A new method of calculating auditory excitation patterns and loudness for steady sounds

A new method for calculating auditory excitation patterns and loudness for steady sounds is described. The method is based on a nonlinear filterbank in which each filter is the sum of a broad passive filter and a sharp active filter. All filters have a rounded-exponential shape. For each center frequency (CF), the gain of the active filter is controlled by the output of the passive filter. The parameters of the model were derived from large sets of previously published notched-noise masking data obtained from human subjects. Excitation patterns derived using the new filterbank include the effects of basilar membrane compression. Loudness can be calculated as the area under the excitation pattern when plotted in intensity-like units on an ERB(N)-number (Cam) scale; no transformation from excitation to specific loudness is required. The method predicts the standard equal-loudness contours and loudness as a function of bandwidth with good accuracy. With some additional assumptions, the method also gives reasonably accurate predictions of partial loudness.     

A revised model of loudness perception applied to cochlear hearing loss

We previously described a model for loudness perception for people with cochlear hearing loss. However, that model is incompatible with our most recent and most satisfactory model of loudness for normal hearing. Here, we describe a loudness model that is applicable to both normal and impaired hearing. In contrast to our earlier model for impaired hearing, the new model correctly predicts: (1) that a sound at absolute threshold has a small but finite loudness; (2) that, for levels very close to the absolute threshold, the rate of growth of loudness is similar for normal ears and ears with cochlear hearing loss; (3) the relation between monaural and binaural threshold and loudness; (4) recent measures of equal-loudness contours. Like the earlier model, the new model can account for the loudness recruitment and reduced loudness summation that are typically associated with cochlear hearing loss.     

响度重振与耳蜗微音电位及耳聋预后的关系

目的了解响度重振与耳蜗微音电位(cochlear microphonic,CM)及耳聋预后之间的关系,探讨重振的形成机制.方法对104例一耳正常,另一耳为感音性听力下降并有响度重振的患者施行双耳CM测试,测试频率为0.5、1 kHz,以高频下降为主者加测2、4、8 kHz.将患者初诊时纯音听阈、双耳CM检测阈值与最终稳定之后的纯音听阈相比较,为便于分析结果,本文提出了CM分型标准Ⅰa型患耳CM检测阈值＜健耳,阈值差≤10dB;Ⅰb型双耳CM检测阈值相等,检测阈≤55dB SPL.Ⅱa型患耳CM检测阈值＞健耳,差值≥15dB SPL;Ⅱb型患耳检测阈值为60～75dBSPL.Ⅲ型患耳CM检测阈值＞75dB SPL或引导不出.结果听力正常组各频率CM绝对振幅在不同个体差异较大,但同一正常个体双耳之间CM幅值及阈值则较接近并稳定,因此不采用平均值而仅以同一个体正常一侧CM幅值的大小来评价患耳的CM幅值.重振耳CM有增大和延长现象.104例单侧感音性聋,95例(91.3%)主观检测有重振的频率出现CM振幅明显增大,其中34例在CM增大同时伴有CM延长(5.8%),与正常耳比较延长1～11个周波,平均时间延长(5.2±2.5)ms.初诊时即遵照CM分型标准分类,随后经6个月以上随诊,发现CM Ⅰ型预后明显好于Ⅱ型和Ⅲ型,Ⅰ型治疗总有效率高达78.19%;Ⅱ型多数预后不佳,治疗有效率仅为2.5%;Ⅲ型治疗均无效;将CM Ⅰ型与Ⅱ型做预后比较,组间差异具有显著性意义(x2=53.709,P＜0.001);Ⅰ型与Ⅲ型比较,差异亦具显著性意义(x2=21.444,P＜0.001);Ⅱ型与Ⅲ型比较,差异无显著性(x2=0.230,P＞0.05).睡眠状态下CM幅值略有增大,与此同时CM阈值减低.结论CM检测可为了解重振发生机理以及重振与CM和耳聋预后之间的关系提供可靠的客观信息.听力下降耳CM幅值正常或增大为重振所特有客观指征.     

A model of loudness summation applied to noise-induced hearing loss

The main contention of this paper is that Zwicker's model of loudness summation is applicable to observers with noise-induced hearing loss when certain parameters of the model are modified. Two types of measurement were obtained in observers with normal hearing and noise-induced hearing loss: loudness summation as a function of level and narrow-band masking. These measurements provided a basis for modifying the parameters of the model. Results suggest that the model of loudness summation is applicable to observers with noise-induced hearing loss when the presence of recruitment and reduced frequency selectivity is taken into account.     

Reorganization of auditory cortex after neonatal high frequency cochlear hearing loss

Cochleotopic representation in cortex (AI) is extensively reorganized in cats having neonatal, bilateral high frequency cochlear hearing loss. Anterior areas of AI, normally devoted to high frequencies, contain neurons which are almost all tuned to one lower frequency. This frequency corresponds, at the level of the cochlea, to the border between normal and damaged haircell regions.     

