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PubMed1986

[The promontory test and electrocochleography with reference to indications for cochlear implant].

A successful cochlear implant demands a functioning auditory nerve. A subjective and qualitative recording can be obtained by promontory testing (PT) whereas cochlear microphonics (CM) give information about the status of the hair-cells in the inner ear. The results of both tests together show different patterns: in sensory deafness in which a cochlear implant is indicated, no CM and no compound action potentials (CAP) can be obtained, whereas the patient reports hearing sensations (PT positive) in response to promontory testing. Deafness caused by lesions close to the second neurone of the auditory pathways can be localized by preserved CM and CAP, but there is no response to promontory testing. A ganglionic deafness ie. of the first neurone can be distinguished by preserved CM, absent CAP and a negative PT. The combined results of electrocochleography and promontory testing help in deciding whether a cochlear implant is indicated, and in localising the origin of the deafness, eg. neural or sensorineural. The possible results are illustrated by examples.

Adult↗
PubMed1989

[Correlation of the latency shift and brain stem potentials in basocochlear hearing loss and the time course of the click stimulus-induced evoked wave in the cochlea].

Frequency-specific information on high tone loss in the inner ear can, and if so only indirectly, be obtained from changes in latency of the click-evoked brain stem potential (ABR). The relationship between latency increases of the Jewett-wave-V in basocochlear hearing loss and the time course of the travelling wave on the basilar membrane will be presented. The latency increases of basocochlear hearing loss at 2 kHz, 1 kHz and 500 Hz correspond to both the computer-simulated time course of the travelling wave and to those of the derived responses. From a pathophysiological standpoint, receptor cells in basocochlear hearing loss are not functional, beginning at the oval window, so that, dependent on the degree of inactivity, a delay corresponding to that of the time course of the travelling wave passes until active hair cells are reached and action potentials released that produce, when summed up a potential of delayed latency.

Acoustic Stimulation↗
PubMed2002

Outer hair cells functionally and structurally deteriorate during reperfusion.

Transient ischemia of the cochlea was induced in 65 albino guinea pigs by pressing the labyrinthine artery, and the effects of cochlear reperfusion on cochlear potentials (endocochlear potential, compound action potential and cochlear microphonics (CM)) and structural changes in hair cells were examined. Although 15 min ischemia did not elevate the post-ischemic CM pseudo-threshold as compared with the pre-ischemic value, ischemia of 30 min or longer significantly elevated the CM pseudo-threshold. CM amplitude tended to progressively decrease during the reperfusion period in the animals subjected to 45 or 60 min ischemia. After transient ischemia, outer hair cells (OHCs) were swollen and exhibited alterations of the nucleus. Severer structural deterioration of OHCs was induced by 4 h reperfusion than ischemia itself when the ischemic period was 45 or 60 min. Perilymphatic perfusion of dimethylthiourea, a hydroxyl radical scavenger, partially ameliorated the elevation of the CM pseudo-thresholds and the structural changes of OHCs. These results indicate that cochlear reperfusion induces functional and structural deterioration of OHC probably by hydroxyl radical generation.

Action Potentials↗
PubMed1993

The protective effects of allopurinol and superoxide dismutase on noise-induced cochlear damage.

Several studies have demonstrated that noise exposure may result in local vasoconstriction of cochlear vessels. The subsequent decrease in cochlear blood flow may lead to hypoxia and predispose to the formation of free oxygen radicals (FORs). If hypoxia occurs in response to noise exposure, then drugs that scavenge or block the formation of FORs should protect the cochlea from damage resulting from hypoxic or ischemic events as well as noise trauma. Rats were exposed to 60 hours of continuous broad-band noise (90 dB SPL) and treated with superoxide dismutase-polyethylene glycol (SOD-PEG), allopurinol, or a control vehicle. Exposure to noise resulted in significant threshold shifts at each frequency tested (3, 8, 12, and 18 kHz) as measured by tone burst-evoked compound action potentials and cochlear microphonics recorded from the round window. Both of these thresholds in drug-treated animals were attenuated compared with animals exposed to noise alone. These findings show that SOD-PEG and allopurinol may preserve cochlear sensitivity associated with noise exposure. This suggests that noise-induced damage to the cochlea may be related to the activity of FORs.

