Public Health Perspectives on Hearing Loss and Aging Outcomes: Age-Related Hearing Loss and the Development of Cognitive Impairment and Late-Life Depression: A Scoping Overview

Age-related hearing loss (ARHL) has been connected to both cognitive decline and late-life depression. Several mechanisms have been offered to explain both individual links. Causal and common mechanisms have been theorized for the relationship between ARHL and impaired cognition, including dementia. The causal mechanisms include increased cognitive load, social isolation, and structural brain changes. Common mechanisms include neurovascular disease as well as other known or as-yet undiscovered neuropathologic processes. Behavioral mechanisms have been used to explain the potentially causal association of ARHL with depression. Behavioral mechanisms include social isolation, loneliness, as well as decreased mobility and impairments of activities of daily living, all of which can increase the risk of depression. The mechanisms underlying the associations between hearing loss and impaired cognition, as well as hearing loss and depression, are likely not mutually exclusive. ARHL may contribute to both impaired cognition and depression through overlapping mechanisms. Furthermore, ARHL may contribute to impaired cognition which may, in turn, contribute to depression. Because ARHL is highly prevalent and greatly undertreated, targeting this condition is an appealing and potentially influential strategy to reduce the risk of developing two potentially devastating diseases of later life. However, further studies are necessary to elucidate the mechanistic relationship between ARHL, depression, and impaired cognition.     

老年性聋助听器选配效果评估问卷的应用

目的:通过对已选配助听器的老年性聋患者进行助听器效果评估问卷的填写,评估其使用效果并有针对性地解决其使用中遇到的问题,提高老年人的生活质量。方法:通过面对面的方式对30例助听器验配患者进行调查和分析。应用SPSS统计学软件分析,初步评估老年性聋患者助听器的使用效果和解决其使用中遇到的问题。结果:调查结果得出老年性聋患者听力障碍问题得到显著改善,对选配的助听器总体比较满意,且听力障碍问题的改善与满意度随时间的延长持续提高。结论:效果评估问卷可以集中反映听力障碍患者助听器使用后的残障改善情况和了解患者使用助听器的满意度,可初步作为康复效果评估的一个可靠主观效果评估指标。     

中药聪耳胶囊干预老年性耳蜗螺旋神经节和疆孔神经损害的实验研究

目的：观察中药健耳Ⅱ号胶囊化裁方——聪耳胶囊对C57小鼠老年性耳蜗螺旋神经节和疆孔神经损害的干预影响并探讨其作用机制。方法：刚出生的C57BL/6J小鼠40只,随机分为对照组和聪耳胶囊组各20只。对照组小鼠为常规饲料喂养;聪耳胶囊组小鼠常规饲料喂至出生后两个月时,以聪耳胶囊溶液代替日常饮水;至7月龄时两组同时终止实验。制作耳蜗切片,在光镜下定量观察比较各组小鼠耳蜗螺旋神经节细胞密度以及疆孔内神经纤维数量。结果：对照组小鼠耳蜗底回螺旋神经节细胞数量明显减少,存活者呈现异常的形态学改变,疆孔内神经纤维数量也有所减少。聪耳胶囊组小鼠蜗轴（特别是底回）内的螺旋神经节细胞密度以及疆孔内的神经纤维数量则减损较轻,其中两组动物的神经节细胞数量呈现极显著差异（P〈0.001）。结论：①中药聪耳胶囊与其源方健耳Ⅱ号胶囊一样,均可延缓C57BL/6J小鼠老年性耳蜗神经系统损害。②中药聪耳胶囊的药理学效应可能在于对相关基因活性表达的调控而阻断了细胞凋亡通路。③小鼠老年性耳蜗损害系由底回开始然后向顶回逐渐蔓延发展。④小鼠老年性听觉周边神经系统的损害可能首先发生螺旋神经节,然后再蔓延到听神经纤维。     

Age-related changes in the guinea pig auditory cortex: relationship with brainstem changes and comparison with tone-induced hearing loss

Elderly people often show degraded hearing performance and have difficulties in understanding speech, particularly in noisy environments. Although loss in peripheral hearing sensitivity is an important factor in explaining these low performances, central alterations also have an impact but their exact contributions remained unclear. In this study, we focus on the functional effects of aging on auditory cortex responses. Neuronal discharges and local field potentials were recorded in the auditory cortex of aged guinea pigs (> 3 years), and several parameters characterizing the processing of auditory information were quantified: the acoustic thresholds, response strength, latency and duration of the response, and breadth of tuning. Several of these parameters were also quantified from auditory brainstem responses collected from the same animals, and recordings obtained from a population of animals with trauma-induced hearing loss were also included in this study. The results showed that aging and acoustic trauma reduced the response strength at both brainstem and cortical levels, and increased the response latencies more at the cortical level than at the brainstem level. In addition to the brainstem hearing loss, aging induced a 'cortical hearing loss' as judged by additive changes in the threshold and frequency response seen in the cortex. It also increased the duration of neural responses and reduced the receptive field bandwidth, effects that were not found in traumatized animals. These effects substantiate the notion that presbycusis involves both peripheral hearing loss and biological aging in the central auditory system.     

