Neuromodulation of the Sensorimotor Network in Parkinson’s Disease: A Therapy and an Investigative Tool
April 3, 2015, 1 p.m.
Helen Bronte-Stewart, MD, John E. Cahill Family Professor of Neurology, Director, Stanford Movement Disorders Center, Division Chief, Movement Disorders, Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, California
Virginia Tech Carilion Research Institute, M106 2 Riverside Circle, Roanoke, VA 24016
The cardinal motor signs of Parkinson’s disease (PD) include resting tremor, slowness of movement (bradykinesia), and stiffness (rigidity), and arise from chronic dopamine denervation in the striatum, one of the deep nuclei of the brain, the basal ganglia. Replacement of dopamine via oral therapy, skin patches, subcutaneous injections, and duodenal infusions have improved the cardinal motor signs but may lead to complications, such as involuntary movements (dyskinesias), a fluctuating and unpredictable response, and unwanted neuropsychiatric effects. Ablative lesions and now high frequency deep brain stimulation (DBS) in downstream basal ganglia nuclei, the Globus Pallidus (GPi) or the Subthalamic nucleus (STN), have emerged as useful treatments of the cardinal motor signs while avoiding the adverse side effects of long-term medication use. Current DBS therapy is in its infancy and its mechanism is still debated. It consists of continuous, open-loop electrical stimulation. The DBS system is blind to the underlying neural activity and cannot adjust its parameters for the state of activity of the patient, nor for independent motor signs.
It is now evident that there are exaggerated and persistent neuronal oscillations and synchronous neural activity in the functionally connected sensorimotor network in PD. A debated hypothesis is that DBS acts like a brain pacemaker and attenuates the abnormal neural synchrony (“neural arrhythmia”), but it is unclear whether this is the underlying cause for DBS induced improvement in mobility. In her lecture, Dr. Bronte-Stewart will discuss the evidence for patient specific neural arrhythmias in Parkinson’s disease and the neuromodulatory effect of different frequencies of DBS on such rhythms. She will also discuss the insights this brings to an emerging theme that brain arrhythmias may underlie other neuropsychiatric diseases.