畸变产物耳声发射在噪声性听力损伤中的应用

目的:比较畸变产物耳声发射(DPOAE)与纯音测听对噪声性聋的敏感性,探讨DPOAE在噪声性聋的检测和诊断中的应用价值。方法:分别对60例正常人(对照组)和62例纯音测听正常的噪声环境工作者(实验组)进行DPOAE检测和纯音测听,比较两组的结果。结果:实验组的DPOAE幅值和引出率在3,4,6 kHz处均明显下降,与对照组比较差异有显著性(P<0.01)。结论:DPOAE对早期监测、评估和诊断职业性听力损失具有应用价值。     

畸变产物耳声发射对3389例新生儿听力筛查的临床分析

目的应用畸变产物耳声发射（DPOAE）法与听性脑干反应（ABR）联合应用，初步探讨该法在我院推广应用的价值。方法应用畸变产物耳声发射（DPOAE）法对3389名新生儿，分别于出生的1～5d及5d～1个月（提前出院而延筛）进行听力筛查，经3次筛查不通过的新生儿联合应用GSI诱发电位仪进行检查，作出听力损伤的结论。结果对3389例新生儿进行DPOAE听力筛选，经1～3次DPOAE筛查通过，通过率为99．93％，复筛未通过者由ABR确诊，共检出听力障碍儿4例，发病率为1．18‰，其中正常新生儿1例，发病率为0．46‰，高危新生儿3例，发病率为19．86‰。结论DPOAE测试具有方便、快速、无创、客观等优点，但其只能反映耳蜗功能，不能用来诊断听神经或中枢听觉通路病损，同时由于假阳性率较高，对未通过DPOAE筛查者不能立即作出听力损伤的结论。ABR测试为比较可靠的新生儿听力筛查工具，联合DPOAE和ABR听力筛查技术，使其相互补充，能提高新生儿听力筛查的精确性、可靠性，具有很好的临床应用价值。     

正常青年女性畸变产物耳声发射测试分析

目的：检查正常青年人DPOAE范围，为临床应用提供良好依据。方法：对30例（60耳）听力正常青年人，用CAPELLA机型耳声发射仪进行DPOAE测试，选择初始音强度L1＝70dBSPL,L2=60dBSPL，水平差10dBSPL。结果：DPOAE总检出率为100％，正常青年人DPOAE幅值差距大，显示出明显个体差异，不同频率处DPOAE幅值有所不同，1KHz，8KHz处幅值最大，信噪比各频率均在10dBSPL以上（明显高出3dBSPL）。结论：发现不同频率下DPOAE图形非光滑曲线，而呈双峰型，双耳显著差异（P＞0．05).     

听神经病患者畸变产物耳声发射特征分析

目的研究听神经病患者畸变产物耳声发射的特征,探讨耳声发射在听神经病诊断中的意义。方法对听神经病患者45例（90耳）和正常人38例（76耳）行畸变产物耳声发射测试,并对2组测试结果进行统计学分析。结果听神经病组和正常对照组的DPOAE全部可引出,听神经病组DPOAE的幅值在所有9个频率点均高于正常对照组,除4.0kHz点（P=0.606）外,2组间差异均有统计学意义（P〈0.01）。听神经病组的DP图幅值与本底噪声的差值（SNR）在0.5、0.7、4.0、6.0、8.0kHz5个频率点低于正常对照组,除4.0kHz点（P=0.126）外,2组间的差异均有统计学意义（P〈0.01）;在1.0、1.4、2.0、3.0kHz处高于正常对照组,1.0k,1.4k2组间差异无统计学意义（P〉0.05）,在2.0、3.0kHz处2组间差异有统计学意义（P〉0.05）。结论畸变产物耳声发射是诊断听神经病的重要听力学依据。     

高血脂豚鼠的畸变产物耳声发射观察

目的 了解高血脂豚鼠的畸变产物耳声发射特点.方法 对20只血脂正常和高血脂豚鼠分别进行畸变产物耳声发射(DPOAE)检测,记录听力图.结果 f0从0.5、1、2、4、8kHz时两组各频率2f2-f1 DPOAE反应幅值检出率均为100%,高血脂组的各频率反应幅值均较血脂正常组低,两组的听力图曲线显示2kHz的反应幅值较其它频率低;8kHz的反应幅值较其它频率高,两组8kHz反应幅值比较差异有显著性(P＜0.05).结论 高血脂可使豚鼠的DPOAE幅值下降,DPOAE是耳蜗早期损伤的敏感指示器,对早期检测蜗性聋有临床指导意义.     

