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PubMed1996

Systematic approach to electrode insertion in the ossified cochlea.

Ossification of the fluid spaces of the cochlea occurs often in candidates for cochlear implantation, especially children. When noted before surgery on computerized tomography, ossification previously was thought to contraindicate cochlear implantation because of possible mechanical obstruction and uncertainty about the level of function that could be achieved by stimulating an ossified cochlea. However, during the preceding 6 years, techniques have been developed that permit implantation in ossified cochleas. We present a systematic approach that has been developed to treat the three clinically important categories of cochlear ossification: round window niche obliteration, inferior segment obstruction, and upper segment obstruction. Case reports are presented for each of these three drill-out procedures, demonstrating results often similar to those expected for implantation of the nonossified cochlea.

Adult↗
PubMed1996

Accuracy of high-resolution computed tomography in cochlear implantation.

Multichannel cochlear implants are a proven method for the auditory rehabilitation of individuals who have severe-to-profound sensorineural hearing loss. These devices typically require insertion into the scala tympani of the cochlea to provide auditory stimulations. A patent scala provides the best chance for an adequate insertion of the electrode array. Preoperative high-resolution computed tomography imaging has traditionally been used to determine the patency of the scala tympani. Its ability to accurately predict the patency of the cochlea has been questioned in several retrospective studies. A prospective study was undertaken in 28 consecutive individuals undergoing cochlear implant surgery to compare the findings on high-resolution computed tomography with the surgical findings in an attempt to determine high-resolution computed tomography's accuracy. Cochlear obstruction caused by ossification was accurately predicted in six of six individuals but overestimated in the round window region in three individuals. High-resolution computed tomography accurately predicted patent cochleas in 19 individuals. No false-negative results were encountered. In this study sensitivity of high-resolution computed tomography was 100%, and specificity was 86%. High-resolution computed tomography appears to be more helpful than previously reported for determining cochlear patency.

Acoustic Stimulation↗
PubMedDate not supplied

An electrophysiologic study of experimental perilymphatic fistula.

This study was undertaken to elucidate the mechanism that causes sensorineural hearing loss in clinical cases with perilymphatic fistula. Perilymph was experimentally aspirated through the round window membrane in 17 guinea pigs. The extent of cochlear damage was examined electrophysiologically as well as histopathologically. Immediately after aspiration, several types of changes in summating potential (SP) were observed. Two animals without a polarity change of the SP showed only slight threshold changes in both cochlear microphonic and action potentials, and no specific histopathologic changes in the cochlea. Reversed polarity of the SP was observed in three animals, of which one showed a high-amplitude negative SP followed by rapidly progressive hearing loss. Bulging of Reissner's membrane was confirmed histopathologically in this case. The SP disappeared in the remaining 12 animals. In animals with profound electrophysiologic changes, bulging or rupture of Reissner's membrane and damaged hair cells were observed. These findings suggest that an abrupt change in perilymphatic pressure produces morphologic changes in the membranous labyrinth, causing changes in the vibration function of the cochlear partition and in the function of the organ of Corti. Abrupt pressure imbalance may be a causative factor of sensorineural hearing loss in the case of perilymphatic fistula.

Acoustic Stimulation↗
PubMed2000

Mathematical decomposition of the round window potential.

We present an algorithm called the median transform which can be used to decompose the round window auditory potential into AC and DC components. The first of these is identified with the cochlear microphonic, and the second with the combined summating and compound action potentials. Elsewhere in this volume, the algorithm is employed as an intermediate step in obtaining the instantaneous frequency of the CM. Since the algorithm is easily implemented and operates entirely in the time domain, it may prove useful to clinicians as well as researchers.

Action Potentials↗
PubMed2000

Effects of AC and DC stimulation on chinchilla SOAE amplitude and frequency.

