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Transcranial Magnetic Stimulation in Parkinson's Disease

2014-08-27 03:56:40 | BioPortfolio

Summary

This study will use transcranial magnetic stimulation (TMS) to explore how the brain controls movement by sending messages to the spinal cord and muscles and what goes wrong with this process in disease. Activity in the motor cortex-the outer part of the brain-will be examined use TMS in patients with Parkinson's disease and in healthy volunteers.

Normal volunteers and patients with Parkinson's disease (stage I to III) 21 years of age and older may be eligible for this study.

All participants will have transcranial magnetic stimulation. For this procedure, an insulated wire coil is placed on the subject's scalp and a brief electrical current is passed through the coil. This creates a magnetic pulse that passes into the brain and generates very small electrical currents in the cortex, briefly disrupting the function of the brain cells in the stimulated area. This may cause muscle twitching or tingling in the face, jaw or limb. During the stimulation, participants will be asked to tense certain muscles slightly or perform other simple actions. The electrical activity of the muscle will be recorded on a computer through electrodes taped to the skin over the muscle. In most cases, the study will last less than 3 hours. Participants will also fill out questionnaires about aspects of personality and will be tested for their ability to perform certain cognitive (thinking) and movement tasks. Patients with Parkinson's disease will, in addition, be administered the Uniform Parkinson's Disease Rating Scale to measure disease severity.

Patients will be requested to stop all Parkinson's disease medications 12 hours before the study. They may resume medications immediately after the study. Patients who so wish may be admitted to the hospital the day or evening before the study while they are off medications and stay there until they feel ready to leave.

Description

Paired pulse transcranial magnetic stimulation (TMS) provides a measure of the balance of inhibitory and facilitatory activity evokable in the motor cortex. Studies in several diverse disorders of basal ganglia outflow and cortical regulation show an alteration in the direction of decreased inhibition or increased facilitation. In general, these have been quite small, data from different interstimulus intervals have been pooled for analysis, and, therefore, disease and state-specific information may have been missed. A deeper understanding of what this technique can tell us about pathological and normal cortical regulation requires detailed studies within populations looking for correlations between physiological and clinical/behavioral variables and large, uniform, head-to-head comparisons between clinical populations. This proposal contains a project that combines the correlational and comparative approaches in Parkinson's disease and healthy individuals. Data from this project will then be comparable to future similar studies in other disorders.

Study Design

N/A

Conditions

Parkinson Disease

Location

National Institute of Neurological Disorders and Stroke (NINDS)
Bethesda
Maryland
United States
20892

Status

Completed

Source

National Institutes of Health Clinical Center (CC)

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:56:40-0400

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Medical and Biotech [MESH] Definitions

Proteins associated with sporadic or familial cases of PARKINSON DISEASE.

A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal dopaminergic neurons. Clinical features include irreversible parkinsonian signs including rigidity and bradykinesia (PARKINSON DISEASE, SECONDARY). MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (Adams et al., Principles of Neurology, 6th ed, p1072; Neurology 1986 Feb;36(2):250-8)

A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.

Parkinsonism following encephalitis, historically seen as a sequella of encephalitis lethargica (Von Economo Encephalitis). The early age of onset, the rapid progression of symptoms followed by stabilization, and the presence of a variety of other neurological disorders (e.g., sociopathic behavior; TICS; MUSCLE SPASMS; oculogyric crises; hyperphagia; and bizarre movements) distinguish this condition from primary PARKINSON DISEASE. Pathologic features include neuronal loss and gliosis concentrated in the MESENCEPHALON; SUBTHALAMUS; and HYPOTHALAMUS. (From Adams et al., Principles of Neurology, 6th ed, p754)

Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)

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