Modeling biomechanical, aero-acoustic, and auditory-motor control mechanisms of vocal hyperfunction

项目摘要/摘要 发声功能亢进(VH)是指由于反复发声的有害模式而导致的慢性疾病 而且它与最常见的发音障碍类型有关。我们中心的目标是 解决增加对病因和病理生理机制的了解的迫切需要 与VH相关，改进VH相关疾病的预防、诊断和治疗。建立在 我们小组在确定关键的潜在物理机制方面取得的进展，额外的努力是 需要更好地了解听觉运动障碍在VH中的作用以及物理机制 为声音创伤患者长期发声奠定基础。确定是什么触发了VH恶性循环 在这些疾病中区分原因和反应是至关重要的。 该项目的第一个目标是确定听觉运动控制在喉部生物力学中的作用。 患有VH的个体。一组集总声带模型和有限元声带模型将合并到一个 建立了语音运动控制的神经计算框架，以研究语音的神经控制 音调、对环境噪音的反应和音质。之前的努力是模拟发病和 VH的补偿机制将扩大到考虑拟议的生理相关 将使用贝叶斯方法开发听觉-运动控制模型和特定于对象的表示法 框架。拟议的听觉-运动框架将允许调查因果影响和 喉运动控制和喉生物力学之间的相互关系，它们不是直接观察到的 从行为反应来看。 第二个目标是确定作为VH统计分类器基础的物理机制 关于动态语音监听。我们的集中元、有限元和物理模型将用于 确定为持续发声模拟的VH机制如何与长期差异相关 在群体和条件之间。此外，数值模型将模拟人口分布在 动态数据以确定VH统计分类背后的潜在物理机制。 我们还将探讨能量耗散剂、水肿、纤维化和愈合使用结构的作用 物理模型和有限元模型中的重塑原则。个别描述将使用以下工具进行增强 基于贝叶斯特定对象模型的动态测量，捕捉潜在的VH病理生理学 评估我们对VH统计分类的结果的机制。完成拟议的目标将 提高对动态监测的认识和临床相关性。

Project Summary/Abstract Vocal hyperfunction (VH) refers to chronic conditions resulting from repeated detrimental patterns of vocal behavior and it is implicated in the most commonly occurring types of voice disorders. Our center aims to address the pressing need to increase the understanding of the etiological and pathophysiological mechanisms associated with VH, to improve the prevention, diagnosis and treatment of VH-related disorders. Building upon the progress made by our group to determine key underlying physical mechanisms, additional efforts are needed to better understand the role of auditory-motor impairments in VH as well as the physical mechanisms underpinning long-term of voice use in phonotrauma. Identifying what triggers a VH vicious cycle and differentiating cause from reaction in these disorders is critical. The first aim of the project is to determine the role of auditory-motor control in the laryngeal biomechanics of individuals with VH. A set of lumped and finite element vocal fold models will be incorporated into an established neurocomputational framework of speech motor control, to investigate neural control of voice in terms of pitch, responses to environmental noise, and voice quality. Previous efforts to simulate onset and compensatory mechanisms of VH will be extended to account for the proposed physiologically relevant auditory-motor control model and subject-specific representations will be developed using a Bayesian framework. The proposed auditory-motor framework will allow for the investigation of causal effects and the interrelation between laryngeal motor control and laryngeal biomechanics, which are not directly observable from the behavioral responses. The second aim is to determine the physical mechanisms that underlie VH statistical classifiers that are based on ambulatory voice monitoring. Our lumped element, finite element, and physical models will be used to ascertain how the VH mechanisms modeled for sustained phonation relate to the long-term differences between groups and conditions. In addition, numerical models will mimic population distributions in the ambulatory data to determine the underlying physical mechanisms behind the statistical classification of VH. We will also explore the role of energy dissipation dose, edema, fibrosis, and healing using structure remodeling principles in both physical and finite element models. Individual descriptions will be enhanced using Bayesian subject-specific model-based ambulatory measures that capture underlying VH pathophysiological mechanisms to assess our findings for the statistical classification of VH. Completion of the proposed aim will improve the understanding and clinical relevance of ambulatory monitoring.