fMRI Correlates of Speech and Voice Impairment in Parkinson's Disease

Northwestern University At Chicago, Evanston IL

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Abstract

PROJECT SUMMARY Approximately 80-90% of individuals with Parkinson's disease (PD) develop motor speech impairments, predominantly in the form of voice dysfunction. It is known that the motor symptoms of PD arise from degeneration of the dopamine producing neurons in the substantia nigra and dysregulation of basal ganglia motor pathways. It is also known that motor cortical activity in PD patients is abnormal during movement. However, it is unclear how the changes in basal ganglia and motor cortical function relate to the speech and voice symptoms of PD. While motor cortical activity is abnormal in PD, it is unknown whether differences in cortical activity appear during sustained vowel production tasks or whether voice-driven motor cortical activity correlates with measures of voice quality in PD. My prior work found that the globus pallidus and subthalamic nucleus are functionally connected to several regions within the healthy speech network. In PD, changes in connectivity of the putamen have been linked to impairments in clinical speech ratings. However, it is not known how connectivity of caudate, globus pallidus, and subthalamic nucleus relate to speech and voice impairments in PD. The specific aims of this proposal will address gaps in existing knowledge about the mechanisms of motor speech impairment in PD. Aim 1 will do so first by examining whether cortical activity is hypoactive in PD patients during sustained vowel production, and second by correlating acoustic measures of voice quality and intensity with levels of motor cortical activation in PD. Aim 2 will address whether global speech impairments in PD are associated with changes in basal ganglia connectivity. It will do so by first examining whether resting- state cortico-basal ganglia connectivity is abnormal in PD patients with clinically detectable speech impairment. Second, it will examine whether voice-driven connectivity of basal ganglia structures in PD subjects is altered in the presence of speech impairments. Together, Aims 1 and 2 will provide insight into the contributions of motor cortical activity and cortico-basal ganglia connectivity to speech production in PD.