老年大鼠听力与耳蜗组织化学,免疫组织化学变化实验观察

自然老年大鼠（２８月龄）和成年鼠（３月龄），用７Ｓｌｌ－Ａ型电反应测试仪确定听阈并记录Ｉ波潜伏期和Ｉ－Ｖ波间期，耳蜗琥珀酸氢酶（ＳＤＨ）、ＰＡＳ、坚牢蓝组化染色和神经特异性和烯醇化酶（ＮＳＥ），Ｓ－１００的免疫组化当色（ＡＢＣ）法，分别观察耳蜗毛细胞、神经节细胞、听神经纤维及鞘膜变化。结果：老年大鼠听性脑干反应阈值升高，ＳＤＨ活性减弱，节细胞人可见多个脂褐素颗粒，神经纤维排列稀疏，节细胞内ＮＳＥ免     

从肾论治老年性聋

“肾主耳”理论是中医藏象学说中的重要内容,文章根据老年人的生理特点,运用中医理论辨证分析老年性聋与肾的关系。提出老年性聋多因肾虚至髓海不足,耳失濡养;扰乱气机,气血运行不畅,耳窍闭塞。故而治疗应注重补肾通窍法,在-临床中防治老年性聋具有重大意义。     

Relative Time Course of Degeneration of Different Cochlear Structures in the CD/1 Mouse Model of Accelerated Aging

Presbycusis (age-related hearing loss) can result from various cochlear pathologies. We have studied the time course of degeneration in a mouse that shows accelerated presbycusis, the CD/1 mouse, as a possible model to investigate stem-cell strategies to prevent or ameliorate presbycusic changes. CD/1 mice from 0 to 72 weeks old were examined by light and electron microscopy. Early pathological changes were detected in basal turn spiral ligament fibrocytes and spiral ganglion, but the latter was variable as both satellite cells and neurons were normal in some cochleae. Light microscopic counts in the spiral ligament of 20-week-old mice revealed that of the five main types (types I–V), only type V fibrocytes showed no reduction in numbers compared with 3-week-old animals, and type IV showed the greatest losses. However, all types of fibrocyte showed subtle damage when examined using electron microscopy, in the form of swollen mitochondria, as early as 2 weeks. The extent of mitochondrial damage showed a degree of correspondence with the light microscopic pattern of fibrocyte loss in that types III and IV fibrocytes had the most abnormal mitochondria and type V the least, especially at early stages. By 10–15 weeks, ultrastructural features of fibrocyte damage were similar to longer term changes reported in gerbils. Stria vascularis, spiral ganglion and hair cells showed few consistent early signs of damage but became increasingly affected, lagging behind the fibrocyte damage. Our data suggest that fibrocyte pathology may precede other presbycusic changes; breakdown of homeostatic mechanisms to which they contribute may cause the subsequent degeneration of the hair cells. Overall, there were many similarities to presbycusic changes in other rodents and humans. Therefore, the features of accelerated aging in this mouse make it a suitable model for rapidly assessing possible strategies to prevent or ameliorate presbycusic changes.     

Cellular correlates of progressive hearing loss in 129S6/SvEv mice

Several strains of mice hear well initially but show progressive sensorineural hearing loss. Affected cochlear cell types include all those known to be affected in human age-related hearing loss (ARHL), or presbycusis. Thus these mice have been offered as models of human ARHL. At present, however, few mouse ARHL models are sufficiently well described to serve as the basis for specific hypotheses about human ARHL. We examined 1-month-old and 15-month-old 129S6/SvEv (129S6) mice and compared them with BALB/cJ and CBA/J mice. Age-related elevation of compound action potential thresholds was interpreted in the light of endocochlear potentials and changes in hair cells, afferent neurons, fibrocytes in spiral limbus and ligament, and supporting cells within the organ of Corti. Aging in 129S6 mice was associated with high-frequency hearing loss. Four components of age-related cochlear degeneration emerged from quantitative analyses, including 1) basal loss of outer hair cells; 2) basal loss of type IV fibrocytes in the spiral ligament; 3) apical loss of fibrocytes in spiral limbus, and 4) anomalies of supporting cells in the cochlear base. Although neuronal loss was not consistently found, two mice showed loss of afferent dendrites and cell bodies in the cochlear apex without inner hair cell loss. Despite multifaceted degeneration, hearing loss in 129S6 mice appears to be best explained by degenerative changes in outer hair cells and in the organ of Corti, conforming to human sensory ARHL. Age-related changes in the apical spiral limbus may promote pathology of the medial organ of Corti and eventual loss of afferent neurons, with possible implications for human neural ARHL.     

