固肾培元方治疗老年性聋临床观察

目的:观察固肾培元方治疗老年性聋的临床疗效。方法:67例老年性聋患者,随机分为两组。对照组口服金施尔康和达纳康,治疗组在口服金施尔康和达纳康的基础上,给予固肾培元方治疗,用药结束后进行疗效观察。结果:治疗组总有效率62.9%,对照组总有效率53.1%。两组总有效率比较无显著性意义(P>0.05),但治疗组总有效率高于对照组。结论:固肾培元方治疗老年性耳聋总有效率优于对照组,提示补肾活血通窍中药可能通过改善内耳局部微循环,促进内耳毛细胞功能恢复,从而起到提高听力的作用。     

JNK信号通路在老年大鼠耳蜗细胞凋亡中的作用

目的探讨c-Jun氨基末端激酶(c-Juna mino-terminal kinase,JNK)信号通路在老年大鼠耳蜗细胞凋亡中的作用,为老年性聋的预防和治疗提供更多的切入点。方法Wistar大鼠24只,其中12只为对照组(3～4月龄),12只为自然衰老组(22～24月龄);听性脑干反应(auditory brainstem response,ABR)检测听力学改变;采用透射电镜观察老年大鼠耳蜗的超微病理变化;用免疫组化及Western blotting方法检测p-JNK和p-c-Jun蛋白的表达。结果老年组大鼠听力〔(72.083±13.345)dBSPL〕较对照组〔(32.083±3.878)dBSPL〕明显下降,差异具有统计学意义(P<0.01);透射电镜下可见外毛细胞有凋亡样改变,螺旋神经节细胞内大量脂褐素沉着;在耳蜗石蜡切片中可观察到p-JNK和p-c-Jun免疫反应阳性细胞,定位于细胞核,老年组与对照组相比,差异具有统计学意义(P<0.05);Western blotting结果显示老年组内耳组织p-JNK和p-c-Jun的蛋白表达明显高于对照组,差异有统计学意义(P<0.05)。结论在大鼠老年性聋的发生过程中,各种损伤因素可能通过激活JNK信号通路而促使耳蜗细胞的凋亡。     

Overview of Central Auditory Processing Deficits in Older Adults

Although there are many reported age-related declines in the human body, the notion that a central auditory processing deficit exists in older adults has not always been clear. Hearing loss and both structural and functional central nervous system changes with advancing age are contributors to how we listen, hear, and process auditory information. Even older adults with normal or near normal hearing sensitivity may exhibit age-related central auditory processing deficits as measured behaviorally and/or electrophysiologically. The purpose of this article is to provide an overview of assessment and rehabilitative approaches for central auditory processing deficits in older adults. It is hoped that the outcome of the information presented here will help clinicians with older adult patients who do not exhibit the typical auditory processing behaviors exhibited by others at the same age and with comparable hearing sensitivity all in the absence of other health-related conditions.     

Hearing threshold levels for an otologically screened population in Spain

Objective: The aim of the present study was to provide thresholds data as a function of age for an otologically normal population in Spain, compared to the current ISO 7029 (2000) standard. Design: A prospective study in an otologically screened population. Study sample: Data was collected from 1175 otologically-normal persons aged between 5 and 90 years. Inclusion criteria involved those listed in ISO 389-1 (1998) and the 8253-1 (2010). Suitability for inclusion was evaluated through interview, based on a questionnaire, and physical examination. Results: The hearing thresholds decreased slightly from 125 to 2000 Hz. From 2000 Hz onwards the thresholds increased; this increase being more pronounced with increasing frequency and age. No statistically significant sex differences were found. The hearing threshold levels in the present study were higher (poorer) than the ones provided by ISO 7029 (2000). Conclusions: Results from this study suggest that the thresholds listed in ISO 7029 (2000) may be too restrictive, and could be useful in formulating the ISO 7029 update.     

Understanding hormone and hormone therapies' impact on the auditory system

Hormones such as estrogen, progesterone, and aldosterone all demonstrate vital roles in sustaining auditory function through either the maintenance of cochlear neurons, up/down regulation of critical molecules (i.e., IGF-1, BDNF, etc.), or generation of the endocochlear potential. With disease and/or age, hormone expression begins to decline drastically, which ultimately affects cochlear structures and the integrity of cochlear cells. The following review explores the latest findings as well as realistic outcomes for hormone therapy treatment in the auditory system. This information could serve as a potential guide for patients considering hormone therapy as a medicinal choice to alleviate the signs of onset of presbycusis—age-related hearing loss. Additional scientific investigations could also be carried out to further enhance recent findings.     

