Abstract
This study examined how gait bradykinesia is changed by the motor programming in Parkinson’s disease. Thirty-five idiopathic Parkinson’s disease patients and nine age-matched healthy subjects participated in this study. After the patients fixated on a visual-fixation target (conditioning-stimulus), the voluntary-gait was triggered by a visual on-stimulus. While the subject walked on a level floor, soleus, tibialis anterior EMG latencies, and the y-axis-vector of the sole-floor reaction force were examined. Three paradigms were used to distinguish between the off-/on-latencies. The gap-task: the visual-fixation target was turned off; 200 ms before the on-stimulus was engaged (resulting in a 200 ms-gap). EMG latency was not influenced by the visual-fixation target. The overlap-task: the on-stimulus was turned on during the visual-fixation target presentation (200 ms-overlap). The no-gap-task: the fixation target was turned off and the on-stimulus was turned on simultaneously. The onset of EMG pause following the tonic soleus EMG was defined as the off-latency of posture (termination). The onset of the tibialis anterior EMG burst was defined as the on-latency of gait (initiation). In the gap-task, the on-latency was unchanged in all of the subjects. In Parkinson’s disease, the visual-fixation target prolonged both the off-/on-latencies in the overlap-task. In all tasks, the off-latency was prolonged and the off-/on-latencies were unsynchronized, which changed the synergic movement to a slow, short-step-gait. The synergy of gait was regulated by two independent sensory-motor programs of the off- and on-latency levels. In Parkinson’s disease, the delayed gait initiation was due to the difficulty in terminating the sensory-motor program which controls the subject’s fixation. The dynamic gait bradykinesia was involved in the difficulty (long off-latency) in terminating the motor program of the prior posture/movement.
Highlights
The cardinal symptom of Parkinson’s disease is difficulty in starting volitional synergic movement; swinging of the arms during walking is diminished, and the gait becomes slow and is usually composed of small steps due to the impaired synergism (Brain and Walton 1969)
The diagnosis of idiopathic Parkinson’s disease was based on the criteria established by the UK Parkinson’s Disease Society Brain Bank (Hughes et al 1992) and the subjects were selected based on similar criteria used in the previous studies (Warabi et al 1986): patients whose primary symptom was bradykinesia without hemiparesis, ataxia, or aphasia
The selfpaced gait mode was due to the motor program initiating the unilateral tibialis anterior EMG activity, and this EMG activity was associated with the unilateral backward bodysway of the same leg (Fig. 1a) (Elble 1997)
Summary
The cardinal symptom of Parkinson’s disease is difficulty in starting volitional synergic movement; swinging of the arms during walking is diminished, and the gait becomes slow and is usually composed of small steps due to the impaired synergism (Brain and Walton 1969). The remained question was the slowness of gait initiation due to difficulty in initiating a new synergic movement or due to difficulty in terminating the preceding posture/movement. Evarts et al (1981) reported that both reaction time and movement time which both reflect the speed of movement tend to be prolonged in Parkinson’s disease. The prolongation of reaction time, which reflects the speed of response initiation, is relatively slight. Their results are incompatible with the hypothesis that the impairment of the ability to initiate a new movement is the primary cause of bradykinesia. If the timing to terminate a preceding posture/movement is distinguished from the timing to initiate a new volitional movement, it is possible to clarify the difficulty of initiating volitional movements in Parkinson’s disease
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