Parkinson Disease Clinical Trial
Official title:
NMDA-Receptor Blockade With Eliprodil in Parkinson's Disease
Patients with Parkinson's disease are missing the chemical neurotransmitter dopamine. This
occurs as a result of destructive changes in an area of the brain responsible for making
dopamine, the basal ganglia. Patients with the disease experience, rigid muscles, stooped
posture, and a shuffling-type walk (gait).
In this study researchers plan to evaluate the effectiveness of the drug eliprodil for the
treatment of Parkinson's Disease. Eliprodil works by blocking special receptors (NMDA) that
are associated with the symptoms of Parkinson's Disease.
Status | Completed |
Enrollment | 20 |
Est. completion date | January 2001 |
Est. primary completion date | |
Accepts healthy volunteers | No |
Gender | Both |
Age group | N/A and older |
Eligibility |
All patients will carry a diagnosis of idiopathic Parkinson's Disease based on the
presence of a characteristic clinical history and neurologic findings. Most will have
relatively advanced disease with associated motor response complications. Males and females between the ages of 18-75. No presence or history of any medical condition that can reasonably be expected to subject the patient to unwarranted risk. No patients with baseline QTc prolongation (greater than 440 msec). No pregnant women nor those not practicing effective means of birth control. |
Endpoint Classification: Safety/Efficacy Study, Primary Purpose: Treatment
Country | Name | City | State |
---|---|---|---|
United States | National Institute of Neurological Disorders and Stroke (NINDS) | Bethesda | Maryland |
Lead Sponsor | Collaborator |
---|---|
National Institute of Neurological Disorders and Stroke (NINDS) |
United States,
Bergman H, Wichmann T, DeLong MR. Reversal of experimental parkinsonism by lesions of the subthalamic nucleus. Science. 1990 Sep 21;249(4975):1436-8. — View Citation
Mitchell IJ, Clarke CE, Boyce S, Robertson RG, Peggs D, Sambrook MA, Crossman AR. Neural mechanisms underlying parkinsonian symptoms based upon regional uptake of 2-deoxyglucose in monkeys exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Neuroscience. 1989;32(1):213-26. — View Citation
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