Mechanisms in noise-induced permanent hearing loss: an evoked otoacoustic emission and auditory brainstem response study

In this study 22 patients (44 ears) with noise-induced permanent hearing loss were audiologically evaluated using transient-evoked otoacoustic emissions (TEOAE) and auditory brain-stem response (ABR). Twenty-one normal subjects (42 ears) without exposure to occupational noise were used as controls. Based upon the hearing loss at 4, 3, 2 and 1 kHz on the pure-tone audiogram, they were classified into four groups. In group 1 (eight ears), emissions were present in all ears but their TEOAE-noise level and their reproducibility (percentage) proved to be weak. The auditory brain-stem response (ABR) indicated that the I/V amplitude ratio, the latency values of wave V and the I-V intervals fell within the normal range in all ears. In Group 2 (14 ears), 40 per cent had no emissions, whereas the remaining ears showed weak emissions. The ABR revealed that in all ears the I/V amplitude ratio became small while wave V peak latency as well as I-V intervals were within the normal range. In Group 3 (10 ears), emissions were absent in 50 per cent, while in the other ears the emissions were very weak. The ABR revealed that the I/V amplitude ratio, which could be calculated in the 60 per cent in which wave I was present, was smaller than in Group 2. Wave V latency as well as I-V intervals were within the normal range. In Group 4 (12 ears), none of the ears showed emissions. The ABR indicated that the I/V amplitude ratio was much smaller when wave I was present (27 per cent) as well as I-V interval values being within the normal range. Wave V absolute latency value (delta V index) indicated a positive index in 17 per cent of this group (two ears) when wave I was absent. In the present study a dynamic process from cochlear outer hair cells to cochlear neurons was seen, correlating with an increasing hearing loss.     

听神经病/听觉失同步化患者的交替短声诱发耳蜗电图

目的 分析听神经病/听觉失同步化(auditory neuropathy/auditory desynchronization.AN/AD)患者交替短声诱发的耳蜗电图特征,探索耳蜗电图在确定听神经病,听觉失同步化病变部位时的应用价值.方法 AN/AD组患者14人,共28耳,所有患者听性脑干反应(ABR)波形缺失或严重分化异常,耳声发射正常:听力正常对照组28人,共35耳.对两组受试者行耳蜗电图(ECochG)检查,使用交替极性短声作为刺激信号.观测AN/AD组和对照组ECochG的波形,并对比:(1)CAP-N1(复合动作电位N1波)的峰潜伏期;(2)-SP(总和电位)和CAP绝对幅度;(3)-SP和CAP幅度比值;(4)CAP反应周值.结果 对照组全部引出分化良好的CAP和-SP.AN/AD组ECochG波形可分为四种类型:(1)可同时引出-SP、CAP,占60.7%;(2)仅有-SP引出,未见CAP引出,占10.7%;(3)仅有CAP引出,占3.6%;(4)-SP、CAP均未引出,占25%.AN/AD组与对照组的CAP潜伏期(P=0.052)无统计学差异;ANIAD组的CAP绝对幅度低于对照组(P<0.001),-SP(P=0.045)绝对幅度、-SP/CAP幅度比(P<0.001)和阈值(P<0.001)高于对照组.结论 在ABR引不出或分化较差时,耳蜗电图是一种比较可靠的评估外周听觉神经功能的方法,在AN/AD的诊断中能够发挥重要作用.     

Electrocochleography in auditory neuropathy

Auditory neuropathy (AN) is a disorder characterized by the absence or the severe impairment of the auditory brainstem responses (ABRs) together with the preservation of otoacoustic emissions and/or cochlear microphonic (CM). We recorded transtympanic electrocochleography (ECohG) evoked by 0.1 ms clicks in one young adult and in four children having distortion product otoacoustic emissions and absent ABRs. In all but one patient CM and summating potential (SP) were present with normal threshold, and their amplitudes appeared comparable to or higher than the values obtained from subjects with normal hearing. The compound action potential (CAP) was absent in two patients while in one subject CM and SP were followed by a highly desynchronized neural activity. A broad CAP was found in two children and the threshold appeared clearly elevated in one of them, while it showed only a mild elevation in the other. No correlation was found between CAP and behavioral thresholds. These results suggest that ECohG can be useful in AN diagnoses since it is the only reliable tool in evaluating the auditory peripheral function in the presence of a desynchronized ABR.     

