Viewing Study NCT00001661



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Last Modification Date: 2024-10-26 @ 9:02 AM
Study NCT ID: NCT00001661
Status: COMPLETED
Last Update Posted: 2008-03-04
First Post: 1999-11-03

Brief Title: Mechanisms of Human Plasticity in the Human System
Sponsor: National Institute of Neurological Disorders and Stroke NINDS
Organization: National Institutes of Health Clinical Center CC

Study Overview

Official Title: Mechanisms of Plasticity in the Human Motor System
Status: COMPLETED
Status Verified Date: 2002-03
Last Known Status: None
Delayed Posting: No
If Stopped, Why?: Not Stopped
Has Expanded Access: False
If Expanded Access, NCT#: N/A
Has Expanded Access, NCT# Status: N/A
Acronym: None
Brief Summary: The purpose of this study is to investigate the physiology associated with plasticity of the motor system Plasticity refers to the process by which neighboring brain cells assume the responsibilities of damaged or diseased brain cells

The mechanisms behind this process are unknown However researchers have several theories about how plastic changes take place Possible explanations include the growth of new connections between brain cells and the use of previously unused connections

Researchers plan to use transcranial magnetic stimulation and drug intervention in order to determine the mechanisms responsible for specific types of plasticity

Previous studies have shown that certain drugs can affect the mechanisms involved in these changes By using one drug at a time researchers plan to evaluate the role of each of several different mechanisms in brain reorganization
Detailed Description: The purpose of this study is to investigate the physiology associated with plasticity of the motor system seen in a number of different circumstances Techniques used will involve the combination of transcranial magnetic stimulation TMS and pharmacologic interventions We propose to use drugs judged to be safe that either potentiate GABA related intracortical inhibition change presynaptic release of excitatory aminoacids like glutamate or decrease the activity of the NMDA receptors mostly antiepileptic drugs If plastic changes expressed as larger motor maps or motor evoked potentials MEP to TMS are secondary to intracortical disinhibition administration of a drug that potentiates intracortical inhibition may result in decreased plasticity and smaller motor maps or MEP This finding would then identify intracortical disinhibition as the mechanism responsible for this type of plasticity Similarly if plastic changes decrease with a drug that inhibits release of excitatory aminoacids or that antagonize the action of NMDA receptors the mechanism underlying plasticity is likely to be mediated by modulation in the release of excitatory aminoacids or activity in NMDA-receptors

Results from this study will then provide information about the relative involvement of intracortical disinhibition modulation in the release of excitatory aminoacids and role of NMDA receptors in different settings of human plasticity

Study Oversight

Has Oversight DMC: None
Is a FDA Regulated Drug?: None
Is a FDA Regulated Device?: None
Is an Unapproved Device?: None
Is a PPSD?: None
Is a US Export?: None
Is an FDA AA801 Violation?: None
Secondary IDs
Secondary ID Type Domain Link
97-N-0048 None None None