高压对耳蜗的影响

目的研究高压环境对人耳蜗的影响,弥补试验手段不足导致的耳蜗在高压环境下听力行为特征研究的缺失,为今后对耳蜗进行针对性研究提供新的思路。方法基于健康人耳蜗CT扫描图像,结合自编程序,利用PATRAN软件建立三维螺旋耳蜗有限元模型。应用NASTRAN软件进行流固耦合频率响应分析和瞬态响应分析,通过数值模拟方法研究高压对耳蜗的影响。结果基底膜12 mm处与镫骨底板中心(卵圆窗的中心)处位移比值模拟结果与已报道的试验结果相吻合,验证了所建模型的正确性。高压环境下,耳蜗中基底膜特征频率点的幅值随着压强的增大而不断减小。结论高压环境最终导致人耳听力的降低。研究结果为临床上研制防治高压的缓冲装置提供理论支撑。     

不同激振位置对压电式人工中耳听力补偿性能的影响

研究不同激振位置对压电式人工中耳听力补偿性能的影响,确定压电式人工中耳最优激振位置。建立人耳有限元模型,并通过和相关实验数据进行对比验证模型的可靠性。基于该模型,分别在鼓膜脐部、砧骨体、砧骨长突和圆窗施加相同的位移驱动,通过检测镫骨足底板位移及基底膜的最大位移,分析这些位置的激振对人工中耳听力补偿性能的影响。结果表明,以镫骨足底板位移为评估标准会低估圆窗激振的高频听力补偿效果。砧骨长突激振下的基底膜特征位置处的运动位移大于激振鼓膜脐部及激振砧骨体时的位移值,其中激振砧骨体时的基底膜特征位置处运动位移最小;激振圆窗时的基底膜特征位置处运动位移在低频段小于激振其他位置时对应的位移值,但在中、高频段其激振效果最好。在频率低于400 Hz时,砧骨长突激励听力补偿效果最好,圆窗激励听力补偿效果最差。当频率大于1 kHz时,圆窗激励听力补偿效果比其他位置好。以传统的镫骨足底板响应为评估标准,将低估圆窗激振式人工中耳的听力补偿效果。     

基于基底膜响应的圆窗激振性能评估偏差研究

目的研究采用传统基底膜位移评价标准评估圆窗激振式人工中耳听力补偿性能的准确性,为圆窗激振式人工中耳的性能评估提供理论基础。方法基于耳蜗几何结构的实验数据,建立耳蜗感声微观有限元模型,通过对比内听毛细胞、外听毛细胞、盖膜等部位位移响应的实验测量值,验证模型的可靠性。基于该模型,对比分析正向激振、圆窗激振下的基底膜位移与内听毛细胞静纤毛剪切位移;以内听毛细胞静纤毛剪切位移作为感声标准,研究圆窗激振时采用传统人工中耳基底膜评价标准的等效声压级偏差。结果在所研究耳蜗微段对应的5 k Hz特征频率处,相同幅值的声压作用下,圆窗激振的基底膜位移和内听毛细胞静纤毛剪切位移均小于正向激振的对应值。结论正向激振下的内听毛细胞更兴奋,感声效果更强。同时,采用正向激振的基底膜位移评价方法评估圆窗激振的听力补偿效果,会高估圆窗激振的听力补偿性能;但偏差较小,是一种相对可靠的评价方法。     

人耳蜗基底膜模型的动力特性有限元数值模拟

目的采用有限元模拟,建立人耳蜗基底膜模型,研究耳蜗结构的动力响应。方法应用有限元方法,利用大型有限分析软件ANSYS求解基底膜简化模型的模态。结果 得到了模型上不同部位产生最大振幅时对应的振动频率。结论 频率不同时,行波传播的远近和最大行波的出现部位不同。振动频率愈低,最大行波振幅出现的部位愈靠近基底膜顶部;相反地,高频率声音引起的基底膜振动,只局限于卵圆窗附近。从一个新的角度验证了行波理论。     

基于中耳与耳蜗集成有限元模型的耳声传递模拟

建立外耳道、中耳和简化耳蜗集成的有限元模型,包含中耳和耳蜗结构、耳道和中耳腔内的空气以及耳蜗内的液体.采用声-结构耦合动力学分析,计算声音由外耳道向内耳的传递过程,获得了鼓膜、镫骨足板的位移、中耳的声压增益、前庭阶的压力分布,同时也模拟了基底膜自蜗底至顶端的频率选择特性.计算结果与相关文献的实验结果具有较好的一致性,说明本模型对中耳传声功能模拟的准确性.结果表明,改进的耳蜗模型可为耳蜗运动功能模拟的探索提供更充分和合理的信息.     