Auditory brainstem responses predict auditory nerve fiber thresholds and frequency selectivity in hearing impaired chinchillas

Noninvasive auditory brainstem responses (ABRs) are commonly used to assess cochlear pathology in both clinical and research environments. In the current study, we evaluated the relationship between ABR characteristics and more direct measures of cochlear function. We recorded ABRs and auditory nerve (AN) single-unit responses in seven chinchillas with noise-induced hearing loss. ABRs were recorded for 1-8 kHz tone burst stimuli both before and several weeks after 4 h of exposure to a 115 dB SPL, 50 Hz band of noise with a center frequency of 2 kHz. Shifts in ABR characteristics (threshold, wave I amplitude, and wave I latency) following hearing loss were compared to AN-fiber tuning curve properties (threshold and frequency selectivity) in the same animals. As expected, noise exposure generally resulted in an increase in ABR threshold and decrease in wave I amplitude at equal SPL. Wave I amplitude at equal sensation level (SL), however, was similar before and after noise exposure. In addition, noise exposure resulted in decreases in ABR wave I latency at equal SL and, to a lesser extent, at equal SPL. The shifts in ABR characteristics were significantly related to AN-fiber tuning curve properties in the same animal at the same frequency. Larger shifts in ABR thresholds and ABR wave I amplitude at equal SPL were associated with greater AN threshold elevation. Larger reductions in ABR wave I latency at equal SL, on the other hand, were associated with greater loss of AN frequency selectivity. This result is consistent with linear systems theory, which predicts shorter time delays for broader peripheral frequency tuning. Taken together with other studies, our results affirm that ABR thresholds and wave I amplitude provide useful estimates of cochlear sensitivity. Furthermore, comparisons of ABR wave I latency to normative data at the same SL may prove useful for detecting and characterizing loss of cochlear frequency selectivity.     

小儿听神经病的误诊和漏诊

目的:探讨小儿听神经病的临床表现。方法:对一组年龄为4～68个月,听力学检查表现为听神经病患儿的临床资料进行回顾性研究。受试者的入选标准为短声听觉脑干反应(ABR)严重异常而畸变产物耳声发射(DPOAE)和(或)耳蜗微音电位(CM)正常。分析其短声ABR、DPOAE、行为听力测试、声导纳以及内耳MRI等结果。结果:①40例听力学表现为双侧听神经病,8例为单侧;②68.2%耳(60/88)在短声ABR的最大输出强度100dBnHL无反应,而有些耳仅在很高的测试强度有波形分化较差的Ⅴ波;③所有耳均可记录到CM,而只有41.5%能记录到DPOAE;④该组患儿的行为听力结果各种各样,为从轻度到极重度的听力损失;⑤4例经内耳MRI诊断为蜗神经发育不全。结论:在听力学表现为听神经病的儿童:①CM的诊断敏感度较DPOAE高;②各种客观听力测试无法预估行为听力;③需作内耳MRI检查,以除外蜗神经发育不全。     

Evaluation of inner hair cell and nerve fiber loss as sufficient pathologies underlying auditory neuropathy

Auditory neuropathy is a hearing disorder characterized by normal function of outer hair cells, evidenced by intact cochlear microphonic (CM) potentials and otoacoustic emissions (OAEs), with absent or severely dys-synchronized auditory brainstem responses (ABRs). To determine if selective lesions of inner hair cells (IHCs) and auditory nerve fibers (ANFs) can account for these primary clinical features of auditory neuropathy, we measured physiological responses from chinchillas with large lesions of ANFs (about 85%) and IHCs (45% loss in the apical half of the cochlea; 73% in the basal half). Distortion product OAEs and CM potentials were significantly enhanced, whereas summating potentials and compound action potentials (CAPs) were significantly reduced. CAP threshold was elevated by 7.5 dB, but response synchrony was well preserved down to threshold levels of stimulation. Similarly, ABR threshold was elevated by 5.6 dB, but all waves were present and well synchronized down to threshold levels in all animals. Thus, large lesions of IHCs and ANFs reduced response amplitudes but did not abolish or severely dys-synchronize CAPs or ABRs. Pathologies other than or in addition to ANF and IHC loss are likely to account for the evoked potential dys-synchrony that is a clinical hallmark of auditory neuropathy in humans.     