The effects of AC and DC current on spontaneous otoacoustic emissions (SOAEs) were studied in normal chinchillas and chinchillas with selective inner hair cell (IHC) loss. Electrical stimulation was delivered through an electrode on the round window or through an electrode in scala media. SOAE frequencies ranged from 4 to 11 kHz and amplitudes ranged from 13 to 51 dB SPL. AC simulation suppressed SOAE amplitude. The suppression contours had a narrowly tuned, low-threshold tip located above the frequency of the SOAE. AC suppression contours were similar to acoustic suppression contours except that the AC suppression contours lacked a high-threshold, low frequency tail. The lowest threshold of the AC suppression contour was 3.9 microA rms whereas the lowest acoustic suppression threshold was 19 dB SPL. AC stimulation, which induced an electrically evoked otoacoustic emission, interacted with the SOAE to generate distortion product otoacoustic emissions (DPOAEs) of up to 26 dB SPL at 2f(S)-f(AC) (f(S)=SOAE). DPOAE amplitude increased with AC current, but saturated at high levels. DC current steps affected both SOAE frequency and amplitude. Positive current at the round window decreased SOAE amplitude and frequency whereas negative current increased SOAE frequency, but had little effect on amplitude. The effects of AC and DC current on SOAEs in animals with IHC loss were similar to those in normal chinchillas.

Animals↗
PubMed2000

Increased noise severity limits potentiation of noise induced hearing loss by carbon monoxide.

This study evaluates the influence of noise intensity and duration on auditory dysfunction due to simultaneous exposure to noise and carbon monoxide (CO). Previous studies have demonstrated that CO potentiates noise induced hearing loss (NIHL). It is not known whether auditory dysfunction due to combined exposure parallels impairment due to noise alone. Based on the 5 dB exchange rate between noise intensity and exposure doubling time, equivalent noise exposure conditions were used. Long Evans hooded rats were divided into groups that received noise alone (95, 100 and 105 dB SPL), and noise plus CO (1200 ppm), for durations of 4, 2 and 1 h, respectively. Controls were exposed to air or CO alone. Thresholds were evaluated 4 weeks later using an electrophysiological endpoint, the compound action potential threshold. Results demonstrate that the 5 dB exchange rate is not conserved under the conditions and subjects used. Moreover, dysfunction due to combined exposure did not parallel dysfunction due to noise alone. Further, although an increase in exposure duration results in increased auditory dysfunction, no further potentiation of NIHL by CO is observed. This suggests that at increasing noise severity, dysfunction due to combined exposure is limited by impairment due to noise alone.

Acoustic Stimulation↗
PubMed2002

The origin of the 900 Hz spectral peak in spontaneous and sound-evoked round-window electrical activity.

