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The Role of Cerebellar Hyperactivity in Parkinson's Disease

Principal Investigator:
Amy
Bastian

The purpose of this work is to study the role of the cerebellum in gait dysfunction for Parkinson's disease (PD) patients. While the symptoms of PD were originally ascribed to dopamine deficiency and basal ganglia dysfunction, recent research has shown that the cerebellum is hyperactive in PD patients during different motor tasks as well. However, whether cerebellar hyperactivity is pathological or compensatory and how it affects gait and balance in PD patients remain open questions.

To elucidate the role of the hyperactive cerebellum in PD, we will use transcranial direct-current stimulation (tDCS) to modulate cerebellar excitability and a paired-pulse transcranial magnetic stimulation (TMS) technique, referred to as cerebellar-brain inhibition (CBI), to study the connection between the cerebellum and the motor cortex.

We hypothesize that if cerebellar hyperactivity in PD is compensatory, anodal tDCS will decrease the CBI response and improve gait. If it is pathological, cathodal tDCS will improve gait. Regardless of the pathological or compensatory nature of cerebellar hyperactivity in PD, we hypothesize that tDCS will be able to modulate it in a way that would reduce gait deficits in patients.

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