Metabolic changes in the auditory cortex in presbycusis demonstrated by MR spectroscopy

In humans, aging is accompanied by the deterioration of the hearing function — presbycusis. The major etiology for presbycusis is the loss of hair cells in the inner ear; less well known are changes in the central auditory system. Therefore, we used 1 H magnetic resonance spectroscopy at 3 T tomograph to examine metabolite levels in the auditory cortex of three groups of subjects: young healthy subjects less than 30 years old and subjects older than 65 years either with mild presbycusis corresponding to their age or with expressed presbycusis. Hearing function in all subjects was examined by pure tone audiometry (125–16000 Hz). Significant differences were found in the concentrations of glutamate and N-acetylaspartate, with lower levels in aged subjects. Lactate was particularly increased in subjects with expressed presbycusis. Significant differences were not found in other metabolites, including GABA, between young and elderly subjects. The results demonstrate that the age-related changes of the inner ear are accompanied by a decrease in the excitatory neurotransmitter glutamate as well as a lactate increase in the auditory cortex that is more expressed in elderly subjects with large hearing threshold shifts.     

Sensorineural Hearing Loss and Neural Correlates of Temporal Acuity in the Inferior Colliculus of the C57bl/6 Mouse

Perception of complex sounds depends on the encoding of the dynamic and static structures within the ongoing stimulus by the auditory system. Aging has been associated with deficits in both areas, thus, the difficulty that the elderly have in speech comprehension could due to hearing loss, or to a loss of temporal sensitivity, or some combination of both. We investigated the effects of sensorineural hearing loss (SNHL) on neural correlates of temporal resolution by recording the responses of inferior colliculus neurons to a gap detection paradigm. We used C57BL/6 (C57) strain of laboratory mouse, which carries the Ahl deafness gene that initiates a progressive high frequency SNHL beginning at about 2 months of age and rapidly progresses to total deafness by 18 months. We compared gap encoding from inferior collicular neurons from young, normal-hearing C57 mice and middle-aged, hearing-impaired, C57 mice, quantifying minimal gap threshold, and recovery functions. The proportion of unit types, spontaneous rates and degree of monotonicity were comparable between young and middle-aged C57 mice. As expected, single unit thresholds were elevated by 30–40 dB in middle-aged C57 mice. However, no significant differences in mean minimal gap thresholds or in the slopes of the gap recovery functions were found between the two age groups. Thus, the results suggest that moderate high frequency SNHL does not affect temporal processing as measured by the gap detection paradigm.     

Earphones in extended high-frequency audiometry and ISO 389-5

Abstract

Objective: To determine common reference equivalent threshold sound pressure levels (RETSPL) for the earphones used in the extended high-frequency (EHF) range, as different earphones are commercially available, but there are not RETSPLs for each model. Design: Hearing threshold sound pressure levels were measured up to 20 kHz for the Sennheiser HDA 200 audiometric earphone, and were compared to the ISO 389-5 (2006) norm and other investigations using that earphone and different ones. Study sample: A total of 223 otologically-normal subjects (aged 5–25 years old) participated in the hearing determination. Results: The results are in good agreement with previous studies of hearing thresholds using the same and other earphones. Conclusions: The results of the present investigation are relevant for the international standard for the calibration of audiometric equipment in the 8 to 16 kHz frequency range, ISO 389-5. The data may be used for a future update of the RETSPL for circumaural and insert audiometric earphones.     

From the Cover: Age-related hearing loss in C57BL/6J mice is mediated by Bak-dependent mitochondrial apoptosis

Age-related hearing loss (AHL), known as presbycusis, is a universal feature of mammalian aging and is the most common sensory disorder in the elderly population. The molecular mechanisms underlying AHL are unknown, and currently there is no treatment for the disorder. Here we report that C57BL/6J mice with a deletion of the mitochondrial pro-apoptotic gene Bak exhibit reduced age-related apoptotic cell death of spiral ganglion neurons and hair cells in the cochlea, and prevention of AHL. Oxidative stress induces Bak expression in primary cochlear cells, and Bak deficiency prevents apoptotic cell death. Furthermore, a mitochondrially targeted catalase transgene suppresses Bak expression in the cochlea, reduces cochlear cell death, and prevents AHL. Oral supplementation with the mitochondrial antioxidants α-lipoic acid and coenzyme Q₁₀ also suppresses Bak expression in the cochlea, reduces cochlear cell death, and prevents AHL. Thus, induction of a Bak-dependent mitochondrial apoptosis program in response to oxidative stress is a key mechanism of AHL in C57BL/6J mice.