外耳道静压对声音传递和耳蜗输入影响数值分析

为分析静压变化对中耳听骨链运动和耳蜗输入的影响,运用有限元模型研究外耳道静压导致的中耳声音传递功能和耳蜗激励输入改变。首先,根据相关实验测量数据并结合有限元分析,拟合了耳道静压力与中耳各构件有效弹性模量关系的经验公式;然后,通过材料参数的改变模拟压力造成的中耳结构刚度增加,分析耳道静压对中耳机动性的影响和不同耳道压力下镫骨底板位移、速度和耳蜗两窗压力差的变化。计算结果与相关的文献实验数据有较好的符合,说明所建立的计算模型在模拟静压条件下中耳传递功能方面的合理性。结果表明在低频范围(0～0.6 kHz)外耳道静压对两窗压力差的影响稍大于对镫骨位移的影响。     

置换部分听骨赝复物后对人耳听力恢复的影响

目的探讨听骨部分置换术中不同的置换方式对患者术后听力的影响。方法根据人体正常右耳CT扫描结果,用自编程序将CT扫描数值化并导入PATRAN重建人耳三维有限元模型,对其进行声音传导动力分析,并与试验数据对比。结果通过正常人耳结构动力响应分析结果与实验数据吻合,验证了模型的正确性;在0.1～10 kHz频率下保留部分锤骨柄置换人工听骨比不保留锤骨柄术后听力恢复更好,听力恢复值在11.56～28.91 dB之间;保留部分锤骨柄时鼓膜处的最大应力值比不保留锤骨柄时更小;厚2.0 mm软骨片在0.1～0.6 kHz,2～10 kHz频率上听力恢复较好;厚0.1 mm软骨片在0.6～2 kHz频率上听力恢复较好。结论在听骨部分置换术中,保留部分锤骨柄比不保留锤骨柄听力恢复效果更好;鼓膜与人工听骨的接触面上垫置的软骨片厚度在0.1～2.0 mm之间对人耳听力恢复效果较好。     

耳蜗基底膜振动模型的建立与应用

人的耳蜗是一个非凡的感觉器件。它可以分辨出强度差别极其微小和频率非常相近的不同的声音。本文首先通过介绍耳蜗基底膜与听觉结构的生理和解剖特性,然后从数学和物理学的角度分析耳蜗基底膜的结构特性,从而建立了耳蜗基底膜的振动模型。最后应用该模型分析,结果发现本文所建立的耳蜗基底膜振动模型得出的结果与临床解剖和生理实验的结果十分吻合。     

基于压电叠堆的砧骨激励式人工中耳低功耗结构设计

目的设计一种具有位移放大结构的压电振子改进方案,用于降低现有砧骨激励式人工中耳压电叠堆振子的功耗。方法首先,基于人耳解剖结构,设计带有位移放大结构和仅仅由压电叠堆构成的两种压电振子,并建立相应压电振子与中耳的耦合力学模型。通过对比该两种耦合力学模型的计算结果,分析引入位移放大结构前后的人工中耳听力补偿性能及功耗。结果引入位移放大结构后,压电振子在10.5 V有效电压驱动下,在1 kHz频率处的等效声压级由之前的100 dB增大至113 dB。此外,由压电叠堆直接激振时,振子在1、2和4 kHz处的功耗分别为6.42、1.56和0.28 mW;引入位移放大结构后,压电振子对应上述3个频率点的功耗分别降低至0.39、0.09和0.01 mW。结论所设计的带有位移放大结构的压电振子能够提高砧骨激励式人工中耳的听力补偿能力,有效降低压电振子的功耗。研究结果将有助于人工中耳结构设计的进一步完善,从而达到更好的听力补偿效果。     

联合使用助听器和增强电子耳蜗的使用者的中文语音识别

目的使用电子耳蜗与助听器联合的声学模拟考察在语音成形噪声中的中文语音识别.方法使用1增/1减的信噪比自适应变化过程,测试了6个具有正常听力、使用中文语言的被试者在语音成形噪声中的中文句子识别门限(speech recognitionthresholds,SRT).结果中文语音识别门限SRT随模拟系统中助听器的低通滤波截止频率变化的曲线呈现与低通滤波的幅频响应相似的形状.结论只要助听器恢复的残存低频声学听力覆盖了说话人的基频范围,这些低频信息就能显著地帮助电子耳蜗使用者在语音成形噪声中识别中文语音,无论电子耳蜗的整体输入频率范围与助听器恢复的频率范围是否交叠.     

