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Abstract Details

Striatal dopamine motor and non-motor network and cortical activity in Parkinson disease: a correlation study between 123I-FP-CIT SPECT and FDG PET
Movement Disorders
P3 - Poster Session 3 (12:00 PM-1:00 PM)
3-013

To examine the correlation of striatal 123I-FP-CIT SPECT (DAT) scan uptake and whole-brain FDG-PET in patients with probable Parkinson's disease (PD).

The utility of DAT in the diagnosis of PD is well-accepted. However, the value of combined use of DAT and FDG-PET to assess circuit dysfunction in PD remains to be elucidated.
We studied 5 consecutive patients with levodopa responsive parkinsonism who were evaluated at the Mayo Clinic, Rochester, MN and underwent DAT and FDG-PET. Images were analyzed using statistical parametric mapping software. 
Five males aged 58.6±7.6 years with average symptom duration of 3.2±2.7 years were studied. All patients were stage Hoehn & Yahr 1-2 . Reduced striatal DAT binding correlated with FDG-PET hypometabolism in the tail but not in the main body of the putamen or caudate p<0.05. Reduced DAT binding also correlated with hypometabolism in the medial thalamus, supplementary motor cortex, sensorimotor cortex, mesencephalon and cerebellum (p<0.05). Conversely, decreased DAT tracer binding correlated with hypermetabolism in the prefrontaland orbitofrontal cortex, and posterior cingulate gyrus bilaterally (p<0.05).
These preliminary results suggest that DAT and FDG-PET provide complementary information regarding circuit dysfunction in PD.  Correlation between reduced dopamine transporter activity and hypometabolism in the tail of the putamen and midbrain on FDG-PET indicate that FDG-PET and DAT  provide similar information regarding  subcortical motor circuit dysfunction. Lack of correlation between DAT and FDG-PET findings in the main body of the putamen and caudate suggests a dissociation between loss dopaminergic terminals and impaired glucose metabolism in most of the striatum. Correlation between decreased striatal DAT uptake and FDG-PET hypermetabolism in cortical areas known to be dysfunctional in PD suggests compensatory response to decreased dopaminergic function and cortical network dysfunction in PD.
Authors/Disclosures
Stuart J. McCarter, MD (Mayo Clinic)
PRESENTER
The institution of Dr. McCarter has received research support from NIH. The institution of Dr. McCarter has received research support from American Academy of Sleep Medicine Foundation.
No disclosure on file
Val J. Lowe, MD (Mayo Clinic) Dr. Lowe has received personal compensation in the range of $10,000-$49,999 for serving as a Consultant for AVID Radiopharmaceutical. Dr. Lowe has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Eisai Inc. The institution of Dr. Lowe has received research support from AVID Radiopharmaceuticals.
Eduardo E. Benarroch, MD, FAAN (Mayo Clinic) Dr. Benarroch has nothing to disclose.
David T. Jones, MD (Mayo Clinic) Dr. Jones has stock in Cephlodyne Neurotechnologies, Inc.. Dr. Jones has received intellectual property interests from a discovery or technology relating to health care.
Bradley F. Boeve, MD, FAAN (Mayo Clinic) Dr. Boeve has received personal compensation in the range of $10,000-$49,999 for serving as an officer or member of the Board of Directors for Rainwater Charitable Foundation. The institution of Dr. Boeve has received research support from Alector. The institution of Dr. Boeve has received research support from EIP Pharma. The institution of Dr. Boeve has received research support from Transposon. The institution of Dr. Boeve has received research support from Cognition Therapeutics. Dr. Boeve has received publishing royalties from a publication relating to health care.
Rodolfo Savica, MD, PhD, FAAN (Mayo Clinic) The institution of Dr. Savica has received research support from ACADIA Pharmaceuticals, Inc.