1241例聋儿40Hz听觉相关电位和听性脑干反应

本文对１２４１例（２４８２耳）聋儿同时作了４０Ｈｚ听觉相关电位（４０ＨｚＡＥＲＰ）和听性脑干反应（ＡＢＲ）测试，均用ＮＩＣＯＬＥＴＰＡＴＨＦＩＤＥＲⅡ型诱发电位仪测试。结果：（１）在用睡眠药组４０ＨｚＡＥＲＰ和ＡＢＲ的引出率均低于不用睡眠药组；（２）４０ＨｚＡＥＲＰ和ＡＢＲ阈值差显示：用睡眠药组４０ＨｚＡＥＲＰ阈值＜ＡＢＲ阈值的占３５６％明显低于不用睡眠药组的５９８９％。表明：（１）４０ＨｚＡＥＲＰ检出残余听力优于ＡＢＲ；（２）服用睡眠剂可使患儿４０ＨｚＡＥＲＰ反应阈值增高     

甲状腺功能低下对ABR和DPOAE的影响

为了探讨甲状腺功能低下（甲低）时听觉功能损害的部位及可能的致病机理，用含甲硫咪唑（０．１５ｇ／Ｌ）的饮用水喂养大鼠制造甲低模型，对甲低前后的大鼠进行听性脑干反应（ＡＢＲ）和畸变产物耳声发射（ＤＰＯＡＥ）的检测。结果发现：甲低后ＡＢＲ阈值明显升高；而ＡＢＲ各波潜伏期及波间期无明显变化。ＤＰＯＡＥ“听力图”显示甲低后ＤＰＯＡＥ振幅明显下降；ＤＰＯＡＥ阈值明显上升。提示耳蜗是甲低时听觉功能损害的主要部位，文中对可能的发病机理进行了讨论。     

新生儿听行为侧听与刺激声类型关系的研究

目的探讨新生儿听行为与刺激声类型的关系,为新生儿听行为筛选测听选择声刺激类型与听反应行为方式提供依据。方法１０２名新生儿,经瞬态诱发性耳声发射（Ｔｒａｎｓｉｅｎｔｅｖｏｋｅｄｏｔｏａｃｏｕｓｔｉｃｅｍｉｓｉｏｎ,ＴＥＯＡＥ）证实其一耳或双耳有正常的ＴＥＯＡＥ波形为研究对象。声场给声,刺激声分别为０５、１、３ｋＨｚ纯音、高频窄带噪声（中心频率３ｋＨｚ,带宽２５４４～３６５２Ｈｚ）以及白噪声。分析恒定强度声刺激下眼睑反应、头部反应、面部反应、肢体反应的反应次数。结果（１）在诱发各种类型听性反应的反应率时,纯音低于噪声,高频窄带噪声低于白噪声;（２）在恒定强度声刺激下,眼睑反应的反应率最高,肢体反应次之;（３）白噪声、高频窄带噪声引出眼睑反应次数无差异。白噪声引出眼睑反应次数与肢体反应次数无差异。结论（１）高频窄带噪声与白噪声是理想的刺激声,眼睑反应与肢体反应是理想的听性反应;（２）高频窄带噪声与眼睑反应、白噪声与肢体反应是最佳组合。     

豚鼠听觉脑干电反应信号小波变换分析

目的：将小波变换这种时频域信号分析方法用于豚鼠听觉脑干电位分析,以了解小波变换是否适用于ＡＢＲ信号分析,较之传统法有否优越之处。方法 雄性纯白豚鼠３０只分成正常,传导性聋,感音性聋三组,每组１０只,要集各组７５ｄＢｎＨＬ短声诱发的ＡＢＲ,用小波处理软件进行变换,将变换前后信号的时域值作配对统计处理,结果 小波２尺度变换使原信号失真,４尺度变换增加原信号的背景噪声,３尺度变换可保持原信号的时域特征,     

正常新生豚鼠听性脑干反应的时域和频域特性

本文对正常新生豚鼠听性脑干反应（ＡＢＲ）时域和频域特性进行了研究。结果表明：正常新生豚鼠ＡＢＲ的反应阈为２２±４ｄＢｎＨＬ（０ｄＢｎＨＬ＝１７ｄＢＳＰＬ），约比正常成年豚鼠ＡＢＲ的反应阈高１０ｄＢｎＨＬ；正常新生豚鼠波Ⅲ潜伏期、Ⅰ─Ⅲ波间期均明显长于正常成年豚鼠（Ｐ＜０．０１），而波Ⅰ潜伏期无显著性差异（Ｐ＞０．０５）；潜伏期─强度函数曲线的斜率大于正常成年豚鼠；功率谱表明，与正常成年豚鼠相比较，０～２００Ｈｚ、５１０～９００Ｈｚ频段谱能量有显著性差异（Ｐ＜０．０５、Ｐ＜０．０１）。     