Discharge patterns in the cochlear nucleus of the chinchilla following noise induced asymptotic threshold shift

Summary Chinchillas were exposed to an 86 dB SPL octave band of noise centered at 4.0 kHz for 3.5–5 days. The noise elevated the hearing thresholds between 4.0 and 16.0 kHz to between 60 and 75 dB SPL. Measurements from single neurons in the cochlear nucleus revealed abnormalities in the response properties of neurons with characteristic frequencies (CF) above 2.0 kHz. Units above 2.0 kHz had elevated thresholds (between 50 and 90 dB SPL) and broad tuning curves due to a greater loss in sensitivity near CF than at lower frequencies. The tuning curve Q₁₀dB values for high frequency neurons were generally less than 3.0 and approached the Q₁₀dB values for basilar membrane displacement. Spontaneous activity rates in units above 2.0 kHz were also low. In a few units, the threshold for single tone inhibition was significantly lower than that for excitation; the best inhibitory frequencies were always below 2.0 kHz. Two-tone inhibition was present in both low and high threshold neurons, but its strength was not assessed. Cochleagrams obtained 12 hours postexposure revealed discrete hair cell lesions in the basal third of the cochlea. The locations of the lesions were consistent with the frequencies of maximum hearing loss. The behavioral thresholds and the thresholds at CF of the most sensitive units were within 10–15 dB of each other. The results indicate that intense sounds reduce the sensitivity, frequency selectivity and spontaneous activity of units in the cochlear nucleus. The findings are similar to those obtained in auditory nerve fibers with ototoxic drugs and hypoxia.     

Capsaicin stimulation of the cochlea and electric stimulation of the trigeminal ganglion mediate vascular permeability in cochlear and vertebro-basilar arteries: a potential cause of inner ear dysfunction in headache

Trigeminal neurogenic inflammation is one explanation for the development of vascular migraine. The triggers for this inflammation and pain are not well understood, but are probably vasoactive components acting on the blood vessel wall. Migraine-related inner ear symptoms like phonophobia, tinnitus, fluctuation in hearing perception and increased noise sensitivity provide indirect evidence that cochlear blood vessels are also affected by basilar artery migraine. The purpose of this investigation was to determine if a functional connection exists between the cochlea and the basilar artery. Neuronally mediated permeability changes in the cochlea and basilar artery were measured by colloidal silver and Evans Blue extravasation, following orthodromic and antidromic stimulation of the trigeminal ganglion innervating the cochlea. Capsaicin and electrical stimulation induced both dose- and time-dependent plasma extravasation of colloidal silver and Evans Blue from the basilar artery and anterior inferior cerebellar artery. Both orthodromic and antidromic activation of trigeminal sensory fibers also induced cochlear vascular permeability changes and significant quantitative differences between the treated and control groups in spectrophotometric assays.These results characterize a vasoactive connection between the cochlea and vertebro-basilar system through the trigeminal sensory neurons. We propose that vertigo, tinnitus and hearing deficits associated with basilar migraine could arise by excitation of the trigeminal nerve fibers in the cochlea, resulting in local plasma extravasation. In addition, cochlear "dysfunction" may also trigger basilar and cluster headache by afferent input to the trigeminal system.     

Micromechanical responses to tones in the auditory fovea of the greater mustached bat's cochlea.

An extended region of the greater mustached bat's cochlea, the sparsely innervated (SI) zone, is located just basally to the frequency place of the dominant 61-kHz component of the echolocation signal (CF2). Anatomic adaptations in the SI zone are thought to provide the basis for cochlear resonance to the CF2 echoes and for the extremely sharp tuning throughout the auditory system that allows these bats to detect Doppler shifts in the echoes caused by insect wing beat. We measured basilar membrane (BM) displacements in the SI zone with a laser interferometer and recorded acoustic distortion products at the ear drum at frequencies represented in the SI zone. The basilar membrane in the SI region was tuned both to its characteristic frequency (62-72 kHz) and to the resonance frequency (61-62 kHz). With increasing stimulus levels, the displacement growth functions are compressive curves with initial slopes close to unity, and their properties are consistent with the mammalian cochlear amplifier working at high sound frequencies. The sharp basilar membrane resonance is associated with a phase lag of 180 degrees and with a shift of the peak resonance to lower frequencies for high stimulus levels. Within the range of the resonance, the distortion product otoacoustic emissions, which have been attributed to the resonance of the tectorial membrane in the SI region, are associated with an abrupt phase change of 360 degrees. It is proposed that a standing wave resonance of the tectorial membrane drives the BM in the SI region and that the outer hair cells enhance, fine tune, and control the resonance. In the SI region, cochlear micromechanics appear to be able to work in two different modes: a conventional traveling wave leads to shear displacement between basilar and tectorial membrane and to neuronal excitation for 62-70 kHz. In addition, the SI region responds to 61-62 kHz with a resonance based on standing waves and thus preprocesses signals which are represented more apically in the CF2 region of the cochlea.     

