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.

项目概要/摘要 运动减退性构音障碍是一种言语障碍，影响 89% 的帕金森病 (PD) 患者。1- 3 它会导致声音强度降低,4-8 和清晰度降低4,6,9 从而剥夺患者的能力 通过言语表达情感 10-12 会损害生活质量。13 言语治疗 (LSVT®) 已成功治疗运动性构音障碍，因为它利用了理论过程 称为“韵律结构的语音编码”14，即发音动作与韵律相关， 当声音强度增加时，发音就会改善。15, 16 然而，这种现象的神经基础 发音强度之间的联系尚不清楚，在我们的治疗和言语运动方面留下了关键差距 控制知识。研究这种效应的神经基础将推动创新治疗方法，并具有 对语言障碍有广泛的影响。该项目的目标是 1) 确定神经学 PD 中语音强度编码的组织和 2) 测试差异贡献 声音强度编码中的皮质和皮质下结构。该项目的目标是 以先前文献为指导，该文献认为初级运动皮层和基底神经节很重要 发音和韵律控制的潜在大脑区域。17-31 作为一个更大项目的一部分， 来自感觉运动皮层的皮层电图记录和来自丘脑底的深度记录 在接受深部脑部检查时收集 PD 患者的细胞核（基底神经节的一部分） 刺激手术。在手术的清醒阶段，患者会说出一些无意义的话 平衡音素和声音强度级别（高与低）。主要目的是解码神经网络 初级运动皮层 (M1) 和丘脑底核中语音强度编码的组织 （STN）通过检查局部场势功率的变化，神经元数量的测量 激活。变异性将解释为口语音素的变化和声音强度的增加。这是 假设将识别出表明局部场电位增加的皮质区域 声音强度的功率，但激活的区域将取决于产生的特定音素。这 第二个目的是研究皮质和皮质下大脑区域对声音强度的影响 控制。在皮质下，基底神经节被认为有助于运动规划和生成 语音前馈命令的数量，32-34，而皮质上，M1 对于语音的执行至关重要。32, 35 次要目标是测试 M1 和 STN 对患者口语声音强度的不同贡献。它 假设 STN 在言语开始之前贡献更大程度，反映运动 准备工作，M1在演讲过程中做出贡献，反映运动执行力。拟议的研究和 培训计划将为申请人提供发展成功所需技能的机会 独立的研究生涯。