We have monitored the spectrum of the (spontaneous) neural noise at the round window (RW) and on the surface of the antero-ventral cochlear nucleus (CN) and the dorsal CN (DCN) of anaesthetised guinea pigs. We have also obtained the average gross extracellular waveform evoked by 20 kHz tone-bursts (0.25 ms and 25 ms) at each of these recording sites, and calculated the spectrum of the average waveforms (SAW). With these tone-bursts, only a small population of neurones in the extreme basal turn of the cochlea near the RW electrode responds, presumably with only a single action potential for each 0.25 ms tone-burst. The RW waveforms recorded between 20 dB and 60 dB SPL were very similar, and are therefore presumably a simple estimate of the shape of the contribution of the firing of a single neurone to the gross RW signal (the unitary potential or UP). In normal animals, the SNN and the SAW were remarkably similar, with peaks at 900 Hz and at 2400 Hz, suggesting that they are not due to neural synchronisation (as suggested previously by others), but are due to an oscillatory waveform produced by each single fibre action potential. Abolition of all spike activity by RW tetrodotoxin left a waveform with only a summating potential and a dendritic potential, and no 900 Hz peak in the SAW or SNN, indicating that the spectral peak is due to neural spiking only. Abolition of the CN contribution to the RW waveforms by CN application of lignocaine or sectioning of the cochlear nerve at the internal meatus (by focal aspiration of the DCN and underlying cochlear nerve) showed that the 900 Hz peak was not simply due to the addition of a delayed and inverted CN contribution: mathematical modelling shows that this would produce a broad spectral peak at about 1200 Hz. Moreover, the 900 Hz spectral peak remains after complete abolition of the CN contribution, although reduced in amplitude. This residual 900 Hz peak can be traced to an oscillation in the gross waveform due to the presence of two peaks (P(1)* and N(2)*) which follow the intact N(1) peak. The P(1)* and N(2)* peaks were present at the RW, but not at the cochlear nerve as it exits the internal meatus, suggesting that they were not due to double-spiking of some of the neurones, but were probably due to a sub-threshold electrical resonance in the peripheral dendrites. We have successfully modelled the production of the SNN and the compound action potential and SAW in response to 0.25 ms and 25 ms tone-bursts at 20 kHz by including only a damped 900 Hz resonance in the UP, without refractory effects, preferred intervals or synchronisation in the timing of neural spike generation. Such resonances in other neurones are known to be due to the activation kinetics of the voltage-controlled sodium (Na(+)) channels of these neurones. The presence of such sub-threshold oscillations probably indicates that the peripheral dendrites are devoid of stabilising potassium (K(+)) channels. We also discuss the role of this membrane resonance in generating burst-firing of the cochlear nerve (as with salicylate) and the role of such burst-firing in generating tinnitus.

Action Potentials↗
PubMed2002

Round window membrane in young and aged C57BL/6 mice.

Although there have been many studies on the round window membrane (RWM), little information has been reported about changes in the membrane associated with aging. We have undertaken morphological studies of RWMs using young (7-8 weeks old) and aged (27-29 months old) C57BL/6 mice. The RWM was thinner in mice from the aged group compared with that of the young group. The cell density in the epithelial and inner layers was also reduced in the aged group. In the middle layer of the RWM in aged mice, transmission electron microscopy revealed many degenerated short and thick elastic fibers. Confocal laser microscopy using fluorescein isothiocyanate(FITC)-wheat germ agglutinin (WGA) staining was used to identify WGA-positive fibers in the middle layer of the RWM, which changed in a similar manner to the fibers in aging skin.

Animals↗
PubMed2003

Influence of pH on the ototoxicity of cisplatin: a round window application study.

Cisplatin is an antineoplastic agent that produces a number of dose-limiting side effects, including ototoxicity. We investigated the effect of pH on cisplatin ototoxicity. Auditory brainstem responses (ABR) were recorded in chinchillas. Then the auditory bullae were opened and acidic (pH=6.5), neutral (pH=7.4) or alkaline (pH=10.2) phosphate-buffered saline (PBS) was applied to the round window membrane. After 30 min, any remaining solution was removed and cisplatin solution was applied to the round window membrane. After 3 days, follow-up ABRs were performed and the cochleae were processed for morphological analysis. Neutral PBS+cisplatin administration resulted in profound threshold changes at all frequencies. Acidic PBS+cisplatin administration showed had a trend of increased threshold changes, but the change did not reach statistical significance. However, the degree of hair cell loss was significantly higher than that of the neutral PBS-cisplatin group. Alkaline PBS significantly reduced cisplatin-induced threshold changes (P<0.05) compared to the neutral PBS group. Because the pH of cisplatin solution was 6.0, pH 6.0 PBS was applied to round window membrane. This acidic PBS solution did not cause any hearing impairment. These results demonstrate that pH can modulate the ototoxic effects of cisplatin.

Animals↗
PubMed2004

Transient focal cooling at the round window and cochlear nucleus shows round window CAP originates from cochlear neurones alone.

