As a higher-level modulator of the supraspinal locomotor network, the primary motor cortex (M1) participates in the control of gait initiation and gait stability.9,10 Previous structural MRI and magnetic resonance spectroscopy studies indicated that a lower grey matter volume and abnormal metabolite ratios were evident in the M1 of subjects with freezing/impaired gait.9,11 By leveraging functional MRI and virtual reality gait paradigms, Shine et al.12 observed a significant decrease in blood oxygen level-dependent response in the bilateral M1 during behavioural freezing compared to stable walking. Since neuroimaging studies were unable to model real gait during scanning, Pozzi et al.13 recently recorded multisite neurophysiological signals (STN and scalp EEG) during walking, and found that FOG was associated with low frequency decoupling between motor cortex regions and the STN, further confirming the involvement of dysfunctional M1 in FOG. However currently, the neurophysiological characteristics specifically related to FOG within the M1 remain largely unknown. In addition, little attention has been paid to the influence of DBS in improving FOG and the corresponding underlying cortical response. This knowledge, though can be challenging to get, is particularly important for translating current findings into improved DBS therapy, e.g. adaptive DBS targeting freezing.14