Action Potentials↗
PubMed1990

Blockade of synaptic transmission from hair cells to auditory afferent nerves by 6-cyano-2,3-dihydroxy-7-nitroquinoxaline, a selective non-NMDA receptor antagonist.

6-Cyano-2,3-dihydroxy-7-nitroquinoxaline (CNQX) is a new, potent and selective competitive antagonist for the non-N-methyl-D-aspartate (non-NMDA) type of excitatory amino acids receptors. We studied the effect of CNQX on the compound auditory nerve action potential (CAP), cochlear microphonics (CM), summating potential (SP) and endocochlear potential (EP). CNQX in doses of 10-20 microM reduced the CAP magnitude and increased the N1 latency without affecting the CM, SP, or EP. Parallel shifts of CAP amplitude- and latency-intensity functions were observed. The CAP suppressed by 10 microM CNQX was completely reversed by a 10-min washout with artificial perilymph. As 10 microM and 20 microM CNQX seem to exert a selective antagonism for non-NMDA receptors, results indicate that non-NMDA receptors play a major role in synaptic transmission from hair cells to auditory afferent nerves.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1997

Postnatal maturation of the organ of Corti in gerbils: morphology and physiological responses.

The organ of Corti, the sensory epithelium of hearing in mammals, matures postnatally in the gerbil. Quantitative analyses of the postnatal development of the organ of Corti, including supporting cells and the basilar membrane, were carried out. The morphological study confirmed that maturation of the sensory cells proceeds with a base-to-apex gradient, with the outer hair cells appearing to mature before the inner hair cells. Maturation of the supporting cells and the basilar membrane commenced first in the middle turn. Expansion of the second row of Deiters' cells began at 6 days after birth in the middle turn, before enlargement of the pillar cell heads at 8 days postnatally. Pillar cell head enlargement continued until 20 days postnatally in the middle turn. The tunnel of Corti and spaces of Nuel appeared first in the middle turn between 8 and 10 days postnatally. The maturation of the basilar membrane involved the thickening of the central hyaline layer and a reduction in the epithelial cells on the tympanic aspect. This process continued until about 20 days after birth. The cochlear microphonic potential, whole nerve action potential, and stimulus frequency otoacoustic emissions were recorded from 12 days after birth onward and related to changes in organ of Corti morphology. The results show that changes in the accessory structures continue throughout the period of onset and development of cochlear responses between 12 and 20 days after birth, and may therefore influence the micromechanical responses of the organ of Corti to acoustic stimuli during this period.

Animals↗
PubMed1999

Auditory deprivation of the central auditory system resulting from selective inner hair cell loss: animal model of auditory neuropathy.

Auditory neuropathy is often characterized by normal thresholds, present otoacoustic emissions, poor speech discrimination, absent acoustic reflexes, absent or abnormal auditory brainstem response waveform, but normal late cortical potential. This paper describes an animal model that has many characteristics of auditory neuropathy. Chinchillas can be deprived of a significant portion of the neural inputs to the central auditory system by administering carboplatin, an antineoplastic agent that selectively destroys inner hair cells (IHCs) and type I auditory nerve fibers. Selective IHC loss has no effect on distortion product otoacoustic emissions or the cochlear microphonic potential, implying normal outer hair cell function. However, selective IHC loss causes the amplitude of the compound action potential to decrease in proportion to the degree of IHC loss. However, the threshold of the CAP shows little increase with mild to moderate IHC loss. Acoustically responsive auditory nerve fibers in ears with mild to moderate IHC loss have normal thresholds and tuning curves with narrowly tuned tips. Although the central auditory pathway is deprived of much of its sensory inputs, the amplitude of the local field potential in the auditory cortex was normal or enhanced, while those from the inferior colliculus were slightly reduced. The results are related to those of a patient with auditory neuropathy.

Animals↗
PubMed1998

Transient deafness due to temperature-sensitive auditory neuropathy.

