PRESBYCUSIS--BIOMEDICAL RISK FACTORS

老年性耳聋是一个常见问题，随着年龄的增长，其患病率正在不断增加 我们社会的老年人数量不断增加。 患病率和 老年性耳聋的严重程度在不同人群中差异很大，但 这种变化的根源尚未确定。 拟议的 研究将探讨老年性耳聋的流行病学 生物医学危险因素，目的是确定相对 与年龄相关的退化和与年龄相关的疾病对：a) 一般性老年性耳聋； b) 功能障碍的主要部位，即耳蜗， 耳蜗后和中央； c) 老年性耳聋的具体类型，即 感觉、神经、纹状和传导。 拟议的研究将获得外围和 已对老年人群的中枢听觉功能进行了调查 患心血管疾病40多年。 这将是第三次 对弗雷明汉队列进行听力评估，这将允许 a) 首个 15 年听力损失发生率纵向分析 老年男性和女性，b) 第一次纵向评估 中枢听觉功能障碍的发生率，以及 c) 有机会 比较听力损失的发生率与听力损失发生率的关系 全身性疾病，包括心血管疾病及其病因 风险因素。 使用相同的方案测试该队列的后代 将为未来的纵向测试建立基线并奠定基础 通过记录以下内容为未来的遗传学研究奠定基础：a) 年龄开始前听力损失的外因 效应和 b) 可能对老年性耳聋的遗传保护。 测试包括纯音阈值、导抗听力测定、 失真产物耳声发射、安静时的言语辨别 以及一系列中枢听觉测试。 将这些测试与其他测试进行比较 9 年前和 15 年前获得的数据可能揭示不明显的变化模式 在横断面研究中。 听力功能的多项测量应 提高我们识别每种类型老年性耳聋的能力并更好地定义 各自的流行程度。 将研究性别相关因素来解释 女性低频丢失更快。 通过比较变化 试镜时会考虑生物医学状况的变化，包括心血管疾病 疾病，我们将检验老年性耳聋和全身性耳聋的假设 血管疾病有共同的危险因素。 知道是否 心血管疾病或其前兆是心血管疾病的辅助因素 某些类型的老年性耳聋的发病机制将允许合理的 预防方法和可能的治疗方法。

Presbycusis is a common problem that is increasing in prevalence as the number of elderly persons in our society increases. The prevalence and severity of presbycusis vary substantially in different populations but the sources of this variability have not been delineated. The proposed research will examine the epidemiology of presbycusis in relation to biomedical risk factors with the goal of determining the relative contributions of agerelated degeneration and age-related diseases to: a) presbycusis in general; b) the major sites of dysfunction, i.e. cochlear, retrocochlear, and central; and c) the specific types of presbycusis, i.e. sensory, neural, strial, and conductive. The proposed research will obtain comprehensive measures of peripheral and central auditory function in an elderly cohort that has been surveyed for cardiovascular disease for over 40 years. This will be the third audiometric assessment of the Framingham cohort, which will permit a) the first 15 year longitudinal analysis of the incidence of hearing loss in elderly men and women, b) the first longitudinal assessment of the incidence of central auditory dysfunction, and c) the opportunity to compare the incidence of hearing loss in relation to the incidence of systemic disorders, including cardiovascular disease and its antecedent risk factors. Testing the offspring of the cohort using the same protocol will establish a baseline for future longitudinal testing and lay the groundwork for future genetic studies by documenting those with: a) exogenous causes of hearing loss prior to the onset of significant age effects and b) possible genetic protection from presbycusis. Tests include pure-tone thresholds, immittance audiometry, distortion-product otoacoustic emissions, speech discrimination in quiet and a battery of central auditory tests. Comparing these tests with those obtained 9 and 15 years earlier may reveal patterns of change not evident in cross-sectional studies. Multiple measures of hearing function should improve our ability to identify each type of presbycusis and better define the prevalence of each. Gender-related factors will be studied to explain the more rapid low-frequency loss in women. By comparing changes in audition with changes in biomedical status, including cardiovascular disorders, we will test the hypothesis that presbycusis and systemic vascular disease share common risk factors. Knowing whether cardiovascular disease or its precursors are co-factors in the pathogenesis of certain types of presbycusis will allow a rational approach to prevention and possible treatment.