Motor Skill Learning in People With Parkinson's Disease

2014-08-27 03:41:40 | BioPortfolio


This study will compare brain changes in people with Parkinson's disease with those of normal control subjects while they learn motor skills. People with Parkinson's disease sometimes have trouble learning new skills, but it is not known why. This study will use repetitive transcranial magnetic stimulation (rTMS), nerve conduction studies, and electroencephaolography (EEG) to look for differences in the way the brain changes with learning in people with Parkinson's disease.

Healthy normal volunteers and people with Parkinson's disease who are between 21 and 80 years of age may be eligible for this study. Participants undergo the following procedures in five visits to the NIH Clinical Center:

Visit 1

Medical and neurological examination.

Visit 2

Motor training. Participants perform a pinching movement once every other second, timed to a metronome, during rTMS. For TMS, a wire coil is held on the subject's scalp. A brief electrical current is passed through the coil, creating a magnetic pulse that stimulates the brain. The subject hears a click and may feel a pulling sensation on the skin under the coil. There may be a twitch in the muscles of the face, arm or leg. rTMS involves repeated magnetic pulses delivered in short bursts of impulses.

Visits 3 and 4

Brain physiology studies using rTMS, nerve conduction studies (electrical nerve stimulation) and EEG. A nerve at the subject's wrist is stimulated with electrical impulses to measure the speed with which nerves conduct electrical impulses and the strength of the connection between the nerve and the muscle. rTMS is performed for 20 minutes. The EEG measures the electrical activity of the brain (brain waves). For this test, electrodes (metal discs) are placed on the scalp with a conductive gel and the brain waves are recorded while the subject moves his or her thumb briskly for 20 minutes.

Visit 5

Subjects undergo rTMS for 20 minutes and have an EEG.




The aims of the present study are to:

1. Clarify that the altered plasticity of the primary motor cortex (M1) in patients with Parkinson's disease (PD) is associated with impaired motor learning by using the paired associative stimulation (PAS) technique, which can enhance or inhibit the M1 excitability with paired stimulation to the contralateral peripheral nerve and cerebral cortex.

2. Elucidate that the altered plasticity of the M1 in patients with PD goes together with impaired sensorimotor integration via the basal ganglia-thalamocortical loop.

Study population

12 right-handed patients with PD

12 right-handed age-matched healthy volunteers


Patients and age-matched healthy volunteers will complete five different sessions: Visit 1: clinical screening; Visit 2: motor learning session; Visit 3 and 4: the paired associative stimulation (PAS) sessions; Visit 5: the control session.

During the motor learning session, subjects will be asked to perform metronome-paced pinch of their index finger and thumb.

During the PAS sessions, they will receive 20 minutes of paired stimulation to the contralateral peripheral nerve stimulation and transcranial magnetic stimulation (TMS) at the appropriate timing for producing changes of the M1 excitability.

During the control session, they will receive 20 minutes of repetitive TMS without the peripheral nerve stimulation.

Outcome measures

For the motor learning session:

- peak acceleration (MPA) of thumb movement

- maximal peak force (MPF) between the index finger and thumb

For the PAS and control sessions:

- peak-to-peak motor evoked potential (MEP) amplitude

- resting motor threshold

- afferent inhibition

- event related desynchronization (ERD) and event related synchronization (ERS)

Study Design



Parkinson's Disease


National Institutes of Health Clinical Center, 9000 Rockville Pike
United States




National Institutes of Health Clinical Center (CC)

Results (where available)

View Results


Published on BioPortfolio: 2014-08-27T03:41:40-0400

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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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