Unilateral hearing losses alter loud sound-induced temporary threshold shifts and efferent effects in the normal-hearing ear

In animals with bilaterally normal hearing, olivocochlear pathways can protect the cochlea from the temporary shifts in hearing sensitivity (temporary threshold shifts; TTSs) caused by short-duration intense loud sounds. The crossed olivocochlear pathway provides protection during binaural loud sound, and uncrossed pathways protect when monaural or binaural loud sounds occur in noise backgrounds. Here I demonstrate that when there is a chronic unilateral hearing loss, effects of loud sounds, and efferent effects on loud sound, in the normal-hearing ear differ markedly from normal. Three categories of test animals with unilateral hearing loss were tested for effects at the normal-hearing ear. In all categories a monaural loud tone to the normal-hearing ear produced lower-than-normal TTSs, apparently because of a tonic re-setting of that ear's susceptibility to loud sound. Second, in the two test categories in which the hearing-loss ear was only partly damaged, binaural loud sound exacerbated TTSs in the normal-hearing ear because it caused threshold shifts that were a combination of "pure" TTSs and uncrossed efferent suppression of cochlear sensitivity. (In normal cats, this binaural tone results in crossed olivocochlear protection that reduces TTS.) Binaural loud sound did not produce such uncrossed efferent effects in the test category in which the nontest ear had suffered total hearing loss, suggesting that this uncrossed efferent effect required binaural input to the CNS. It is noteworthy that, in the absence of this uncrossed efferent suppression, the pure loud sound-alone induced TTSs after binaural exposure were low. Thus in the absence of any efferent effect, the normal-hearing cochlea had a reduced susceptibility to loud tone-induced damage. Finally, the results suggest that, with respect to cochlear actions at high sound levels, uncrossed and crossed efferent pathways may exert different effects at the one type of receptor cell.     

Bandwidth dependency of cochlear centrifugal pathways in modulating hearing desensitization caused by loud sound

Centrifugal olivocochlear (OC) pathways modulate cochlear hearing desensitization induced by loud sounds, but there is a null point, determined by sound bandwidth, for this effect. In a previous study, using loud sounds from the region of greatest hearing sensitivity in cats, OC pathways did not affect desensitization induced by 2-kHz wide noise, but did to narrower bandwidth (tones) or broader bandwidth (3.5 kHz-wide or 5 kHz-wide noise) trauma from the same cochlear region. The bandwidth null-point effect occurred in three very different conditions in which OC pathways modulated losses to narrower or broader bandwidth traumata, confirming the robustness of this phenomenon, and was also true for sub-component OC pathways: neither crossed nor uncrossed OC pathways individually modulated desensitization to that 2 kHz-wide noise. The medial olivocochlear system (MOCS) that is most likely to have modulated desensitization in that study, varies in its cochlear distribution; in cats, densest innervation is in the region of greatest hearing sensitivity and the decrease away from that region means MOCS effects there may not translate to other regions. This hypothesis was now tested in lower- (around 4 kHz) and higher- (around 18 kHz) frequency cochlear regions. Across this fairly large cochlear swath, no OC modulation of desensitization occurred to 2-kHz-wide bandwidth sounds, but did to broader bandwidth; thus the bandwidth dependency was constant across this swath. However, when OC effects did occur, the pattern of effects of OC sub-components could be idiosyncratic to sound bandwidth and cochlear region even for similar net OC effects.     

Early and late reaction of the guinea pig cochlea to impulse noise

Guinea pigs (GP) were exposed to 10 impulses of 164 dB (SPL). Measuring of cochlear microphonics (CM) at frequencies between 0.5 and 10 kHz and morphological examination of the cochlea by the surface preparation technique followed 2 hours, 2 and 6 weeks after exposure to impulse noise. During the 2 hours following noise exposure the amplitudes of CM decreased in all tested frequencies, while recovery of CM never could be observed at this time. Subsequent morphological changes in the structure of the organ of Corti could be found. They varied considerably between the tested animals. 2 and 6 weeks after exposure to 10 impulses all GP had irreversible defects in the cochlea in an extent from an incomplete pattern of outer hair cells up to a total lack of areas of the organ of Corti. Only in GP with morphological damages in a small extent CM were recordable again. A good agreement of functional and morphological results was established. It can be concluded that exposure to few single impulses with peaks of sound pressure of sufficient intensity will produce irreversible morphological defects in the cochlea, resulting in marked functional injury, if the damaged area is large enough.