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.