Pitch perception and auditory stream segregation: implications for hearing loss and cochlear implants

Pitch is important for speech and music perception, and may also play a crucial role in our ability to segregate sounds that arrive from different sources. This article reviews some basic aspects of pitch coding in the normal auditory system and explores the implications for pitch perception in people with hearing impairments and cochlear implants. Data from normal-hearing listeners suggest that the low-frequency, low-numbered harmonics within complex tones are of prime importance in pitch perception and in the perceptual segregation of competing sounds. The poorer frequency selectivity experienced by many hearing-impaired listeners leads to less access to individual harmonics, and the coding schemes currently employed in cochlear implants provide little or no representation of individual harmonics. These deficits in the coding of harmonic sounds may underlie some of the difficulties experienced by people with hearing loss and cochlear implants, and may point to future areas where sound representation in auditory prostheses could be improved.     

Distortion-product emissions and auditory sensitivity in human ears with normal hearing and cochlear hearing loss.

Distortion product emissions (DPEs) at 2f1-f2 frequencies were measured in 53 human ears; 21 of them exhibited cochlear hearing loss. DPEs were obtained as a function of stimulus level (DPE growth curves) at seven frequency regions between 707 Hz and 5656 Hz. Several distinctly different shapes or patterns of DPE growth curves were observed. These included single-segment monotonic growth curves with and without saturation at moderate and high stimulus levels, diphasic growth curves with nulls at moderate stimulus levels, and non-monotonic growth curves with negative slopes at high stimulus levels. Low-level, irregularly shaped segments were more frequent in normal-hearing ears, suggestive of normal low-level active nonlinearities from the outer-hair-cell subsystem. High-level, steeply sloped segments were frequent in hearing-impaired ears, suggestive of residual nonlinearities from a cochlear partition without functional outer hair cells. The stimulus level at which the DPE could just be distinguished from the noise floor, the DPE detection threshold, demonstrated moderate positive correlations (r's from 0.50 to 0.81) with auditory thresholds when all ears, both normal and impaired, were considered together. Those correlations were not strong enough to quantitatively predict auditory thresholds with any great accuracy. However, DPE thresholds were able to predict abnormal auditory sensitivity with some precision. DPE thresholds correctly predicted abnormal auditory sensitivity 79% of the time in the present study, and up to 96% of the time in previous studies. These results suggest that DPE thresholds may prove useful for hearing screening in cases where cooperation from the subject is limited or where corroboration of cochlear hearing loss is required. Different patterns of DPE growth curves suggest underlying micro-mechanical differences between ears, but the differential diagnostic value of those patterns remains to be determined.     

Inaccuracies in the measurement of auditory brainstem response data in normal hearing and cochlear hearing loss

In a test-retest experiment inaccuracies in the measurement of the peak latencies and threshold of the auditory brainstem response were determined for a group with normal hearing and for a group with cochlear hearing loss. The inaccuracy of the auditory brainstem response threshold is less than 4 dB in both groups. The inaccuracy in latency was measured as a function of stimulation level. In both groups the latency inaccuracy of peak V varies from 0.1 ms at levels well above threshold to 0.2 ms near the response threshold. Analysis of variance showed that in subjects with normal hearing the intra- and interindividual variabilities of the peak V latencies contribute about equally to the total variance at all stimulation levels. The implications that these findings have for the determination of the horizontal shift of the latency-intensity curve are discussed.     

The effect of cochlear hearing loss on auditory brain stem response latency.

The effect of audiometric configuration on the auditory brain stem response was studied in a large patient sample, and wave I latencies, wave V latencies, and the I-V interwave intervals were compared to those from a previous report. Patients with notched hearing losses showed longer wave V latencies and I-V interwave intervals than those with other audiometric configurations, but the magnitude of the effect was relatively small, and the confidence limit for cochlear diagnosis was essentially the same as that based upon a cochlear hearing loss population without regard to audiometric configuration.     

A cochlear schwannoma presenting with sudden hearing loss

A cochlear schwannoma is a rare tumor that arises from the cochlear nerve. Clinically, a cochlear schwannoma mimics the clinical features of sudden deafness or Meniere's disease. We report a case of cochlear schwannoma that presented with sudden hearing loss, which was diagnosed with gadolinium-enhanced magnetic resonance imaging and removed using a transotic approach.     

Effect of hearing loss of cochlear origin on the auditory brain stem response.

