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Effects of Rhythmic Context on Time Perception in Individuals with Parkinson Disease

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Effects of Rhythmic Context on Time Perception in Individuals with Parkinson Disease EFFECTS OF RHYTHMIC CONTEXT ON TIME PERCEPTION IN INDIVIDUALS WITH PARKINSON DISEASE Nathaniel S. Miller A Dissertation Submitted to the Graduate College of Bowling Green State University in partial fulfillment of The requirements for the degree of DOCTOR OF PHILOSOPHY December 2010 Committee: J. Devin McAuley, Advisor Dale Klopfer Sheryl Coombs Alexander Goberman Graduate Faculty Representative ii ABSTRACT J. Devin McAuley, Advisor Parkinson disease (PD) is a neurodegenerative disorder of the basal ganglia (BG) that results in a significant loss of dopaminergic neurons. Previous studies have shown that individuals with PD show impairments in both the perception and production of duration, supporting the involvement of the BG and dopamine (DA) in perceptual and motor timing. One such DA-dependent timing impairment is gravitation in the remembered duration of an isolated (single) time interval toward the mean of a set of experienced time intervals (Malapani, et al., 1998). This dissertation extends research on time perception in PD to an investigation of the effects of rhythmic context on perceived duration. The basis for the project is a paradigm previously shown to produce large effects of rhythmic context on perceived duration in young adults (Barnes & Jones, 2000; McAuley & Jones, 2003). In this paradigm, participants are asked to compare the duration of two empty time intervals marked by pairs of tones (a fixed standard interval followed by a variable comparison interval) with the instruction to ignore a preceding tone sequence (i.e., context rhythm). Previous studies have shown that participants are unable to ignore the context rhythm, as evident by relative duration judgments about the standard-comparison pair of intervals being more accurate when the tone marking the end of the standard interval is ‗on time,‘ relative to a periodic extrapolation of the context rhythm, than when the tone marking the end of the standard interval is ‗early‘ or ‗late.‘ The resulting ∩-shaped pattern of performance has been termed a temporal expectancy profile. Two experiments tested two hypotheses about the strength of the expectancy profiles in young adults, older adults, and individuals with PD. The first hypothesis is a period-correction hypothesis that posits that increasing the number of repetitions of the standard interval will eliminate (or at least weaken) the expectancy profile. The second iii hypothesis is a DA-mediated distortion hypothesis that posits that larger effects of rhythmic context will be observed when individuals with PD are tested off their DA-enhancing medication than when tested on medication. Moreover, the loss of DA in individuals with PD will result in larger effects of rhythmic context than observed with older adult controls or young adults. Experiment 1 tested young adults in order to provide a baseline measure of performance and to provide an initial evaluation of the period-correction hypothesis, whereby effects of rhythmic context on perceived duration were predicted to be eliminated (or at least weakened) by increasing the number of repetitions of the standard interval. Experiment 2 compared the performance of individuals with PD (both on- and off-medication) to older adult controls and to the young adults tested in Experiment 1. In general, support for the period-correction hypothesis was found. Increasing the number of equal standard intervals reduced the effects of rhythmic context on perceived duration in all groups. Mixed support was found for the DA-mediated distortion hypothesis. Although no group differences were observed in the strength of expectancy profiles for the one-standard interval condition, increasing the number of equal standard intervals differentially affected individuals with PD on- and off-medication. Increasing the number of equal standard intervals served to weaken expectancy profiles for PD participants when they were on medication, but not when the same participants were off their medication. Taken together, the present findings provide the first evidence for the potential involvement of DA in period-correction processes. iv This dissertation is dedicated to the memory of Eva J. and John C. Miller. I am forever grateful for all that I have learned from you. v ACKNOWLEDGMENTS Before I acknowledge everyone who has helped me throughout this dissertation, I must first thank my family for their love and support. Roger Miller and Kathy Carns, thank you for supporting me in all of my life endeavors. John and Eva Jean Miller, you have influenced my life in ways that I am only just beginning to realize. While I miss you more every day, I consider myself fortunate for all the great years we had together. Finally, thank you Michelle Renzetti for being my ‗sister‘ and putting up with me since 8th grade. Special acknowledgement is also due to both Drs. J. Devin McAuley and Alexander Goberman. Devin has provided invaluable mentoring and support throughout my graduate training, for which I am forever thankful. Alex took me under his wing, introduced me to the Northwest Ohio Parkinson community, and taught me about conducting research on Parkinson disease. I am forever indebted to his continual support and willingness to listen and share ‗wild‘ testing stories. I must also thank my other committee members, Drs. Dale Klopfer and Sheryl Coombs, for their ideas and comments that have shaped this dissertation. Finally, Drs. Laura Dilley and Mary Hare must also be thanked for their advice and valuable comments throughout my graduate training. I have been fortunate to meet so many great people in Bowling Green who have provided amazing levels of support during graduate school. Sarah Domoff, you have been my rock throughout everything. I appreciate your understanding, sacrifices, and undying support throughout this dissertation—I owe you big time. I must also thank Molly Henry, Kavita Desai, Mo Wang, Guyla Davis, and Eileen Delaney for their continuing friendship. Thank you for your support and willingness to listen; I cannot imagine what graduate school would have been like had you six not been there for me. vi I would also like to acknowledge both the Bowling Green State University and Michigan State University branches of the Timing, Attention, and Perception Lab, who have contributed helpful comments and outstanding support during several research projects. Additionally, I must thank everyone who has helped with various stages of this dissertation: Jessica Zavadil, Shanta' Coleman, Claire Hoover, Daniel Percival, Alicia Cornell and Kelly Kaltenbach–you have made my life much easier and the time spent organizing these datasets much shorter. I must also extend appreciation to the participants of Experiment 2. Not only did they give me hours of their time, but also they were more than happy to have a relative stranger come into their home in the ‗wee‘ hours of the morning with several carloads of testing equipment. I am especially grateful to the members of the Parkinson Foundation of Northwest Ohio who have provided tireless assistance and support throughout this project and others. vii TABLE OF CONTENTS CHAPTER 1: INTRODUCTION ................................................................................................... 1 CHAPTER 2: BACKGROUND ON PARKINSON DISEASE ..................................................... 9 Description and Classification ............................................................................................ 9 Pathophysiology of PD ..................................................................................................... 13 Treatments for PD ............................................................................................................. 16 Pharmacological Therapies ................................................................................... 17 Levodopa................................................................................................... 17 DA agonists. .............................................................................................. 19 Catechol-O-methyl transferase inhibitors. ................................................ 20 Monoamine oxidase B inhibitors. ............................................................. 20 Amantadine. .............................................................................................. 20 Anticholinergics. ....................................................................................... 21 Pharmacological therapies for non-motor symptoms of PD. .................... 21 Ablative Surgeries ................................................................................................. 22 Deep Brain Stimulation......................................................................................... 23 CHAPTER 3: PERCEPTION AND PRODUCTION OF TIME INTERVALS—THEORY, DATA, AND NEURAL BASES .................................................................................................. 28 Theories of Timing ........................................................................................................... 28 Interval Theories ................................................................................................... 28 Entrainment Theories ............................................................................................ 32 Theory of the Neural Bases of Timing ................................................................. 34 Data ..................................................................................................................................
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