坑道作业人员的听力损伤

部队坑道作业场所内的大型发电、通风、降湿设备运转时产生较强的噪声 ,其发电机组噪声可达95～ 1 0 5dB(A) ,风机噪声在 85～ 95dB(A)之间 ,大功率电机噪声都在 85dB(A)以上 ,以 2～ 4kHz稳态噪声为主 ,风机噪声还有 6～ 8kHz成分。坑道工作人员长时间在这种环境下工作 ,其听力易受到损伤。我们对 83例坑道工作人员进行听力调查 ,现分析报告如下。1　资料与方法1 .1 　 临床资料坑道工作人员 83例 ,均为男性。按参加坑道工龄分组。 <2年组 39例 ,年龄 1 8～ 2 5岁 ,平均2 1岁 ;2～ 5年组 2 5例 ,年龄 2 0～ 30岁 ,平均 2 3岁 ;>5年组 1…     

早期噪声性听力损失伴耳鸣患者的掩蔽效果分析

目的:观察耳鸣掩蔽疗法在早期噪声性听力损失伴耳鸣患者中的掩蔽效果,为临床该类耳鸣患者的治疗提供依据。方法:对68例早期噪声性听力损失伴耳鸣患者进行常规听力学检查和耳鸣检测,所有患者掩蔽治疗6个月后对其疗效进行比较分析。疗效评估采用耳鸣残疾评估量表及主观视觉模拟量表,测试比较其治疗前后的最小掩蔽声大小。结果:耳鸣检测结果显示该类患者的耳鸣主频绝大部分(59例,86.8%)为4kHz,残余抑制试验完全阳性者居多(44例,64.7%),掩蔽治疗效果好,有效率达83.8%,其中3例耳鸣完全消失;治疗前后耳鸣残疾评估量表得分、主观视觉模拟量表得分和最小掩蔽声大小比较均差异有统计学意义(均P<0.01)。结论:早期噪声性听力损失伴耳鸣患者的掩蔽治疗效果显著,值得推广。     

一种耳鸣分类调查表的介绍（附225例主观耳鸣分析）

耳鸣是临床上常见症状，由于耳鸣的病因非常复杂，耳鸣发生机制仍不清楚，所以耳鸣的治疗也极其困难，耳鸣已经成为临床上迫切需要解决而又难以解决的顽症之一。在采集病史或描述耳鸣时，常常需要对耳鸣进行分类，由于耳鸣的分类方法很多，以致常常遗漏某些重要特征，为此，特设计了一种耳鸣分类调查表。１ 耳鸣分类调查表 该表除一般项目（姓名、性别、年龄、利手、职业等）外，主要用１４个英文字母和２个阿拉伯数字来描述耳鸣，它们是：ＳＯＤＭ，ＡＢＣ，Ｃ－Ｃ－ＣＬＡＰ，ＡＶ９５。它们所代表的意义是：Ｓ－主观耳鸣，Ｏ－客观耳鸣，…     

以听力突然下降为特征的分泌性中耳炎（附24例报告）

目的：提高对以听力突然下降为特征的分泌性中耳炎的确诊率。方法：回顾性分析24例（28耳）以听力突然下降为特征的分泌性中耳炎的临床资料,结果：11例患者被误诊或漏诊,各频率的平均气导阈值在60．2－66．5dBHL,平均骨导阈值在40．5－58．6dBHL,听力图示感音神经性聋9耳,混合性聋19耳,鼓室压图为B型,治疗后听力明显改善,结论,鼓室积液影响圆窗及卵圆窗间的相位差,导致听力突下降,它们的听力图无特征,并对产生误诊的原因进行了讨论。     

172例耳聋学生听力情况的调查报告

我们于1996～1997年对哈尔滨市盲聋哑学校172例聋生进行了有关听力情况的调查,现报告如下.     

