Fig. 10. A summary of cortico-subthalamic motor control and mechanism of therapeutic effect of STN-DBS in PD.

(Left) In PD, MC activities are increased, with fewer spatiotemporal changes upon movement. STN bursts are longer and less variable, and thus less responsive to different MC drives. There are consequently decreased α oscillations electrophysiologically and poor initiation (akinesia) as well as deranged automatic program transitions (bradykinesia) behaviorally. Here “akinesia” denotes difficulties in the initiation of both a movement and a non-motor cognitive process, and thus may include the deficiency of initiatives in PD. On the other hand, the impaired operations of the MC-STN (cortex-basal ganglia re-entrant loops) lead to deranged autonomic shifts of motor (and/or non-motor) programs and thus slowing the speed of execution of a set of movement (i.e. bradykinesia). It is of note that even in such a deranged system of PD, α augmentation upon movement is preserved, suggesting that α augmentation is an essential attribute of movement. (Right) In PD with STN-DBS, MC activities are decreased, with more spatiotemporal changes upon movement and restoration of α oscillations. STN bursts are decreased in number, and are shorter as well as more variable, and thus more responsive to different MC activities. However, if the STN is overly stimulated and depolarized, burst discharges would be excessively inhibited (few or no bursts). The principal role of STN burst discharges for an immediate check or “brake” for the cortical output is very much weakened. α oscillations are decreased again, with possibilities of impulsive initiation of a movement or even the other cognitive processes (e.g. ballism) and an unchecked automatic program transitions (propulsion or a movement without interim interruptions, such as the type 2 movement in Fig. 8).