The frequency specificity of the ABR threshold evoked by a 1000-Hz filtered click was determined in subjects with sloping cochlear hearing losses, both high- and low-frequency in character. The results show that the ABR threshold evoked by this stimulus is low-frequency specific. The standard error in estimating the 1000-Hz pure-tone threshold (PTT) is 10.4 dB, which equals that for estimating the 3000-Hz PTT from the routinely used click-evoked ABR threshold. The ABR threshold evoked by a 1000-Hz filtered click can therefore be regarded as an accurate tool to predict the pure-tone hearing loss at 1000-Hz. In comparison with the ABR threshold evoked by a click masked with 1590-Hz high-pass noise, the ABR threshold evoked by a 1000-Hz filtered click has a larger dynamic range, yields a larger number of useful responses and is less time consuming. For clinical low-frequency-specific ABR threshold assessment, the 1000-Hz filtered click is therefore preeminently useful.
In this study, the frequency specificity of the ABR threshold to stimulation with a click masked with 1590-Hz high-pass noise was determined in subjects with sloping cochlear hearing losses both high- and low-frequency in character. The results show that the ABR threshold elicited by this stimulus is low-frequency specific. The standard error in estimating the 1000-Hz pure-tone threshold from the high-pass-noise-masked click-evoked ABR threshold is 10.2 dB which equals that for estimating the 3000-Hz pure-tone threshold from the routinely used unmasked click ABR threshold. The ABR threshold elicited by a click masked with 1590-Hz high-pass noise can therefore be regarded as an accurate tool to predict the pure-tone hearing loss at 1000 Hz. However, this method is less suitable for routine clinical testing because of the masking noise needed: the occasional high loudness level adversely affects the response quality and reduces the dynamic range of pure-tone hearing losses to be assessed. A third disadvantage is that determining the masking level electrophysiologically for each ear is time consuming. The search for a method with no or less masking noise should therefore continue.
In this study, the frequency specificity of the auditory brainstem response (ABR) threshold to. a click masked with 1590-Hz high-pass masking noise is compared with the frequency specificity of the unmasked click-evoked ABR threshold. The ABR threshold to the high-pass-noise-masked click stimulus is low frequency specific and corresponds with the 1 000-Hz pure-tone threshold. Although the ABR threshold to the unmasked click stimulus corresponds with the '3000'-Hz pure-tone threshold, the frequency specificity seems much less pronounced than that of the low-frequency-specific stimulus. This study shows, however, that this apparent lack of frequency specificity can be attributed to the selection of pure-tone hearing losses. The ABR threshold evoked by an unmasked click stimulus is, therefore, preeminently useful as a high-frequency point of a two-point audiogram. The possible reasons why the ABR threshold evoked by a broad-band stimulus as the unmasked click corresponds with the higher frequencies of the pure-tone audiogram are discussed.
Monaural and binaural auditory brainstem response (ABR) thresholds to clicks masked by high-pass noise with a cut-off frequency of 1,590 Hz were measured in normal-hearing subjects. In sleeping normal-hearing subjects, the 1,000-Hz frequency-specific ABR threshold for binaural stimulation amounted to 12 dB nHL and for monaural stimulation to 18 dB nHL. No significant difference in latency was found between monaural and binaural stimulation. Binaural ABR threshold was 5.5 +/- 1.4 dB (mean +/- SEM) lower than the mean monaural ABR threshold. This difference is statistically significant (Student's t test; p less than 0.005).
In normal-hearing subjects and in subjects with a flat cochlear hearing loss, auditory brainstem responses (ABR) were recorded at various levels of a 1,000-Hz filtered click stimulus with and without high-pass filtered masking noise. The difference in latency of the major peak in the ABR for the masked and unmasked condition was zero at the ABR threshold. We regard this as proof of the frequency specificity of the 1,000-Hz filtered click-stimulated ABR threshold. The difference between ABR threshold and the subjective puretone threshold at 1,000 Hz amounted to 19 dB in normal-hearing subjects and to 10 dB in subjects with a flat cochlear hearing loss. This is probably related to loss of temporal integration and an abnormal loudness growth (recruitment).
In normal-hearing subjects and in subjects with a flat cochlear hearing loss, auditory brainstem responses (ABR) were recorded at various levels of a 1,000-Hz filtered click stimulus with and without high-pass filtered masking noise. The difference in latency of the major peak in the ABR for the masked and unmasked condition was zero at the ABR threshold. We regard this as proof of the frequency specificity of the 1,000-Hz filtered click-stimulated ABR threshold. The difference between ABR threshold and the subjective puretone threshold at 1,000 Hz amounted to 19 dB in normal-hearing subjects and to 10 dB in subjects with a flat cochlear hearing loss. This is probably related to loss of temporal integration and an abnormal loudness growth (recruitment).