262例耳鸣患者听力损失情况的临床调查

目的对耳鸣患者的听力损失情况进行临床调查,为进一步探讨耳鸣的发病原因提供临床资料。方法对262例以耳鸣为第一主诉的患者进行纯音听阈测定,并详细询问耳鸣与听力损失发生的时间和部位,据此将耳鸣与听力的关系分为四种情况：听力正常,听力损失与耳鸣无相关性,听力损失与耳鸣有相关性,听力损失与耳鸣可能相关。结果262例患者中,50%的患者耳鸣与听力损失有相关性,其中27.5%的患者明确有相关性,22.5%的患者可能有相关性;50%的患者耳鸣与听力损失无明显相关性,其中28.2%的患者听力正常,21.8%的患者听力损失与耳鸣无明确的相关性。年龄分布中,20～60岁占78.6%,20岁以下及60岁以后较少。结论耳鸣与听力损失并非总是相伴相随,对耳鸣的发病原因及机理须从多角度进一步研究。     

无自觉听力障碍的耳鸣患者462例听力分析

目的:探讨耳鸣的危险因素,为耳鸣的预防提供科学依据。方法:通过分析462例以耳鸣为惟一主诉的患者听力情况及其耳鸣调查表中所提供的病史,了解各型听力曲线的患者年龄分布、性别特点及所占比例,分析其与噪声接触史、耳毒药物、基础疾病之间的关系。结果:①高频下降型、低频下降型、正常型、中频切迹型、覆盆型及其他型听力曲线所占比例依次为:46.10%、15.80%、14.07%、11.04%、7.58%、5.41%;②年龄分布:高频下降型主要分布在30～40岁患者,低频下降型、正常型、中频切迹型主要分布在20～30岁患者,覆盆型主要分布在50岁以上患者;③男女比例:高频下降型、低频下降型、正常型、中频切迹型、覆盆型及其他型依次为158/55、14/59、29/36、12/39、20/15、9/16;④危险因素:高频下降型、低频下降型、中频切迹型、覆盆型主要危险因素分别为:噪声接触、疲劳或/和精神压力、长期接触乐器、高龄;正常型及其他型未发现明确的危险因素。结论:无自觉听力障碍的耳鸣患者中,听力异常率高达86.00%,其中高频下降型高达46.10%,噪声为主要危险因素,男性为主要受害者;低频下降型占15.80%,疲劳或精神压力为主要危险因素,女性为主要受害者;中频切迹型占11.04%,长期接触乐器为主要危险因素;覆盆型占7.58%,高龄为主要危险因素。     

工厂生产车间噪声对工人听力的影响及其对策

目的探讨工厂生产车间噪声对工人听力的影响。方法对在噪声达85～95dB(A)的工厂生产车间工作的71名工人进行问诊及纯音测听检查。结果所有被调查的工人均伴有不同程度耳鸣、头痛、头昏、烦燥易怒、注意力和记忆力下降、消化不良、食欲不振等症状，均有不同程度听力损伤，随工龄增加听力损伤发生率增加且程度加重。结论噪声对听功能的影响，主要表现在听敏度下降，听阈升高；听力损伤程度与接触噪声的强度、暴露时间有密切关系。     

甲硫氨酸对噪声性听力损失的预防作用研究

目的：探讨口服甲硫氨酸对噪声性听力损失的预防作用。方法将解放军某部健康男性军人203例随机分为试验组（113例）和对照组（90例）,均给予脉冲噪声（峰值160～170 dB SPL）暴露1小时,暴露前3天试验组口服甲硫氨酸片1500 mg/日×3天,对照组则口服等剂量安慰剂（淀粉）。两组受试者噪声暴露前后行纯音测听、听性脑干反应听（ABR）检查,对检查结果进行统计学分析。结果噪声暴露后1天,两组各频率纯音听阈均高于暴露前（P＜0．05或 P＜0．01）,暴露后7天,对照组纯音听阈仍升高（P＜0．05）,而试验组与暴露前比较差异无统计学意义（P＞0．05）;噪声暴露前、暴露后1天、7天,试验组 ABR 反应阈分别为40．5±9．3、51．7±12．3、44．1±11．4 dB nHL,对照组分别为41．5±8．9、62．4±13．7、47．6±12．5 dB nHL,试验组 ABR I－V 波间期分别为3．72±0．21、3．99±0．36、3．82±0．25 ms,对照组分别为3．71±0．22、4．45±0．37、3．85±0．34 ms,噪声暴露后1、7天两组间 ABR 反应阈、I－V 波间期比较差异有统计学意义（P＜0．05或 P＜0．01）。结论噪声暴露前口服甲硫氨酸片能有效减轻噪声暴露后噪声性听力损失的发生。     

Tinnitus and Patterns of Hearing Loss

Tinnitus is strongly linked with the presence of damaged hearing. However, it is not known why tinnitus afflicts only some, and not all, hearing-impaired listeners. One possibility is that tinnitus patients have specific inner ear damage that triggers tinnitus. In this study, differences in cochlear function inferred from psychophysical measures were measured between hearing-impaired listeners with tinnitus and hearing-impaired listeners without tinnitus. Despite having similar average hearing loss, tinnitus patients were observed to have better frequency selectivity and compression than those without tinnitus. The results suggest that the presence of subjective tinnitus may not be strongly associated to outer hair cell impairment, at least where hearing impairment is evident. The results also show a different average pattern of hearing impairment amongst the tinnitus patients, consistent with the suggestion that inner hair cell dysfunction with subsequent reduced auditory innervation is a possible trigger of tinnitus.     

