Dystonia, Parkinson’s Disease Share Motor Cortex Synchronization

Brain wave
Brain wave
The disorders react similarly to basal ganglia deep brain stimulation.

CHICAGO – Isolated dystonia and Parkinson’s disease are both disorders of the basal gangliothalamocortical network. Both respond to similar subcortical targets in deep brain stimulation (DBS), suggesting a pathophysiological overlap.

Svjetlana Miocinovic, MD, PhD, of the University of California, San Francisco, and colleagues hypothesized that the association between isolated dystonia and Parkinson’s has to do with elevated cortical neuronal synchronization. In order to investigate this relationship, the researchers launched an observational study of 36 patients scheduled to undergo DBS from May 1, 2008 through April 1, 2015. Their findings were published to coincide with the American Neurological Association 2015 Annual Meeting from September 27 – 29, 2015 in Chicago.

Among the patients included in the study were eight with dystonia with apparent arm involvement (DYST-AMR), 14 with dystonia without arm involvement (DYST), and 14 with akinetic rigid Parkinson’s disease. Cortical phase-amplitude coupling (PAC) was present in primary motor and premotor arm-related areas for all groups, however the DYST group was less likely to show increased PAC (P=.008). Subthalamic DBS reversibly decreased PAC in a group of patients with dystonia. At rest, broadband gamma (50-200Hz) in the primary motor cortex was greater in the DYST-ARM and PD groups than the DYST group, while alpha (8-13Hz) and beta (13-30Hz) power was comparable across all three patient groups. The DYST-ARM group showed impaired beta and low gamma desynchronization in the primary motor cortex during movement.

The researchers found that isolated dystonia and Parkinson’s indeed have a physiologic overlap with respect to high levels of motor cortex synchronization and reduction of cortical synchronization by subthalamic DBS, which explains the similar therapeutic response to basal ganglia stimulation. 


  1. Miocinovic S et al. JAMA Neurol. 2015; doi:10.1001/jamaneurol.2015.2561.