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Functional effects of striatal dysfunction in Parkinson disease
V A Holthoff-Detto1, J Kessler, K Herholz
1Max-Planck-Institut für Neurologische Forschung, Köln, Germany.
Archives of Neurology
|February 1, 1997
Summary
Parkinson disease motor deficits are linked to putamen dopamine dysfunction, while cognitive decline in advanced stages is associated with caudate dopamine issues. This study differentiates striatal pathway involvement in Parkinson's symptoms.
Area of Science:
- Neuroscience
- Neurology
- Medical Imaging
Background:
- Basal ganglia organization involves segregated pathways linking putamen and caudate function to motor and cognitive performance.
- Parkinson disease (PD) presents with both motor and cognitive impairments, suggesting potential disruptions in nigrostriatal dopaminergic pathways.
Purpose of the Study:
- To investigate if motor and cognitive impairments in Parkinson disease are selectively linked to disturbances in nigrostriatal dopaminergic function.
- To examine the role of regional cerebral glucose metabolism in these impairments.
Main Methods:
- Twenty patients with probable Parkinson disease underwent positron emission tomography (PET) scans.
- PET measurements included dopaminergic nigrostriatal function (using fluorodopa F 18) and regional glucose metabolism (using fludeoxyglucose F 18).
- Patients also underwent memory testing and evaluation of locomotor disability.
Main Results:
- All Parkinson disease patients showed significantly reduced striatal uptake rates of fluorodopa F 18 compared to controls.
- Putaminal fluorodopa F 18 uptake correlated with locomotor disability, but not memory performance.
- In advanced PD, reduced caudate fluorodopa F 18 uptake correlated with memory impairment (delayed recall), but not locomotor disability.
- No significant changes in regional glucose metabolic rates were observed.
Conclusions:
- Motor impairment in Parkinson disease is associated with altered dopamine neuronal integrity in the putamen.
- Cognitive impairment, specifically memory deficits in advanced PD, is linked to dysfunction in the caudate nucleus.
- These findings support a model of selective striatal pathway involvement in Parkinson disease symptomatology.