We have measured the compound action potential (CAP) evoked by very brief high-frequency tone-bursts (20 kHz, 1/4 ms) at the round window (RW) and at the surface of the cochlear nucleus (CN) in guinea pigs before, during and after a localised chilling of either the cochlea or CN, with a non-toxic 'freeze spray'. CN chilling almost abolished the negative-going component of the CAP measured in the CN (generated by the CN and here called the cochlear nucleus response or CNR), leaving a positive-going localised response from the cochlear neurones as they leave the internal auditory meatus. Within 3 min, the CNR recovered to control values. During that time, the N(1) component of the RW CAP was slightly increased and the P(1) was larger, even though the CNR was abolished, indicating that the P(1) was not due to electrotonic spread of current from the CN. The N(2) and successive peaks at the RW were also abolished, but returned after 30 s. When the cochlea was chilled, the RW CAP was initially reduced in amplitude, presumably due to a drop in the number of cochlear neurones spiking in response to sound, but recovered within 3 min to be larger than the control waveform, with a more prominent N(1) peak which was delayed slightly, making the CAP more monophasic. At the same time, the CNR was smaller, presumably due to fewer cochlear neurones responding, but overall the CN CAP was altered little in waveshape. These experiments indicate that that RW CAP is generated almost solely by cochlear neurones. We also suggest that some of the changes in the RW CAP during the chills were due to changes in the firing of the lateral olivo-cochlear system of efferent neurons.

Acoustic Stimulation↗
PubMed2004

K(+) currents produce P(1) in the RW CAP: evidence from DC current bias, K(+) channel blockade and recordings from cochlea and brainstem.

Tone-burst-evoked compound action potentials (CAP) from the guinea pig round window (RW) are altered by DC current injection through the RW. The CAP waveform consists of a series of interleaved negative and positive peaks (N(1), P(1), N(2), P(2) etc.) of decreasing amplitude. During positive DC current injection (around +50 microA) the positive peaks are depressed substantially and there is an overall negative baseline shift of the waveform following the N(1). Negative current injection (around -50 microA) increased the positive peaks, in particular P(1), and produced an overall positive baseline shift following the N(1) peak. Results support our hypothesis that the first and dominant N(1) peak in the RW CAP is due to depolarising Na(+) currents into the primary afferent dendrites and axons within the cochlea, and that the P(1) potential is largely due to the exit of the hyperpolarising K(+) currents in the same cells. We have reached this conclusion on the basis of the sign and latency of the N(1) and P(1) components at the RW, beneath the myelin layers around the spiral ganglion cells, at the internal auditory meatus (IAM) within the brain case, and on the basis of the differential susceptibility of the various peaks to perfusion of lidocaine in the cochlear nucleus, sectioning of the cochlear nerve at the IAM, application of the K(+) channel blockers 4-amino-pyridine and tetraethylammonium within the cochlea, and DC current biasing at the RW.

4-Aminopyridine↗
PubMed2004

Determinants of the spectrum of the neural electrical activity at the round window: transmitter release and neural depolarisation.

In this paper we summarise the changes we have observed in the electrical activity at the round window (RW) of guinea pigs during transient cooling of the RW or cochlear nucleus (CN), transient hypoxia, low frequency acoustic biasing, ablation of the CN, and DC current injection into the basal cochlear turn. We have measured the compound action potential (CAP), the spectrum of the average CAP waveform (SAW) evoked by brief tone-bursts, and the spectrum of the neural noise (SNN). We discuss how the changes we have observed can be understood in terms of changes in transmitter release from inner hair cells (that controls stochastic neural firing), or changes in the membrane potential of the primary afferent neurones (that controls the neural firing waveshape and the spectral content of the SAW and SNN). We note that changes in sound intensity produce a simple increase in the stochastic release of transmitter from inner hair cells, without much change in the waveform of the neural response, but manipulations of the auditory brainstem, cooling and current injection all appear to alter neural firing rate and the neural response waveform, producing a baseline shift in the CAP and changes in 1000 Hz peak and low frequency content of the SAW and SNN. We also discuss the use of the CAP, SAW and SNN as an indication of cochlear and auditory brainstem neural activity.