OBJECTIVE: To define mechanisms accounting for transient deafness in three children (two siblings, ages 3 and 6, and an unrelated child, age 15) when they become febrile. DESIGN: Audiometric tests (pure-tone audiometry, speech and sentence comprehension), tympanometry, middle ear muscle reflex thresholds, otoacoustic emissions (OAEs), and electrophysiological methods (auditory brain stem responses [ABRs], sensory evoked potentials, peripheral nerve conduction velocities) were used to test the children when they were afebrile and febrile. RESULTS: ABRs, when afebrile, were abnormal with a profound delay of the IV-V and absence of waves I-III. The ABR in one of the children, tested when febrile, showed no ABR components. Measures of cochlear receptor function using OAEs were normal in both febrile and afebrile states. Cochlear microphonic potentials were present in the three children, and a summating potential was likely present in two. When afebrile, there was a mild threshold elevation for all frequencies in the 15-yr-old and a mild elevation of thresholds for just low frequencies in the two siblings. Speech comprehension in quiet was normal but impaired in noise. One of the siblings tested when febrile had a profound elevation (>80 dB) of pure-tone thresholds and speech comprehension was absent. Acoustic reflexes subserving middle ear muscles and olivocochlear bundle were absent when febrile and when afebrile. No other peripheral or cranial nerve abnormalities were found in any of the children. Sensory nerve action potentials from median nerve in one of the children showed no abnormalities on warming of the hand to 39 degrees C. CONCLUSION: These children have an auditory neuropathy manifested by a disorder of auditory nerve function in the presence of normal cochlear outer hair cell functions. They develop a conduction block of the auditory nerves when their core body temperature rises due, most likely, to a demyelinating disorder of the auditory nerve. The auditory neuropathy in the two affected siblings is likely to be inherited as a recessive disorder.

Acoustic Impedance Tests↗
PubMed1982

Cochlear microphonic evidence for mechanical propagation of distortion products (f2 - f1) and (2f1 - f2).

The present cochlear microphonic (CM) study was undertaken to help resolve a conflict in the literature regarding cochlear nonlinear properties. The CM studies of Dallos and his coworkers have concluded that "(up to 70-80 dB SPL [re 20 mu Pa]), all orders of distortion components...do not seem to be accompanied by traveling waves of their own" (Dallos, P. (1973): The Auditory Periphery: Biophysics and Physiology. Academic Press, New York). However, studies of spatial distributions of cochlear nerve fiber responses, acoustic distortion products in the ear canal, and related modeling studies of Kim et al. (Kim, D.O. and Molnar, C.E. (1975): in: The Nervous System, Vol. 3: Human Communication and Its Disorders. Editor: D.B. Tower. Raven Press, New York; Kim, D.O., Molnar, C.E. and Matthews, J.W. (1980): J. Acoust. Soc. Am. 67, 1704-1721) have led to conclusions to the contrary. In the present study, CM data were obtained from the second and third turns of the chinchilla cochlea using fluid-filled glass micropipettes in scala media and nichrome wire electrodes in scala vestibuli and scala tympani. We sought responses containing predominant distortion products (f2 - f1) and (2f1 - f2) by fixing a distortion frequency (fD) near the characteristic frequency (CF) of the recording site and varying the stimulus frequencies f1 and f2 and SPLs (with L1 = L2). By subsequently varying the distortion frequency around the CF, e.g., fixing f1 well above the CF and varying f2, we measured the tuning characteristics of the distortion products (f2 - f1) and (2f1 - f2). Tuning characteristics of single-tone responses were measured by applying single-tone stimuli of various frequencies with a constant SPL at the eardrum. We have observed, with SPLs as low as 25 dB, that these distortion products in CM display tuning similar to the single-tone response which is consistent with above neural results. From these tuning similarities, we conclude that our CM data reflect the presence of mechanically propagated distortion products at low SPLs, in agreement with the above studies by Kim et al. Validity of our results is supported by the sensitivity and sharp tuning of our CM data and, in the case of the scala media recordings, by the presence of a normal d.c. endolymphatic potential. Plausible explanations for the opposing conclusions of previous studies of Dallos et al. and the present study are discussed.