Using concha electrodes to measure cochlear microphonic waveforms and auditory brainstem responses

During electrocochleography, that is, ECochG or ECoG, a recording electrode can be placed in the ear canal lateral to the tympanic membrane. We designed a concha electrode to record both sinusoidal waveforms of cochlear microphonics (CMs) and auditory brainstem responses (ABRs). The amplitudes of CM waveforms and Wave I or compound action potentials (CAPs) recorded at the concha were greater than those recorded at the mastoid but slightly lower than those recorded at the ear canal. Wave V amplitudes recorded at the concha were greater than those recorded at the ear canal but lower than those recorded at the mastoid. There was not a significant difference between the amplitudes recorded at the concha and at the ear canal. For CM and Wave I or CAP, the latency recorded at the concha was longer than at the canal but shorter than at the mastoid; for Wave V, the reverse was true. However, these differences were not statistically significant and may be due to the distance to response generators. Aside from the advantages that the regular ECoG has over otoacoustic emission (OAE) testing, the concha electrode was also easier and safer to place and may be suitable for children, newborn screening, participants with canal conditions, and remote clinics which could have concerns with the availability and cost of a canal electrode. Using concha electrodes, we also experienced fewer postauricular artifacts than when using a mastoid electrode.     

Auditory neuropathy characteristics in children with cochlear nerve deficiency

OBJECTIVE: To describe a group of children exhibiting electrophysiologic responses characteristic of auditory neuropathy (AN) who were subsequently identified as having absent or small cochlear nerves (i.e., cochlear nerve deficiency). DESIGN: A retrospective review of the clinical records, audiological testing results, and magnetic resonance imaging (MRI) studies. Fifty-one of 65 children with AN characteristics on auditory brain stem response (ABR) testing had MRI available for review. Nine (18%) of these 51 children with ABR characteristic of AN have been identified as having small (N = 2; 4%) or absent (N = 7; 14%) cochlear nerves on MRI. RESULTS: Of the nine children with cochlear nerve deficiency, five (56%) were affected unilaterally and four (44%) bilaterally. Eight of nine presented after failing a newborn infant hearing screening, whereas one presented at 3 yr of age. On diagnostic ABR testing, all 9 children (9 of 13 affected ears; 69%) had evidence of a cochlear microphonic (CM) and absent neural responses in at least one ear. In the unilateral cases, AN characteristics were detected in all affected ears. In bilateral cases, at least one of the ears in each child demonstrated the AN phenotype, whereas the contralateral ear had no CM identified. Only one ear with cochlear nerve deficiency had present otoacoustic emissions as measured by distortion-product otoacoustic emissions. In children with appropriate available behavioral testing results, all ears without cochlear nerves were identified as having a profound hearing loss. Only 4 (31%) of the 13 ears with cochlear nerve deficiency had a small internal auditory canal on MRI. CONCLUSIONS: Children with cochlear nerve deficiency can present with electrophysiologic evidence of AN. These children frequently refer on newborn screening examinations that use ABR-based testing methods. Similar to other causes of AN, diagnostic ABR testing will show a CM with absent neural responses. Given that 9 (18%) of 51 children with available MRI and electrophysiologic characteristics of AN in our program have been identified as having cochlear nerve deficiency makes this a relatively common diagnosis. These findings suggest that MRI is indicated for all children diagnosed with AN. Moreover, electrophysiologic evidence of unilateral AN in association with a profound hearing loss should make the clinician highly suspicious for this problem. Although children with cochlear nerve deficiency who have a small nerve may benefit from cochlear implantation or amplification, these interventions are obviously contraindicated in children with completely absent cochlear nerves.     

Electrophysiological measures of auditory function in the neurofilament-deficient mutant quail (Quv)

Auditory pathway electrophysiological studies were performed on the mutant quail 'Quv'. This mutation is known to result in neurofilament deficiencies of both the peripheral and central nervous systems. Auditory evoked brainstem responses (ABRs), electrocochleograms (EcochGs) and middle latency responses (MLRs) were evaluated. ABRs in Quv quails demonstrated markedly altered waveforms exhibiting longer latencies, absence of the later peaks and lower amplitudes. The EcochG showed normal cochlear microphonics with no obvious abnormalities in amplitude or latency and normal latencies for peak N1. Quv quails had a mild threshold elevation with a normal latency for the first peak of the ABR (P1). The Quv MLRs showed no significant differences in amplitude but they revealed a latency prolongation for peaks N0, Pa and Na relative to the controls. We have discovered abnormal findings of auditory evoked potentials in the neurofilament-deficient quail (Quv). We suggest that the smaller axonal size and axonal hypotrophy due to altered neurofilament expression underlies these abnormal auditory evoked potential responses.     