The mechanism of hearing loss in Paget's disease of bone

OBJECTIVES/HYPOTHESIS: The mechanism of hearing loss (HL) in Paget's disease of bone was investigated. The present study was a systematic, prospective, controlled set of clinical investigations to test the hypothesis that there is a general underlying mechanism of HL in Paget's disease of bone and to gain additional insights into the auditory and otologic dynamics of this disease. Specific questions were 1) whether the mechanism is cochlear or retrocochlear and 2) whether the bone mineral density of the cochlear capsule is related to hearing levels. STUDY DESIGN: Several double-blinded, cross-sectional, prospective, correlational studies were conducted in a population of elderly human subjects with skull involvement with Paget's disease versus a control population of elderly subjects free of Paget's disease. Demographic and clinical data were recorded. Longitudinal observations were made in subjects under treatment. METHODS: Subjects were recruited from a Paget's disease clinic. Pure-tone auditory thresholds, word recognition, and auditory brainstem responses (ABRs) were recorded. The dimensions of the internal auditory canals were measured using computed tomographic (CT) images and digital image analysis. The precision, accuracy, and temporal stability of methods to measure the bone mineral density of the cochlear capsule and an adjacent area of nonotic capsule bone were validated and applied. Correlations were sought between hearing levels and cochlear capsule bone mineral density. RESULTS: ABRs were recorded in 64 ears with radiographically confirmed Paget's disease involving the skull. Responses were absent in eight ears, all of which had elevated high pure-tone thresholds. ABRs were interpreted as normal in 56 ears; none were abnormal. The mid-length diameter and minimum diameter of the internal auditory canal of 68 temporal bones from subjects with Paget's disease were found to have no statistically significant relationship to hearing thresholds. The Pearson product-moment correlation coefficients (age- and sex-adjusted) in the group with Paget's disease involving the temporal bone were -0.63 for left ears and -0.73 for right ears for high-frequency air conduction pure-tone thresholds (mean of 1, 2, and 4 kHz) versus cochlear capsule density. Correlation coefficients (age- and sex-adjusted) between cochlear capsule density and air-bone gap (mean at 0.5 and 1 kHz) for the affected group were -0.67 for left ears and -0.63 for right ears. All correlations between hearing thresholds and cochlear capsule density in pagetic subjects were significant at P <.001. The regressions were consistent throughout the ranges of hearing level. There were no significant correlations between cochlear capsule mean density and hearing level in the volunteer subjects. CONCLUSIONS: The evidence supports the existence of a general, underlying, cochlear mechanism of pagetic HL that is closely related to loss of bone mineral density in the cochlear capsule. This mechanism accounts well for both the high-frequency sensorineural HL and the air-bone gap. Early identification, radiographic diagnosis of temporal bone involvement, and vigorous treatment with third-generation bisphosponates are important to limit the development and progression of pagetic HL.     

Effects of aging on peripheral and central auditory processing in rats

Hearing loss is a hallmark sign in the elderly population. Decline in auditory perception provokes deficits in the ability to localize sound sources and reduces speech perception, particularly in noise. In addition to a loss of peripheral hearing sensitivity, changes in more complex central structures have also been demonstrated. Related to these, this study examines the auditory directional maps in the deep layers of the superior colliculus of the rat. Hence, anesthetized Sprague–Dawley adult (10 months) and aged (22 months) rats underwent distortion product of otoacoustic emissions (DPOAEs) to assess cochlear function. Then, auditory brainstem responses (ABRs) were assessed, followed by extracellular single‐unit recordings to determine age‐related effects on central auditory functions. DPOAE amplitude levels were decreased in aged rats although they were still present between 3.0 and 24.0 kHz. ABR level thresholds in aged rats were significantly elevated at an early (cochlear nucleus – wave II) stage in the auditory brainstem. In the superior colliculus, thresholds were increased and the tuning widths of the directional receptive fields were significantly wider. Moreover, no systematic directional spatial arrangement was present among the neurons of the aged rats, implying that the topographical organization of the auditory directional map was abolished. These results suggest that the deterioration of the auditory directional spatial map can, to some extent, be attributable to age‐related dysfunction at more central, perceptual stages of auditory processing.     

多学科协作干预对老年性耳聋佩戴助听器者生活质量的影响

目的探讨多学科协作(MDT)干预对老年性耳聋佩戴助听器者生活质量的影响。方法将53例老年性耳聋患者随机分为干预组28例,对照组25例,干预组成立由耳鼻喉科医师、配验师、康复师、专科护士、社区护士、心理咨询师等组成的MDT团队,对照组采用社区常规健康教育。1个月后比较2组的相关知识掌握率、助听器佩戴依从性,3个月后比较2组的生活质量。结果 1个月后干预组相关知识掌握率、助听器佩戴依从性均高于对照组(P0.05),3个月后生活质量方面的改善也显著优于对照组(P0.05)。结论 MDT模式下的路径干预能提高老年性耳聋患者相关知识掌握率、助听器佩戴依从性,改善生活质量。     

Glycine immunoreactivity and receptor binding in the cochlear nucleus of C57BL/6J and CBA/CaJ mice: Effects of cochlear impairment and aging

Glycinergic neurons in the cochlear nucleus (CN) of C57BL/6J (C57) and CBA/CaJ (CBA) mice were studied by using immunocytochemical and receptor-binding techniques. Adult C57 mice exhibit progressive cochlear pathology as they age, whereas aging CBA mice retain good hearing. In the CN of old C57 mice (18 months) with severe hearing loss, the number of glycine-immunoreactive neurons decreased significantly. The number (B_max) of strychnine-sensitive glycine receptors (GlyR) decreased significantly in the dorsal CN of old C57 mice. Significant effects were not observed in the CN of middle-aged C57 mice (with less-severe hearing loss) or in very old CBA mice (which do not exhibit severe hearing loss). The data suggest that the combination of severe hearing loss and old age results in deficits in one or more inhibitory glycinergic circuits in the CN. J. Comp. Neurol. 385:405–414, 1997. © 1997 Wiley-Liss, Inc.     

中国老年聋的研究现状和对策

老年聋严重影响老年人的语言交流和生活质量.在中国,老年聋及其后果已引起足够重视.虽然老年聋的预防和治疗的研究取得了不少进展,但是由于缺乏该病流行病学的人口统计学的系统研究,有关老年聋的有效治疗、听力的恢复和临床管理方面仍存在许多问题.本文根据国内已发表的论文,分析了中国老年聋的研究现状和对策,提出了老年聋的防治研究应重视听觉中枢处理过程障碍(central auditory processing disorder,CAPD)流行病学,老年聋和认知障碍的相关性研究.助听器的使用是老年聋获得听力的重要途径.最后,作者讨论了国内老年聋研究滞后的原因和解决的方法.