Auditory brain stem response (ABR) testing is widely used to detect lesions of the auditory neural pathways. The ABR waves depend not only on the integrity of the neural pathways, but also on the condition of the cochlea. To properly interpret the ABR response, it is necessary to understand the effects of cochlear hearing loss on the ABR wave latencies. We studied two populations of subjects with cochlear hearing loss: one with varying degrees of high-frequency hearing loss and the other with varying degrees of flat configuration hearing loss. The degree of cochlear hearing loss was quantified in several different ways and subjected to one linear and three nonlinear regression analyses to test for accuracy in predicting ABR wave latencies and interpeak intervals (waves I, III, V, I-V, I-III, and III-V) for three click intensities. Hearing loss levels from 2 to 6 kHz, in particular 4 kHz, were superior to other audiometric test frequencies as predictors of ABR wave latencies for the group with the high-frequency losses. No particular characterization was found to be superior for the flat hearing loss configurations. From these results, modeled predictions of wave latencies as a function of degree and configuration of hearing loss were made. The modeled predictions are then used to suggest guidelines for interpretations of ABR results where hearing impaired patients are involved.     

隐性听力损失的一种新机制——短暂性听神经脱髓鞘

以往认为,听阈正常的人听觉处理能力是正常的(即使是从噪声暴露导致的暂时性阈移中恢复过来的听阈正常者),其所出现的听力缺陷问题被归因为中枢问题.但是,最新的动物和临床研究表明,中等强度的噪声暴露或者年龄因素能够导致一种新型的外周听力损失,即隐性听力损失(hidden hearing Loss,HHL).HHL在生理学上能被检测出来,其特征是听阈正常,而声诱发的螺旋神经元(spiral ganglion neuron, SGN)动作电位AP(ABR波Ⅰ峰值)阈上幅值降低,以及由毛细胞产生的ABR波的峰值(总和电位SP)与AP之间的比值改变.隐性听力损失中神经活性降低会导致阈上声音时阈编码的退化以及言语分辨力和言语理解力的缺陷,特别是在嘈杂环境中.但是,言语分辨能力和理解能力的缺陷并不能用来诊断HHL,因为它们也可能是由于中枢处理缺陷引起.目前为止,内毛细胞突触的损失或者功能障碍是唯一被提到过的HHL的发生机制.     

An improved model for loudness coding during auditory adaptation

A comparison of loudness adaptation measured at four baseline intensities and at test values 10 and 20 dB above the baseline intensities revealed an orderly decline. The magnitude of the decline in loudness adaptation with the increasing difference between the test values and the baseline was shown to agree with earlier theories. A method for closely estimating the change in loudness adaptation is presented in convenient graphic form and in algebraic equations.

Résumé

Nous avons, pour quatre intensités de base, comparé les valeurs d'adaptation de la sonie pour des intensités de test: 1) égales à l'intensité de base; 2) supérieures de 10 dB à l'intensité de base et 3) supérieures de 20 dB à l'intensité de base. Nous avons observé une diminution régulière de la valeur de l'adaptation avec l'augmentation de l'écart entre les intensités de test et les intensités de base, en accord avec les théories émises par Hood [1950], Small [1963] et Stevens [1956]. Nous présentons une méthode sous forme graphique et algébrique qui permet d'estimer les valeurs d'adaptation de la sonie.     

Interaction of click intensity and cochlear hearing loss on auditory brain stem response wave V latency.

Auditory brain stem responses (ABRs) to 95, 80, 60, 40, and 30 dB nHL clicks were retrospectively studied from 103 patients (194 ears) with various degrees of cochlear impairment. Hearing loss and sample size were balanced across gender. Results indicate that the slope of the wave V latency versus 4000 Hz hearing loss function doubles as click intensity is decreased from 80 (0.01 msec/dB HL) to 60 nHL (0.02 msec/dB HL). Overall results indicate a slope increase of 0.0004 msec for each decibel decrease in click intensity from 95 to 30 dB nHL. Intersubject variability increased with increased hearing loss and/or decreased stimulus intensity. The effects of hearing loss on wave V latency are minimal, and intersubject variability is less if high-intensity clicks (greater than or equal to 95 dB nHL) are used. No differences in the effects of hearing loss on wave V latency were seen between males and females. Latency corrections for cochlear hearing loss should, therefore, consider stimulus intensity.     

Progressive sensorineural hearing loss and cochlear otosclerosis: A prospective study

The association of otosclerosis with reduced bone conduction is well known but no experimental or valid clinical relationship has been established to confirm this relationship. The purpose of this presentation is to demonstrate a clinical relationship between otosclerosis and sensorineural hearing loss. Experimental proof will await the accumulation and study of temporal bones of those individuals who, in life, exhibited the clinical relationship to be developed in this dissertation. The material presented is from the author's private practice during the years 1974, 1975 and 1976. Patients presenting the clinical problem of progressive sensorineural hearing loss were examined in depth including diagnostic audiology and polytomography of the petrosa. This thesis shows that a high percentage of such diagnostic problems are due to cochlear otosclerosis, the diagnosis being clinically supported roentgenologically.