Acoustic Stimulation↗
PubMed1993

Ototoxicity in dogs and cats.

Ears are special sense organs whose principal functions are hearing and maintaining equilibrium. Aminoglycoside antibiotics, erythromycin, polymyxin B, and cisplatin can affect either or both of these functions by binding with, injuring, and/or destroying special receptor cells associated with these functions. Severe hearing loss manifests itself as deafness, whereas loss of equilibrium will present as abnormal righting reflexes, nausea, and vomiting. Damage is proportional to levels of these ototoxins in the endolymphatic fluids. Evidence suggests that toxicity may be influenced by endolymphatic calcium concentrations, and levels of cAMP and cGMP are altered in specialized cochlear cells during ototoxicity, suggesting an additional mechanism for ototoxicity. The administration of salicylates and loop diuretics may potentiate the action of ototoxins, especially aminoglycoside antibiotics, probably by increasing the levels of these toxins in the endolymphatic fluid. Although many of these assessments have been made in laboratory animals, applicability may also be expected in small domestic animals, and extreme care should be taken in prescribing potentially ototoxic drugs to small animals. Cochlear damage from ototoxic compounds occurs initially in the cells detecting high-frequency sounds located at the lower basal region. In aging dogs and humans, this sensitivity of receptors in the lower basal region is enhanced. Early auditory damage is detectable by BAER and cochlear microphonic potentials. Vestibular responses can also be detected early as vestibular ocular reflexes and visual-vestibulo-ocular reflexes. Early detection is especially important because early changes can sometimes be reversible. Cavinton (apovincaminic acid) and fosfomycin represent examples of experimental agents being evaluated in laboratory animals for application as potential treatments to limit the ototoxicity associated with various drugs.

Aminoglycosides↗
PubMed1983

Comparative ototoxicity of four aminoglycosidic antibiotics during the critical period of cochlear development in the rat. A functional and structural study.

The comparative ototoxicity of four aminoglycosides (amikacin, dibekacin, gentamicin and tobramycin) was evaluated in the rat during the critical period of cochlear development. Newborn rats received a daily subcutaneous injection of one of the four antibiotics for 8 consecutive days, starting on day 8 after birth (amikacin: 225 mg/kg, dibekacin: 60 mg/kg, gentamicin and tobramycin: 45 mg/kg). Evaluation of ototoxicity was assessed one month after the end of the treatment using cochlear recordings (action potential and cochlear microphonic), surface preparations and scanning electron microscopy. No functional or structural evidence of ototoxicity was found in animals treated with dibekacin. Tobramycin had a weak ototoxic effect characterized by a slight increase in N1 latency and moderate damage to OHC stereocilia (fusion and formation of giant cilia). Gentamicin-treated animals demonstrated more severe evidence of ototoxicity including increased thresholds for CM, and a higher incidence of missing hair cells and damage to OHC stereocilia. The maximal cochlear damage was observed in amikacin-treated animals: both AP and CM thresholds were severely impaired, cell counts and SEM showed extensive loss of hair cells.

Action Potentials↗
PubMed1996

[Hearing preservation and tinnitus following removal of acoustic neurinomas].

