Some patients with Parkinson’s disease benefit from a treatment known as deep brain stimulation. The loss of dopamine disrupts the activity of structures deep within the brain called the basal ganglia, which normally control movement.
These symptoms occur when neurons that produce the chemical dopamine die. Symptoms include uncontrollable shaking or tremor, and difficulty with large or fast movements. Parkinson’s disease is a disorder of the nervous system that affects more than 1% of people over the age of 60. We propose that insufficient recruitment of fast gamma bursts during movement may underlie bradykinesia as one of the cardinal symptoms in Parkinson’s disease. Burst amplitude and duration were unaffected by the medication state. In the dopamine-depleted state, gamma power and burst rate significantly decreased, particularly when peak velocity was slower than ON medication. The gamma burst rate highly correlated with averaged power, increased gradually with larger movements and correlated with symptom severity. These effects relied on movement-related bursts of transient synchrony in the gamma band. In 16 patients undergoing deep brain stimulation surgery, movements of different velocities revealed that subthalamic gamma power peaked in the sensorimotor part of the subthalamic nucleus, correlated positively with maximal velocity and negatively with symptom severity. Here, disease-specific characteristics of this synchronization and the dopamine-dependence of its scaling in Parkinson’s disease are investigated. Gamma synchronization increases during movement and scales with kinematic parameters.
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