Examining the Links Among Motor Symptoms in Vocal Hyperfunction, Auditory Acuity, and Auditory-Motor Function

项目摘要 声音障碍是常见的，在任何给定时间影响高达9%的美国人口，并且大多数美国人都有声音障碍。 被转诊到多学科语音诊所的患者患有功能亢进性语音障碍（HVD;例如，声带 结节和肌肉紧张性发音困难）。在临床上，HVD的特征是发声疲劳、发声困难， 发声时肌肉活动失调然而，相对较少的是了解有关的病理生理学 这些迹象和症状的基础。阐明引起和维持HVD的机制是必要的 指导有效的治疗研究。最近的研究已经确定了运动障碍，包括 非典型嗓音基频听觉辨别与非典型适应性发声学习 在HVD患者的一个子集中，对听觉反馈扰动的反应。HVD患者显示 除了F0之外，还可以在语音的多个参数（例如强度和语音质量）上进行非典型发声。是 这些行为可能与发声感觉运动控制的广泛听觉运动障碍有关。因此，在本发明中， 拟议的研究将通过检查听觉， 敏锐度和适应性声乐学习在两个重要参数的声乐感觉运动控制： 强度。除了了解HVD患者的运动障碍程度外， 这种损害和这些疾病的临床特征之间的关系是至关重要的指导 临床研究到目前为止，运动障碍和肌肉失调之间的直接关系 发声期间的激活（HVD的标志）尚未建立。对侧咽周共同收缩 当说话者增加他们的发声努力时，肌肉发生，并且被认为发生在HVD的发声期间。在 研究达到运动，共同收缩发生在肢体，以响应反馈扰动， 以稳定运动，并随着参与者适应扰动而减少。重要的是， 感觉运动控制也表明较差的感觉敏锐度降低了适应性。因此，我们建议， 咽周围共同收缩可响应于听觉反馈扰动而发生， 喉，并将减少与适应性声乐学习。此外，在某些说话者中， HVD可能与非典型适应性发声学习和持续性咽周共刺激有关。 与没有HVD的扬声器相比收缩。因此，目标1将比较自适应声乐学习和 个体对fo和听觉反馈强度扰动的咽周共同收缩反应 有（n = 26）和无（n = 26）HVD。目的2将评估非典型听觉敏锐度的患病率为声乐 在同一组说话人中的fo和强度。在目标3中，听觉敏锐度、适应性声乐 学习和咽周共同收缩。这项工作将是第一次检查喉 听觉反馈扰动后的稳定反应，并可能确定一个潜在的机制 HVD患者发声过程中运动障碍与肌肉激活失调之间的联系。

Project Summary Voice disorders are common, affecting up to 9% of the U.S. population at any given time, and the majority of patients referred to multidisciplinary voice clinics have hyperfunctional voice disorders (HVDs; e.g., vocal fold nodules and muscle tension dysphonia). Clinically, HVDs are characterized by vocal fatigue, dysphonia, and dysregulated muscle activation during voicing. Yet, relatively little is understood about the pathophysiology underlying these signs and symptoms. Elucidating the mechanisms that cause and sustain HVDs is necessary to guide impactful treatment research. Recent studies have identified auditory-motor impairments, including atypical auditory discrimination of voice fundamental frequency (fo) and atypical adaptive vocal learning in response to fo auditory feedback perturbations, in a subset of individuals with HVDs. People with HVDs display atypical voicing across multiple parameters of voice, such as intensity and voice quality, in addition to fo. It is possible that these behaviors relate to a broad auditory-motor impairment for vocal sensorimotor control. Thus, the proposed studies will address the specificity of auditory-motor impairment in HVDs by examining auditory acuity and adaptive vocal learning across two important parameters for vocal sensorimotor control: fo and intensity. In addition to understanding the extent of auditory-motor impairment in HVDs, determining the relationship between such impairments and the clinical characteristics of these disorders is critical to guide clinical research. To date, a direct relationship between auditory-motor impairment and dysregulated muscle activation during voicing, a hallmark of HVDs, has not been established. Co-contraction of opposing perilaryngeal muscles occurs when speakers increase their vocal effort, and is thought to occur during voicing in HVDs. In studies of reaching movements, co-contraction occurs in the limbs in response to feedback perturbations in order to stabilize movements, and decreases as participants adapt to the perturbations. Crucially, studies of limb sensorimotor control also suggest that worse sensory acuity reduces adaptation. Thus, we propose that perilaryngeal co-contraction may occur in response to auditory feedback perturbations in order to stabilize the larynx, and will decrease with adaptive vocal learning. Furthermore, impaired auditory acuity in some speakers with HVDs may be associated with both atypical adaptive vocal learning and persistent perilaryngeal co- contraction compared to speakers without HVDs. Therefore, Aim 1 will compare adaptive vocal learning and perilaryngeal co-contraction in response to perturbations of fo and intensity of auditory feedback in individuals with (n = 26) and without (n = 26) HVDs. Aim 2 will evaluate the prevalence of atypical auditory acuity for vocal fo and intensity in the same groups of speakers. In Aim 3, relationships among auditory acuity, adaptive vocal learning, and perilaryngeal co-contraction will be examined. This work will be the first to examine laryngeal stabilization responses following auditory feedback perturbations, and may identify a potential mechanistic connection between auditory-motor impairment and dysregulated muscle activation during voicing in HVDs.