冲击波对豚鼠螺旋神经节细胞谷氨酸免疫反应及听阈的影响

豚鼠经平均压力峰值１８４ｄＢ（ＳＰＬ）的冲击波一次暴露后，分别测８、２４、７２小时、７天的螺旋神经节（ＳＧ）细胞谷氨酸免疫反应（Ｇｌｕ－ＩＲ）阳性产物的光密度值，均较对照组明显增高（Ｐ＜０．０１）。以８小时者光密度最大，７天者最小。免疫透射电镜发现，爆震后８小时豚鼠ＳＧⅠ型、Ⅱ型细胞浆内ＬＵ－ＩＲ阳性产物明显增多。不同时间组ＡＢＲ阈移与Ｇｌｕ－ＩＲ阳性产物光密度的变化率成正相关（ｒ＝０．９１９，Ｐ＜０．０５）。提示冲击波所致听力损伤与ＳＧ细胞内Ｇｌｕ变化有关。     

儿童脑干中线病变ABR特征分析

作者报告５例儿童脑干中线病变。其ＡＢＲ测试结果有下列特征性表现：双耳波Ⅰ～Ⅴ波间潜伏期均明显延长，但双侧相近；△Ⅴ值双耳呈正值；双耳波Ⅰ～Ⅴ波间期差及双耳波Ⅴ潜伏期差（ＩＬＤ）却在正常范围。这是出于脑干中线病变不同于单侧桥小脑角病变，它对两侧听神经通路压迫、阻断程度接近所致。临床上应重视上述特征，以期及早作出电生理诊断。     

Auditory nerve and brain stem responses in homozygous jaundiced gunn rats

Summary In humans, functional evidence based on recording cochlear microphonic, auditory nerve, and brain stem responses has shown that the site of lesion in hearing loss following neonatal hyperbilirubinemia is the auditory nerve (with sparing of the hair cells). Structural damage to the central nervous system (CNS) including the cochlear nuclei has been demonstrated in adult, homozygous Gunn rats which develop hyperbilirubinemia shortly after birth. In an attempt to use the Gunn rat as an experimental model for bilirubin-induced CNS damage, auditory nerve and brain stem responses (ABR) were recorded in jaundiced (homozygous) and non-jaundiced (heterozygous) Gunn rats and in Sabra (Wistar) rats. All of the rats including the jaundiced Gunn rats had normal ABR and responded behaviorally to sound stimuli. These results suggest that the adult jaundiced Gunn rat retains auditory function and in this way differs from human patients in whom neonatal jaundice has lead to hearing loss. Therefore, the adult homozygous Gunn rat probably cannot serve as a model for hearing loss due to hyperbilirubinemia.     

Habituation and rate effect in the auditory cortical potentials evoked by trains of stimuli

Summary The effects of the stimulus repetition rate over the habituated auditory cortical evoked responses were studied. The stimulation pattern consisted of trains of pure tone bursts with interstimulus interval (ISI) of 1 s, and intertrain interval (ITI) of 5 s, delivered with constant time and intensity parameters during 93 min. The analysis of the responses was based upon across averaging of the trains, each single response being evaluated in the latency and amplitude parameters. Two time-dependent factors affected the responses in a distinct way: the habituation throughout the whole stimulation and the rate effect within the train. The linear regressions of the time/amplitude functions of the responses were calculated in relation to the duration of ISI and ITI. By introducing a correction factor depending on the repetition rate it was possible to evaluate the relationships between habituation and repetition rate. Changes in the repetition rate do not have any effect on the habituation process. The two phenomena are completely distinct, and they probably have neurophysiologic substrates corresponding to different levels in the central nervous system (CNS).     

Aspects in diagnostics of central neural hearing disorders

Summary The central neural hearing disorders — in contrast to central cortical lesions — can be concretely defined audiometrically, and they can be localized realiably within the 2nd–4th neurons. For this purpose a definite test program is needed; especially indicative are the behavior of the acoustico-facial stapedius reflex and the results in dichotic discrimination and ERA. SISI and difference limen mostly point to a neural dysfunction, but — in distinct patterns of impairment — they may correspond to the picture of a peripheral hearing disorder as well. A fatigue of hearing apparently only appears if the myelin is damaged, at — perhaps additional — axonal lesions it shows up less clearly or not at all. The deficiency pattern of the stapedius reflex reflects the course of the reflex arc within the brain stem; accordingly, more central lesions of the auditory pathway do not affect the reflex. ERA mostly makes perceivable a lesion of synchronization, which only becomes noticeable at fast repetition rates with ultra short stimuli (1/4 ms), i.e., solely in the responses of the brain stem. The cortical responses, on the contrary, are not impaired more than the subjective threshold renders to be expected, they even show the same values of the pure tone audiogram. The dichotic discrimination is nearly always disturbed unilaterally, at processes of the brain stem homolaterally, at cortical foci predominantly leftside, perhaps because the left hemisphere dominates in speech discrimination. The otologist should know how to make use of the possibility of neuro-otologic diagnostics.Presented at the Annual Meeting of the Deutsche Gesellschaft für Sprach- und Stimmheilkunde, Mainz, May 30, 1981