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Results for “Cochlear Microphonic Potentials”

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At least 253 records · Page 14Linked to original sources
PubMedDate not supplied

Cochlear and brain stem responses in hearing loss following neonatal hyperbilirubinemia.

The site of lesion in hearing loss following neonatal hyperbilirubinemia is unclear. Histopathological studies have implicated the brain stem auditory nuclei while other investigations have hinted at a lesion in the cochlea. In order to clarify this issue, attempts were made to record responses from the auditory pathway in 13 patients with hearing loss following neonatal hyperbilirubinemia. The neural response from the auditory nerve was absent in 11 of the 13 patients and present only in response to high intensity stimuli in 2 patients. However, the response of the cochlear hair cells (cochlear microphonic potential) was present in 9 of the 13 patients. In most other cases of sensorineural hearing loss, with no history of hyperbilirubinemia, the hair cell response was absent. This is functional evidence for auditory nerve damage in cases of hearing loss following neonatal hyperbilirubinemia while the hair cells are spared.

Adult↗
PubMedDate not supplied

Generators of the frequency-following response in the guinea pig.

Generators of the frequency-following response (FFR) were assessed in 13 guinea pigs by cooling of the whole body and by experimental lesions of the brain stem. In the temperature study, the amplitude-temperature function of the FFR contained a significant cubic component that was absent from that of the cochlear microphonic potential (CM) recorded from the round window. The phase shift of the FFR increased with decreasing body temperature. In experimental lesions of the brain stem, a significant phase shift of the FFR was obtained following contralateral postcollicular section. The FFR amplitude with transection of the auditory nerve was similar to that found before surgical sections of the brain stem. The duration of the FFR after the transection corresponded precisely to that of the round window CM. These results indicate that the origin of the FFR contains both nonneural (ie, cochlea) and neural (ie, involving the inferior colliculus) generators.

Animals↗
PubMed2000

Basic and clinical physiology of the inner ear receptors and their neural pathways in the brain.

The six receptors of the inner ear (cochlea, two otolith organs and three semicircular canals) share a common transduction unit made up of a sensory hair cell, a first order sensory neuron and the synapse between them. Displacement of the stereocilia in a particular direction leads to excitation of the hair cell and activation of the neuron. Electrical and mechanical reflections of these stages of transduction can be recorded non-invasively in humans and in animals. These include cochlear microphonic potentials, otoacoustic emissions, auditory and vestibular evoked potentials. The ability to record these activities can be used to track the development of inner ear function in the fetus and neonate and to study the effects of various ototoxic agents (e.g. noise) and drugs.

Animals↗
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↗
PubMed1994

Influence of calcitonin-gene related peptide on cochlear blood flow and electrophysiology.

Intra-arterially infused calcitonin gene-related peptide (CGRP) induced dose-dependent decreases in both systemic blood pressure and cochlear blood flow (CBF). However, when subjects were pretreated systemically or locally with the specific receptor antagonist CGRP(8-37), CBF increased, despite decreases in systemic blood pressure in response to CGRP infusions. Micro-infusions of CGRP directly into the supplying arterial network of the cochlea induced dose-dependent increases in CBF that were blocked by CGRP(8-37) pretreatment. Cochlear electrophysiology, as assessed by cochlear action potential and cochlear microphonics, remained unchanged following each condition tested. These results indicate that CGRP is involved in systemic regulation of blood pressure and contributes to the regulation of CBF.

Animals↗
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↗
PubMed2001

Reversible and irreversible damage to cochlear afferent neurons by kainic acid excitotoxicity.

Kainic acid (KA) selectively damages afferent synapses that innervate, in chickens, mainly tall hair cells. To better understand the nature of KA-induced excitotoxic damage to the cochlear afferent neurons, KA, at two different concentrations (0.3 or 5 mM), was injected directly into the inner ear of adult chickens. Pathologic changes in the afferent nerve ending and cell body were evaluated with light and transmission electron microscopy at various time points after KA application. The compound action potential (CAP) and cochlear microphonic (CM) potential were recorded to monitor the physiologic status of the afferent neurons and hair cells, respectively. Hair cell morphology and function were essentially normal after KA treatment. However, afferent synapses beneath tall hair cells were swollen within 30 minutes after KA at both low (KA-L) and high (KA-H) doses. In the KA-L group, the swelling disappeared within 1 day and the morphology of the postsynaptic region returned to near normal condition. In the KA-H group, by contrast, the vacant region beneath tall hair cells remained evident even 20 weeks after KA. The number of cochlear ganglion neurons in the KA-H group decreased progressively from 1 to 8-20 weeks, whereas hair cells in the basilar papilla remained morphologically intact out to 20 weeks after KA. There was no significant change in neuron number in the KA-L group. Temporal changes in the CAP amplitude paralleled the anatomic changes, although the CAP only partially recovered. These results suggest that KA induces partially reversible damage to cochlear afferent neurons with low KA concentration; above this level, KA triggers irreversible, progressive neurodegeneration.

Action Potentials↗
PubMed1996

A comparative study on the effect of pure-tone exposure of the guinea pig cochlea.

Electrophysiological methods were applied to 160 healthy adult male guinea pigs in order to investigate the effects of pure-tone exposure for 24 h on the inner ear. A reduction in cochlear microphonics (CM), action potential (AP) and endocochlear potential was observed following exposure to 110 dB at 100 Hz, 100 dB at 200 and 600 Hz and 95 dB at 2 kHz. The observed K+ endolymphatic concentration during 40 min anoxia remained unchanged. In contrast K+ decreased in control animals and following exposure to pure tones varying from 110 dB at 60 Hz to 85 dB at 2 kHz. These findings indicate that high frequency tones have a greater effect on inner ear functions than those of lower frequency, decreasing the maximum output voltage of CM and AP but not changing K+ endolymphatic concentration.

Acoustic Stimulation↗
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↗