畸变产物耳声放射法在新生儿听力筛查中的应用价值

目的：应用畸变产物耳声发射法对新生儿进行听力筛查,探讨其在小儿听力障碍诊断、干预中的应用价值。方法对1170例婴儿采用畸变产物耳声发射法进行听力筛查,对第一次筛查未通过者,与出院前和出生后42 d分别进行复查,若两次复查仍未通过,则通过脑干听觉诱发电位进行确诊。结果1170例婴儿通过检测,通过率为96.8%,未通过率为3.2%。经过脑干反应检查异常者3例,听力障碍发生率为2.56‰,其中单耳聋为2例,双耳聋为1例。结论畸变产物耳声发射法适合小儿听力筛查,有利于及早发现儿童听力障碍,以便早期进行干预。     

突发性聋畸变产物耳声发射与预后的关系

我们于1999年3月～2000年12月对29例突发性聋(突聋)患者进行了耳声发射(OAE)检查,旨在了解突聋患者耳声发射的变化、预后与耳声发射的关系。     

畸变产物耳声发射对伪聋的诊断价值

目的探讨畸变产物耳声发射对伪聋的诊断价值。方法运用畸变产物耳声发射（DPOAE）技术对伪聋组、感音神经性聋组和正常对照组进行DPOAE检查。结果伪聋组和正常对照组DPOAE的平均检出率分别为96．92％和97％，两组比较差异无统计学意义（P〉0．05）；感音神经性聋组的平均检出率为18％，与伪聋组和正常对照组比较差异有统计学意义（P〈0．001），且当听闻〉50dB时检出率为零。结论DPOAE检查可作为识别伪聋的客观检查方法。     

畸变产物耳声发射在新生儿听力筛查中的应用

<正>随着我国新生儿听力筛查工作的推广,现在很多医院都逐渐开展了新生儿听力筛查。听力障碍是常见的出生缺陷之一,婴幼儿听力损失直接影响其语言的形成,主要表现为发音不清,严重者甚至可导致聋哑。同时,语言发育的落后还可以影响儿童心理、智力和社会交往能力的发展,给社会、家庭带来沉重的负担。笔者所在医院应用畸变产物耳声发射     

Emerging treatments for noise-induced hearing loss

Introduction: Approximately 5% of the population worldwide suffers from industrial, military or recreational noise-induced hearing loss (NIHL) at a great economic cost and detriment to the quality of life of the affected individuals. This review discusses pharmacological strategies to attenuate NIHL that have been developed in animal models and that are now beginning to be tested in field trials.

Areas covered: The review describes the epidemiology, pathology and pathophysiology of NIHL in experimental animals and humans. The underlying molecular mechanisms of damage are then discussed as a basis for therapeutic approaches to ameliorate the loss of auditory function. Finally, studies in military, industrial and recreational settings are evaluated. Literature was searched using the terms ‘noise-induced hearing loss’ and ‘noise trauma’.

Expert opinion: NIHL, in principle, can be prevented. With the current pace of development, oral drugs to protect against NIHL should be available within the next 5 – 10 years. Positive results from ongoing trials combined with additional laboratory tests might accelerate the time from the bench to clinical treatment.     

噪声性听力损伤药物防治的研究进展

噪声是一种常见的严重危害人类身心健康的环境因素,噪声危害在不断增加,其危害范围也在不断扩大。关于噪声引起的听力损伤的研究一直是一项重要的研究内容。噪声性听力损伤的产生有多种机制,耳蜗内大量氧自由基的形成和与Ca2+失衡引起的血管微循环障碍可能是重要原因。目前用于防治噪声性听力损伤的药物主要是神经营养剂、血管调节剂、抗氧化剂等。本文对噪声性听力损伤药物防治方面的一些研究进展进行了综述。     

The effects of lead on otoacoustic emissions and auditory evoked potentials in monkeys

