足月新生儿听觉脑干电反应的特性

本文工作根据北京市儿童医院临床的需要,在临床实验条件下对足月新生儿的ABR进行了测量,以期分析足月新生儿ABR的电反应特征。 新生儿听觉脑干反应(ABR)的波形是Ⅰ、Ⅲ、Ⅴ波为主的连续波复合体;新生儿在声强80dB(HL)刺激频率20次/秒的短声刺激条件下,I、Ⅲ、Ⅴ波潜伏期大体为2.50,5.00和7.00ms;新生儿ABR潜伏期—刺激强度函数的斜率是30—60μsec/dB(声刺激强度从80到50dB(HL),声刺激频率20次/秒);新生儿ABR Ⅴ波对Ⅰ波的比率大于1.0(短声强度80dB(HL),刺激频率20次/秒);在80dB(HL)短声条件下,改变声刺激频率(从20次/秒增止100次/秒),Ⅴ波潜伏期约延长0.6—1.0ms;新生儿ABR阈值在30—60dB(HL)的范围。综上所述新生儿ABR电反应特性,可以为其听力和脑干功能的临床诊断提供可靠的指标和依据。     

有关猫听觉脑干电反应（ABR）两耳干涉作用的研究

用不同声强稳态白噪声和短声同时分别刺激两耳,观察白噪声负荷侧耳蜗破坏前后另一侧ＡＢＲ的改变,探讨两耳干涉作用及其可能的机制。结果显示,对侧耳蜗破坏前,４０ｄＢ和７５ｄＢ白噪声对０ｄＢ、４５ｄＢ、７０ｄＢ和７５ｄＢＳＰＬ的短声诱发的ＡＢＲ各波振幅均有明显影响（Ｐ＜０．０５０．０１）。耳蜗破坏后,同样条件下记录的ＡＢＲ振幅基本无明显变化（Ｐ＞０．０５）。提示白噪声对短声有一定的干涉作用。短声为７０ｄＢＳＰＬ时ＡＢＲＰ１波振幅的减小可能与中枢离中控制相关。     

白噪声对听觉脑干电反应(ABR)和耳蜗电图(ECochG)的影响

本文通过20例听力正常人和10例听力正常豚鼠研究了白噪声对耳蜗电图(ECochG)和听觉脑干电反应(ABR)的干涉作用。实验结果表明,白噪声比短声(信号)的声强级低30dB(SL)以上时,ECochG和ABR的振幅仅轻微减小。白噪声与短声的声强级相等时,ECochG与ABR的振幅和出现率会明显受到干涉而减小,甚至完全消失。但是,此时的耳蜗微音器电位(CM)并未观察到有明显的变化。这意味着白噪声对ECochG和ABR的干涉作用主要与围绕毛细胞基底部的突触产生的抑制密切相关。由于白噪声对ABR各波的干涉有些差异,所以认为这种抑制,可能既包括脑中抑制也包括侧方抑制。     

我国正常成人脑干听觉电反应各波潜伏期的测定

在10名正常被试者的20只耳,用不同强度的短声测定了脑干听觉电反应(BSR)的7个波的潜伏期(数值见表1),结果表明,各波的潜伏期都随刺激声强的减弱(80到0 dB)而延长,且呈直线函数关系,并且这种延长主要来自1波。由每个被试者两耳所诱发的 BSR 各波的潜伏期及其与刺激声强的变化关系都较为恒定和对称。V 波振幅较大,出现率较高,接近主观听觉阈值,是 BSR 中的主波,其潜伏期(声强80 dB 时为5.7±0.6毫秒)如明显超出此范围(6.3毫秒)或两侧不对称时,应考虑为异常。我们还在半数测试例中记录到Ⅷ波,关于它的生理意义,尚不清楚。     