单侧低频感音神经性聋：附40例分析

文中对40例单侧低频感音神经性聋患者进行分析,发现患者主诉中有耳鸣的最多(87.5%)、耳聋次(75%)、眩晕和耳闷者各为35%及25%.纯音测听均为低频感音神经性聋,其低频与高频听阈均值之差为26.32 dB.40例中36例听性脑干反应正常.并讨论了产生低频感音神经性聋可能的原因,耳鸣、低频听力损害与内淋巴积水的关系,并提出对低频感音神经性自应有统一的划定标准.     

Resistance to Noise-Induced Hearing Loss in 129S6 and MOLF Mice: Identification of Independent,Overlapping, and Interacting Chromosomal Regions

Noise-induced hearing loss (NIHL) is a prevalent health risk. Inbred mouse strains 129S6/SvEvTac (129S6) and MOLF/EiJ (MOLF) show strong NIHL resistance (NR) relative to CBA/CaJ (CBACa). In this study, we developed quantitative trait locus (QTL) maps for NR. We generated F1 animals by intercrossing (129S6 × CBACa) and (MOLF × CBACa). In each intercross, NR was recessive. N2 animals were produced by backcrossing F1s to their respective parental strain. The 232 N2-129S6 and 225 N2-MOLF progenies were evaluated for NR using auditory brainstem response. In 129S6, five QTL were identified on chromosomes (Chr) 17, 18, 14, 11, and 4, referred to as loci nr1, nr2, nr3, nr4, and nr5, respectively. In MOLF, four QTL were found on Chr 4, 17, 6, and 12, referred to as nr7, nr8, nr9, and nr10, respectively. Given that NR QTL were discovered on Chr 4 and 17 in both the N2-129S6 and N2-MOLF cross, we generated two consomic strains by separately transferring 129S6-derived Chr 4 and 17 into an otherwise CBACa background and a double-consomic strain by crossing the two strains. Phenotypic analysis of the consomic strains indicated that whole 129S6 Chr 4 contributes strongly to mid-frequency NR, while whole 129S6 Chr 17 contributes markedly to high-frequency NR. Therefore, we anticipated that the double-consomic strain containing Chr 4 and 17 would demonstrate NR across the mid- and high-frequency range. However, whole 129S6 Chr 17 masks the expression of mid-frequency NR from whole 129S6 Chr 4. To further dissect NR on 129S6 Chr 4 and 17, CBACa.129S6 congenic strains were generated for each chromosome. Phenotypic analysis of the Chr 17 CBACa.129S6 congenic strains further defined the NR region on proximal Chr 17, uncovered another NR locus (nr6) on distal Chr 17, and revealed an epistatic interaction between proximal and distal 129S6 Chr 17.     

Relationship of Pathology to Function in Congenital Hearing Loss: I. The Pathology of Congenital Hearing Loss

New sources of information on the pathology of congenital hearing loss allow the otolaryngologist to evaluate more confidently the number of functional elements present or absent in a given hearing loss. Information is obtained from two sources: histo-pathological studies on temporal bones of deceased hearing-impaired children, and polytomogram studies on living children. These sources reveal that varieties and modifications must be added to the classic pathologies described by Mïchel, Mondini, Scheibe, and Alexander, necessitating changes in our estimates of the hearing function of hearing impaired children. Variations occur in recessive and dominant genetic hearing loss, in viral labyrinthitis, in chromosomal abnormalities, and in iatrogenic hearing loss. Temporal bone slides and polytomograms of these entities are shown and their functional elements described.     

