Difficulty in terminating posture of three-dimensional gait bradykinesia in Parkinson’s disease

Abstract This study investigated whether difficulty in initiating volitional gait in patients with Parkinson’s disease stems from impaired termination of the preceding posture or impaired initiation of new movement. Participating were 41 patients with Parkinson’s disease and 15 age-matched controls. While participants fixated on a conditioning visual target, a visual cue test stimulus prompted participants to initiate volitional gait. Three-dimensional sole-floor reaction forces during coordinated gait movement, antagonist/agonist electromyography (EMG), and levodopa (L-DOPA) therapy were recorded. From the visual cue, gait initiation was measured by tibialis anterior EMG burst onset (EMG-on latency) and coordinated gait movement onset, whereas preceding postural termination latency was measured by the pause in antagonist soleus tonic EMG activity (EMG-off latency). Three visual fixation paradigms were used: no-gap (fixation and test targets turn-off simultaneously), gap (fixation turned off 200 ms before test stimulus), and overlap (fixation turned off 200 ms after test stimulus). In all three tasks, antagonist EMG-off latencies were prolonged in the patients. Agonist EMG-on latencies remained within physiological range in the gap and no-gap tasks but were prolonged for the overlap task in the patients. In three tasks, all coordinated gait movement latencies and overlap-task EMG-on latencies were prolonged among the patients and correlated with prolonged EMG-off latencies of the preceding movement/posture termination. Differences in unsynchronized EMG-off/on latency correlated with slow, short-step, small three-dimensional gait, and L-DOPA therapy, suggesting that the initiation difficulty in Parkinson’s disease is related to difficulty in terminating the preceding movement/posture rather than difficulty in generating new movement.