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

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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.