Graduation Date

Fall 12-16-2016

Document Type


Degree Name

Doctor of Philosophy (PhD)


Medical Sciences Interdepartmental Area

First Advisor

Max Kurz, PhD


This dissertation explored motor control in individuals with multiple sclerosis (MS) by quantifying the behavioral and neurophysiological deficits present in these individuals. We behaviorally quantified the precision of the ankle plantarflexor musculature of individuals with MS. Our results indicated that the individuals with MS had a greater amount of variability in the precision of the isometric ankle torques, and that this greater variability was related to decreased walking performance. To further explore whether these motor control deficits were due to aberrant cortical activity associated with planning motor actions, we used magnetoencephalography to assess the motor planning and execution stages of movement during a goal directed target matching task performed with the knee joint. Interestingly, we found no differences between groups in the cortical activity during the planning and execution stages of movement. However, we did find that individuals with MS had a weaker post-movement beta rebound in the precentral and postcentral gyri relative to healthy controls. These results suggest that the internal model is faulty in individuals with MS. We further explored if the faulty internal model could be due to sensory processing deficits by examining somatosensory gating in these individuals using paired-pulse tibial nerve stimulation. Our results showed reduced somatosensory gating for the individuals with MS, suggesting the inhibitory intracortical circuits may be altered in these individuals. Finally, we examined the cortical responses to single-pulse tibial nerve stimulation at rest and during movement, in order to assess the performance of the sensory system during active movement. Our results indicated that the individuals with MS were unable to properly suppress the somatosensory responses during movement. All together, the results of this dissertation provide evidence that the impaired motor control of individuals with MS may be due to a faulty internal model, which has become corrupt due to demyelination, and cannot be properly updated due to impaired sensory processing.

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