Author's School

Graduate School of Arts & Sciences

Author's Department/Program

Movement Science


English (en)

Date of Award


Degree Type


Degree Name

Doctor of Philosophy (PhD)

Chair and Committee

Gammon Earhart


Many persons with Parkinson's disease: PD) experience difficulty turning that can lead to freezing of gait, falls, and an increased risk of fall-related injuries. We hypothesized, based on previous literature, that turning difficulty and freezing during turning may be related to deficits in the ability to switch from one motor pattern to another: Chapter 2). We further hypothesized that deficits in oculomotor control, particularly in the case of voluntary saccades, also contribute to the pathogenesis of turning difficulty since turning is normally initiated with an eye movement: Chapter 3). Finally, we hypothesized that current treatment approaches including pharmacological and surgical interventions would improve turning performance and oculomotor performance in individuals with PD: Chapter 4). To determine whether individuals with PD have trouble switching motor patterns with the eyes and whether they experience similar deficits in the lower limb, we tested healthy controls and persons with PD during an orientation switch task. The PD group delayed orientation switching that was attributable to bradykinesia, and there was a correlation in the amount of impairment across body parts. These results suggest that while individuals with PD may take longer to switch from one motor pattern to another, bradykinesia may be the driving factor as opposed to an internal deficit in the ability to switch motor programs. Regardless of mechanism, delays in switching motor patterns may play a role in freezing and turning difficulty. To determine if oculomotor function is abnormal in PD during turning and whether this contributes to turning difficulty, participants with PD and healthy controls performed in-place 90┬║ and 180┬░ turns. Turn performance was worse in PD: i.e., longer time to turn, more steps) and those with PD made more saccades during the turns. Further, the saccade initiating the turn was smaller, slower, and exhibited altered timing relative to the first step of the turn in those with PD compared with controls. Finally, saccade performance was correlated with turn performance in those with PD. Our results suggest that the oculomotor strategy used by those with PD is altered and less efficient as compared with controls, and that oculomotor dysfunction may be a contributing factor in turning difficulty. To determine if therapeutic interventions could improve oculomotor function and related turning performance, we tested individuals with PD and deep brain stimulation: DBS) of the subthalamic nucleus. Gait parameters and turn duration improved with both levodopa therapy and DBS, but only DBS was successful in improving concurrent oculomotor function. The amplitude and velocity of the first saccade improved with DBS, while the latency of the first saccade decreased relative to the onset of head rotation and the first step. Taken together, these studies corroborate previous knowledge that voluntary saccades are dysfunctional in PD. Further, these studies relate oculomotor impairment to a functional task and give insight into the role of therapeutic interventions for improving turning difficulty in PD. These results also provide support for using visual cueing to improve turning performance and therefore, future research should examine the efficacy of such cues on turning performance.


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