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UBC Theses and Dissertations

Manual tracking in Parkinson's disease : implications for L-dopa-induced dyskinesias Stevenson, James


Though Parkinson’s disease (PD) is considered to be a prototypical basal ganglia disorder, it has become increasingly clear that this traditional view does not capture the complexity of the disease pathophysiology. For instance, imaging studies demonstrate altered cerebellar activity in PD that may compensate for and/or contribute to the symptoms of the disease. L-dopa-induced dyskinesias (LID) are involuntary writhing movements that commonly occur as a side effect of L-dopa therapy, and despite the prevalence of LID their underlying mechanisms are poorly understood. Altered cerebellar activity in PD may contribute to the pathophysiology of LID, and due to altered ‘forward models’ lead dyskinetic subjects to more heavily rely on ambiguous visual feedback. The principal aim of this thesis was to investigate the ability of PD subjects to de-weight ambiguous visual feedback during motor performance, while examining this ability as well as subtle differences in motor performance across dyskinetic and non-dyskinetic PD subjects. To this end we designed a large-amplitude visually guided tracking task where the target ‘jittered’ about the desired trajectory, and used root mean square (RMS) error and linear dynamical system (LDS) models to quantify tracking performance. The three major findings of this work were: 1) in addition to their known susceptibility to speed, PD subjects off medication were significantly more susceptible to increasing visual uncertainty than control subjects, 2) despite similar RMS error during non-ambiguous tracking the damping ratio parameter of the LDS models was significantly lower for dyskinetic subjects off medication, and 3) dyskinetic PD subjects were significantly more susceptible to visual uncertainty than non-dyskinetic and control subjects, and though L-dopa improved their overall tracking ability, this came at the price of a greater response to and reliance on ambiguous visual feedback. From this work we conclude that PD subjects demonstrate an impaired ability to de-weight ambiguous visual input, possibly due to inadequate forward models, and which may be specific to LID pathophysiology. The presence of motor abnormalities while dyskinetic subjects are off medication and not actively experiencing LID is suggestive of persistent neural plasticity. We argue these findings are related to altered cerebellar function in PD.

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