Sensorimotor mechanisms of vocal hyperfunction

项目摘要 在美国3%-9%的嗓音障碍人群中，发声功能亢进(VH)是一种非常普遍的特征。 以喉部和咽周过度和/或不协调的张力为特征，其病理生理学 被归因于许多潜在的原因，如不良的声音卫生，心理因素，反流，以及 非典型自主神经系统(ANS)功能。我们最近的发现支持我们的中心假设，即 一些VH患者的听觉-运动功能受损：我们发现说话者的听觉受损 对自己语音基频(Fo)记录的差异的敏感度及其对 人为地改变了自己的声音。在这个循环中，我们建议进一步阐明干扰的病因学作用。 目的：探讨VH患者的听觉运动功能，并评价具有临床应用价值的听觉运动功能指标。 在目标1中，有VH和对照的个体将参与任务，以在有和没有VH的情况下获得适应性反应 一种同时的认知应激源，以引起ANS的唤醒。越来越多的证据表明，非典型的ANS起作用 是VH的潜在致病因素，ANS觉醒水平可能与 听觉运动功能。因此，我们将直接评估ANS和听觉运动功能是否中断 在VH的病因学中代表共同的内表型(相关的易感因素)。在目标2中，Fo敏锐度和 适应性反应将在VH中进行纵向研究。我们的试点数据显示，许多患有 VH和非典型听觉-运动特征在发声后立即表现出适应反应的改善 心理治疗。这可能代表了潜在病因的正常化。相反，发声疗法可能 提供改善发声质量的策略，但不解决个人潜在的神经脆弱性 发展为VH，听觉-运动适应的改变是次要的。我们预计，拥有 治疗后立即出现的非典型听觉运动特征对治疗的长期反应较差， 听觉-运动控制障碍是脑性痴呆发生和持续的一个病因因素 VH。在目标1和目标2中使用的fo摄动法需要对仪器和 良好控制的声学环境，限制了它们的临床生存能力。因此，在目标3中，潜在的“临床友好型” 关联(听觉敏锐度与标准声音的音调变化和语音产生在前、中、后 在暴露在嘈杂环境中诱发伦巴第反应后)将接受心理测量评估 就其同时效度和重测信度而言。成功完成这些目标将提供 理论和临床洞察力，直接有助于所有中心的目标：描述病因和 VH的病理生理学，VH的更特异的表型，以及改进的预防、诊断和治疗方法 VH的治疗。这种理解可以使评估对每个患者的具体情况敏感 内表型，允许基于潜在机制的个性化治疗方法。

Project Summary Vocal hyperfunction (VH) is a highly prevalent feature in the 3 – 9% of the U.S. population with voice disorders. Characterized by excessive and/or incoordinated laryngeal and perilaryngeal tension, its pathophysiology has been attributed to many potential etiologies, such as poor vocal hygiene, psychological factors, reflux, and atypical autonomic nervous system (ANS) function. Our central hypothesis, supported by our recent findings, is that auditory-motor function is impaired in some individuals with VH: we found impairments in speakers' auditory acuity to differences in recordings of their own voice fundamental frequency (fo) and their adaptive responses to artificial shifts in their own voice fo. In this cycle we propose to further elucidate the etiologic role of disrupted auditory-motor function in VH and to evaluate measures of auditory-motor function that have clinical applicability. In Aim 1, individuals with VH and controls will participate in tasks to derive fo adaptive responses with and without a simultaneous cognitive stressor to elicit ANS arousal. Converging evidence suggests that atypical ANS function is a potential etiologic factor in VH, and that the level of ANS arousal may be associated with impairments in auditory-motor function. Thus, we will directly assess whether disrupted ANS and auditory-motor function represent a shared endophenotype (related predisposing factors) in the etiology of VH. In Aim 2, fo acuity and adaptive responses will be investigated longitudinally in VH. Our pilot data indicate that many individuals with VH and atypical auditory-motor features show improvement in their adaptive responses immediately after voice therapy. This may represent normalization of an underlying etiologic factor. Conversely, voice therapy may provide strategies to improve vocal quality, without addressing the underlying neural vulnerability of individuals to develop VH, with changes in auditory-motor adaptation that are secondary. We anticipate that individuals with atypical auditory-motor features immediately post-therapy will have poorer long-term responses to therapy, with the implication that disrupted auditory-motor control is an etiologic factor in the development and persistence of VH. The fo perturbation methods employed in Aim 1 and Aim 2 require precise calibration of instrumentation and well-controlled acoustic environments, limiting their clinical viability. Therefore, in Aim 3, potential “clinic-friendly” correlates (auditory acuity to shifts in the fo of a standard voice and production of speech before, during, and after being exposed to a noisy environment to induce a Lombard response) will be psychometrically evaluated in terms of their concurrent validity and test-retest reliability. Successful completion of these Aims will provide theoretical and clinical insight, contributing directly to all Center Aims: delineation of the etiology and pathophysiology of VH, more specific phenotyping of VH, and improved methods for prevention, diagnosis, and treatment of VH. This understanding could allow for assessments that are sensitive to each patient's specific endophenotype, allowing personalized therapy approaches based on underlying mechanisms.