A comparison between pure-tone audiometry and brainstem electric response audiometry was made in 25 children with a conductive hearing loss due to otitis media with effusion. Pure-tone audiometry, including bone and air-conduction thresholds, was recorded using standard procedures. BERA was used to construct a latency-intensity function and from this the conductive hearing loss could be estimated. For all frequencies except for 2000 Hz a good correlation was found between the conductive loss in the pure-tone audiogram and the conductive loss as estimated by BERA. The moderate correlation for 2000 Hz is due to a ‘Carhart’ -notch-like phenomenon in the pure-tone audiogram.
The resultant hearing loss can be variable if cis-dichlorodiammineplatinum is given to guinea pigs. In order to find out more about these differences, we used brainstem audiometry to study the start and development of hearing loss over time for several frequencies. Our results confirmed previous observations that hearing loss starts at the higher frequencies but can also occur at lower frequencies. Furthermore, there were great differences in the start and the rate of the increase of hearing loss found in the individual animals. The individual differences in susceptibility can not be explained by one factor alone, but by the combination of three factors, namely deviation point, slope and length of survival.
The difference in the hearing threshold before and after treatment with cis-diaminnedichloroplatinum (DDP) is analysed in 69 patients. Hearing loss due to DDP treatment is mainly limited to 8,000 Hz and the incidence is about 40%. The effect of DDP is dose-related, although even at the lowest dose 20% of the patients are affected. The age of the patients is not an important factor. Loss of hearing due to DDP treatment occurs independent of any pre-existent hearing loss although those patients with great pre-existent hearing loss do not show a further loss. Of the patients with hearing loss, 39% show a difference of 20 dB or more between the left and the right ear. Hearing loss due to DDP is of minor importance compared with many of the other side-effects of DDP.
Gentamicin-induced cochlear degeneration in the guinea pig was studied by complete hair-cell counting (cytocochleograms) and phase-contrast and interference microscopical examination of the stria vascularis and Reissner's membrane. Gentamicin (100 mg/kg/day) was administered over a period of 7–17 days. The first loss of hair cells (OHC) occurred in a region 6–8 mm from the round window. From this ‘degeneration point’, the loss of haircells progressed towards the round window (fast) and the apex (slowly). The stria vascularis showed no signs of degeneration. Reissner's membrane, on the other hand, showed intracellular vacuolization of the endolymphatic cells over the complete length of the cochlea after 12 or more days' intoxication. Hearing loss was measured by electrocochleography with skin electrodes. The histologic findings were compared with the objective audiograms.
Cis-diammine-dichloroplatinum-II (DDP)-induced cochlear degeneration in the guinea pig was studied by complete hair-cell counting (cytocochleograms) and transmission electron microscopy. The DDP (1.5 mg/kg/day) was administrated over a period of 5–20 days. The degeneration of the organ of Corti started sporadically in almost every outer hair-cell (OHC) with a strong prevelance in the OHC 1 in the basal turn.No distinct starting point for the degeneration of the organ of Corti could be found. It seemed that the ototoxic effects of DDP are rather different from the ototoxic changes due to aminoglycoside antibiotics.This study showed that the animals with hearing loss due to DDP also had a clear loss of body weight. Perhaps DDP induces toxic effects (loss of body weight) which can amplify the ototoxic effects.Untersuchung der Cis-Platin-Wirkung auf das Cortische Organ des Meerschweinchens mittels Zytocochleogramm und Elektronenmikroskopie. Die Schädigung begann stets an den äußeren Haarzellen der Basalwindung. Der Beginn der Degeneration konnte nicht exakt bestimmt werden. Tiere mit Hörverlust zeigten einen Verlust des Körpergewichtes. Vielleicht trägt der letztere zur Verstärkung des ototoxischen Effektes bei.
Cis-diammine-dichloroplatinum-II (DDP)-induced cochlear degeneration in the guinea pig was studied by complete hair-cell counting (cytocochleograms) and transmission electron microscopy. The DDP (1.5 mg/kg/day) was administrated over a period of 5–20 days. The degeneration of the organ of Corti started sporadically in almost every outer hair-cell (OHC) with a strong prevelance in the OHC 1 in the basal turn.