有关猫交叉听力及其对检测耳影响的初步研究

目的研究猫的交叉听力现象及其产生机理,初步探讨交叉听力对检测耳ABR振幅的影响。方法用彻底破坏一侧耳蜗的方法,观察16只听力正常家猫的交叉听力现象及其对检测耳的影响。结果①当短声强度≥75dB(SPL)时,开始出现交叉听力波形,声强增至95dB时,交叉听力波形最典型。②95dB短声产生的交叉听力波形可被40或45dB(SPL)的稳态白噪声（SWN）完全屏蔽掉。③在同一时间轴中比较95dB短声诱发的ABR和交叉听力波形,发现交叉听力之波谷恰与ABR之pⅢ、pⅣ波峰相对应。④两耳均正常时对侧耳负荷的40dBSWN可使95dB短声诱发的ABR之pⅢ、pⅣ波振幅增大,且具统计学意义（P＜0.01）。结论交叉听力对ABR振幅的影响取决于两者的波峰与波谷在同一时间轴上的对应情况,声强较大时记录到的ABR,实质上是交叉听力与刺激侧产生的ABR在同一时间轴上的综合电位。     

脑干缺血对听觉脑干反应影响的实验研究

目的 :探讨脑干缺血模型ABR变化特点及其在脑缺血早期诊断中的应用价值。方法 :阻断猫基底动脉不同部位血流 ,观察记录阻断血流后不同时间ABR变化特点及其规律。结果 :①夹闭基底动脉上、下段或小脑下前动脉 10min左右 ,ABRP3 ,P4振幅明显减小 (P <0 .0 1,P <0 .0 5 ) ,60min恢复夹前水平 ;②夹闭基底动脉上段 10～60minP5明显减小 (P <0 .0 5 ) ,直到 12 0min尚未恢复至夹前状态。结论 :①猫的ABRP3脑区的血供主要来自小脑下前动脉 ,P1,P2产生部位基本不依赖基底动脉供血 ;②轻度暂短性脑缺血时ABR振幅比潜伏期更敏感 ,振幅减小的程度与脑干缺血的程度密切相关 ;③ABR可用于脑缺血定位诊断及脑功能动态观察的电生理检测。     

孤独症谱系障碍儿童听觉脑干反应特征分析

摘要 目的：探讨孤独症谱系障碍(autism spectrum disorder,ASD)儿童听觉脑干反应(auditory brainstem response,ABR)各波潜伏期和波间期特征与ASD行为表型间的关联。方法：对2019年7月-2020年12月来我科就诊的26例明确诊断的2~6岁ASD儿童的患儿进行声导抗,听性脑干反应,畸变产物耳声发射及多频稳态听觉诱发电位测试,以38例正常儿童为对照组,进行同样的测试,并对其测试结果进行统计分析。分析ASD儿童左右耳各波潜伏期,波间期特征及与ASD临床表型的关联。结果：ASD儿童左右耳Ⅰ,Ⅲ,Ⅴ波潜伏期分别为(1.42±0.09)ms,(3.67±0.09)ms,(5.65±0.13)ms;(1.45±0.11)ms,(3.69±0.08)ms,(5.62±0.15)ms。ASD组的右耳I,III波的潜伏期均值大于正常组 (P 值均＜0.05);ASD儿童两组间左耳III-V,右耳III-V,右耳I-V的波间期分别是(1.97±0.07)ms,(1.93±0.10)ms,(4.15±0.14)ms;ASD组的左耳III-V,右耳III-V,右耳I-V波间期均小于正常组(P 值均＜0.05);ASD组中小于等于3岁组与大于3岁组间ABR波间期差异不具有统计学意义。关联性分析发现,ASD儿童语言能力与右耳III波潜伏期,右耳最小阈值V波潜伏期负相关;社会行为能力与右耳I-III波间期负相关;社会生活能力与左耳最小阈值V波潜伏期负相关;而ABC评分与ASD儿童右耳III波潜伏期,左耳I-III波间期,右耳I-III波间期正相关。结论：ASD儿童存在异常的听觉脑干反应特征,且异常程度与 ASD 儿童语言,社会行为能力,社会生活能力的严重程度存在明显关联。     

