Abstract
Abnormality in gait is a cardinal feature of Parkinson's disease. Walking is characterized by relatively preserved sequencing of trunk and limb movements, but diminished velocity, shortened stride length, increased base, and diminished double stance support time. The principle problem producing the gait abnormalities is dopamine deficiency, which is hypothesized to disrupt pallido-thalamic modulation of cortical motor regions that automatically regulate walking. Deep brain stimulation currently is directed at either the globus pallidum internus (GPi) or subthalamic nucleus (STN) and improves many of the abnormal characteristics of parkinsonian gait with efficacy similar to dopamine replacement. The optimal target for stimulation remains uncertain and is currently being addressed in a large VA cooperative study. Our studies show that unilateral stimulation of GPi or STN improves gait to a similar extent. Functional and quantitative gait analyses confirm sustained improvement in gait dynamics with bilateral stimulation for periods for more than several years. Parkinsonian gait is also improved with rehabilitation training, primarily using external visual or auditory cues. The combination of deep brain stimulation, pharmacotherapy, and rehabilitation training may result in more effective comprehensive approaches to the reduced mobility associated with Parkinson's disease.
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