Persistent Auditory Nerve Damage Following Kainic Acid Excitotoxicity in the Budgerigar (<Emphasis Type="Italic">Melopsittacus undulatus</Emphasis>)

Permanent loss of auditory nerve (AN) fibers occurs with increasing age and sound overexposure, sometimes without hair cell damage or associated audiometric threshold elevation. Rodent studies suggest effects of AN damage on central processing and behavior, but these species have limited capacity to discriminate low-frequency speech-like sounds. Here, we introduce a new animal model of AN damage in an avian communication specialist, the budgerigar (Melopsittacus undulatus). The budgerigar is a vocal learner and speech mimic with sensitive low-frequency hearing and human-like behavioral sensitivity to many complex signals including speech components. Excitotoxic AN damage was induced through bilateral cochlear infusions of kainic acid (KA). Acute KA effects on cochlear function were assessed using AN compound action potentials (CAPs) and hair cell cochlear microphonics (CMs). Long-term KA effects were assessed using auditory brainstem response (ABR) measurements for up to 31 weeks post-KA exposure. KA infusion immediately abolished AN CAPs while having mild impact on the CM. ABR wave I, the far-field AN response, showed a pronounced 40–75 % amplitude reduction at moderate-to-high sound levels that persisted for the duration of the study. In contrast, wave I latency and the amplitude of wave V were nearly unaffected by KA, and waves II–IV were less reduced than wave I. ABR thresholds, calculated based on complete response waveforms, showed no impairment following KA. These results demonstrate that KA exposure in the budgerigar causes irreversible AN damage, most likely through excitotoxic injury to afferent fibers or synapses as in other species, while sparing ABR thresholds. Normal wave V amplitude, assumed to originate centrally, may persist through compensatory mechanisms that restore central response amplitude by downregulating inhibition. Future studies in this new animal model of AN damage can explore effects of this neural lesion, in isolation from hair cell trauma and threshold elevation, on central processing and perception of complex sounds.     

Prevalence of auditory neuropathy/synaptopathy in a population of children with profound hearing loss

OBJECTIVE: To examine the prevalence of auditory neuropathy/synaptopathy (AN/AS) in a cohort of children with profound hearing loss. METHODS: From 1997 until 2004, 5190 children, aged 1-15 years, whose hearing ability was uncertain or who had risk factors for hearing impairment were investigated with subjective and objective hearing tests. Three thousand four hundred and fifteen from these children were screened for AN/AS using pure-tone audiometry, impedance measurement, transient evoked otoacoustic emissions (TEOAE) and click-evoked auditory brainstem responses (ABR). RESULTS: From 3415 patients who participated in an ABR and TEOAE assessment, 379 children showed absent or elevated (> or = 80 dB nHL) ABR thresholds. Within this group we found 32 cases with evidence of AN/AS via visible TEOAE and/or cochlear microphonics (CM) coupled with absent ABR. In the remaining 3036 children, AN/AS, could be ruled out by means of detectable ABR-thresholds and coherent findings in pure-tone audiometry and TEOAE assessment. This results in a prevalence of AN/AS of 0.94% within the group at risk for hearing loss, compared to 8.44% among profoundly hearing impaired children. CONCLUSION: This study shows that AN/AS is a common finding in the population of hearing impaired infants. In the majority of our AN/AS children (50%, n=16), an early audiological diagnosis was made under the age of 12 months. Therefore, clinicians and other health care professionals should generally be sensitised for AN/AS in infants, so that an appropriate treatment can promptly be initiated. Further research on clinical and pathophysiological aspects is necessary to better identify and manage patients suffering from AN/AS.     