猫听觉脑干诱发电反应中P_(2a)和P_(2b)波的起源

在33例猫将普鲁卡因或海人酸微量注入耳蜗核(CN)和上橄榄复合体(SOC)内,观察ABR的相应改变,以分析P_(2a)和P_(2b)波的来源。猫P_(2a)波的出现率与电极导联有关,颅顶-颈后为90％,颅顶-乳突仅为18％。普普卡因注入CN后,同侧耳短声诱发的ABR仅保留P_1波,对侧耳的则无改变。海人酸注入CN后,P_1和P_(2a)存留,P_(2a)不减小反而增大。普鲁卡因注入双侧SOC,可使P_3、P_4和P_5消失。这些结果提示,P_(2a)波主要起源于CN区域内的第一级听觉传入神经元轴突并受第二级神经元负电位的影响,P_(2b)波主要起源于SOC以下的第二级听觉传入神经元,猫的P_(2a)和P_(2a)波与对侧脑干结构无关。     

杏仁体影响兔内膝体双耳神经元的声反应

实验在２３只三碘季胺酚麻痹的新西兰兔上进行。采用记录单个神经元放电的方法,观察了刺激杏仁体对内膝体（ｍｅｄｉａｌｇｅｎｉｃｕｌａｔｅｂｏｄｙ,ＭＧＢ）６５个双耳神经元声反应的影响。实验结果表明：杏仁刺激对其中２１个神经元的活动产生抑制性影响（占３２．３％）。刺激杏仁外侧核或基底核,既能抑制内膝体神经元对单侧耳声刺激的反应,也可抑制该神经元对双耳声刺激的反应。杏仁体所产生的这种抑制性影响的潜伏期最短为２ｍｓ,表明是经由杏仁－内膝体单突触联系。一般认为,接受双耳信息的神经元与声源定位有关,因此可以推测杏仁体的活动可以干预动物对声源的定位。     

豚鼠脑干听觉中枢的立体定位

用常规组织学、声诱发电位、HRP逆行追踪等方法确定了豚鼠耳蜗核、上橄榄复合体、外侧丘系核及下丘的定位坐标值。对320—700g的豚鼠,耳蜗核中心位置的模坐标值为P 2.3,LL/RL 3.0,H1.5;上橄榄复合体为P2.3,LL/RL1.6,H-1.5;外侧丘系核为P0.8,LL/RL 2.0,H-1.5;下丘为A2.0,LL/RL 2.2,H5.5。对每一脑干中枢,当记录电极插至中心位置时短声诱发电位的振幅最大,主波为负。     

Auditory brain stem responses in characterization of dolphin hearing

Summary Auditory brain stem responses (ABR) were recorded from the head surface of non-anesthetized and non-relaxed bottle-nosed dolphins, Tursiops truncatus. The region of best ABR recording was shown to be located 6–9 cm caudal to the blowhole. The threshold values were about 1 mPa for noise bursts and –3 dB re 1 mPa for tone bursts of the optimal frequency (80 kHz). The maximum frequency at which ABR could be evoked was 140 kHz. The duration of temporal summation reached 0.5 ms at intensities near the threshold and decreased with an increase in intensity. When the stimuli were paired clicks of the same intensity, the time to complete recovery from the second response was about 5 ms, while that to its 50% recovery was 0.7 ms. When the conditioning click exceeded the testing one in intensity, prolongation of the recovery period was observed. A 40-dB intensity difference led to an approximately 10-fold prolongation of this period.Abbreviations ABR auditory brain stem response - EP evoked potential     

Effect of stimulus mode on middle latency auditory evoked potentials in humans

Middle Latency Auditory Evoked Potentials (MLAEPs) were recorded in 35 healthy subjects; all underwent monaural stimulation and 18 of them additionally underwent binaural stimulation. The aim of the study was to determine the effect of stimulus mode on MLAEP Na, Pa and Nb components and to assess normative data for clinical purposes. MLAEPs were respectively obtained from Cz-ipsilateral ear lobe (monaural mode) and from Cz-A1 and Cz-A2 (binaural mode) by twice averaging 1000 responses to 65 dBHL alternating clicks delivered at a repetition rate of 8.1 Hz. Time base was 100 msec; analogical band-pass filter setting was 5-1000 Hz (off-line digital badpass: 20-100 Hz). The statistical analyses (paired t-test, repeated measures analysis of variance) were not able to demonstrate any differences that derived from differing sides of stimulation (monaural mode) or from differing recording derivations (binaural mode); on the contrary, we demonstrated a slight increase in waveform amplitudes when the binaural mode was employed. In particular, we observed an increase in Na-Pa peak-to-peak amplitude, whereas Pa-Nb amplitude was unmodified. This finding is explicable in terms of a binaural interaction effect. Finally, we propose some guidelines for the correct performance and evaluation of MLAEPs in clinical practice.     