Action Potentials↗
PubMed1996

Electrophysiological and morphological evaluation of the acute ototoxicity of sodium nitroprusside.

Nitric oxide (NO) is a messenger molecule that mediates several physiological functions and pathological processes. Sodium nitroprusside (SNP), a potent vasodilator, when given clinically as an anti-hypertension agent, exerts its function by releasing NO. It was reported recently that SNP causes a loss of auditory nerve compound action potential (CAP) after topical application of SNP on guinea pig round window membrane (RWM). The current study was designed to investigate the ototoxic target of SNP through both electrophysiological and morphological approaches. The CAP threshold at frequencies ranging from 2 to 36 kHz, the cochlear microphonic quadratic distortion product (cmQDP, F2-F1, where F1 = 17.1 kHz; F2 = 18 kHz), and the cochlear microphonic (CM) at the frequency of F1 were recorded via a round window electrode before and up to 2 h after RWM application of 1 microliter of drug solution. Cochlear blood flow (CBF) and arterial blood pressure were monitored. The cochleae were then processed for morphological examination. The effect of SNP on endocochlear potential (EP) was also studied. Results showed that cmQDP, CM, and CAP, as well as EP, were suppressed in varying amounts, while CBF was substantially increased following drug application. Morphological evaluations showed swelling of the afferent inner radial dendrites within the basal cochlear turn in the higher concentration groups of SNP, while the hair cells presented no evidence of damage at the light microscopic level. The results indicate that SNP has an acute ototoxic effect in a concentration- and time-dependent manner. The targets of SNP ototoxicity are at least the afferent dendrites and stria vascularis.

Action Potentials↗
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↗
PubMed1997

Auditory nerve neurophonic tuning curves produced by masking of round window responses.

In response to low-intensity, low-frequency, phase-locked tonal stimuli with non-alternating polarity, the time-average round window (RW) response of the gerbil is a mixture of the auditory nerve neurophonic (ANN) and cochlear microphonic (CM), with the former often being of equal or greater magnitude than the latter. Forward masking (using a conservative 25% amplitude reduction criterion) can be used to generate ANN tuning curves (TC). Most of these TCs are sharply tuned V-shaped functions. Harmonic distortion is often present in the ANN, especially in response to the lower-frequency (< or = 1 kz) or higher-intensity (> or = 50 dB) stimuli. The TCs created by forward masking of the harmonics are similar in appearance to those generated by masking the fundamental frequency of the ANN. When lower-frequency probe stimuli (< or = approximately equal to 1 kHz) are used, the frequency of the TC tip tends to be higher than that of the probe; with higher probe frequencies, the tip tends to be lower. Regardless of the frequency of the probe, the TC tip threshold occurs at an intensity level lower than that of the probe. The sharpness of these TCs generally increases as a function of the frequency of the probe stimulus and the values of Q10dB are comparable to those of FTCs of cochlear nerve fibers of the gerbil. The amplitude of the ANN is often enhanced in response to a limited intensity range of forward maskers over a restricted range of frequencies that are outside the high-frequency boundary of the forward masker TC. By alternating the polarity of the probe stimulus, the CM can be canceled, allowing the effects of simultaneous maskers to be evaluated.

Acoustic Stimulation↗
PubMed1997

Expression and function of adenosine receptors in the chinchilla cochlea.