Wireless Connectivity for People with Hearing Loss: The Acoustic Transparency of Waterproof Smartphone Cases

Phone use is a critical communication event in many people''s lives. Audiologists have aimed to assist individuals with hearing loss and phone usage through the use of technology and counseling. To counsel effectively, all contributions to hearing difficulty on the phone must be considered, including the effects of smartphone cases. The purpose of this study was to evaluate the effects on dB output caused by waterproof smartphone cases that cover the ear-level speaker. One waterproof case was tested with three smartphones, two iPhones, and one Android. A second waterproof case was tested with the two iPhones. Results revealed there was significant attenuation of the audio-signal by both waterproof smartphone cases that was great enough in one case/phone combination to potentially result in a complete lack of intelligibility of the signal.     

语后聋人工耳蜗植入者的心理健康状况分析

目的探讨重度听力损失者借助人工耳蜗重获听力后的心理健康状况及其与听力正常人群的差异。方法采用症状自评量表(symptom checklist 90,SCL-90)和艾森克人格问卷(Eysenck personality questionnaire,EPQ)对18例语后聋人工耳蜗使用者(耳蜗组)的心理健康状态及人格特质进行评估,并与45例听力正常组(对照组)进行比较。结果①SCL-90评分结果显示:耳蜗组在人际关系、焦虑、敌对、恐怖、偏执、精神病性六个因子方面的得分均明显高于对照组(P<0.01);躯体化、强迫、抑郁三个因子的得分两组间差异无统计学意义(P>0.05)。②EPQ评定结果显示:耳蜗组在人格特质的内外倾、神经质、精神质三个维度评分与对照组相当,两组差异无统计学意义(P>0.05)。结论植入人工耳蜗有利于改善重度聋患者的心理健康状况,但人工耳蜗植入者在社会交往过程中仍存在人际关系敏感、焦虑、偏执等不良心理状态,提示在进行听觉言语康复的同时,还应关注其心理和社会交往状况,以帮助其改善生活质量、回归主流社会。     

Progressive Hearing Loss and Increased Susceptibility to Noise-Induced Hearing Loss in Mice Carrying a <Emphasis Type="Italic">Cdh23</Emphasis> but not a <Emphasis Type="Italic">Myo7a</Emphasis> Mutation

Exposure to intense noise can damage the stereocilia of sensory hair cells in the inner ear. Since stereocilia play a vital role in the transduction of sound from a mechanical stimulus into an electrical one, this pathology is thought to contribute to noise-induced hearing loss. Mice homozygous for null mutations in either the myosin VIIa (Myo7a) or cadherin 23 (Cdh23) genes are deaf and have disorganized stereocilia bundles. We show that mice heterozygous for a presumed null allele of Cdh23 (Cdh23^v) have low- and high-frequency hearing loss at 5–6 weeks of age, the high-frequency component of which worsens with increasing age. We also show that noise-induced hearing loss in 11–12-week-old Cdh23^v heterozygotes is two times greater than for wild-type littermates. Interestingly, these effects are dependent upon the genetic background on which the Cdh23^v mutation is carried. Noise-induced hearing loss in 11–12-week-old mice heterozygous for a null allele of Myo7a (Myo7a^4626SB) is not significantly different from wild-type littermates. CDH23 is the first gene known to cause deafness in the human population to be linked with predisposition to noise-induced hearing loss.     

Increased Sensitivity to Noise-Induced Hearing Loss by Blockade of Endogenous PI3K/Akt Signaling

The PI3K/Akt signaling pathway is involved in mediating survival of sensory hair cells. Here, we investigated the involvement of PI3K/Akt in noise-induced hearing loss in both temporary and permanent threshold shift noise models. The PI3K regulatory subunit p85α and phosphorylation of Akt on serine 473 (p-Akt S473) are downregulated in sensory hair cells, including both outer and inner hair cells, and supporting cells of the mouse organ of Corti 1 h after exposure to permanent-threshold-shift-inducing noise (PTS noise), but not with temporary-threshold-shift-inducing noise (TTS noise). In contrast, the PI3K catalytic subunit p110α and phosphorylation of Akt on threonine 308 (p-Akt T308) do not change with PTS or TTS noise. Additionally, mice pretreated with p85α small interfering RNA (siRNA) have decreased expression of p-Akt1 (S473) in their sensory hair cells and increased sensitivity to TTS noise-induced hearing loss. Finally, Akt1-knockout mice also have enhanced sensitivity to TTS noise-induced hearing loss. In conclusion, this study suggests that endogenous PI3K/Akt signaling is an intrinsic protective mechanism of the inner ear. Blockade of PI3K/Akt signaling pathways increases sensitivity to TTS noise-induced hearing loss.