Thirty-five cases of unilateral acoustic neurinomas were analyzed with special reference to the postoperative eighth cranial nerve function. An additional three cases of bilateral acoustic neurinomas associated with neurofibromatosis were also analyzed. Out of a total of 40 neurinomas in all, 38 cases were retrospectively reviewed. The thirty-five cases of unilateral acoustic neurinomas were summarized as follows. The patients' age ranged from 23 to 69 years old. The tumor size varied as follows; 7 cases were confined to the internal acoustic meatus, 4 cases were 20 mm or less in their maximum diameter, 13 cases were 30 mm or less, and 11 cases were more than 30 mm. The consistency of the tumor was classified as being solid in 27 cases, and being cystic in 8 cases. Hearing had been maintained in 27 cases on admission, serviceable in 17 cases, unserviceable in 10 cases and deaf in 8 cases. Operations were performed via the retromastoid suboccipital approach in all cases. The facial nerve was anatomically preserved in all cases. On the other hand, the cochlear nerve was anatomically preserved in 14 out of 35 cases (40%). The preservation ratio of the cochlear nerve showed a negative correlation to the tumor size. In 17 cases with preoperative serviceable hearing, preservation of the cochlear nerve was attempted, which resulted in a 65% anatomical preservation. However, hearing was preserved in 4 cases (36%). Serviceable hearing was preserved in only 2 cases. Tinnitus developed in 20 cases preoperatively, and then occurred postoperatively in 11 cases. Tinnitus was prominently aggravated in 2 cases in which the cochlear nerves were preserved, which resulted in unserviceable hearing. There was a statistically significant correlation between cochlear nerve preservation and the postoperative presence of tinnitus (Fisher's exact probability test: P = 0.0106 < 0.05). Tinnitus was aggravated just after the operation. However, it gradually improved and vanished as the hearing showed a recovery to a slight degree in one case. Three cases of bilateral acoustic neurinomas in neurofibromatosis were also summarized. One case received the operation only on the unilateral side. The remaining two cases were operated bilaterally. To preserve serviceable hearing on at least one side, partial removal of the tumor was performed under the monitoring of auditory brain stem response and/or cochlear microphonic potential. Serviceable hearing on at least one side was maintained in all three cases. In conclusion, hearing preservation can be expected after removal of the acoustic neurinomas under the following situations; hearing acuity of less than 50-60dB in preoperative pure tone audiogram, tumor size of less than 20 mm in maximum diameter, cases with preservation of cochlear nerve and of the internal auditory artery during the operation, and no injury to the labyrinth during the operation. In some cases, tinnitus becomes aggravated in the case with cochlear nerve preservation associated with unserviceable hearing. Furthermore, the degree of tinnitus shows a decrease as postoperative hearing improves in some cases.

Adult↗
PubMed2003

Synchronization of a nonlinear oscillator: processing the cf component of the echo-response signal in the cochlea of the mustached bat.

Cochlear microphonic potential (CM) was recorded from the CF2 region and the sparsely innervated zone (the mustached bat's cochlea fovea) that is specialized for analyzing the Doppler-shifted echoes of the first-harmonic (approximately 61 kHz) of the constant-frequency component of the echolocation call. Temporal analysis of the CM, which is tuned sharply to the 61 kHz cochlear resonance, revealed that at the resonance frequency, and within 1 msec of tone onset, CM is broadly tuned with linear magnitude level functions. CM measured during the ongoing tone and in the ringing after tone offset is 50 dB more sensitive, is sharply tuned, has compressive level functions, and the phase leads onset CM by 90 degrees: an indication that cochlear responses are amplified during maximum basilar membrane velocity. For high-level tones above the resonance frequency, CM appears at tone onset and after tone offset. Measurements indicate that the two oscillators responsible for the cochlear resonance, presumably the basilar and tectorial membranes, move together in phase during the ongoing tone, thereby minimizing net shear between them and hair cell excitation. For tones within 2 kHz of the cochlear resonance the frequency of CM measured within 2 msec of tone onset is not that of the stimulus but is proportional to it. For tones just below the cochlear resonance region CM frequency is a constant amount below that of the stimulus depending on CM measurement delay from tone onset. The frequency responses of the CM recorded from the cochlear fovea can be accounted for through synchronization between the nonlinear oscillators responsible for the cochlear resonance and the stimulus tone.

Acoustic Stimulation↗
PubMed1978

A correlation of the effects of normoxia, hyperoxia and anoxia on PO2 of endolymph and cochlear potentials.

Change in PO2 in endolymph, endocochlear potentials and cochlear microphonics have been tested in normoxia, hyperoxia and anoxia on 24 guinea pigs. The polarographic method and construction of oxygen-sensitive microelectrodes is described in detail. The normal level of PO2 in endolymph vaires between 20 and 30 mm Hg. One-minute anoxia induced by breathing 100% N2 caused a decline in PO2, EP and CM, but during recovery only PO2 returned with over-correction to the preexposure level. Hyperoxia evoked by breathing 100% oxygen failed to increase the cochlear potentials and the PO2 in the endolymph. This suggests that vasoconstriction most likely occurs proximal to the capillaries bed of the stria vascularis.

