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PET Scanning in Parkinson's Disease - Article


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Water Pollution


Clinical Trial: PET Scanning in Parkinson's Disease

This study is currently recruiting patients.

Sponsored by: National Human Genome Research Institute (NHGRI)
Information provided by: Warren G Magnuson Clinical Center (CC)

Purpose

This study will compare brain blood flow and the brain's use of dopamine in patients with Parkinson's disease, their family members and normal volunteers. Dopamine is a chemical normally found in the part of the brain involved in controlling movement. This chemical is lacking in people with Parkinson's disease, and patients have difficulty initiating or controlling some body movements. Usually, Parkinson's disease develops in people without any known cause. In a few families, however, three or more people are affected, suggesting these families may have a genetic alteration that makes them more prone to develop the disease.

Normal healthy volunteers and members of families in which three or more people have Parkinson's disease may be eligible for this study. Candidates will have a physical examination and provide a personal and family medical history. Volunteers will also have a neurological examination.

Participants will undergo PET scanning. One hour before the scan, subjects are given a medication called Carbidopa, which maximizes the usefulness of the scans. For the procedure, the subject lies on a table in the scanner, a catheter (thin plastic tube) is inserted into an arm vein, and a baseline scan is done. Radioactive water is then injected through the catheter and another scan is done. During this scan, the subject is asked questions to stimulate blood flow in certain areas of the brain. Up to 10 injections are given, with different questions asked each time. The total time for the scans is not more than 1 hour. A final scan, which may last up to 2 hours, is then done. Dopamine is injected into the catheter before the scan begins. When it is completed, subjects are instructed to empty their bladder immediately and then every 2 hours for the rest of the day to reduce the exposure to radioactive material.

Shortly afterwards, the subject has a magnetic resonance imaging (MRI) scan. This scan is used to help interpret the information obtained from the PET scans. MRI uses radio waves and a magnetic field to image structural and chemical changes in tissues. For this procedure, the subject lies still on a table that is moved into the middle of a narrow circular scanner. An intercom system permits communication with the staff member performing the study at all times during the procedure.

Condition Treatment or Intervention
Parkinson Disease
 Drug: 18F-Fluoro-L-dopa
 Drug: O-15 Water

MedlinePlus related topics:  Parkinson's Disease
Genetics Home Reference related topics:  Parkinson disease

Study Type: Observational
Study Design: Natural History

Further Study Details: 

Expected Total Enrollment:  200

Study start: September 17, 2001

This is an in vivo study of regional cerebral dopamine neurochemistry and blood flow in normal volunteers, persons with sporadic Parkinson's disease and individuals from families with inherited Parkinson's disease (PD), including clearly affected individuals, those with equivocal signs, and those at risk but showing no signs of the disease. Using positron emission tomography (PET) with 6-[F-18] Fluoro-L-dopa (6FD) and (15)O-H2O in a single scan session, both presynaptic dopaminergic function and cerebral blood flow are assessed. The kinetic rate constant (Ki) for striatal dopamingergic uptake is calculated. Using bivariate analysis we compare Ki in all three family groups (affected, unaffected, equivocally affected individuals) with aged match healthy volunteers to detect any abnormalities in striatal and putamenal presynaptic F-dopa uptake. Futhermore, we also draw comparisons between subjects with inherited and sporadic Parkinson's disease to determine whether the PET phenotype is the same in both groups. Each subject is further screened with an MRI to rule out structural abnormalities and also to further delineate areas of interest in the PET scan. The results of the PET scan will help to phenotypically categorize clinically equivocal/unaffected family members and strengthen the linkage analysis study to which those with inherited PD have already consented to participate. Information about the PET scans results will not be communicated back to the individuals or families involved as part of this study.

Eligibility

Genders Eligible for Study:  Both

Accepts Healthy Volunteers

Criteria

INCLUSION CRITERIA:
Individuals over the age of 18 from families in which an autosomal dominant form of Parkinson's disease is suspected based on pedigree analysis.
Each sugject will hava a medical history and brief neurological examination.
The diagnosis in probands must be supported by accepted clinical criteria: tremor, bradykinesia, and responsiveness to L-DOPA.
Equivocally affected individuals will also be included in order to aid in their phenotypic classification as will at risk individuals who show no neurological signs.
Healthy volunteers who do not have a family or clinical history of Parkinson's disease will also have a PET can on the same day. Volunteers will be age, gender and handedness-matched for statistical purposes.
EXCLUSION CRITERIA:
Individuals not capable of understanding the consent will be excluded.
Individuals taking medications (such as antidepressants) which affect dopamine transporters will also be excluded.

Location and Contact Information


Maryland
      National Human Genome Research Institute (NHGRI), 9000 Rockville Pike,  Bethesda,  Maryland,  20892,  United States; Recruiting
Aideen McInerney-Leo  3014020160    amcinern@nhgri.nih.gov 

More Information

Detailed Web Page

Publications

Gasser T, Muller-Myhsok B, Wszolek ZK, Oehlmann R, Calne DB, Bonifati V, Bereznai B, Fabrizio E, Vieregge P, Horstmann RD. A susceptibility locus for Parkinson's disease maps to chromosome 2p13. Nat Genet. 1998 Mar;18(3):262-5.

Kitada T, Asakawa S, Hattori N, Matsumine H, Yamamura Y, Minoshima S, Yokochi M, Mizuno Y, Shimizu N. Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism. Nature. 1998 Apr 9;392(6676):605-8.

Polymeropoulos MH, Lavedan C, Leroy E, Ide SE, Dehejia A, Dutra A, Pike B, Root H, Rubenstein J, Boyer R, Stenroos ES, Chandrasekharappa S, Athanassiadou A, Papapetropoulos T, Johnson WG, Lazzarini AM, Duvoisin RC, Di Iorio G, Golbe LI, Nussbaum RL. Mutation in the alpha-synuclein gene identified in families with Parkinson's disease. Science. 1997 Jun 27;276(5321):2045-7.

Study ID Numbers:  010232; 01-HG-0232
Record last reviewed:  August 24, 2004
Last Updated:  April 6, 2005
Record first received:  September 23, 2001
ClinicalTrials.gov Identifier:  NCT00024622
Health Authority: United States: Federal Government
ClinicalTrials.gov processed this record on 2005-04-08


Source: ClinicalTrials.gov
Cache Date: April 9, 2005


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