Mechanisms of Human Plasticity in the Human System

Spinal Cord Injury Clinical Trial

Official title:

Mechanisms of Plasticity in the Human Motor System

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00001661
• Other study ID #: 970048
• Secondary ID: 97-N-0048
• Status: Completed
• Phase: N/A
• First received: November 3, 1999
• Last updated: March 3, 2008
• Start date: December 1996
• Est. completion date: March 2002

Study information

• Verified date: March 2002
• Source: National Institutes of Health Clinical Center (CC)
• Contact: n/a
• Is FDA regulated: No
• Health authority: United States: Federal Government
• Study type: Observational

Clinical Trial 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.

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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 260
• Est. completion date: March 2002
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: Both
• Age group: N/A and older

Eligibility

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.

Study Design

N/A

Related Conditions & MeSH terms

• Blindness
• Cerebrovascular Accident
• Spinal Cord Injuries
• Spinal Cord Injury
• Stroke

Locations

Country	Name	City	State
United States	National Institute of Neurological Disorders and Stroke (NINDS)	Bethesda	Maryland

Sponsors (1)

Lead Sponsor	Collaborator
National Institute of Neurological Disorders and Stroke (NINDS)

Country where clinical trial is conducted

United States, 

References & Publications (3)

Brasil-Neto JP, Valls-Solé J, Pascual-Leone A, Cammarota A, Amassian VE, Cracco R, Maccabee P, Cracco J, Hallett M, Cohen LG. Rapid modulation of human cortical motor outputs following ischaemic nerve block. Brain. 1993 Jun;116 ( Pt 3):511-25. — View Citation

Cohen LG, Bandinelli S, Findley TW, Hallett M. Motor reorganization after upper limb amputation in man. A study with focal magnetic stimulation. Brain. 1991 Feb;114 ( Pt 1B):615-27. — View Citation

Ziemann U, Lönnecker S, Steinhoff BJ, Paulus W. Effects of antiepileptic drugs on motor cortex excitability in humans: a transcranial magnetic stimulation study. Ann Neurol. 1996 Sep;40(3):367-78. — View Citation