Neural encoding of phoneme and vocal intensity interactions in the motor cortex and basal ganglia

运动皮层和基底神经节中音素和声音强度相互作用的神经编码

• 批准号: 10447486
• 负责人: Christina Dastolfo-Hromack
• 金额: $ 0.25万
• 依托单位: UNIVERSITY OF PITTSBURGH AT PITTSBURGH
• 依托单位国家: 美国
• 财政年份: 2020
• 资助国家: 美国
• 起止时间: 2020-09-01 至 2022-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10447486
• 关键词: Affect; Analysis of Variance; Area; Articulation; Basal Ganglia; Behavior; Brain; Brain region; Communication; Deep Brain Stimulation; Dysarthria; Electrocorticogram; Electrodes; Electrophysiology (science); Epidemiologist; Expressed Emotion; Frequencies; Functional disorder; Future; Generations; Goals; Impairment; Interdisciplinary Study; Intervention; Knowledge; Life; Linear Models; Link; Literature; Location; Loudness; Measurement; Measures; Mentorship; Motor; Motor Cortex; Movement; National Institute on Deafness and Other Communication Disorders; Neurologic; Neurons; Operative Surgical Procedures; Outcome; Parkinson Disease; Patients; Performance; Population; Precentral gyrus; Preparation; Process; Production; Quality of life; Research; Research Personnel; Research Training; Signal Transduction; Social isolation; Speech; Speech Disorders; Speech Therapy; Structure; Structure of subthalamic nucleus; Testing; Time; Training; United States; awake; brain behavior; career; experience; improved; innovation; motor control; neurophysiology; relating to nervous system; skills

PROJECT SUMMARY/ABSTRACT Hypokinetic dysarthria is a speech disorder that affects 89% of patients with Parkinson disease (PD).1- 3 It causes reduced vocal intensity,4-8 and decreased intelligibility4, 6, 9 which deprive patients of the ability to express emotion through speech 10-12 and contributes to impaired quality of life.13 Speech therapy (LSVT®) has been successful in treating hypokinetic dysarthria because it utilizes a theoretical process called `the phonetic encoding of prosodic structure'14 that is, articulatory movements are linked to prosody, and articulation improves when vocal intensity is increased.15, 16 However, the neural basis of this articulation-intensity link is not understood, leaving a critical gap in our treatment and speech motor control knowledge. Investigating the neural basis of this effect will fuel innovative treatments and have a broad impact on speech disorders. The project goals are to 1) determine the neurological organization of phonetic-intensity encoding in PD and 2) test the differential contributions of cortical and subcortical structures in vocal intensity encoding. The aims of this project are guided by prior literature which identifies the primary motor cortex and basal ganglia as important potential brain regions for both articulatory and prosodic control.17-31 As part of a larger project, electrocorticography recordings from the sensorimotor cortex and depth recordings from the subthalamic nucleus (part of the basal ganglia) were collected in patients with PD while undergoing deep brain stimulation surgery. During the awake portion of the surgery, patients spoke nonsense words that were balanced for phoneme and vocal intensity level (high vs. low). The primary aim is to decode the neural organization of phonetic-intensity encoding in the primary motor cortex (M1) and subthalamic nucleus (STN) by examining the variability in local field potential power, a measurement of neuron population activation. Variability will be explained changes in phoneme spoken and vocal intensity increases. It is hypothesized that regions of cortex will be identified which demonstrate an increase in local field potential power for vocal intensity, but the region activated will depend on the particular phoneme produced. The secondary aim is to investigate the influence of cortical and subcortical brain regions on vocal intensity control. Subcortically, the basal ganglia has been proposed to contribute to motor planning and generation of feedforward commands for speech,32-34 while cortically, M1 is critical for execution of speech.32, 35 The secondary aim will test the differential contributions of M1 and STN to patients' spoken vocal intensity. It is hypothesized that the STN will contribute a greater extent prior to speech onset, reflecting motor preparation, and M1 will contribute during speech, reflecting motor execution. The proposed research and training plan will offer the applicant the opportunity to develop the skills necessary for a successful independent research career.

项目摘要/摘要 运动性构音障碍是一种言语障碍，影响%的帕金森病患者。1- 它会导致发声强度降低，4-8和智力下降4，6，9，从而剥夺患者的能力 通过言语表达情感10-12并有助于降低生活质量。13言语疗法 (LSVT®)已成功用于治疗运动性构音障碍，因为它利用了一种理论过程 称为韵律结构的语音编码14，即发音动作与韵律相关联， 当声音强度增加时，清晰度会改善。15，16然而，这一点的神经基础 发音-强度联系还不清楚，在我们的治疗和言语运动中留下了一个关键的缺口 掌握知识。研究这种效应的神经基础将推动创新的治疗方法，并有 对言语障碍的广泛影响。该项目的目标是1)确定神经学上的 帕金森病语音强度编码的组织和2)检验差异贡献 在声强编码中的皮质和皮质下结构。这个项目的目标是 以先前的文献为指导，认为初级运动皮质和基底节是重要的 发音和韵律控制的潜在大脑区域。17-31作为更大项目的一部分， 来自感觉运动皮质的皮质电记录和来自丘脑底核的深度记录 帕金森病患者在接受脑深部手术时采集了核团(部分基底节)。 刺激手术。在手术的清醒部分，患者说的是无稽之谈 平衡音素和声音强度水平(高与低)。其主要目的是对神经进行解码 初级运动皮质(M1)和丘脑底核的语音强度编码组织 (STN)通过检查局部场电位功率的可变性，这是对神经元数量的测量 激活。变异性会被解释为音素发音的变化和发声强度的增加。它是 假设大脑皮层的区域将被识别为显示局部场势增加的区域 声音强度的能量，但激活的区域将取决于产生的特定音素。这个 第二个目的是研究大脑皮质和皮质下区域对发声强度的影响。 控制力。在皮质下，基底节被认为对运动规划和生成有贡献。 语音的前馈命令，32-34，而实质上，M1对于语音的执行是关键的。32，35 次要目的是测试M1和STN对患者发声强度的不同贡献。它 假设STN在言语开始之前有更大程度的贡献，反映运动 准备，而M1将在说话过程中做出贡献，反映运动执行。拟议的研究和 培训计划将为申请者提供发展成功所需技能的机会 独立研究生涯。