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Home > "M" Clinical Trials Conditions > Mechanisms of Human Plasticity in the Human System  Mechanisms of Human Plasticity in the Human System
Mechanisms of Human Plasticity in the Human System
For Condition: Blindness,Cerebrovascular Accident,Spinal Cord Injury
Status: Completed
Sponsor(s): National Institute of Neurological Disorders and Stroke (NINDS) ,
Synopsis: 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.
Details: 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.
Eligibility:
Study Type: Observational, Natural History
Minimum Age/Maximum Age: /
Genders: Both
Protocol Entry Criteria: Must be over 18 years of age. Must not have personal history of seizures, loss of consciousness, hypertension, psychosis, heart conditions or allergies to any of the drugs. Women must not be nursing or pregnant. Patients may have amputations, spinal cord injuries, blindness or large hemispheric lesions from stroke.
Total Enrollment: 260
Location and Contact Information:
National Institute of Neurological Disorders and Stroke (NINDS)
Bethesda, Maryland, 20892
United States
Additional Information:
Study ID Numbers: 970048; 97-N-0048
Study Start Date: December 23, 1996
Record last reviewed: March 27, 2002
Additional information available at: clinicaltrials.gov
Clinicaltrials.gov Reference link: NCT00001661
Other Spinal Cord Injury Studies:
1. Evaluation of Eye Movement Tracking Systems for Visual Rehabilitation
2. Brain Plasticity of Verbal Memory in the Blind
3. Diabetic Retinopathy Study (DRS)
4. The Connection Between Areas in the Brain of Blind Patients
5. Mechanisms of Human Plasticity in the Human System
Related Studies:
Other Spinal Cord Injury Clinical Trials
Other Maryland Clinical Trials
Other Bethesda Clinical Trials
Mechanisms of Human Plasticity in the Human System
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