microphonics (CM) enabled us to distinguish between neural and sensory deafness. On the basis of a careful history and serological tests in 19 cases of unilateral deafness we found that the hearing loss was probably caused by mumps. In all patients except one auditory sensations could be obtained by electric stimulation of the acoustic nerve whereas no CM were detectable even with strong stimuli of 100 dB tonepips. In view of the electrophysiological findings, doubt is cast on the neural genesis of deafness following mumps as assumed by Lehnhardt (1962).

Audiometry, Evoked Response↗
PubMed1992

Study of the effect of 350-Hz tone exposure on electrophysiological function of the inner ear of guinea pigs.

The effects of noise exposure were studied in fifty-nine 4- to 5-week-old albino Hartley guinea pigs with normal hearing (body weight 250-300 g). The following experiments and results were carried out: exposure to 350 Hz pure tones at 115 dB for 40 h and exposure to 350 Hz tones at 120 dB for 64 h. In order to investigate the effects of low-frequency tone exposures on the hearing of the guinea pigs, cochlear microphonics (CM), whole nerve action potentials (AP) and endocochlear potentials (EP) were measured. With a high-sound pressure, a decrease was observed in the CM maximum output voltage in the test frequencies of 2, 4 and 6 kHz while the CM threshold (pseudothreshold) of 6 kHz was elevated. Output voltage of the N1 potential of the AP using a 7-kHz tone burst decreased while the threshold of the N1 potential was elevated. An extension of latency and a decrease in the absolute value of the negative potential in EP were also observed.

Acoustics↗
PubMed1989

Correlative changes of auditory nerve and microphonic potentials throughout sleep.

Gross cochlear potentials in response to alternating clicks and pure tone bursts were recorded in guinea-pigs with chronically implanted electrodes in the round window during sleep and the awake state. A significant increase in both averaged potentials, the compound auditory nerve action potential (cAP) and cochlear microphonics (CM) occurred in slow wave sleep (SWS) with a subsequent diminution in paradoxical sleep (PS) periods. The cAP, CM, amplitude and area averages were similar during quiet wakefulness and in PS. Moreover, as an episode of PS progressed, the recorded potentials continued to decrease. On the other hand, increased averaged values were again observed during a subsequent episode of SWS. An involvement of the efferent olivo-cochlear bundle is postulated, first, because it is the only known pathway connecting the CNS and the auditory periphery and, second, because several key pre-receptor variables (middle ear muscles and ossicles and sound-source ear relation) were either abolished or altered dramatically.

Acoustic Stimulation↗
PubMed1981

Electrocochleographic study of patients with cerebral vascular lesions.

Electrocochleographies were performed on three patients with deafness resulting from cerebral vascular lesions. Recording was made by the transtympanic needle electrode technique. In a patient who had anterior-inferior cerebellar artery aneurysm that showed fluctuating hearing loss, auditory nerve action potential (AP), cochlear microphonics (CM), and summating potential fluctuate in amplitude in concert with episodes of ischemic hearing loss. This indicates the pathophysiology of reversible impairment of the cochlear nerve and of sensory epithelium of the inner ear caused by disturbance of blood flow into the inner ear. It was also conjectured that the cochlea is hardly impaired in the case with normal AP and CM responses despite the increased threshold in pure-tone audiometry and that the cochlea undergoes irreversible organic changes in the patient who has no AP or CM response in tests after a long period.

Action Potentials↗
PubMed1986

Differential effects of benzodiazepines on cochlear and auditory nerve responses.

The influence exerted by chlordiazepoxide or midazolam upon auditory nerve compound action potential (cAP) and cochlear microphonic (CM) has been analyzed in chronic as well as in acutely prepared guinea pigs. Pre-receptorial variables were carefully controlled. The benzodiazepines dissociated the cochlear recorded potentials, increasing the cAP amplitude, in response to clicks, and decreasing the CM area, produced by a coherent pure tone pip. Both responses were dose related. A direct effect upon the cochlea was eliminated by local infusion of the drugs. It was also demonstrated to be a specific benzodiazepinic action because the use of an antagonist, Ro 15-1788, abolished the effect. Benzodiazepines could have increased the GABAergic activity at the pontine origins of the olivo-cochlear bundle or in the reticulo-cochlear fibers. These are the only central pathways that could be responsible for the effects obtained at the cochlea or auditory nerve levels. We suggest that this is the cause of the withdrawal of inhibitory tonus from the primary afferent fibers mediated by the efferent system (lateral superior olive), as may occur during dishabituation. It may also be the cause of the CM decrement, but the effect in this case would be exerted mainly through another set of efferent fibers (trapezoid body nucleus).

Action Potentials↗
PubMed1992

The effects of moderate cooling on gross cochlear potentials in the gerbil: basal and apical differences.

Changes in the threshold of the compound action potential (CAP) response in the gerbil to low- and high-frequency tonebursts were monitored during uniform cooling of the cochlea by 7-8 degrees C below normal body temperature. Recordings of the endocochlear potential (EP), cochlear microphonic (CM), and summating potentials (SP) were also obtained from the base and apex of the cochlea under the same conditions. Cooling-related changes in the CAP, as well as the CM and SP response obtained near the best frequency of the recording location, were greater in the base than in the apex. In contrast, reductions in the EP appeared uniform throughout the cochlea. Thus the greater vulnerability of CAP thresholds in the base does not result from a greater vulnerability of the stria vascularis in this region. Our results suggest that the enhanced susceptibility to cooling of the CAP in the cochlear base reflects changes in hair cell mechanisms.