Auditory functioning was assessed in two groups of adult rhesus monkeys (11 years of age). One (n = 11) received modest exposure to lead early in life and the other (n = 8) served as controls and did not receive any lead supplementation. Two lead-exposed monkeys had abnormal distortion product otoacoustic emissions (DPEs) and smaller amplitude or absent evoked potentials. These monkeys had the highest blood levels recorded in their respective groups. For the remaining lead-exposed monkeys there was little difference between their DPEs and the DPEs of the control monkeys with one exception. DPE amplitudes of the control monkeys increased more rapidly as a function of stimulus level than those of the lead-exposed monkeys at most frequencies. There was also a significant but modest effect of lead exposure on the auditory brain stem evoked responses (ABRs) of these lead-exposed monkeys. There was no apparent effect on the middle latency evoked responses (MLRs), although that result could be due to the relatively greater variability of the MLR.     

60例高危新生儿听性脑干反应和畸变产物耳声发射结果分析

目的 探讨听性脑干反应(ABR)及畸变产物耳声发射(DPOAE )两种测试方法在高危新生儿听力筛选中的意义。方法　对60名高危新儿(120耳)采用ABR及DPOAE检测技术对其进行了听力监测。结果　120耳经DPOAE检测。在未通过DPOAE的44耳中有26耳通过ABR检测,而在通过DPOAE的76耳中有14耳未通过ABR。结论 对高危新生儿的听力筛查,建议联合应用ABR与DOPAE方法,以免漏诊、误诊。     

Perinatal exposure to Aroclor 1254 impairs distortion product otoacoustic emissions (DPOAEs) in rats.

Polychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants that are a potential health hazard to human and wildlife populations. Low-frequency auditory impairments have previously been documented in Aroclor 1254 (A 1254)-exposed rats, including elevated behavioral auditory thresholds and decreased amplitude and prolonged latency auditory evoked brain stem responses (ABRs). Furthermore, outer hair-cell loss on the basilar membrane of the cochlea has been documented, demonstrating that the cochlea is a target organ for PCB ototoxicity. The current experiment assessed the effects of A1254 on cochlear function by measuring distortion product otoacoustic emissions (DPOAEs). ABRs were measured to determine the effects of A1254 on the central nervous system auditory pathways. Pregnant Long-Evans rats received either 0 or 6 mg/kg A1254 (po) in corn oil from gestation day 6 to lactational day 21. The auditory function of male and female offspring was assessed at approximately 18 months of age. The rats were anesthetized and a probe-unit, consisting of 2 insert earphones and a microphone, was positioned in the ear canal. DPOAE amplitudes were reduced and thresholds increased in the A1254-exposed rats. The deficits were most pronounced at the lowest frequencies tested (2.1-3.2 kHz), but deficits were also observed at higher frequencies (3.7-8.6 kHz). Males and females were equally affected at the lower frequencies, but females were more impaired at the higher frequencies. In contrast, ABR latencies and amplitudes were not altered by A1254 exposure. These findings provide the first functional evidence supporting a cochlear site of damage in PCB-induced hearing loss.     

Early investigational drugs for hearing loss

Introduction: Sensorineural hearing loss (HL) is becoming a global phenomenon at an alarming rate. Nearly 600 million people have been estimated to have significant HL in at least one ear. There are several different causes of sensorineural HL included in this review of new investigational drugs for HL. They are noise-induced, drug-induced, sudden sensorineural HL, presbycusis and HL due to cytomegalovirus infections.

Areas covered: This review presents trends in research for new investigational drugs encompassing a variety of causes of HL. The studies presented here are the latest developments either in the research laboratories or in preclinical, Phase 0, Phase I or Phase II clinical trials for drugs targeting HL.

Expert opinion: While it is important that prophylactic measures are developed, it is extremely crucial that rescue strategies for unexpected or unavoidable cochlear insult be established. To achieve this goal for the development of drugs for HL, innovative strategies and extensive testing are required for progress from the bench to bedside. However, although a great deal of research needs to be done to achieve the ultimate goal of protecting the ear against acquired sensorineural HL, we are likely to see exciting breakthroughs in the near future.     

