Ph.D., University of Washington, Seattle
For most of us reaching to grasp an object seems an almost effortless task, despite the profound difficulty of the underlying control problems. How the central nervous system accomplishes such feats of motor skill is one of my overarching research interests. The central network that solves this control problem involves several motor-related regions of cortex and portions of the basal ganglia, cerebellum and thalamus. A specific goal of mine is to tease apart the relative roles of the basal ganglia and the motor cortices in learning and controlling skillful arm movements. Recent results from my lab show that the motor circuit through the basal ganglia is not necessary for the selection and execution of well-learned motor sequences. Future extensions of this work will examine the importance of the basal ganglia versus motor cortices in various forms of motor learning and adaptation.
A related topic of ongoing interest is how pathology within the basal ganglia, such as the degeneration of dopamine cells in Parkinson’s disease, leads to specific and distinct disorders of movement. Although great strides have been made in understanding the essential pathologic changes that underlie Parkinson’s disease, we have only a rudimentary understanding of how that local pathology gives rise to a cluster of specific behavioral impairments. Currently, we are testing the hypothesis that the different parkinsonian signs (akinesia, bradykinesia and rigidity) are related to distinct abnormalities in neuronal activity in the motor cortices.
High frequency electrical stimulation through electrodes implanted deep in the brain (i.e., Deep Brain Stimulation, DBS) is a highly effective therapy for Parkinson’s disease, dystonia, and several other medically intractable disorders. Despite that fact that this form of brain-machine therapy is being applied to an ever-widening range of disorders, we are only now beginning to understand the fundamental physiologic mechanisms by which DBS produces a therapeutic effect. An ongoing project in my lab investigates the mechanisms of action of DBS by studying the changes in neuronal activity in the motor cortices during DBS-induced modulations of symptom severity.
The primary experimental approach used in my lab is to correlate regional brain activity with measures of task performance or impairment. Most experiments are conducted in non-human primates trained to perform motor tasks, but some experiments are in humans, including those undergoing neurosurgical therapies for movement disorders. We design tasks to dissociate behavioral and neuronal correlates of multiple independent motor control processes. We also study the roles of different motor control pathways by manipulating local neuronal activity using pharmacologic agents.
Ultimately, I hope that studies in my lab will both advance our understanding of how the brain controls of movement and improve the treatment of common disorders of movement.