Auditory sensitivity in children using the auditory steady-state response

OBJECTIVE: To determine the effectiveness of auditory steady-state response (ASSR) as a measure of hearing sensitivity in young children suspect for significant hearing loss. DESIGN: Within-subject comparisons of click auditory brainstem response (ABR) thresholds and ASSR thresholds. SUBJECTS: The study population comprised 42 children suspect for hearing loss and subsequently referred for hearing assessment using electrophysiologic techniques. MAIN OUTCOME MEASURES: Electrophysiologic threshold responses for click ABR and ASSR stimuli (0.5, 1, 2, and 4 kHz) for right and left ears. RESULTS: Based on ABR and ASSR thresholds, 50% of the subjects demonstrated significant hearing loss in the severe to profound range. In some subjects, ASSRs were present at higher stimulus levels when click ABRs were absent. Significant correlations (P<.05) were found between high-frequency ASSR and click ABR thresholds for this study sample. For some subjects, ASSR findings suggested differences between ears that were not observable from the no-response click ABR results. CONCLUSIONS: Auditory steady-state response testing may provide additional information for children who demonstrate hearing levels in the severe to profound range. This information may be helpful when selecting the ear for cochlear implantation for a young hearing-impaired child. Multiple objective methods, such as ABR and ASSR testing, may be needed to determine accurate hearing sensitivity for young children being considered for sensory devices, and in particular, cochlear implants.     

儿童孤独症患者脑干听觉诱发

目的通过观察儿童孤独症患者脑干听觉诱发电位的改变,探讨听觉诱发电位检测在听觉障碍儿童孤独症诊断中的临床意义.方法按DSM-IV诊断标准确诊的15例孤独症患儿和14例正常对照组,同期接受听觉诱发反应检测,比较两组间波I～V各波峰潜伏期、波峰潜伏期差和波幅的差异.结果孤独症患儿左侧波V、右侧波II峰间潜伏期和右侧I～III、I～V峰间潜伏期差较对照组显著延长(P<0.05～0.005),孤独症组右侧波III振幅较对照组增高(P<0.05),其他各指标两组间无显著性差异.结论孤独症患儿脑干听觉诱发电位的突出改变是潜伏期有延长的趋势;对就诊于耳鼻咽喉科的听阈正常而有听觉障碍,言语交往能力差,脑干听觉诱发电位检查潜伏期延长的儿童,应警惕孤独症或其他神经精神发育障碍.     

Estimation of the status of spiral ganglion neurons and Schwann cells in the auditory neural degeneration mouse using the auditory brainstem response

Conclusion: The auditory brainstem response (ABR) wave I threshold, latency and amplitude are insensitive to spiral ganglion neurons (SGNs) degeneration, but are sensitive to the degeneration of Schwann cells and can estimate the status of Schwann cells in a neural degeneration mouse model. The thorough pre-operative ABR assessment would be helpful in predicting cochlear implant performance.

Objectives: This study aimed in finding a non-invasive electrophysiological method to evaluate the status of the auditory nerve and the Schwann cells in sensorineural hearing loss (SNHL) and auditory neuropathy (AN) ears, and providing useful information for candidates screening and outcome prediction in cochlear implantation.

Methods: The frequency-specific acoustic ABR was recorded in mice. The immunohistochemical staining was performed to detect the SGNs and Schwann cells in mice cochlea. The correlations between ABR wave I metrics and SGNs, Schwann cells were investigated.

Results: In SNHL and AN mice cochlea, statistically significant correlations between ABR wave I thresholds, latencies and amplitudes at 8, 16, and 32?kHz and their corresponding SGNs densities were found only in wave I amplitude at 8?kHz. While the ABR wave I metrics at all three frequencies showed strong significant correlations with their corresponding Schwann cells densities.     

Transient evoked otoacoustic emission measurement in infants

Transient evoked otoacoustic emissions (TEOAEs) were measured and evaluated in 194 ears of 101 subjects under 4 years old who were suspected of hearing loss, using a ILO88 Otoacoustic Emission Analyzer, to study the basic characteristics of this measure and its utility for hearing screening. The mean time necessary to record TEOAEs in both ears was short, about 3 minutes. In 58 ears judged as normal hearing within 30 dB in ABR, TEOAE levels in infants aged less than 2 months were significantly higher than in those aged more than 1 year, especially in the high frequency bands (4-kHz and 5-kHz bands). One case which had been judged as bilateral moderate-to-profound hearing impairment in initial ABR testing showed good responses in TEOAEs, indicating normal cochlear function, and obvious wave Vs in follow-up ABRs recorded at 30 dB nHL confirmed normal auditory function. Therefore, in a case like this one, suspected of retardation in brain stem maturation, TEOAE is more useful than ABR as a hearing screening technique. Since external and middle-ear factors caused poor TEOAE responses in some cases which had been judged as normal hearing by ABR. TEOAE seems to be more sensitive in detecting external and middle ear problems than ABR. Moreover, TEOAE measurement of infants was easy and noninvasive. We conclude that TEOAE is an excellent tool for screening auditory function in infants.     

