Abstract

In addition to locomotor disability, cognitive impairment and dementia are sometimes concomitant in Parkinson's disease (PD). Reduced glucose metabolism and blood flow in some part of the cerebrum have also been observed in PD patients using positron emission tomography (PET) and/or single photon emission computed tomography (SPECT). Especially, in PD patients with dementia (DPD), decreased cortical glucose metabolism has been observed in the temporo-parietal association cortex, in a manner similar to that seen in patients with Alzheimer's disease. Using 18F-dopa PET and statistical parametric mapping (SPM) on a voxel-by-voxel basis, we have demonstrated a significant dysfunction bilaterally in the anterior cingulate area and ventral striatum and in the right caudate nucleus in DPD. Additionally, the mini-mental state examination (MMSE) score significantly correlated with the 18F-dopa influx constant (Ki) in the right caudate nucleus. These findings are consistent with the hypothesis that impairment of mesolimbic and caudate dopaminergic function plays an important role in the dementia of PD. To reinforce this hypothesis, we investigated the relation between dopaminergic impairment and cortical dysfunction in PD patients using 18F-dopa and 18F-fluorodeoxyglucose (FDG) PET. We have demonstrated positive correlations between the Ki value in the caudate nucleus and the glucose metabolic value in the posterior cingulate area and temporo-parietal association area. These results suggest that impairment of the dopaminergic system is correlated to cortical dysfunction in PD. Furthermore, even though in PD without dementia, occipital and posterior parietal hypoperfusion has been observed and hypoperfusion in the right visual association area is likely to underlie impairment of visual cognition according to the Raven's colored progressive matrices (RCPM) test. To clarify the relation between cortical dysfunction and the decline of RCPM score in PD, we are investigating the brain areas activated at RCPM test using 1 5O–H 2O PET.

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