Apical-to-basal gradients in age-related cochlear degeneration and their relationship to "primary" loss of cochlear neurons

The predominant conceptual framework for understanding human age-related hearing loss (ARHL, or presbycusis) holds that three different cochlear elements (organ of Corti, afferent neurons, and stria vascularis) can degenerate independently, and exert independent influences on hearing. Within this framework, temporal bones from subjects with ARHL may be classified as exemplifying sensory (referring to organ of Corti), "primary" neural (loss of afferent neurons without loss of their hair cell targets), strial, or mixed ARHL. While there is general agreement as to the types of cochlear cells most affected by aging, there is less agreement about how to classify ARHL, and whether contributions of particular structures to hearing loss can be isolated. The cochlear apex of humans and animals is particularly prone to apparent primary loss of neurons that may represent an aspect of neural ARHL. We recently reported that in 129S6/SvEv mice apical neuronal loss is often accompanied by abnormalities of spiral limbus, pillar cells, and Reissner's membrane (Ohlemiller and Gagnon [2004] J Comp Neurol 469:377-390). We proposed that the initial pathology occurs within limbus, leading to disruption of perilymphatic ion homeostasis, and eventual loss of neurons as one consequence. We have now examined this issue quantitatively in young and old mice of four different strains (129S6/SvEv, CBA/J, C57BL/6, and BALB/c). Abnormalities of apical spiral limbus were found to correlate only weakly with neuronal loss. Strong correlations were found between neuronal loss and abnormalities of both pillar cells and Reissner's membrane, however. Apical neuronal loss and apical-to-basal progression of pathology of limbus, pillar cells, and Reissner's membrane run counter to most reported age-related cochlear trends. Our findings suggest that these changes share a common triggering influence.     

Metabolic Presbycusis: Differential Changes in Auditory Brainstem and Otoacoustic Emission Responses with Chronic Furosemide Application in the Gerbil

Auditory characteristics of metabolic or strial presbycusis were investigated using an animal model in which young adult Mongolian gerbils (Meriones unguiculates) were implanted with an osmotic pump supplying furosemide continuously to the round window. This model causes chronic lowering of the endocochlear potential (EP) and results in auditory responses very similar to those seen in quiet-aged gerbils (Schmiedt et al., J. Neurosci. 22:9643–9650, 2002). Auditory function was examined up to one week post-implant by measurement of auditory brainstem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs). Emission threshold was defined as the stimulus level required to reach a criterion emission amplitude. Comparing all responses on a threshold-shift diagram, where emission threshold increases were plotted versus ABR threshold increases, the following results were obtained: (1) On average, the increase of the emission threshold was about 55% of the increase in ABR threshold, with comparatively little scatter. (2) The main dysfunction in metabolic presbycusis appears to be a decrease in the gain of the cochlear amplifier, combined with an additional, smaller increase in neural threshold, both effects caused by a chronically low EP. (3) For ABR threshold increases over 20 dB, the points for the chronic low-EP condition were largely separate from those previously found for permanent acoustic damage. The threshold-shift diagram therefore provides a method for noninvasive differential diagnosis of two common hearing dysfunctions.     

Age-Related Hearing Loss in C57BL/6J Mice has both Frequency-Specific and Non-Frequency-Specific Components that Produce a Hyperacusis-Like Exaggeration of the Acoustic Startle Reflex

