## Abstract The soleus Hโreflex excitability during gait initiation was investigated in Parkinson's disease. Eleven patients participated in this study. Patients stepped forward as soon as the start signal flashed. Soleus Hโreflex was evoked from the trailing leg 100, 300, or 600 msec after the sta
Gait initiation in parkinson's disease
โ Scribed by Regina Rosin; Dr. Helga Topka; Johannes Dichgans
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 724 KB
- Volume
- 12
- Category
- Article
- ISSN
- 0885-3185
No coin nor oath required. For personal study only.
โฆ Synopsis
Abstract
We studied the kinematic patterns of gait initiation in 31 patients with Parkinson's disease and in 20 ageโ and sexโmatched normals by using an optoelectronic tracking system (ELITE). Position markers were attached to the skin overlying the ankle, knee, hip, elbow, shoulder, and zygomatic bone. Subjects were instructed to start walking immediately after an acoustic go signal. Gait initiation was defined as the phase between standing motionless and steadyโstate locomotion. This phase was subdivided into a movement preparation period (the time between go signal and movement onset) and a movement execution period (the time between movement onset and the end of the first stride). Onset and duration of ankle, knee, hip, trunk, and arm motion within the first stride were analyzed. Movement preparation time was significantly increased in Parkinson's disease (p = 0.01), whereas movement execution times were similar in both groups (p = 0.23). Initiation of ankle, knee, hip, arm, and trunk movements was delayed in patients as compared with healthy subjects, but the relative timing and the sequence of submovements was comparable in both groups, indicating that the overall pattern of submovements was preserved in the patients. Our data suggest that gait initiation deficits in Parkinson's disease cannot be explained by a disordered sequence of limb and trunk submovements. More likely, gait initiation problems originate from the basal ganglia's internal cueing deficit for movement sequences, delaying onset and slowing the execution of all subcomponents.
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