Previous studies indicate the presence of adenosine receptors in the cochlear tissues obtained from different animals. This study was initiated to determine the subtypes of adenosine receptor (AR) present in the chinchilla cochlea and to assess their function. Radioligand binding studies demonstrate the presence of both the A1AR and A3AR in membranes prepared from the cochlea, using the radioligands [3H]DPCPX and [125I]APNEA. Estimates of the number (Bmax) of A1AR and A1AR plus A3AR by saturation curves were 118 +/- 13 and 417 +/- 120 fmol/mg, respectively, with the respective equilibrium dissociation constants (Kd) averaging 2.7 +/- 0.2 and 26.3 +/- 13.8 nM. No significant number of A2aAR were detected using [3H]CGS21680. The nonhydrolyzable adenosine analog R-phenylisopropyladenosine (R-PIA, 1 microM) elicited a small but significant degree of inhibition of forskolin-stimulated adenylyl cyclase activity (10.4 +/- 2.5%) in cochlear membrane preparations, which was insensitive to blockade by theophylline (100 microM). Furthermore, R-PIA elicited an increase in inositol 1,4,5-trisphosphate production in dissociated cell preparations obtained from the cochlea. No significant effect of R-PIA was observed on auditory measures such as auditory brainstem evoked response, cochlear action potential and endocochlear potential following round window application. However, round window application of R-PIA elicited significant increases in the activities of antioxidant enzymes such as superoxide dismutase and glutathione peroxidase and significantly reduced the levels of malondialdehyde, a marker of lipid peroxidation. These results suggest a potential cytoprotective role of adenosine in the cochlea against oxidative damage.

Adenosine↗
PubMed1997

Enhanced cochlear responses after sound exposure.

Alternating potentials produced in Hensen's cells of Mongolian gerbils by sinusoidal stimuli were enhanced or depressed after exposure to broad-band sound of moderately high intensity, depending on exposure- and stimulus intensities. Since Hensen's cell responses have been shown to be identical in phase and directly proportional in magnitude to outer hair cell (OHC) responses (Oesterle, E.C., Dallos, P., 1989, J. Acoust. Soc. Am. 86 (3), 1013-1032.; Zwislocki, J.J., Slepecky, N.B., Cefaratti, L., Smith, R.L., 1992, Hear. Res. 57, 175-194), it was assumed that these changes were reflections of changes in OHC receptor potentials, which were of main interest. The indirect method of intracellularly recording the Hensen's cell potentials rather than OHC potentials was used to minimize damage to the organ of Corti and reduce technical difficulties associated with repeated recordings from OHCs. Continuous magnitude and phase transfer functions (TFs) were obtained before and after the exposure over a range of sound pressure levels (SPLs) extending from 40-90 dB by using frequency sweeps ranging from 0.125-18 kHz. Cochlear microphonic (CM) TFs were also acquired over the same frequency and intensity ranges for monitoring purposes. The exposure stimuli were set at 80, 86, 90 or 100 dB SPL for periods ranging from 10-40 min. When response enhancement occurred, it was most clearly seen in the peak of the transfer function determined at 90 dB SPL. Enhancement ranged from approximately 12-230% of the original peak. In contrast, control Hensen's cell recordings obtained over periods of up to 130 min revealed great response stability. In all reliable recordings, response enhancement was associated with a phase lead or no phase change. The strongest exposure stimuli tended to produce sensitivity loss accompanied by phase lag at the lower SPLs, in agreement with previous work in this laboratory (Zhang and Zwislocki, 1995). In some preparations, both sensitivity loss at lower SPLs and enhancement at higher SPLs occurred simultaneously, suggesting involvement of two different mechanisms.

Acoustic Stimulation↗
PubMed1997

Steady state EP is not responsible for hearing loss in adult chickens following acoustic trauma.

The steady state DC endocochlear potential (EP) in young chicks shows a large decrease after acoustic overstimulation followed by a rapid recovery that parallels the recovery of threshold (Poje et al., Hear. Res. 82 (1995) 197-204). These results raise a question as to whether or not the EP could account for the hearing loss and make a significant contribution to the recovery of the threshold. In contrast to results in young chicks, we show that acoustic overstimulation, which causes extensive hair cell damage, does not cause a decrease in the steady state EP in adult chickens. However, there is a significant reduction in the negative EP seen during anoxia which persists even after 4 weeks of recovery. Thus, our results indicate that the steady state EP cannot account for the hearing loss observed in adult chickens.

Acoustic Stimulation↗