Auditory brainstem-evoked response (ABR) thresholds were obtained in a longitudinal study of C57BL/6J mice between 10 and 53 weeks old, with repeated testing every 2 weeks. On alternate weeks, acoustic startle reflex (ASR) amplitudes were measured, elicited by tone pips with stimulus frequencies of 3, 6, 12, and 24 kHz, and intensities from subthreshold up to 110 dB sound pressure level. The increase in ABR thresholds for 3 and 6 kHz test stimuli followed a linear time course with increasing age from 10 to 53 weeks, with a slope of about 0.7 dB/week, and for 48 kHz a second linear time course, but beginning at 10 weeks with a slope of about 2.3 dB/week. ABR thresholds for 12, 24, and 32 kHz increased after one linear segment with a 0.7 dB slope, then after a variable delay related to the test frequency, shifted to a second segment having slopes of 3–5 dB/week. Hearing loss initially reduced the ASR for all eliciting stimuli, but at about 6 months of age, the response elicited by intense 3 and 6 kHz stimuli began to increase to reach values about three times above normal, and previously subthreshold stimuli came to elicit vigorous responses seen at first only for the intense stimuli. This hyperacusis-like effect appeared in all mice but was especially pronounced in mice with more serious hearing loss. These ABR data, together with a review of histopathological data in the C57BL/6 literature, suggest that the non-frequency-specific slow time course of hearing loss results from pathology in the lateral wall of the cochlea, whereas the stimulus-specific hearing loss with a rapid time course results from hair cell loss. Delayed exaggeration of the ASR with hearing loss reveals a deficit in centrifugal inhibitory control over the afferent reflex pathways after central neural reorganization, suggesting that this mouse may provide a useful model of age-related tinnitus and associated hyperacusis.     

褪黑素对豚鼠老年性聋的拮抗作用

目的:观察褪黑素对豚鼠老年性聋的拮抗作用.方法:80只豚鼠随机分为4组:正常对照组(A组),老年性聋模型组(B组),褪黑素治疗的老年性聋模型组(C组0.3 mg/(kg·d和D组1.0 mg/(kg·d).以腹腔注射D-半乳糖制作老年性聋模型,4周后测量各组ABR、耳蜗组织谷胱甘搿-过氧化物酶(GSH-Px)含量,耳蜗铺片观察毛细胞变化情况.结果:与A组比较,B、C组ABR阈值、Ⅰ波潜伏期、Ⅲ波潜伏期及Ⅰ、Ⅲ波间期均升高,GSH-Px含量降低(P＜0.05或0.01).D组上述各指标与A组相比,差异无统计学意义(P＞0.05).耳蜗铺片结果,B组耳蜗基底膜各周外毛细胞排列紊乱,大小不一,胞内颗粒染色变浅,可见细胞点状缺失;A、D组外毛细胞排列整齐,无缺失;C组介于B、D组之间.结论:褪黑素对老年性聋豚鼠听力及耳蜗毛细胞有保护作用,且与剂量有关.     

Contralateral suppression of distortion-product otoacoustic emissions declines with age: a comparison of findings in CBA mice with human listeners

OBJECTIVES/HYPOTHESIS: The auditory efferent system plays presumed roles in enhancing signals in noise, maintaining the cochlea for optimal acoustic signal processing, and may have a protective role in preserving auditory function in the face of ototoxic events. The objective of the study was to measure age-related changes of the medial olivocochlear efferent system in mice by comparing distortion-product otoacoustic emissions generated with and without contralateral white noise stimulation. Consistent with prior work, distortion-product otoacoustic emissions were typically reduced in magnitude when white noise was presented to the contralateral ear. This contralateral suppression is attributed to activation of the medial olivocochlear efferent system, which has an inhibitory effect on the cochlear hair cell system. By studying contralateral suppression on cochlear output in subjects of different ages, it is possible to describe aging effects on the medial olivocochlear system. STUDY DESIGN: CBA mice were divided into three age groups: young adult, middle-aged, and old-aged animals (21, 13, and 22 animals per group, respectively), and auditory brainstem responses were obtained before distortion-product otoacoustic emission testing to assess overall hearing abilities. METHODS: 2f1-f2 distortion-product otoacoustic emission recordings were obtained from individual subjects (anesthetized with ketamine/xylazine) in each age group under two conditions: 1) in quiet and 2) in the presence of a contralaterally applied wideband noise. RESULTS: Principal findings were that distortion-product otoacoustic emission levels decreased with age for mice in a way similar to humans, when correcting for the absolute difference in life spans. In addition, contralateral suppression declined in middle-aged and old-aged groups relative to the young adults for mice in a manner similar to humans. The contralateral suppression decline at low frequencies preceded that of the decline in distortion-product otoacoustic emissions with age. CONCLUSION: Functional decline of the medial olivocochlear efferent system with age precedes outer hair cell degeneration. Loss of medial olivocochlear suppressive function may play a role in the development of presbycusis in both clinical cases and animal models.