Acoustic Stimulation↗
PubMed1992

Fine structure of the intracochlear potential field. II. Tone-evoked waveforms and cochlear microphonics.

1. Extracellular evoked potentials to low-frequency pure-tone stimuli were recorded in the second cochlear turn of the anesthetized guinea pig. Spatial variations of the field potentials were characterized by advancing and withdrawing micropipettes along radial tracks in scala tympani (ST) and scala vestibuli (SV). Compound action potentials (CAPs) and cochlear microphonics (CM) are the major components of the evoked responses to 50- to 1,600- Hz stimuli. The relative contribution of CM and CAP to the evoked potentials varies with cochlear scala and location within the scala as well as with stimulus frequency and intensity. 2. In the 50- to 800-Hz frequency range, the largest CM in the second turn was recorded from scala media (SM). Below 500 Hz the CM in SV is larger than in ST, whereas above 500 Hz a larger CM is present in ST. The CM in SV is nearly in phase with the CM in SM, although it is smaller by a factor of two to four. The CM diminishes by another factor of two over a 100-microns depth range as an electrode is withdrawn out of SV through the spiral ligament. While the electrode is in SV or in the fluid outside the spiral ligament, the CM magnitude does not change by greater than 10%. The shape of the radial CM magnitude profile along tracks in SV shows little or no dependence on intensity in the 65- to 105-dB SPL range or on frequency in the 50- to 800-Hz range. 3. Unlike the CM profiles in SV, the shape of the CM magnitude and phase profiles in ST are a complex function of frequency and intensity. Below 500 Hz, the CM goes through a 140-180 degree radial phase shift over a 100-microns distance near the spiral ligament bordering ST. Concomitant with the large radial phase shift is a local minimum of the CM magnitude. The location of this "virtual ground point" can shift radially by as much as 100 microns over a 30-dB intensity range. The CM magnitude deep in ST is always larger than the CM outside the spiral ligament bordering ST. However, the ratio of the CM magnitudes at these two locations can vary from 0.1 to 0.8, the ratio tending to increase with intensity in the 200- to 800-Hz range.(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗
PubMed1983

Chronological changes of electrocochleogram in experimental endolymphatic hydrops. Special reference with AP output potential and hair cell cilia.

Chronological changes of the whole nerve action potential (AP), cochlear microphonics (CM) and summating potential (SP) in experimental endolymphatic hydrops in guinea pigs were studied during a period from 1 week to 13 months after the endolymphatic sac obliteration. Endolymphatic hydrops became extensive in month 3 and persisted thereafter. The threshold of AP increased with the lapse of time but good AP output potential was obtained, being maximum in month 3. The threshold of CM increased with the lapse of time. The CM output potential was the highest around week 3 when endolymphatic hydrops was slightly formed, and it decreased thereafter. SP responses at the frequencies of 8, 4, 1 and 0.5 kHz showed the reversed polarity of -SP in month 3 and changed towards potential 0 thereafter. In animals showing super-normal AP output potential, the cilia in the third row of outer hair cells were disarranged. This seems to be involved in recruitment.

Action Potentials↗
PubMed1984

Single unit responses in the cochlear nucleus of the deaf quivering mouse.

Mice homozygous for the autosomal recessive gene quivering do not have a classical Preyer reflex and appear to be deaf. Round window recordings including both cochlear microphonics and compound action potentials failed to reveal any abnormality. However, auditory-evoked potentials recorded from the inferior colliculus (IC) are small with long latencies, and the thresholds are at least 50 dB higher than those recorded in controls. This suggests that the auditory deficit arises in the auditory pathway between the cochlear nerve and IC and underlines the need for a description of the functioning of the cochlear nucleus (CN). Single units were recorded extracellularly from the CN in 9 mutants (qv/qv) and 11 control animals (+/qv, or +/+) in the age range 60-120 days. The spike response pattern in mutant animals was broadly similar to that in the controls: a sustained response with monotonic rate-intensity functions. In addition the mean Q10dB for units in the mutants was similar to that of the controls. However, in mutants the group mean threshold at the characteristic frequency was higher and the latency to the first evoked spike at 20 dB above threshold was longer than in controls. Some unit responses in the mutants were similar to those of the controls. Nevertheless, in the quivering mouse, evidence now exists of single unit dysfunction in the cochlear nucleus.

Acoustic Stimulation↗
PubMed1982

Cochlear potentials in the Bronx waltzer mutant mouse.

The Bronx waltzer mutant mouse has a unique cochlear abnormality in which the outer hair cells appear normal but the inner hair cells are absent. Potentials recorded from the round window indicate that the gross cochlear nerve action potential is very small or absent and cochlear microphonics are present but of small amplitude. Positive and negative summating potentials can both be recorded, indicating that mammalian outer hair cells are capable of producing both positive and negative DC potentials.

Animals↗