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Spinocerebellar Atrophy (SCA) clinical trials

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NCT ID: NCT01983670 Completed - Clinical trials for Spinocerebellar Atrophy (SCA)

The Investigation of the Pre-movement Facilitation of Agonist-antagonist Muscles and the Effect of the Feedforward Rehabilitation in Individuals With Hypermetria

Start date: July 2009
Phase: N/A
Study type: Interventional

In individuals with spino-cerebellar atrophy (SCA), the delayed onset of antagonist muscle firing has been reported to be the cause of hypermetria. Hypermetria is a common deficit in individuals with spino-cerebellar atrophy SCA when they perform ballistic goal-directed movement. Based on the previous studies, ballistic goal-directed movements are controlled by a triphasic pattern of agonistic and antagonistic muscle activation. The origin of the EMG pattern is a central program, whereas the delayed onset of antagonistic muscle firing has been reported to be the cause of hypermetria. To develop a therapy method, the difference in temporal pattern and intensity of supraspinal excitability of agonist and antagonist bursts between healthy adults and individuals with SCA when performing rapid and slow goal-directed movements should be further investigated. Traditional rehabilitations of individuals with cerebellum lesion were limited to improve the functional performance of movement. Since the deficits of the goal-directed movement are at pre-movement programming, only feedforward training will be possible to re-establish an appropriate program. Previous showed that peripheral stimulation resulted in a facilitation of motor cortex. Our group also found that this facilitation in individuals with SCA was similar to the ones without SCA. Therefore, it is possible to adjust the control pattern of supraspinal excitability of agonist and antagonist busts of SCA patient with passively providing electrical stimulation contains normal control pattern of healthy human. The present study sought to investigate the difference in temporal pattern and intensity of supraspinal excitability of agonist and antagonist bursts between healthy adults and individuals with SCA when performing rapid and slow goal-directed movements.