Examination of central gait control mechanisms in Parkinson's disease using movement-related potentials

Abstract Gait disorders are common in people with Parkinson s disease. The pathophysiology of these disorders is not fully understood. Movement-related potentials reflect supplementary motor area activity associated with the preparation and execution of voluntary movement. Our aim was to investigate movement-related potentials associated with gait disturbances in patients with Parkinson s disease, as reflected by gait hypokinesia and initiation difficulties, in order to better understand the role of the basal ganglia in the pathogenesis of these conditions. Movement-related potentials were back-averaged from electroencephalography recordings performed on 11 participants with Parkinson s disease with no gait initiation difficulties, 9 participants with Parkinson s disease who suffered from gait initiation difficulties, 12 young healthy adults, and 8 healthy older adults. Participants took 3 steps forward, stepping off a force plate. Trigger signals from the force plate and electromyographic activity of the tibialis anterior muscle were used to identify gait initiation time. Participants stride length was also measured using a 3-dimensional motion analysis system. Movement-related potentials showed significant group differences between the healthy young adults and the 2 Parkinson s disease groups as well as the Parkinson s disease group as a whole. No significant difference was found between the participants with Parkinson s disease and age-matched controls. A significant inverse relationship between movement-related potentials and stride length was found in patients with Parkinson s disease who did not experience gait initiation difficulties but not in those who did have this symptom. Gait-generated movement-related potentials appear to show electrical evidence of cortical disturbances correlated with stride length reduction in patients with Parkinson s disease without gait initiation difficulties.