婴幼儿单侧听神经瘤

目的：探讨婴幼儿单侧听神经病（AN）神经生理学特点。方法：对3例单侧AN患儿在采集病史和耳科检查的基础上,行系统的听力学检查,包括声阻抗、镫骨肌反射、听性脑干反应（ABR）、耳蜗微音电位（CM）、诱发耳声发射（EOAE）、中潜伏期反应（MLR）和事件相关电位（ERP）以及CT和（或）MRI及周围神经系统检查。结果：3例患儿鼓室图均呈“A”型,健耳的同侧和交叉镫骨肌反射可正常引出,而患耳的同侧和交叉镫骨肌反射未引出。3例患儿双侧EOAE有效引出,健耳的ABR正常引出,思耳的ABR未引出,但CM均正常。3例患儿双耳均记录到MLR及ERP。影像学和周围神经系统未见异常。结论：单侧AN与双侧AN有相似的神经生理学特点。对婴幼儿单侧AN的诊断应着重分析其神经生理学特点,建议联合应用EOAE、ABR、CM和影像学检查。应对AN患儿定期随访。     

蹄蝠听性脑干诱发电位特点分析

目的对野生蹄蝠进行短纯音（ToneBurst）和短声（Click）诱导听性脑干反应（ABR）分析,对其ABR特点与已有的研究进行比较,分析其中差异,加深我们对回声定位蝙蝠听觉功能的认识。方法捕捉并饲养野生蹄蝠,运用美国TDT公司（Tucker-Davis Technologies）TDT System Ⅲ诱发电位仪对蝙蝠进行短声和短纯音的听阈测定,分析其波形变化规律,确定其短纯音听阈阈值,分析听力图的特点。结果（1）蹄蝠听阈呈“W”形分布,经统计学分析各听阈区段有统计学意义（P〈0．05）。存在2个听敏区：28kHz处为最敏感的第一听敏区,阈值最低可达15dBSPL,平均29.1dBSPL;40kHz附近出现第二个听敏区,阈值最低25dBSPL,平均35．9dBSPL;在12kHz～64kHz听阈不超过55．9dBSPL。（2）短声引出的蹄蝠ABR可见4个相对稳定的波峰：波I的潜伏期为1．26ms：波Ⅱ较高且尖,潜伏期为1．94ms;波Ⅲ相对稳定,潜伏期为2．47ms;波Ⅴ潜伏期为3．40ms。随着短声强度的上升,在20～80dBSPL声强范围,各个波振幅逐渐增大、潜伏期缓慢缩短。（3）短纯音引出的蹄蝠ABR各波随刺激频率的提高而潜伏期缓慢地缩短,在64kHz以上潜伏期又逐渐延长;在28kHz、80dBSPL条件下,各波潜伏期分别为I波1．74ms,Ⅱ波2．72ms,Ⅲ波3．60ms,Ⅳ波4．58ms,Ⅴ波5．76ms。频率28kHz、声强在45～100dBSPL范围内上升时,主波振幅逐渐增大;但在部分蝙蝠出现主波振幅在达到最大后,随着声强的上升．振幅逐渐减小。（4）在高声强诱发下,短纯音和短声诱发的ABR均可见Ⅰ波分化为2个波峰,Ⅰa和Ⅰb波。（5）越接近敏感频率,ABR波形就越典型,振幅越大。结论（1）蹄蝠听闯呈“W”形分布,类似我们已知的其他回声定位蝙蝠,存在2个听敏区：28kHz处达到最敏感的第一听敏区,40kHz附近出现第二个昕敏区,在12kHz。64kHz听阈不超过55．9dBSPL。（2）从蹄蝠主波与声强、频率的关系可以看出,蝙蝠主波振幅与声强存在一定的正相关。随着接近其敏感听觉频率,波形逐渐变得更为典型,波幅也愈来愈高,反应阈值愈来愈低。但部分蹄蝠在声强高于80dBSPL时,出现振幅随声强增加而下降的趋势,提示可能与中枢某种调节性抑制有关。（3）在高声强诱发下,蹄蝠ABR可以看到Ⅰ波分化为2个波峰,Ⅰa和Ⅰb波,这可能与蝙蝠耳蜗的某些特化结构的“听黄斑”相关。