Cerebral Glucose Metabolism of Parkinson’s Disease Patients with Mild Cognitive ImpairmentLyoo C.H. · Jeong Y. · Ryu Y.H. · Rinne J.O. · Lee M.S.
Departments of aNeurology and bRadiology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, and cDepartment of Brain and Bioengineering, KAIST, Daejeon, Korea; dTurku PET Center, University of Turku, Turku, Finland
Background: Half of Parkinson’s disease (PD) patients with mild cognitive impairment (MCI) develop dementia. We studied topographic distribution of cerebral hypometabolism in PD with different types of MCI. Methods: This study included 61 nondemented PD patients and 14 age-matched controls. PD patients were grouped into normal cognition (PD-NC, n = 20), single amnestic (PD-SA, n = 12), single nonamnestic (PD-SN, n = 11), and multidomain MCI (PD-MD, n = 18). Using [18F]-fluorodeoxy-glucose PET, cerebral glucose metabolism of MCI groups was compared with that of controls and the PD-NC group. Results: In comparison with controls, PD-NC and PD-SA groups showed no hypometabolic brain areas. However, the PD-SN group showed hypometabolism in parieto-temporo-occipital cortices. The PD-MD group showed widespread hypometabolism that predominantly involved parieto-occipital cortices. In comparison with the PD-NC group, only the PD-MD group showed hypometabolism in lateral frontal, cingulate, and parieto-temporo-occipital cortices. Conclusions: The distribution of hypometabolic brain areas of the PD-MD group suggests that PD-MD seems to be caused by a common pathology with PD dementia. PD-SA and PD-SN seem to be caused by very mild or topographically heterogeneous cerebral dysfunction. Longitudinal clinical and neuroimaging studies are needed to define whether PD patients with single domain MCI progress to PD-MD and finally to dementia.
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