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No PET scan differences between PDD and DLB
This research compares 8 patients with PDD (Parkinson disease with dementia), 6 patients with DLB (dementia with Lewy bodies), and 9 non-demented PD patients, using PET scans with different radioactive tracers. Significant differences between PDD and DLB were not found through any of the tracers used.
Neurology. 2010 Feb 24. [Epub ahead of print]
Neurotransmitter changes in dementia with Lewy bodies and Parkinson disease dementia in vivo.
Klein JC, Eggers C, Kalbe E, Weisenbach S, Hohmann C, Vollmar S, Baudrexel S, Diederich NJ, Heiss WD, Hilker R.
From the Department of Neurology (J.C.K., S.B., R.H.), Goethe-University, Frankfurt am Main; Department of Neurology (C.E., E.K.), University of Cologne; Cognitive Neurology Section (INM-3) (E.K.), Research Centre Juelich; Department of Epileptology (S.W.), University of Bonn; Max-Planck Institute for Neurological Research (C.H., S.V., W.D.H.), Cologne, Germany; and Department of Neurosciences and Interdisciplinary Sleep Laboratory (N.J.D.), Centre Hospitalier de Luxembourg.
OBJECTIVE: Although Parkinson disease with dementia (PDD) and dementia with Lewy bodies (DLB) show a wide clinical and neuropathologic overlap, they are differentiated according to the order and latency of cognitive and motor symptom appearance. Whether both are distinct disease entities is an ongoing controversy. Therefore, we directly compared patients with DLB and PDD with multitracer PET.
METHODS: PET with (18)fluorodopa (FDOPA), N-(11)C-methyl-4-piperidyl acetate (MP4A), and (18)fluorodeoxyglucose (FDG) was performed in 8 patients with PDD, 6 patients with DLB, and 9 patients with PD without dementia vs age-matched controls. Data were analyzed with voxel-based statistical parametric mapping and region of interest-based statistics.
RESULTS: We found a reduced FDOPA uptake in the striatum and in limbic and associative prefrontal areas in all patient groups. Patients with PDD and patients with DLB showed a severe MP4A and FDG binding reduction in the neocortex with increasing signal diminution from frontal to occipital regions. Significant differences between PDD and DLB were not found in any of the radioligands used. Patients with PD without dementia had a mild cholinergic deficit and no FDG reductions vs controls.
CONCLUSIONS: Patients with dementia with Lewy bodies and Parkinson disease dementia share the same dopaminergic and cholinergic deficit profile in the brain and seem to represent 2 sides of the same coin in a continuum of Lewy body diseases. Cholinergic deficits seem to be crucial for the development of dementia in addition to motor symptoms. The spatial congruence of cholinergic deficits and energy hypometabolism argues for cortical deafferentation due to the degeneration of projection fibers from the basal forebrain.
PubMed ID#: 20181924 (see pubmed.gov for this abstract only)