Auditory brain stem responses to monoaural stimulation registered in symmetrical areas of cat's brain cortex

In five anaesthetized cats (Nembutal 35 mg/kg) with 14 chronically implanted recording epidural electrodes the auditory brain stem responses (ABR) to monoaural stimulation (click) in symmetrical areas of the brain cortex were recorded. Each ABR to acoustic stimulus of sufficient intensity is formed by a complex of alternating five positive (P1-P5) and four negative (N1-N4) peaks; two further small peaks often follow on this complex. The amplitude of ABR peaks N3, P4, N4 and P5 to monoaural stimulation in symmetrical areas of cat's cortex was always higher in records from the hemisphere contralateral to the stimulated ear than in records from the ipsilateral one. The amplitude of P3 ABR peak behaved to the contrary--it was higher on ipsilateral hemisphere. On the other hand the amplitude of ABR peaks P1, N1, P2 and N2 to monoaural stimulation in symmetrical areas of the brain cortex showed no degree of lateralization in our experimental animals. The present findings support indirectly the presumption that each peak of the ABR is generated by a particular acoustic brain stem structure.     

Brainstem auditory evoked potentials in the rabbit.

Eight white New Zealand rabbits were submitted to auditory stimulation in order to obtain normative BAEP parameters. A monaural alternating 0.1 ms click stimulation at 20 Hz, 90 dB was used. Two series of 1000 responses were averaged (10 ms time-base, 160-3000 Hz band-pass) and highly reproducible peaks were obtained. Peaks P1, P2, P3, P4 were obtained in all ipsilateral recordings, whereas peak P5 was detectable in only 6 animals. In contralateral recordings P1 was absent and the following peaks were similar to those of ipsilateral recordings. Normative values of absolute and interpeak latencies, peak amplitudes and amplitude ratios were obtained. The procedure was repeated 24 hours after basal recordings and measures of test-retest variability were obtained.     

The modulation rate transfer function of a harbour porpoise (Phocoena phocoena)

During echolocation, toothed whales produce ultrasonic clicks at extremely rapid rates and listen for the returning echoes. The auditory brainstem response (ABR) duration was evaluated in terms of latency between single peaks: 5.5 ms (from peak I to VII), 3.4 ms (I–VI), and 1.4 ms (II–IV). In comparison to the killer whale and the bottlenose dolphin, the ABR of the harbour porpoise has shorter intervals between the peaks and consequently a shorter ABR duration. This indicates that the ABR duration and peak latencies are possibly related to the relative size of the auditory structures of the central nervous system and thus to the animal’s size. The ABR to a sinusoidal amplitude modulated stimulus at 125 kHz (sensitivity threshold 63 dB re 1 μPa rms) was evaluated to determine the modulation rate transfer function of a harbour porpoise. The ABR showed distinct envelope following responses up to a modulation rate of 1,900 Hz. The corresponding calculated equivalent rectangular duration of 263 μs indicates a good temporal resolution in the harbour porpoise auditory system similar to the one for the bottlenose dolphin. The results explain how the harbour porpoise can follow clicks and echoes during echolocation with very short inter click intervals.     

