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

NCT ID: NCT01983670

Last Updated: 2013-11-14

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Clinical Phase

NA

Total Enrollment

40 participants

Study Classification

INTERVENTIONAL

Study Start Date

2009-07-31

Study Completion Date

2012-06-30

Brief Summary

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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.

Detailed Description

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Conditions

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Spinocerebellar Atrophy (SCA)

Keywords

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Pre-movement facilitation Fast goal directed movement Triphasic EMG pattern Temporal electrical stimulation, Spinocerebellar Ataxia

Study Design

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Allocation Method

RANDOMIZED

Intervention Model

PARALLEL

Primary Study Purpose

TREATMENT

Blinding Strategy

NONE

Study Groups

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health group 1

Health subjects received 30 mins delay antagonist activation temporal ES.

Group Type EXPERIMENTAL

Temporal electrical stimulation

Intervention Type OTHER

SCA group 1

SCA subjects received four weeks temporal ES assisted home training program.

Group Type EXPERIMENTAL

Temporal electrical stimulation

Intervention Type OTHER

health group 2

health subjects controlled group

Group Type NO_INTERVENTION

No interventions assigned to this group

SCA group 2

SCA subjects controlled group

Group Type NO_INTERVENTION

No interventions assigned to this group

Interventions

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Temporal electrical stimulation

Intervention Type OTHER

Eligibility Criteria

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Inclusion Criteria

* Clinical diagnosis of spinocerebellar ataxia
Minimum Eligible Age

20 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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Chang Gung University

OTHER

Sponsor Role lead

Responsible Party

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Ya-Ju Chang

Associate Professor

Responsibility Role PRINCIPAL_INVESTIGATOR

Locations

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Chang Gung University

Taoyuan District, , Taiwan

Site Status

Countries

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Taiwan

References

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Huang YZ, Chang YS, Hsu MJ, Wong AM, Chang YJ. Restoration of Central Programmed Movement Pattern by Temporal Electrical Stimulation-Assisted Training in Patients with Spinal Cerebellar Atrophy. Neural Plast. 2015;2015:462182. doi: 10.1155/2015/462182. Epub 2015 Aug 31.

Reference Type DERIVED
PMID: 26417459 (View on PubMed)

Other Identifiers

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98-0951B

Identifier Type: -

Identifier Source: org_study_id