噪声致听力损伤豚鼠穴位注射神经生长因子疗效分析

目的探讨神经生长因子（NGF）对噪声所致听力损伤豚鼠的修复作用。方法取健康雄性豚鼠48只随机分成4组,分别为对照组（正常组）、腹腔注射组、穴位注射组、模型组（听力损伤）,除对照组以外,其余3组豚鼠均24h放置在声压级100dB（A）的白噪声中,共7d,每组豚鼠均用畸变产物耳声发射（DPOAE）来判断其幅值、信噪比;然后通过注射NGF,观察其对各组豚鼠听觉通路上GJB2基因、SLC26A4基因表达的影响。结果穴位注射组DPOAE幅值测试结果和性噪比测试结果,提示除f0为0．25Hz处P〉0．05外,其余频区P〈0．01：穴位注射组GJB2基因、SLC26A4基因表达分别为8．45和6．65（OD／dL）,显著低于其他观察组（P〈0．05）。结论神经生长因子穴位注射不失为一种治疗噪声性听力损伤安全有效的新方法。     

Potentiation of noise-induced hearing loss by low concentrations of hydrogen cyanide in rats.

Noise-induced hearing loss is the most prevalent occupational injury in the United States despite the adoption of clear permissible exposure limits and protocols for hearing conservation. This study identifies low-level chemical asphyxiant exposure as a risk factor capable of potentiating noise-induced hearing loss. Rats were exposed to 10, 30, and 50 ppm hydrogen cyanide (HCN) alone for 3.5 h (n = 28) or in combination with 2 h octave band noise exposure (100 dB(lin); n = 28). Additional groups received noise exposure alone (n = 16) and no treatment other than placement in an inhalation chamber with clean air and quiet (n = 16). Pure tone compound action potential (CAP) thresholds were determined 4 weeks following the exposure in order to assess pure tone auditory sensitivity and permanent threshold impairment. Cochleae from an additional 13 subjects were processed for light microscopy to permit assessment of hair cell loss. The results demonstrate that the noise exposure alone impaired CAP threshold by about 10 dB, averaged between 12-40 kHz, and produced a 5% loss of outer hair cells at the base of the cochlea, but no inner hair cell loss. The combined exposure to noise and HCN caused a cyanide dose-dependent CAP threshold impairment that exceeds the noise exposure alone. This effect reached statistical significance at a HCN level of 30 ppm. Combined exposure also produced more outer hair cell loss than noise alone. HCN alone did not cause significant hearing loss or hair cell loss. A risk assessment analysis was conducted for the auditory threshold data using benchmark dose software published by the U. S. EPA (BMDS version 1.3). A continuous model showed that the data could be described by a linear function. For a benchmark response corresponding to a 5 dB increase in auditory threshold above the effect of noise alone, the lower bound on the 95% confidence interval for the benchmark dose was 9 ppm. The benchmark dose that impaired auditory threshold 10% above the effect of noise alone had a lower bound of 2 ppm. The lower bound to the HCN dose that produced a 1 SD elevation in noise-induced hearing loss was 16 ppm. These exposure levels provide a range of concentrations below to slightly above the short-term exposure limit for HCN. However, if these levels are adjusted for an 8 h time-weighted average (TWA), the resulting levels are below the permissible exposure level (PEL) for HCN.     

The effects of early lead exposure on auditory function in rhesus monkeys

Thirty-one female rhesus monkeys were randomly assigned to three lead exposure conditions (none, birth to 1 year, and birth to 2 years). Blood lead levels were maintained at 35–40 μg/dl beginning shortly after birth and continuing for 1 or 2 years postnatally. Auditory function was assessed in these monkeys at least 1 year after exposure to lead. The outcome measures included tympanometry to assess middle ear function, otoacoustic emissions (OAEs) to assess cochlear function, and auditory brainstem-evoked responses (ABRs) to assess the auditory nerve and brainstem pathways. There were no significant differences among the three experimental groups for any of the tympanometric variables measured suggesting no effect of lead exposure on middle ear function. Suprathreshold and threshold distortion product OAEs (DPOAEs) were comparable among the three groups. Finally, the auditory-evoked response at levels from the auditory nerve to the cerebral cortex did not significantly differ as a function of lead exposure. The lead exposure in this study had little effect on auditory function.