Freezing of gait (FOG), defined as the ‘episodic absence or marked reduction of forward motion of feet despite the intention to walk’,1 is one of the most debilitating symptoms in Parkinson’s disease.2,3 Although deep brain stimulation (DBS) of the subthalamic nucleus (STN) well controls cardinal symptoms of Parkinson’s disease such as tremor and motor fluctuation, current DBS therapy provides modest and highly heterogeneous benefits to FOG.4–8 Revealing the neurophysiological patterns directly associated with FOG and the underlying modulation effects induced by DBS will foster optimized DBS therapy targeting FOG.