Animals↗
PubMed1997

Changes in cochlear function after double-membrane rupture in the guinea pig.

We measured the transiently evoked otoacoustic emissions (TEOAEs), compound action potentials (CAPs) and cochlear microphonics (CMs) in guinea pigs after rupture of the round window membrane alone (n = 5) or of the round window membrane with localized cochlear damage (n = 10). The localized cochlear damage entailed rupture of Reissner's membrane with damage to the stria vascularis. We determined the time course of changes in the total echo power (TEP) in TEOAEs and the minimal detectable levels of CAPs and CMs. The endocochlear potential (EP) was measured in the cochlea with localized damage. There were no changes in TEOAEs, CAPs or CMs in the guinea pigs subjected to round window membrane rupture alone, but the minimal detectable levels of CAPs and CMs were increased in all the guinea pigs in which TEOAEs were absent after rupture of the round window membrane with localized cochlear damage. Our results suggest that double-membrane rupture (rupture of the round window membrane with localized cochlear damage) produces acute sensorineural hearing loss. The hearing loss appeared to be related to damage to the cochlea, which may be induced by influx of potassium-rich endolymph into the perilymph, and by morphological damage to the scala media.

Acoustic Stimulation↗
PubMedDate not supplied

[The history of audiology].

INTRODUCTION: The paper presents historical data on development of audiology as a medical speciality. It gives the chronological overview of the most significant discoveries which have contributed to the progress and constant development of the science of hearing. The insights and discoveries encompass the ancient, medieval and contemporary medical science. THE TERM "AUDIOLOGY" AND FIRST ASSOCIATIONS OF AUDIOLOGISTS: The paper reviews the origin of the term "audiology" and the time of its occurrence. The First World Congress of Audiologists was held in 1948, and the Conference of Audiologists and Phoniatrists of Yugoslavia was established in 1974. HISTORICAL OVERVIEW: The ancient scientists and philosophers mentioned in the paper are as follows: Democritus, Hippocrates, Empedocles, Plato, Aristotle, and Galenus. Discoveries of Vesalius, Fallopio, Eustachio, Duverney, Schelhammer, Catugno and Helmholtz marked their epochs and made a great contribution to the development of the entire medical science, including audiology. A significant contribution to audiology was made by Schwartz in 1920 and Fletcher in 1926, constructors of audiometers. Fowler, Weigel and Fletcher promoted an audiogram in 1922. Wever and Bray first introduced the cochlear microphonic potentials. The first modern audiometer with a flat zero line for all pitches was constructed in 1937. In 1947, Bekesy constructed the automatic audiometer, and the theory of mobile waves was introduced in 1928. Fletcher and Steinberg promoted speech audiometries in 1929. Mendel and Goldstein described medium latency responses in 1969. The first hearing aids worn within the ear appeared in the same year. William House pioneered the cochlear implantation in adults in 1969, and the program of infant cochlear implants. Jewett described the evoked auditory potentials in 1970. James Jerger classified tympanometric curves into three tympanogram types (A, B, C). Portmann and Arran introduced transtympanic electrocochleography in 1971. Kemp introduced otoacoustic emission in 1978. INSTEAD OF CONCLUSION: finally, the paper lists the titles of available dissertations and sub-specialisations in the field of audiology defended in Novi Sad and Belgrade.

Audiology↗
PubMed1981

Development of surface-recorded cochlear and early neural potentials in the cat.

The development of the surface-recorded cochlear and early neural potentials has been studied in the cat from birth to the 8th post-natal week. CM, SP, and each of the neural waves has a characteristic temporal developmental pattern and mature threshold. Wave IV is the most resistant to reduction in stimulus intensity levels, while the thresholds of both cochlear potentials are high. Animals with hereditary unilateral deafness constitute a most convenient model for the study of functional maturation in the auditory pathways, particularly with regard to precise latency estimations.

Aging↗