Real-time imaging of neural activity during binaural interaction in the guinea pig auditory cortex

Spatio-temporal patterns of binaural interaction in the guinea pig auditory cortex (AC) were observed using optical recording with a 12 × 12 photodiode array and a voltage-sensitive dye. The amplitudes of the sound-induced light signals from the cortex were transformed into sequential two-dimensional images every 0.58 ms. Binaural sound stimuli evoked an excitatory response followed by a strong inhibition, and contralateral stimuli evoked a strong excitatory response followed by a weak inhibition. Ipsilateral sound stimuli evoked a weak response. Binaural stimulation induced two types of ipsilateral inhibition: a fast binaural inhibition which was detected only after the contralateral and ipsilateral responses were subtracted from the binaural responses, and which appeared 12–25 ms after the onset of stimulation, and a slow binaural inhibitory effect which was clearly observed in the binaural responses themselves, appearing 70–95 ms after the onset of stimulation. The fast binaural inhibition was observed in the same area as the contralateral excitatory response. The inhibited area became stronger and more widespread with increasing intensity of ipsilateral stimulation. We did not observe the specialized organization of binaural neurons as electrophysiologically found in the cat AC, in which binaural neurons of the same binaural response type are clustered together and alternate with clusters of other response types. Accepted: 14 August 1997     

Responses of auditory cortical neurons to paired clicks

In cats immobilized with tubocurarine, a paired-click method was used to determine the duration of the refractory period of 75 auditory cortical neurons responding to clicks with a latent period of up to 30 msec. Sixty-eight of the neurons exhibited no spontaneous activity, while in the other seven spontaneous activity was infrequent and irregular. It was found that a click makes responding neurons refractory to a second click for a long time. The duration of this refractory period is 3 to 700 msec; it is constant for each neuron, but varies from one neuron to another. A direct relationship was found between the number of neurons responding to the second click and the interval between the first and second clicks: the shorter the interval the fewer neurons respond to the second click. It is postulated that this dependence lies at the basis of the neurophysiological mechanism of perception and discrimination of short time intervals.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 2, No. 3, pp. 227–235, May–June, 1970.     

Dopaminergic modulation of the P50 auditory-evoked potential in a computer model of the CA3 region of the hippocampus: its relationship to sensory gating in schizophrenia

 We modeled the neuronal circuits that may underlie a sensory-processing deficit associated with schizophrenia. Schizophrenic patients have small P50 auditory-evoked responses to click stimuli compared to normal subjects. The P50 auditory-evoked response is a positive waveform recorded in the EEG approximately 50 ms after the auditory click stimulus. In addition to relatively small amplitudes, schizophrenic patients do not gate or suppress the P50 auditory-evoked response to the second of two paired-click stimuli spaced 0.5 s apart. Neuropleptic medication, which decreases dopaminergic neuronal transmission, increases the amplitude of the P50 auditory-evoked response but does not improve gating. Normal subjects have large P50 auditory-evoked responses to click stimuli when compared to unmedicated schizophrenic patients, and they gate their response to paired click stimuli or have smaller P50 auditory-evoked response amplitudes to the second of two click stimuli spaced 0.5 s apart. Schizophrenic patients do not gate and have similar response amplitudes to both clicks. We hypothesized that the small amplitudes of unmedicated schizophrenic subjects were due to a state of occlusion whereby excessive background noise in local circuits reduced the ability of cells to respond synchronously to sensory input, thereby reducing the amplitude of the P50 waveform in the EEG. Because the P50 auditory-evoked potential amplitudes increased with neuroleptic medication, which reduces dopaminergic neuronal transmission, we hypothesized a role for dopamine in modulating the signal-to-noise (S/N) in the local circuits responsible for sensory gating. To test the hypothesis that modulation of the S/N ratio reduces sensory gating, we developed a model of the effects of dopaminergic neuronal transmission that modulates the S/N in neuronal circuits. The model uses the biologically relevant computer model of the CA3 region of the hippocampus developed in the companion paper [Moxon et al. (2003) Biol Cybern, this volume]. Modified Hebb cell assemblies represented the response of the network to the click stimulus. The results of our model showed that excessive dopaminergic input impaired the ability of cells to respond synchronously to sensory input, which reduced the amplitudes of the P50 evoked responses. Received: 3 December 2001 / Accepted: 23 October 2002 / Published online: 28 February 2003 Correspondence to: K.A. Moxon (e-mail: karen.moxon@drexel.edu, Tel.: +1-215-8951959, Fax: +1-215-8954983) Supported by USPHS, MH01245 & MH58414, MH-01121, and research grants from the Department of Veterans Affairs and the National Alliance for Research on Schizophrenia and Depression.