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: 10268199
• 负责人: Christina Dastolfo-Hromack
• 金额: $ 4.85万
• 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/10268199
• 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.

项目总结/摘要 运动功能减退性构音障碍是一种语言障碍，影响89%的帕金森病（PD）患者。 3它会导致声音强度降低，4-8和可理解性降低，4，6，9剥夺了患者的能力 通过语言表达情感10-12，并有助于降低生活质量。 (LSVT®）已经成功地治疗运动不足性构音障碍，因为它利用了理论过程， 称为“韵律结构的语音编码”14，也就是说，发音运动与韵律有关， 当声音强度增加时，发音会得到改善。15，16然而，这种情况的神经基础 发音强度的联系是不理解的，留下了一个关键的差距，在我们的治疗和语言运动 控制知识。研究这种效应的神经基础将推动创新治疗， 对言语障碍的广泛影响。该项目的目标是1）确定神经系统 组织的语音强度编码在PD和2）测试的差异贡献 皮质和皮质下结构在声音强度编码中的作用。该项目的目标是 在先前文献的指导下，将初级运动皮层和基底神经节确定为重要的 发音和韵律控制的潜在脑区。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底丘脑的深度记录 在接受脑深部手术时收集PD患者的核（基底神经节的一部分） 刺激手术在手术的清醒部分，病人说一些无意义的话， 平衡音素和声音强度水平（高与低）。主要目的是解码 初级运动皮层（M1）和丘脑底核中语音强度编码的组织 (STN)通过检查局部场电位功率的变化， activation.变异性将被解释为音素的变化和声音强度的增加。是 假设皮层区域将被识别为显示局部场电位增加 功率的声音强度，但激活的区域将取决于特定的音素产生。的 第二个目的是研究皮层和皮层下脑区对声音强度的影响 控制在皮质下，基底神经节被认为有助于运动规划和生成 32-34，而在皮层，M1对执行语音至关重要。 第二个目标是测试M1和M2对患者口语声音强度的不同贡献。它 假设在言语开始之前，前额叶皮层将在更大程度上起作用，反映运动神经元的运动， M1将在言语过程中发挥作用，反映运动执行。拟议的研究和 培训计划将为申请人提供机会，以发展必要的技能，成功的 独立的研究生涯。